Post on 03-Dec-2014
this is for non-commercial usage by Russian-speakers only! if you are not a Russian-speaker deLete this file immediately!
,qaHHblH CKaH npe,qHo3Ha .... eH nHWb p,!1.R :
1. PYCCKHX nOllb30BaTellel-1-
Bpa4el1 H Y'let-lblX, B OCo6eHHOCTI1
2. cBo6oAHoro, HeKOMMep"lecKoro J.1
6ECnllATHoro pacnpocTpaHeHI1.R
CKaHJ.1pOBaHO nOTOM J.1 KPOBbto MYCAH;II 3'I' WoH'I' . P¥
3rd edition
Michael J. Murphy · Ronald L. Cowan ' Lloyd I. Sederer
... r.ot r .,...- &al e I '" "" Ole ,l1li11 'lPOAill<>< ! ..
BLUEPRINTS p_S_yC __ H __ I_AIRy ___________ ___________ _ Third Edition
Michael J. Murphy, MD, MPH Instructor in Psychiatry Harvard Medica l School Boston, Massachusetts Assistant Psychiatrist Mclean Hospita l Belmo nt, Massachusetts
Ronald L. (owan, MD, PhD Assistant Professor of Psychiatry Assista nt Professor of Radiology and Radiological Sciences Vanderbilt Unive rsity Medical Cente r Nashvill e, Tennessee
Facul ty Advisor
Lloyd I. Sederer, MD Executive De puty Commissioner for Mental Hygiene Department of Health and Mental Hyg iene The City of New York New York, New York
flJ Blackwell Publishing
© 2004 by Blackwell Publishing
Blackwell Pl1hli~hing, Inc., 350 Main Street, Malden, Massachusetts 02 148-50 18, USA Blackwell Publishing Ltd, 9600 Garsington H.oad, Oxford OX4 2DQ, UK Blackwell Science Asia Pty Ltd , 550 Swanston Street, Carlton, Victoria 3053, Australia
All rights reserved. No part of this publication may be reproduced in any form or by any electronic or mechanica l means, including infommtion storage and retrieval systems, without permission in writing from th~ publisher, except by a reviewer who may quote: brief passages in a revie¥.·.
03 04 05 06 5 4 3 2 1
ISBN, 1- 4051 -0334-5
fjfmary of Congress Cataloging-in-Publication Data
Murphy, Michael, 1966-Blueprints psychiatry / Michael 1. Mtirphy, Ronald L. Cowan; faculty
advisor, Uoycll. Sederer.-3rd ed. po. ; cm.-(Blueprints)
IncJudes index. ISBN 1-405 1-0334-5 1, Psychiatry-Examinations, questions, etc.
2. Physicians-Lic.enses- 15nited States--Examinations-...<;tudy guides. [DNLM: 1. Mental Disorders-Outlines. 2 . Psychotropic
Drugs-Outlines. WM 18.2 M978b 2004] I. Cowan, Ronald. U. Sederer; Lloyd I. n1. Ti tle. rv; Series.
RC457.t-187 2004 61 6.89'OO76-dc2 1 200300 1499
A cata logue record for Ulis title is available from the British Library
Acquisitions: Nancy Anastasi Duffy Development: Julia Casson Production: Debra Lally Cover design: Dick Hannus Interior de~ign : Mary McKeon 'I)-'pesettf'r: SNP Best-set Typesetter Ltd. , Hong Kong Printed and bound by Capital City PreSs "in Berlin! VT
For fmther information on Blackwel l Publishing, visit our website : wW\v.blackwellpublishing.com
l'\olicc: Th~ indkations ami dusages of all drugs in this book have been recommended in tht~ medicalliteraturE" and cnnfnrm to the practices of the general community. 111e- medicatiolls described do not necessarily ha ... e spt.'Cifil· appro ... al by the r ood and Dru~ Administration for uSC' in thE' diseast':.'i and dosagt'.5 fnr which th~y are rt'commended. The package in~rt ror each dmg .shcluld be u lnsulted ft-lf lIS~ and dosage as appro ... ed by the FDA. Because standards for usage change, it is advisable to keep abreast of revised recommendations, particu_ larly thpse conc~ning new d~ ...
Contributors . ...... . ........ . ... . .... . ... . ... • ...••...•....•...... .• ........... . vi Reviewers ......... ...... •..•.....•. .• • ... •. ... . ...••. . • . . .• . ...• • .. . ......... . vii Preface ............. .. •... .. . . .• . ..••............ •...•........• •... .......... . viii Acknowledgements .........• . .... ...••....... ..... ...•... . •• ... • ...• • ... ...... jx
Abbreviations ......... ...... ..•........• .... • ... •. ..•...• • ...•.... • ...•........ .x
1 Psychotic Disorders .....•............ • ... .....•....... . •.. .• •... .. . . ••...... 1
2 Mood Disorders .......... .. .. .. .•. .. •... . . . . . ... . . ..... ... .. ... . ...•....... 8
3 Anxiety Disorders .......... •....... .... .•...••... . ...•...•.... •... .•...... 14
4 Personality Disorders ...... .....• ..... . . .•..• . ....•......•• • .. •• .. • ••...... 20
5 Substance-Related Disorders ...... ....... . ...••...•........................ 25
6 Eating Disorders .............................•...•....•...•.... • ...•.... . .32
7 Disorders of Childhood and Adolescence ...........•... • ... • •...• . .. •• ..... .36
8 Cognitive Disorders ......................... •• . . . ....• •... •.. . • . .......... 44
9 Miscellaneous Disorders ..... ... .•...•...•....•........ . ...•.... •.......... 49
10 Special Clinical Settings .............. . . ................... . ... .. . ......... .55
11 Antipsychotics ............... .... ............•....•...•........ • .......... 58
12 Antidepressants, ECT, and Phototherapy .. ...•. .. . ........•...•.. ..•. ........ 63
13 Mood Stabilizers .... ........ . ........... ... .. ....•. ...• • ...... . ...• •...... 68
14 Anxiolytics ..................... . ...• . . . • ... .•.... ....• • . .. ....• ... ....... 73
15 Miscellaneous Medications ........•...•...•.... . .......••...•...••........ .77
16 Major Adverse Drug Reactions .............. . .. .. ..... . .... .. . .............. SO
17 Psychological Theories . ...... .....•.• ..... •. ..... ....... . ... • ... . ... .. ..... 84
18 Legall"ues . ..... ....... ........ ... .......... . ................. . ......... 88
Questions .... . ...... • ...••... •...• .. ...... • .. .•• ..•• . .. • . ...•. . .• . ............ 90 Answers . .... .. •• ...•.... .. . . • .......• •...•.. .•• ............•................ . 100 References . .....•...• • .... ...• • .. .•...•.. . • • .. . • .. .• • ...•.... •...• ....•...... . 107 Index . .............• • ...•...••.......•...••... •...••...•........ •........... . 108
Marketa Wills, MD Clinical Fellow in Psychiatry, Harvard Medical School Resident in Adult Psychiatry, MGH/Mclean Program Boston, Massachusetts
Julia Coleman, MD Clinical Fellow in Psychiatry, Harvard Medical School Resident in Adult Psychiatry, MGH/Mclean Program Boston, Massachusetts
Todd Pollack Class of 2003 Temple University School of Medicine
Philadelphia, Pennsylvania
Emery Chang, MD Resident, Internal Medicine and Pediatrics Tulane University New Orleans, Louisiana
Heather Maim, MD Resident York Hospital York, Pennsylvania
vii
viii
I n 1997, the first five hooks in the Blueprints series were published as board review for medical students, interns and residents \vho wanted high-yield, accurate clinical content for USMLE
Steps 2 & 3. Six years later, we are proud to report that the original hooks and the entire Blueprints brand of review materials have far exceeded our expectations.
'Ine feedback we've received from our readers has been tremendously helpful and pivotal in deciding what direction th" third edition of the core books will take. The student-ta-student approach was highly acclaimed by our readers, so resident contributors have been recruited to ensure that the third edition of the sene: continues to provide content and an approach that made the original Rlueprints a success. It was suggested that the review questions should reflect the current format of the Boards, so new board-format questions have been included in this edition with full explanations provided in the answers. Our readers asket! for an enhanced art program, so a second color has heen added to this edition to increase the usefulness of the figures and tables.
'Vhat we've also learned from our readers is that Blueprints is more than just Board review for lJSMLE, Steps 2 & 3. Student.~ use the hCXlh during their clerkship rotations and subinternships. Residents studying for USMLE Step 3 often use the books for reviev.ing areas that were not their specialty. Students in physician assistant, nurse practitioner and osteopath programs use Blueprints either as a companion or in lieu of review materials written specifically for their areas.
However you use Blueprints, we hope that you find the hCXlks in the series informative and useful. Your feedback and suggestions are essential to our continued success. Please send any comments you may have about this book or any book in the Blueprints series to blue@bos.bl.ackwellpublishing.com.
The Publisher Blackv.,.·ell Puhlishing
W e would like to acknowleJ ge the faculty, staff, and trainees of the Mclean Hospital and Harvard Medical School for their ongoing inspiration.
Ronald L. Cowan, MD, PhD Michael J. Murphy, MD, MPH
l1lis third edi tion stands as a testimonial to the fine work of my collea!,'lJes, Drs. Cowan and Murphy, and to the lessons we have all learned from our patients and our students.
Lloyd I. SeJerer, MD
AA Alcoholics Anonymous ICU Intensive care unit
ABG Arterial blood gas 1M Intramuscular
AClS Advanced cardiac life support IPT Intrapersona l therapy
ADHD Attention-deficitJhyperactivity disorder IQ Intelligence quotient ASP Antisocial personality disorder IV Intravenous
BAL Blood alcohol level LP Lumbar puncture
BID Twice daily LSD Lysergic acid diethylamine CBC Complete blood count MAOI Monoamine oxidase inhibitor
CBT Cognitive-behavioral therapy MCV Mean corpuscular volume
CNS Central nervous system MDMA Ecstasy
CO, Carbon dioxide MR Mental retardation CPR Cardiopulmonary resuscitation MRI Magnetic resonance imaging CSF Cerebrospinal flu id NIDA National Institute on Drug Abuse
CT Computerized tomography NMS Neuroleptic malignant syndrome
CVA Cerebrovascular accident OeD Obsessive-compulsive disorder
DBT Di.:lIectical behavior therapy PCA Patient controlled analgesia
DID Dissociative identity disorder PMN Polymorphonuclear leukocytes
DT Delirium tremens PO By mouth
ECT Electroconvulsive therapy PTSD Posttraumatic stress disorder
EEG Electroencephalogram QD Each day
ECG Elearocardiogram REM Rapid eye movement
EPS Extrapyramidal symptoms SES Socioeconomic status
EW Emergency ward SSRI Selective serotonin reuptake inhibitor
FBI Federal Bureau of Investigation TO Tardive dyskinesia
SHIAA S-hydroxy indoleacetic acid T4 Tetra-iodo thyronine
SHT S-hydroxy tryptamine T3 Tri-iodo thyronine
GABA Gamma-amino butyriC acid TeA Tricyclic antidepressant
GAD Generalized anxiety disorder TID Three times daily
GHB Gamma-hydroxybutyrate TSH Thyroid-stimulating hormone
GI Gastrointestinal WBC White blood cell count
HPF High power field WISC-R Wechsler Intelligence Scale for
HIV Human immunodeficiency virus Children- Revised
,
Psychotic disorders are a collection of disorders in which psychosis predominates the ~-ymptom
complex. Psychosis is defined as a gross impairment in reality testing. Specific psychotic symptoms include delusions, halJucinations, ideas of reference, and disorders of thought. Tahle I - I lists the Diagnostic mid Statistical Mamlal of Mental Disorders, 4th edition (DSM-IV) classification of the psychotic disorders.
It is important to understand that psychotic disorders are different rrom mood disorders with psydIotic features. Patients can present \'lith a severe episode of depression and have delusions or with a manic episode v.,'ith delusions and halluci nations.. These patients do not have a primary psychotic disorder; rathe r, their psychosis is secondary to a mood disorder.
The diagnoses described below are among the most severely disabling of mental disorders. Disabi lity is due in part to the extreme degree of social and occupational dysfunction associated with these disorders.
• SCHIZOPHRENIA
Schizophrenia is a disorder in which patienL" have psychotic symptoms and social andlor occupational dysfunction that persists for at least 6 months.
Epidemiology
Schizophrenia affects I % of the population. The typica l age of onset is the ea rly 20s for men and the late 20s for women. Women are more likely to have a ~firS l break~ later in life; in fact, about one third of women have an onset of illness after age 30. Schizo-
phrenia is diagnosed disproportionately among the lower socioeconomic classes; although theories exist fur this finding, none have been substantiated.
Etiology
The etiology of schizophrenia is un known. There is a clear inheritable component, but familial incidence is sporadic and schizophrenia does occur in families with no history of the disease. Schizophrenia is wi dely believed to have a neurobiological basis. The most notable theory is the dopamine hypolhesis, which posits that schizophrenia is due to hyperacti vity in brain dopaminergic pathways. This theory is consistent with the efficacy of antipsychotics (which block dopamine receptors) and the ability of drugs (such as cocaine or amphetamines) tl1 at stimulate dopaminerglc activity to induce psychosis. Postmortem studies also have shown higher numbers of dopamine receptors in specific subcortical nuclei of schizophrenics than in normal brains. More re.cent studies have focused on structural and functional abnormalities through brain imaging of schizophrenics and control populations. No one finding or theory to dale is adequate in exp laining the etiology and pathogenesis of this complex disease.
Clinical Manifestations
History and Mental Status Examinat;on
Schizophrenia is a disorder characterized by what have been termed positive and n~ativc symploms, a pattern of social and oc(."llpat.ional deterionttion, and persistence of the illnes. .. for at least 6 mOllths. Positi\'e symptoms are characterized by the presence of unusua l thoughts, perceptions, and behaviors (e.g.,
< not foc sal .. ! 0> < He lll1R npo.u"""" ! :>
2 • Bluepritlt6 Psychiatry
• TABLE 1-1
Psychotic Disorders
Schizophrenia Schizophreniform disorder Sct)izoaffective disorder
Brief psychotic d isorder Shared psy<hotic d isorder DellJsional disorder
hall ucinations, delusions, agitation) ; negative symptoms are characterized hy the abscm:c of normal social and mental functions (e.g., lack of moti vation , isolation, anergia, and poor self-care) . The positive versus negative cUstinction was made in a nosologic attempt to identify subtypes of schizoph renia and because some medications seem to be more effective .1.n treating negative symptoms. C lin ically, patients often exhibi t both posit ive and negative symptoms at the same time. Table 1-2 lists common posjtive and negative symptoms.
To make the di agnOSis, two (o r more) of the fo llowing criteria must be met: hallucinations, dt'lusions, disorganized speech, grossly disorganized or catatonic (mute and/or posturing) behavior, or negative symptoms. There lllust also be social .and/or occupational dysfunction . The patient must be ill for at least 6 months.
Patients with schizophrenia generally have a history of abnormal p remorbid functioning. The prodranK' of schizophrenia includes poor social skills, social Withdrawal, and unusual (although not frankly deluSional) thinking. Inquiring ah6ut the premorbid history may help to distinguish schizophrenia
• TABLE 1-2
Posmve and Negative Symptoms of Schizophrenia
from a psychotic illness secondary to mania or drug ingestion.
Schizophrenics are at high risk for suicide. Approx.imately one third wi ll attempt suicide and 10% wil l complete suicide. Risk factors for suiLide include ma le gender, age <30 years, chronic course, prio r depression , and recent hospital d ischarge.
DSM-N recogni zes fi·ve subt)."pes of schizophrenia: paranoid, disorganized, catatonic, undifferenti ated, and residual. The subtypes of schizophrenia are useful as descriptors but have not been shown to be reliable or valid . Table 1-3 describes these subtypes.
Differential DiagnosiS The differential cUagnosis of an acute p!»'chotic episode is broad and challenging (Table 1-4) . Ontto' a medical or substance-related condition has been ruled out , the task is to differentiate schizophren ia from a schizoaffective disorder, a mood disorder with psychotic features, a delusional d isorder, or a personality disorder.
Management
Antipsychotic. agents (a lso called neuroleptics) are primaril y used in treatment. These mt!dications <Ire used to treat acute psychotic episodes and t.o maintain p<lt ients in remission o r with chronic ill ness. Antipsychotic medications are discussed in Chapter 11 _ Combinations of several cla.'iSt'S or mt:!dications are ofte n prescrihed in severe or refractory cases. ]lsychosodaJ treatments, including stable reality-
Negative symptoms Affective flattening
Alogia
Decreased expression of emotion, such as lack of expressive gestures
Asociali ty
Positive symptoms
Hallucinations
Delusions
Bizarre behavior
Literally "lack of Words,· inclUding poverty of speech and of speech content in response to a question
Few friends, activi ties, inte rests; impaired intimacy. little sexual interest
Auditory, visual. tactile, and/or olfactory hallucinations; voices that are commenting
Often described by content; persecutory, g randiose, paranoid, re ligious; ideas of reference., thought broadcasting, thought insertion, thought withdrawal
Aggressive/agitated, odd dothing or appearance, odd social behavior, repetitive-stereotypep behavior
Adap\ed from Andr !'il~en Nc.llIack ow. Introductory te~tbook of psychfatry. 3ft! eel. 'Namirlgton, OC American Psychiatrk" Publi5hing, 20014
.( not; ( o r """h, I J> .( "" AmI rlPO_ ! ,.
Chapter 1 I Psychotic Disorde rs • 3
TABLE 1-3
~oI5cIIiIqJIIrorO
Paranoid Catatonk
Paranoid delusions, frequent auditory hcJlucination, affect not flat
Motoric immobility or exce5siYe, purposeless motor activity, maintenance of a rigid echolalia
Disorganized
Undifferentiated (probably most common)
Residual
Disorganized speech, disOfganized behavior, flat or inappropriate affect; not catatonic
Delusions, hallucinations, disorganized speech, catatonic behavior, negative symptoms Criteria nor met for paraooid, catatonic. or din)fgonized
Met criteria for schizophrenia, now resotved, i.e~ no hallucinations, no prominent delusions, etc.. but residual negative symptoms or attenuated de4usions, hallucinatiOns, or thought diMlrder
Adapled from AndreaseJ1 NC. Bl1I(k OW, Introductory lex!booka P$YChlatry. lrd I'd Wasl'iil"og1on. DC: Ameriom Psy<,hlatrlc Publishing. 2001 .
TABLE 1-4
Major psychiatric disorders Acute exacerbation of schizophrenia Atypkal psychoses (e.g.. schizophreniform) Depression with psychotic features Mania
Drug abuse and withdrawal Alcohol withdrawal Amphetamines and cocaine Phencyclidine (PCP) and hallucinogens Sedative-hypnotic withdrawal
Prescription drugs Anticholinergic Ct9E!nts Digitalis toxicity Glucocorticoids and adrenocorticotropic hormone
IAaH) Isoniazid L-Dopa and other d opamine agonislS Nonsteroidal antt-inflammatory agents Withdrawal fmm MAOls
Other toxic agents carbon disulfide Heavy metals
NeurolOgic cause .. AIDS encephalopathy
Brain tumor Complex partial seizures Early Alzheimer's or Pick's disea~ Huntington's disease HYIXlXic e ncephalopathy Infectious viral encephalitis Lupus cerebritis Neurosyphilis Stroke Wilson's disease
Metabolic causes Acute intennittent porphyria Cushing's syndrome Early hepatic encephalopathy Hypc>- and hypercalcemia Hypoglycemia Hypo- 3M hypenhyrotdism Paraneoplastic syndromes (limbic encephalitis)
Nutritional cauSt3 Niacin deficiency (pellagra) Thiamine deficiency (Wernkke-Korsakoff syndrome) Vitamin Bl l deficiency
Reproduced wllh penniMion (rom Hyman Sf.. fI.rMa aN. Rowflbaum Jf. l-Wldboolr. of P')<hiallk dUI9 lho>rapy. 4lh l'd. Philadelphia: UppincOIl,Wi.\am511rodWiI<im, 2000.
< no t f o c sal .. ! ;> < He llJUI npollant ! :;>
4 • Blucprirw Psychiatry
oriented psydlOtherapy, family SLlpport j psychoeducation , social and vocat ional skills training, and atlentio n to details of living situation (hou~ing,
roommates, daily activities), are critical to the long-term management of these p<ltients. Poorer prognosis occurs with early onset, a history llf head trauma, or comorbid sub:.-tam.:e abuse..
iii KEY POINTS 1)1
1. Schizophrenia is characterized By psychosis and social/occupational dysfunction.
2. Symptoms must last for at least 6 months. 3. Schizophrenia has a 10% suicide rate (approxi:
mately one third attemp~) .
4. It is treated With antipsychotic> and psychosocial support.
• SCHIZOAFFECTIVE DISORDER
Patients with sdlizoaffectivl~ disorder have psychotic episodes that resemble schi;.r.ophrenia but \\~th
prominent mood di~"turbances . T heir psycbotic symptoms, however, mLlst persist for some time in the ahw nce of any mood syndrome.
Epidemiology
Lifetime prevalence is estimated at 0 .5% to 0.8%. Age of onset is similar to schi"ophrenia (late teens to early 20s) . Schizo<lffective patients are more likeJy than S(;hizophrenics but less likdy than mood-disordered patients to have a remission after treatment.
Etiology
'The etiology o/" schizoaffectivC" disorder is unknown. It may be a variant of schi zophrenia, a variant of a mood disorder, a distinct' psychotic syndrome, or simply superimposed mood disorder and psychotic disorder.
Clinical Manifestations
History and Mental Status Examination
Patients with schizoaffective disorder have the typical sytnp~oms of schizophren ia and coincidentally a major mood disturbance, such as a manic or depressive episode. They must also have periods of
illness in w hich they have psychotic symptoms without a .najor mood disturbance. Mood disturhances need to be. present for a substantial portion of t.he illness.
There are two subtype.; of schizoaffecti ve disorder recognized in the DSM-IV, depressive and bipolar, which are detennined by the nature. of th~~ mooddisturbance episodes.
Differential DiagnOSis
Mood disorders with p!>ychotic features, as in mania or psychotic depression, are different from schizoaffeLtive disorder in that schizoaffective patients have persistence (for at least 2 \\reeks) of the psychotic symptoms after the mood symptoms haw resolved. Schizophrenia is d ifferentiated from schizoaffective disorder by the absence of a prominent mood diso rder in the course of the illness.
It is important to distinguish the prominent negati ve symptoms of the schizophrenic from the lal:k of encrgy or anhl'.donia in the depressed patient with schi70affect ive disorder. More distinct symptoms of a mood disturbance (such as depressed mood and sleep disturhanceJ should indicate a true coincident mood disturbance.
Management
Patients are trt::ated with medications that target the psychosis and the mood disorder. Typically, these patients require the lnmbinatioll of all antipsychotic medication and a mood stabilizer. Mood stab ilizers are described in Chapter 13. An antidepressant or electroconvulsive therapy may be needed for an acute depressive episode. Psychosocial trf."atments are ,similar for schizoaffective disorder and schizophrenia. Prognosis is better th an ror schizophrenia and \\forse thlln for bipolar disorder or major depression .
• " KEY POINTS , _;
1. 1n schizoaffective disorder, there are mood disturbances with psy<:hotic episodes ,snd there are periods of psychosis without a mood disturbance.
2. Treatment is with antipsychotics and mood stabilizers.
3. The prognosis for schizoaffective disorder is better than for schizophrenia but worse than for a mood disorder.
.. not to r sale l ,,< I!e PJ!R Il~"""" I "
• SCHIZOPHRENIFORM DISORDER --- --- -- -------- ----------.-------------------Essenti ally, lhis is sd lizophrenia that fails to last fo r 6 mont.hs and dOt!S not involve soda] withdrawal.
Epidemiology
The validity of this diagnosis js under question_ Outcome studies of this disorder indicate that most patienu. may go on to develop full-blown schizophrenia, v·:hereas others appear to develop a mood d isorder. The d iagnosis of schizophrenifonn d.isorder may, hOWl;:vt1", help to avoid p remature diagnosis of paLlents with schizophrenia before some other disorder, stich <'IS hipolar disorder, manifest.~ itself
Etiology
At this ti me, the etio logy is unknown_ At least one study found similaritit's in brain structure abnormaliti l.!S bt!tween schizophrenics and tho.<;e w ith schi 7-Ophreniform d isorder.
Clinical Manifestations
History and Mental Status Examination
Schi7.ophre.nifonn disorder is essentially !>ho rt-mUl"sc st:hi7.ophrcnia without the requirement of SOl:ial withdrawal. Patients With this disorder have what appears to he <'I "full -bkl\\'n" t'pisode of schizophrenia, including delusions, hallucination~, disorgani ...-.ed speech, or neg(ltive symptoms, but the duration of ill ness induding prodromal, actlve, and residu;tl phases, is fro m 1 to 6 months. The diagnosis changes ( 0 sdlizophrenia once the symptoms have extelH.k·J past 6 months, eVt'1l if only residual symptoms afe left.
Differential Diagnosis
Cart must be take n to d istinguish schizophreruform d isorder from a manic or depres!>ive episode with psychotic fea tu res. Olht.'.f caU .. "es of an acute psychosis must ~ ruled out (substance-induced or due to a general mt':d ical condi tion)..
Management
The disorder is by de hn it ion self-limited . When symptoms cause severe impairment , Lreatml:nt b similar to that fo r the acute treatment of psychosis in schizophrenia.
Chapter 1 I Psychotic Disorders • S
KEY POINTS
1_ Schizophreniform disorder resembles schizophrenia.
L It resolves completely in less than 6 months. 3 .. It most often results In either SChizophrenia or
biPQlar disordef. 4. It is self-timited .. ft
• DELUSIONAL DISORDER ---.- -- ~ ----_. ------~ ~ --_ .. -_. --------- ---De lusio nal disorder is characteri zed by nonbizarre delusio ns without other p~ychntic symptoms. It ls rare, it.'> coun;e is t:hronic, and tre<'l tment is supporthre.
Epidemiology
ThIS disorde r j~ rare, with a prevalence o ( <0.05%. Genera lly, o nset is ill midd le to late life; it affects women mOre o ften than men. Its course i!> chronif.: and unrL"lli ittiug.
Etiology
T he et iology is unknown_ Often. psychosocial stresSOTS 3ppear to he et iologic, for e-"Xarnple, follOwing m.igration. Ju migratio n psychosis, the recently immigrated person develops persecutory delusions. Many patients with ddusional disorder have a paranoid character premorbidly. Paranoid personality di sorder has been found in rami[i~ of patients with delusional disorder.
Clinical Manifestations
History and Mental Status Examination
This disorder is characterized by well-systematized nonbizarrc ddusions ahout things that could hap)Jt.'ll in real life (such as being followed, poi~ned, infected, loved at a distance, haVing a disease, being deceived by one 's spouse or significant other) . The delusions must he prt::St:n t for at leJ,!!'>t I month . O ther than the de lusion, the pat ient's social adju.:.1:ment may be normal.
The pal"i{' nt must not 1l1cet criteria for schiZOphrenia. Any mood di~rcler must be brief relative to the duration of the ilIne .... "_ The DSM-IV rt'L"Ognizes seven subtypes of delusional disorder (Table 1-5),
< not f o e s ale! :> < H .. ll.JUI npo,Ilano ! ::>
6 • Blucprinw Psychiatry
" TABLE '-5
Delusional Disorder Subtypes
Erotomanic
Grandiose
A person becomes false ly convinced that another person is in love with him or her.
A person becomes false ly convinced that he or she has special abilities or is in other ways,m~ch more important than reality indicates.
Jealous
Persecutory
A person becomes fa lsely convillced that his Of her lover is unfaithful.
A per!>on becomes false ly convinced that others are out to harm him or her and that he or she is being conspired against in general.
So."atic A person becomes falsely convinced that he or she has a bodily function disorder, (or
example or'gan dysfunction, body odor, or parasite infection.
Mixed
Unspecified
Diagnosed when no single delusional theme predominates
Diagnosed when a single delusional theme cannot be determined or when the predominant delusional theme does not match subtype criteria
Differential DiagnOSis
It is important to rult' out other psychiatric or medical i11nesses that could have caused the delusions. Thereafter, delusional disorder must be distinguished from major depression wi th psychotic features, mania, schizophrenia, and panmoid personality.
Management
lhals of anti psychotics are appropriate but are often ineffective. The p rimary treatment is ps}'chothcrapy, taking care to neither support nor refute the delusion but to mainta in an aLliance with th e p.:dtient. Without such an alliance, most patients fall out of treatment; with an alliance, over time, the patient may relinquish the delusions.
• KEY POINTS •
1. Delusional disorder is characterized by nonbizarre delusions.
2. It is chronic and unremitting. 3. Treatment involves making a therapeutic alliance.
In brief psychotic disorder, the patient experiences a full psychoLic episode that is short-Ji,'cd . It can be temporally related to some stressor or occur postpartum, but is also seen without :lny apparent :lntecedl'nt.
Epidemiology
There is insufficient data available to determine prevalence and sex ratio.
Etiology
Etiology is unknown. H owever, it seems to be associated with borderline personality disorder and schizC"ltypal personality disorder.
Clinical Manifestations
History and Mental Status Examination
In hrief psychotic disorder, the patient develops psychot ic symptoms that last for at least I day hut no more than I 111Ol1th, followed by eventual return to premorbid functioning. Patients can exhibit any combination of delusions, hallucinat ions, disorga-· nized speech, or grossly disorganized behavior. There are three recognized subtypes: with marked strcsso rs (formerly known as brief reactive psychosis), without markl~d strcssors , and postpartum. Patients with the postpartum subtype typically deve10p symptoms within I to 2 weeks after delivery that resolve within 2 to 3 months.
Differential Diagnosis
It is important to rule out schizophrenia, especially if the disorder worsens or persists for more than a month (except for postpartum psychosis, \vhich may last 2 to 3 months) . A mood disorder such as mania or depression with psychotic features must be ruled out.
< lIot f () { .... l el ,. "" lie JlnR np<lJIall:>l >
Management
Hospitalization may he necessary to protect the palient. Trelltment with antipsych otics is commOn, although the condition is by de1initlon self- li mited and no ~-peci fic t reatment is required. The containing e nvironment of the hospital milieu may be suffident to help the pat ient recover.
Chapter 1 I Psychotic Disorders • 7
, KEY POINTS I ;:
1. Brief psychotic disorder is characterized by typical psychotic symptoms.
2. lhe condition is short-lived. larung from 1 to 30 day<
3. It can be pre<:eded by a stressOf or can be postpartum.
4. It may occur without an antecedent. S. The condition is self-limited.
Mood disorders 3re among tht: most common diagnoses in psychiatry. Mood is a pt'.rsistent emotional !'tate (as difft:r~ntiated from affect, which is the external display of feelings). T here are three major categories of mood disorders according to the Diag~ lJOslic and SlarL~rilXll Manual of Memal Di.sorder.~, 4th edition: unipolar mood disorders (maj or dt'pressive disorder, dysthymic disorder) , b ipolar mood uis~ orders (bipolar I disorder, bipolar II disordt'.r, and cyclothymi<.: disorder), and mood d isorders haVing a kno"l/n etiology (suhstance-induced mood disorder and mood disorder due to a general mt'dical condi~ ti on) (Table 2~ 1) .
The hest availahle evidence suggests that mood disorut'rs lie on a continuum with norma l mood. Although mania and deprtSSion are oftt'n viewed as oppoltite ends of the mood spectrum, they can occur !>imultaneously in a single individual within a hrief period, giving rise to the com:ept of mixed mood states.
UNIPOLAR DISORDERS
Unipolar disorut'.rs are major dt=pressive disordtr and dysthymic disorder.
Major Depressive Disorder
Major depressive disordt'r i.s d.iagnosed afttr a single episode of major depre>sion (Table 2~2) . It is d,ar. acterized hy ~motional changes, primarily depressed mood, and by so~called vegetati ve changes. consisting of altNations in sleep, appetite, and energy le,rels.
Epidemiology
The li fe_time prevalence (will occur at some point in a pt'_rson's life) rate for major depressive disorder is
5% to 20%. The fema le-malt' ratio is 2 ; L R;tce dis~ trihutions appe:-lr equal, and socioeconomic variahles do not seem to he a faLior. The incidence (rate of new case .. ) is J,rreatest between the ag-es of 20 and 40 and Jecrta.SeS after the agt' of 65.
Etiology
Psychologica l theories of depression generally view interpersonal Ios.c;es (actual or perceived) as risk factors for developing depres.. .. ion_ In fac.."1., avail able evidence suggefOLc; that childhood loss o f a parent or loss of a spouse are associated WiU1 dcpreS&10n. Classic psychoanalyti c theories center on ambi\la~
lenee toward the lost object (person), although more recent tht'Ories focus on the critical importance of the object relatio nship in maintaining psychic equilibrium and self~regard . The cognitive-behavioral model views cognitive distortions as the primary events that foster a negative misperception of the wor'ld, which in tum generate negative emotions. The learned help lessl1e>s model (based on animal studies) ~"Uggests that depression arises when individuals come to believe they have no control over the stresses and pains that beset them.
Biologic, fami lial, and genetic data supper! u1e idea of a biologiC diathet.is in the genesis of depression. Genetic studies show that depression is found to be concordant more often in monozygotic twins than in dizygotic twins. Unipolar depression in a parent leads to an increased incidence in the offspring of both unipolar and bipolar mood disorders..
Neurotransmitter evidence points to ahnormalities in amine neurotrammitters as medi<ltors of depressive states: The evidence is stronge .. t for deh~ ciencies in norepint=phrine and serotonin.
Neuroendocrine abnonnalities in the hypotha la~ mic-pituitary.adrenal axis are often present III
depression and suggest a neuroendocrine li nk.
TABLE 2-1
Clas5lficadon at Mood Disorders
Unipolar Bipolar Etiologic:
Major depressive Bipolar I Substance-induced disorder disorder mood d isorder
Dysthymic Bipolar II Mood disorder disorder disorder due to general
Cyclothymic medical disorder condition
, TABLE 2-2
c.tferio fOf MaJo. 1leptH_ Episode
Mood: depressed mood most of t he day, nearly every d,y
,Sleep: insomnia or hypersomnia
Interest: marked decrease in interest and pleasure ill most activities
Guilt: feelings of worthlessness or inappropriate guilt
Energy; fatigue or low energy nearly every day
Concentration: decreased concentration or increased indecisiveness
Appetite: increased or decreased appetite or weight gilin or loss
Psychomotor: psychomotor agitation or retardation
Suicidality: recurrent thoughts o:f death, suicidal ideation, suiCidal plan, suicide attempt
Ger.eral criteria for II major c\epre1Sive epi50de require five or moreo! the ~ ~ymptorm to be ~t for al least.2 weeks; ooe symptom must be clepmsed mood or loss or interest or plemure The!re sylflPtoms ml3t be a ch;)nge hom prior functioning and cannot be due til a rnedkal condition, Cilnnot be,sub.r~lnduced.and Cilnnot be due to bereilvement. The symptoms must also CaUse distre<Sorimpofrment Reptlnted wlt1l pl'rmis';on hom the Dii'lgl105tic and Statistical Manual of Meota! Disorders, Fourtl) Edition, Te.;t ~ion. Copyright 2000 Arnerkan Psychiat(i( Associiltion ,
steep disturhances are near universaJ wmplaints in depressed persons. Objective evidence from sleep studies reveals that deep sleep (delta sleep, stages 3 and 4) is decreased in depression and that rapid-eyemovement (REM) sleep (l lteratlons include increased time spent in REM and earlier onset uf REM in the sleep cycle (decreased latency to REM).
Clinical Manifestations
History and Menta l Status Examination A major depressive disorde.r is d iagnosed if a patient has a t least one episcx.le of major depn'ssioll and does
Chapter 2 / Mood Disorders • 9
Flut meet criteria for bipol ar disorder or dialogic mood di'>order. Major depression i ~ characterized by emotional and vegetative changes. Emotional changes most commonl y indude depre~~ed mood with feelings of sadne.<>s, hopelessness, guilt, and despair. Irritability may be the primary mood complaint in some cases. Vegetative symptoms include alterations in sleep! appetite, energy, and libido.
Major depression is frequently rCCtlrrcnt. The usual duration of an untreated episode (li"ig. 2-1 A) is 6 to 12 m onths. Fifteen percent of patients diagnosed with m ajor depression die by suicide at some point in their lifetimt-_
Differentia l Diagnosis Mood disorders secondary to (induced h y) medical ill n.esses or substance abuse are the primary differential diaj:ploses. PsydlOtk depression must be differentiated from schizophrenia; negative symptoms of schizophrenia can mimi c depression. Persons with major depression may eventually meet criteria for hipolar disorder.
Management
Depression IS responsive to psychotherapy and pharmacotherapy, Milder cases may be treated With brief
Mania
Hypomania
El.Jthymla
~\( II Dysthymia
DeprESSion 0 2 4
A years
Mania
Hypomania
Euthymia I--
/ Dyslhyrnia
Depression 0 2 4
B Years
Figure 2-1 • Unipolar mood disorders. (A) Major depressive di!.· order and (B) dysthymic disorder,
. < oot foe sal .. ! :. < H .. JlMI flPOJlan1
10 . Bluqmnw Ps}'chiatry >
psychotherapy inter\'t~ntions alone. Fur mure severe case;;. antidepressant medications combined with psychotherapy are supeIiOt to medications or psy· c.hotherapy alone. Among the p.<;y<.:hntherapies, supportive, cOgnitive-hchavi(.lral. and brief inkrrl"rSoll:tJ therapies have tht' O1ost data to ~upport their errlcacy. There is a long tratiitilm of ps}rchodynamk psychotherapy in treating deprt:'..s!>ion, although it has not ix-ell t!tnpirically well ~1UWOO.
There arc many classes of antidepres.·"ants availahle thai are effective and art:' lIloually chosen according to side·effect profiles. Presendy, availahlt.' Ua5.'.l"S of antldeprcssants include tril:.ydk antidepressants, sdl;'(..tive serotonin reuptake inhihitors, monoamine o)..idase inhibitors, and atypi<.:al antidepn.ossanL, In addi tion, lithium. thyroid hormone, and psychostimul ants may be used as au~mentati\'e treatml·nt~. Elel.· tTOl.Onvulsivc therapy (ECn is u~d in psychotic, sevt ~rt; or treatment n:rra( tory depressions or wht::n medications are contrainuicated (e.g., in the e1dl.>rly or dt,hililated). AntipsydlOlii.: medications arc an essential adjunct to :mtidepressants in psychotic depreSSions. Anxiolyti cc; rna)' be llsed as adjuncts to antidepressants in depression \vith high Ie.vels o f an).. iety, although more .<;t:dutillg antidepressants may ~urti<.:e. Phototherapy can be used for seasonal mood disord<'rs.
KEY POINTS
1. Major depression is a unipolar mood disorder. 2. It is often recurrent. 3. Major depression has a , 5% suicide rate. 4. Combined psychotherapy and pharmacotherapy
are the best treatment.
Dysthymic Disorder
DysthymiL disonl~r is l:I mild , t:hronic form nf major depression.
Epidemiology
The lir(~ lime prevalellu' 1.<; 6%.
Etiology
B~ausc.' dyslhymla is often con<.:t:ptualized as a milder, chronic form or major deprosion, !->imilar etiologies an: gcnt:.raUy attrihutl!d lo dysthymia.
Clinical Manifestations
History and Mental Status Examination Dysthymit di.:.orde.r is a chronic and less sevue form of major depression. The dillgnosis of dysthymia requires a minimum of 2 years of chronically depressed mood most of th~ time (Fig. 2-1 S). Associated .!o·ymptoms and <.:omplaints may include change in appetite and sleep, rati~'Ut', decreased com.:entralion, Hnd hopelessness. Dysthymia can he chronic and ditllCUh to treat. At limes, major I.kprt'!>-Sivt epiMKlt'!o may co·occur, givl ng ri~ to the term double depression.
Differential DiagnOSiS
Major depression and etiologiC" mood di<;orders are the major differen tial diagnostic considerations.
Management
Treatment is sim il ar to major depression e);cept that p.\)'chotberapy may playa larger role and the course or treatment may he more protracted.
• KEY POINTS •
I. Dysthymia is a unipolar mood dlsorder. 2. It is chronic. lasting at least 2 years. 3, It is often treatment refractory.
TIle bipolar disorderlo are bipolar I disorder, bipolar JI disorder, and cyclothymia.
Bipolar I Disorder
Bipo lar I disorder i~ the most serious of the bipolar disorders and is diaItno.o;eJ after at least one episode or mania (Table 2-3) Patients w1 dl hipolar I disordtl tYPIcally also have major depressive episodes In th< ' C"I.)urse of their lives.
Ep;demio/ogy
Thc lifetime prevail-nee is 0.4% Lo 1.691.1 <Ind the male-female ratio is t:'qual . There are no racial variat ions in incidence.
Etiology
G(~nt:t;l. and familial studies few'al that bipolar I di ~· (.lnler is assnoateJ \vith incu:a.:,cd bipolar 1, bipolar II , and major J epre!.Sive disorders in first.Jegree n' l~
<; not r,, ~ ..... h ol :. "" ... , /U'IfI ~ I ..
TABLE 2-3
CritAIria for Monk Episode
Three to four of the following criteria are required dUring the e levated mood period:
Self-esteem: highly inflated, grandiosity
Sleep: decreased need (or sleep, rested afte r only a few hou" Speech: pressured
Thoughts; racing thoughts and flight of 'ideas
Attention: easy distractibility
Activity: increased goal-directed activity
Hedonism: high excess involvement in pleasurable activities (sex, spending, travel)
G6ler,,1 aitl'iia fOf 11 ffia,.k episode reqube" deilI' perkld ofpenk· tefltIy dntol~ ~mI\If; Of ;",'IDbIt'mood t.ming 1 week or seve-l' enDI.l!lh to .eq~Je ~atWtlol'\. IlIese lymptuns mU\.C be .. CMfl9I! from priof functioning "nd C<I'''\OI be due 10 a medical condition lI"d c,",nor "'" sob5tall(f'-ind\Ked. The ~oms alw _ OIUlie di$l:U!U or "'paifment. DiagllOSlic and Stat\s1kal Maowl QI' Mmrnl DIso~, Fourth &litiol'l, rext ~. W~OII, DC: A.rnerialn ~ychlatric A~sodaliorl, 2<XXl.
arives. X linkage has been demonstrated in some sturue:; but remains controversial. Man.ia can be prt dpitakd by psychoSQCial stressors, and lhl..'rc is evidence that sl<-~tv/\vake cycle pcrturhations may p redispose a person to mania.
Clinical Manifestations
History and Mental Status Examination Bipolar J disorder is ddined by the OCCUffl~nCl~ (.If
m ania (or a mixed epi!'ode). /\ single manic episode is sufficil:n t to meet uiagnostic require me.nts; most patient .. , howe\'~r, have recurrent epi:;odes of mania typically intermixed with depressive episodes. The criteria for a manic episode are outlined in '!'ablt! 2-3.
The fu'St episode of man ia usually nccurl> in the early 20s. Man il.: episodes are typicall), briefer than depres.<;i,'e l~pisodes. ~J be transition hetweelt mani a and depression occurs wi tho ut an intervening perioO of euthymia in about two ofth ree patient!' (Fig. 2·2A) . Lifetime suicide ra tes range from 10% to 15%.
Different ial Diagnosis Mania may hl' induced by antidepressant tTe;Jtnll. . .'Jlt, includ ing antidepressant medications, psychost imu· laolS, ECT, and photo therapy. When th is occurs, tht~ pat;{~nl is diagnosed with suhstance-induced mood disorder, not bipolar d isorder. Mood disorder due to
Chapler 2 I Mood Disorders 11
Mani<!
Hypomania
Euthyrnia
Dysthymia
Depression
o A
Mania
Hypomania
Elithymia
Dyslhymia
J 1
~ 2
Yeats
L
•
DepresSIon LJ"'='--___ -!~='-_ ___ ~. o 2 •
B Years
MM'a
Euthymia
Depression!:-_ _____ -;;-______ -' o 2 •
c Yeats
Figure 2-2 · Bipolar mood disorders. (A) bipolar I (B) bipolar II disorder, (e) cyclothymic disorder.
a general medical condition is tht~ other major dif· feft~nlial mnsideration . Schizoa lTective d~)rd(-'r, horderline personality disorder, and depression with agitation an : at~() consjdt~ral i (Jns.
Management
Pt:r!'OIlS experil'ncing 3 Ill anic episode often have poor insight and resist treatment. Pharmacological interventions fo r acute mania indude antipsyt:hotics in n,lnjunc..tion with bcnzodiazt'pincs (for rapid tran· quilization) and initiatio n of mood stahilizcr medication. Antipsychotics are fn:."{jllen tly USL.J in m ania
< not for sale! :> < He .Il)lR np<JJlIlD! ! :>
12 • B1uI::prinT6 Psychiatry
with and without psychotic features. Lilhium is th e mo~t cnmmonly llsed mood ~tabilizer, but valproic acid is quite e rrective and is more effecti ve for the rapid-cycling variant of mania. Ca rbamazepine, lamotrigine, gabapentin, and long-acting benzodiazepines are used if first-lim' t realments fail. ECf is used in patient" with medication intoler::mce and where a more immediate response is medically or psychi atric;ally needed.
Mood stabilizer maintenance Lherapy is essential in preventing the recurrence of mania and appears to dec reasf' the recurrence of depression . Psychotherapy is used to encoura ge medication compliance, to help patients come to terms with their illness, and to help repa ir some of the interpersonal damage done while ill (e.g. , infidel ity, hostility, squa ndering money) . Care m ust be taken when prescribing ant idepressants for depression or dysthymia becau..'>t' of their role "in prompting more severe or more freq uen t manic episodes.
• KEY POINTS h 1. Bipolar I disorder is a biphasic mood disorder. 2. It is cyclic. 3. It has a suicide rate of 10% to 15%. 4. Maintenance treatment with mood stabilizers is
required.
Bipolar II Disorder
Bipolar 11 disorder is Similar to bipolar 1 disorder except that mania is absent in bipolar 11 disorder and hypomania (a milder form of elevated mood thtln mania) i.~ the ~sen t ial diagnostic finding.
Epidemiology
Lifetime prevalence is about O.SlJrI. Bipolar U disorder may be more COmtl1<,111 in women.
Etiology
Current evidence impli cates the same factors as for bipolar l.
Clinical Man;festations
Histo ry and Mental Status Examination Bipolar [J disorder is chamcterized by the occurrence of hypomania ::md episodes of major depression in an individual , ·vilO has never met criteria for mania Of a mixed stat e.. Hypomania is determined by the same
symptom complex as ma nia but the symptoms are less severe, cau~e les-<; impairment, and usually do not require hospita lization . Bipotar H disorder is cydic (see Fig. 2-213 for course of untreated bipolar U). Suicide ocwrs in 10% lo 15%.
Differential Diagnosis Samt:' as for bipolar J.
Management
Treatment is th e same as for bipolar I disorder, although hypomanic episodes typically do not require as aggressive a treatment regimen as mania. Care m ust be taken in prescribing antidepressants for depressiOll or dysthymia because of their role in prompting more severe or frequent hypo manic episodes.
• KEY POINTS •
1. Bipolar 11 disorder is a biphasic mood disorder with hypomania.
2. It is recurrent. 3. It has a suicide rate of 10% to 15%.
Cyclothymic Disorder
Cyclothymic disorder is a recu rrent, chronic, m ild fann of bipolar disorder in \vhich mood typica lly oscillates between hypoman ia anJ dysthym ia. It is not d iagnosed if ~ person has had either a manic episode or a major depressivt' episode.
Epidemiology
TIle lifetime prevalence of cyclothymic disorder is 0.4% to 1 %. The rate appears equal in men and women, though women more often seek treatment.
Etiology
Fam ilial 311J g<>netic studies reveal an association with ot her mood disorders.
Clinical Man;festations
History and Mental Status Examination Cyclothymic d isorder is a milder form of bipolar d isorder consisting of rL'Currcnt mood di sturbances between hypoma nia and dysthymic mood. A single episode of hypomania is suf6cient to d i3gnose cyclothymic disorder; however; most individua ls also have dysthymic periods. The diagnosis of
cyclothymic disorder is never made w hen there is a hi<;tory of m ania or major depressive episode or mjxed episode. The COll.rSe of untreated cyclothymic disorder is depicted in Figure 2-2C.
Differential Diagnosis The principal differential is among other unipolar and bipolar mood disorders, ~ubstance-induced mood disorder, and mood disorder due to a general medica1 condition. Personality disorders (especially borderl ine) with labile moml may be confused with cyclothymic disorder.
Management
Psychotherapy, mood stabilizers, and antidepressants are used. H owever, persons with cyclothymia may never seek medi cal at tention for their mood symptoms.
II KEY POINTS .,
'1. Cydothymic disorder is a biphasic mood disorder without frank mania Qr depression.
2. It is chronic and recurrent.
MOOD DISORDERS WITH KNOWN ETIOLOGY
Substance-Induced Mood Disorder
Substance-induced mood disorder is diagn()sed w hen med ications, other psychoact ive substancel, Ecr, o r phutotherapy are proximate events and the likely cause of the rnood d isturbance. All arore mentioned types o f mood disorder (e.g., llnipolar, bipo lar) may ()(.~cur.
Mood Disorder Due to a General Medical Condition
This categury is for moud disturbances apparently caused by a med ical illness. Endocrine disorders, such as thyroid antI adrena l dysfunction, are common eti-
Chapter 2 I Mood Disorders • 13
ologies. Postpartum mood disorders are excluded from the criteria; they are modifiers of unipolar and bipolar mood disorders (see above).
• SUBTYPES AND MODIFIERS
Various diagnostic specifiers can be applied to specific subtypes of mood disorders. These have prognostic and treatment implica t ions and may prove tu have etiologic implications.
Melancholic: Melancholic depression is a severe form of depression associated with guilt, remorse, l os..~ of p leasure, and extreme vegetative symptoms.
Postpartum : Postpartum depression occurs · ..... ithin 4 weeks o f delivery. The presence of one episode of postpartum mood disorder is strongly predictive of a recurrence.
SeasOJ!al: Seasonal mood disorder.> show a C011.<'islent seasonal pattern o f variation. TIle most common pattern is a worsening of depression during tht' fa ll and w inter \vith improVt'ment in the spring. The reverse is sometimes true. If the depression is a component of a bipolar disorder, the marne and hypomanic episodes may show a seasona l association.
AtypicaL: Atypical depressions show a pat tern of hypersom nia, increased appetite or weight gain, mood react ivity, long~standing rejection sensitivity, anergia, and leaden paralysis.
Rapid Cye/ing: Patients with bipolar disorder may have frequent (rapid) cycles. To meet criteria for rapid cycling; four muod disturbances per year must be presen t. The suicide rate may be h igher than in non-rapid cyclers.
Catntmlic: The catatonic .~pecifier is applied to mood disorders when then: are pronounced m{wement abnormalities, ind uding motoric immubility or excessive purposeless motor activity, maintenance of a rigid posture, nlutism, .stereotyped movement, echolalia (repetition of a word or phf'"dse just spoken by another person)! or echoprax ia (repet ition of movements made by another person).
The term anxiL>ty refers to many states in which the sufferer experiences a sense of impending threat or doom that is not well defined or realistically based. Anxiety can be adaptive or pathnlo1:,>1.c, transient or chronic, and has a variety of psychological and physical manifestations. Anxiety disorders are a heterogeneous group of disorders in which the feeling of anxiety L" th e major element. They are the most prevalent group of psychiatric d isorders; according to the Epidemiological Catchment Area study, 7.3% of all Americans meet the Diagnostic alld Statistical Manual of Mental Disorders, 3rd edition (DSM-llI ; the DSM version used at the time) criteria at a given point in time (so-called point prevalence). Anxiety disorders listed in the Dia!,'uoslic and Statislical Manual of Metltal Disorders, 4th edition (DSM-IV) are shown in Table 3- 1.
• PANIC DISORDER AND AGORAPHOBIA
Panic disorder is characteri:t.ed by recurrent unexpected panic attacks that can occur witlt or without agoraphobia. Agoraphohia is a disabling condition in which patients fear places in which escape might be difficult. Whether occurring as distinct disorders or together, panic disorder and agoraphobia are common, sometiInes disabling, conditions.
Epidemiology
Panic disorder occurs more frequently in women, with a lifetime prevalence of 2% to 3%. The typical onset is in the 20s, with most cases beginning before age 30.
Agoraphobia also occurs more freq uently in women, \vith a lifetime prevalence of between 2% and 6%. Only one third of patients with agoraphobia also havt' panic disorder. However, most patients with agoraphobia seen clinically also have panic disorder. This apparent contradiction is due to the fact that patients with agoraphobia alone are unlikely to seek trealment.
Etiology
The etiology of panic disorder is unknown. There art' several popular biologic theories involving carbon dioxide (C02 ) hypersensitivity, abnormalities in lactate metabolism, an abnormality of the locus coerul eus (a reglon in the brain that regulates level of arousal), and elevated central nervous system catecholamine levels. The gamma-amino butyric acid (GABA) receptor also has been implicated as etiologic since patients respond well to benzodiazepines and panic is induced in patients with anxiety disorders using GABA antagonists.
TIleorists posit that panic attack.<; are a conditioned response to a fearfu l situation . For example, a person has an automobile accident and experiences severe anxiety, including palpitations. Thereafter, pal pitations alone, experienced during exercise or any sympathetic nervous system response, may induce the conditioned response of a panic attack.
Clinical Manifestations
History and Mental Status Examination
Panic disorder is characteri zed by recurrent unexpected panic attacks that can occur with or without
TABLE 3-1
Anxiety DiIorders
Panic disorder with agoraphobia Panic disorder without agoraphobia Agoraphobia Social phobia Specific phobia Obsessive-compulsive disorder Generalized anxiety d isorder Acute stress disorder Posttraumatic stress disorder Substance-induced anxiety disorder Anxiety disorder due to a geOff':'! medical condition Anxiety d isorder not otherwise specified
agor:1phobia (see below ). PaniE att2('ks typically come un suddenly, peak within minutes, and last 5 tt) 30 m inutes_ The patient must experience 4 of 13 typical symptoms of panic outlined in Table 3-2.
To warrant the diagnosis, onc of the fo llow:ing must occur for at teast I month : per!iistent concern about having additional attacks, worry abou t the implications o f the attack (losing control, ngoing crazyQ), or a significant change of behavior rein ted to the attacks [e.g. , restrict ion of activities').
Agoraphobia is a d isabling complication of pa nic disorder but can also occur in patients with no histo ry of panic disorder. It is characterized by an inl £'J)s£' f£,ar of places or situations in which escape m ight be d iHicu lt [or embarrassing). Pat.ients with agoraphobia and panic disorder typ icall y fear haVing a panic attack in a public p lace and heing e.mharrassed or unable to escape. Those ",dth agoraphobia alone (two thirds of those with agoraphobia) simply avoid public arenas but do not have panic attacks. Although Some agoraphobic patienL~ are so dis.'1bled that they are homebatmd/ many are comforted by the presence of a companion , allowing th em to enter SOme publi c places with less anxiety.
Differential Diagnosis Panic attacks should be distinguished &om the dirt.'Ct physiologic effects of a s\lb~ance' or a general medical condition. ' 111e panic attacks also cannot be accounted for by another mpntal disorder [Stich as soci<ll phobia o r obses.<;ive-compulsive disorder [OCD]) .
Chapter 3 I Anxiety Disorders 15
TABLE 3-2
DSM-IV Criteria foI Panic Attack
A discrete perlod of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within 10 minutes:
Palpitations, pounding heart o r accelerated heart rate S...veating
• Trembling or shaking • SensaqOf]S of shortness of breath or smothering • Feeling of choking • Chest pain or discomfort
Nausea or abdominal distress Feeling dizzy. unste03dy, lightheaded. or faint Derealization (feelings of unreality) or depersonalization (being detac!1ed from oneself) Fear of losing control or going O'azy Fear of dying Paresthesias
• Chills or hot flushes
Ad~pted from Diagnostk afld st<ltisticlll mMI\ J<lI of ll1ent~ 1 rn.orde .... 4th rn. Washington. PC: Ametk~n Psyt:hl~tr,( ASSOC:idTlon, 1994:39S,
Management
Not surprisingly, the m ain trf' <ltments for pan ic disorder <lre pharmacotherapy and cognitive-behavior<ll therapy o r their combi na tion. Specific triC;ydic antidepressants (TeAs), specific monoamine oxidase inhibitors [MAO Is), selfftivc serotonin reuptakc inhibito rs (SSR ls), anJ high-potency hen zodiazepiJl<'_'i have been show n to be effel"tive in cont rolled studies. Cognitive-behavioral thel".Jpy (CfiT) i.n\'olves thf' usc of relaxation exercises and desen.,.itization co mbined with education aimed at help ing patients to undcrst<lnd th<lt their panic attack.-; are a result of misinterpret ing bodily sensa tions. Pat ier)ts can then learn that the sensations arc innocuous and sel f-limited, which diminishes th e panicky response. EXl-lOSurC therapy, in whic.b the pati("m incrementally confront., a feared st i mulu~. has bee11 shown to be effective in treating agoraphobia.
<: not f o r sal e ! :> < He ll/UI np<J,Ilant ! :>
16 • Blucpri!'\t6 Psychiatry
• KEY POINTS •
1. Panic disorder is characterized by' recurrent IJne)(pected panic attacks.
2. Panic disorde r can be seen with or without agoraphobia.
3. Panic disorder is treated with antidepressants and benzodiazepines and cognitive-behavioral techniques.
4. Agoraphobia is fear of not being able to (or being too embarrassed tal escape a place or situation.
5. Agoraphobia most often Occurs alone (without panic).
6. Agoraphobia can be a complication of panic disorder.
7. Agoraphobia is treated with exposure therapy.
Spec ific phobia is an anxiety disorder characterized by intense fear of particular C)bjects or si luat ions (e.g., snakes, heightsl lt is the most common psychiatric disorder.
Epidemiology
Sperific phobias are more prevalent in 'Nomen than men and occur with a lifet ime preva lence of 25%. Typical onset is in chi ldhood, with 1l1OSl ca ses occurring before age 12.
Etiology
Phob ic disorder ... , including specific phobia , tend to run in fami lies. Behavioral theorists nrgtle that phobias are learned by being paired \'."ith t raumatic events.
Clinical Manifestations
History and Mental Status Examination
A phobia is an imltiona! fear of a specific object, place, activity, or situation that is o ut of proportion to any actual danger. To meel the DSt>/l-IV criteri a for speCific phobia, ., patient must experi ence a marked, persistent fear lhat is recognized by the patien t to b e excessive or unreasonable and is cued by the presence or anticipation of a specific object or situation. in addition, exposure to the stimulus must
almost invariahly provl,lke the anxiety reaction, and the aVQidance of or distress over the feared situation tntlst impair everyday al:ti vili es Qr rel ationships. F<Jr thQse younger than age 18, S}Tll.ptoms must persist ror at least 6 months.
Differential Diagnosis
The prindp<1 l differential diagnosis is another mental disC)rder (such as avoidance o f school in sepa rati(m anx iety disorder) presenting w ith anxiety or rearfuJness.
Management
Specific child hood phobias tend to remit sponta~
neously with age. \Vhen they persist into adulthood, they often becom e dlronic. However, they rarely callse disability. Exposure therapy in the form of systematic desensitization or flooding is the treatment of choice. There is no role for medication.
• KEY POINTS •
1. Specific phobia is an intense fear of a certai n object, place, activity, or situation.
2. It occurs in 25% of the population at some poInt in tl-)eir Iffetime, usually with onset before age 12.
3. It is treated with systematic desensitization and flood ing.
SOCIAL PHOBIA
Social phobia is an allxiety disorder in \vh iCh patients have an intense fear of being scrutinized in social or public situations (e.g. , giving a speech, speaking in class). The d isorder may be gCllc1'3 lizcd or limited to specinc situations.
Epidemiology
Social phobias occur equall y among men and women and arrect 3% to 5% of the population. The typical onset ls in adolescence, w ith most cases occurring berore age 25.
Etiology
Phobic disorders, including social phobia , tend to run in families. Behavioral theorists argue lhat phobias
nnt f o r ,,. l e, l ;> < " " ,IIJ1R nJ'OA'l""" ! ;>
are lea rned by being paired with traumatic events. Some thetlrists posit that hypersensitivity to rejecl ion is a psychological antecedt:nt of social phobia.
Clinical Manifestations
History and Mental Status Examination Social phobias ;I re characterized by the fear of situations in which the person is exposed to unfamiliar people o r to possible scrutiny by o thers. Exposure to
the fea red social situation must almost invariably provoke an anxiety reaction . Avoidance of Or Ji!ttress over the feared situation must impair everyday activi ti~s or relationships. F(lr those younger than age J 8, symptoms must persist fo r alleast 6 months. Social phobia can either be generalized (the patie.nt fears nearly all situations) or limited to specifi c situations.
Differential Diagnosis The principal d iffe rential diagnosis is another mental disorder (such 3S avoidance of school in separation anx iety d isorder) prt'sent in g with anxiety or fearfulness.
Management
Mi ld cases of social phobia can be treated with e S'.1; btlt many cases req uire medication. MAOls, betablock~rs. SSRls, alprn w lam, and gabapentin h,we proven successful in t reating social phobia. CB'f uses the expo.~ure thernpy tech niques of flooding and syslemnlic desensitiza tion to reduce anxiety in feared situ~tions. Supportive ind ividual and grlJup psy, holherapy is helpful t(l restore self-esteem and to
encourage venturing into feared sitllations,
.' KEY POINTS ......
1. Social phobia is fear of exPOsure to scrutiny by others.
2. It has a lifetime prevalence of 3% to 5%, typically occurring before age 25.
3. It can be generalized or limited. 4, It is treated with MAOIs, beta-blockers, SSRIs,
alprazdam. or gabapentin and with CST.
Chapter 3 ! Anxiety Disorders • 17
• GENERALIZED ANXIETY R !~!J!!~_~!lJ G~~L. .. __ . ____ _ GA D is charac: te rized by intenst' pervasive worry over virtua ll y every aspect of life associated with pbysiwl manile..talions of anxiety.
Epidemiology
TIle lifetime prevalence of GAD is approximatel y 5 ~X,. The typical age of onset is in the early 20s, but the di sorder In.'l y begin at any age.
Etiology
' I\ \l in studies suggest lhat GAD has both inherited and enviromnentnl etiologies. SerotllOe.rgic, noradrt':nt':rgic, and GAllA-ergic neurotrnnsmitter 5}'S
Le Ins haw been studied in relation to GAD, but th t:: bio logic etiology rem.a.in<; obscure_ Cognitivebehavioral theorists pOSit that GAD is due to cognitive disto rtion.<; in \\Ihidl patients mispen::eive situat ions as dangerou.<; when they are noL
Clinical Manifestations
History and Mental Status Examinat;on Patients with generalized anxiety rus(lTder worry excessively about virtually every a<;pect of their lives Uob performance, health , marital relations, and social life), They do noL have panle attacks, phobias, obsessions, or compu lsions; rathe r, they experience pervasive nnxlety and worry (apprehensive expectatiun) aboul n number ( I f e vents or act ivities that occur mo::.t days fo r at It'asl fi monlhs. They mu!>t also have difliclllty contrdUng the worry, and it must be associated w ith at least three of the followin~ s)'TIlptoms,! restlessness, easily fat igued, difficulty concentrating or mind going bl ank, irritability, muscle tension , nod sleep disturbanct'_
Differential Diagnosis ~rne focu.~ of the anxiety an~1 worry in GAD must not be symptomatic of another axis I dic;order. For example, the anxiety anc.I worry carmot be about having a panic attack (as in panic disorder) or being embarrassed in public (as in social phobia).
18 - Blut'prirrtt;. Psychiatry
Management
The pharmacolo~ic treatment of GAl) is \'lith hL'tIzodiazepincs. buspirone (8 non-benzodiazepine an>. iolylic), gah:dpentin, or hcrn-hhlckers. Although benzod iazepines are vcry effc( tive, the duration of trea lmt:nt is limited by the ri.~k uf tult"rance and dependence. Relaxation ICLl1niqucs arC' also usC'd in tr~t.ment with some success.
• KEY POINTS •
, . GAD [s intense wony over every aspect of life. 2. GAD Is characterized by difficulty contro1l1ng the
worry. 3. It is associated with physical manifestations af
anxiety. 4. GAD is treated with benzodiazepine, buspirone.
beta-blockers. gabapentin, and relaxation techn;quE!'S.
POSTTRAUMATIC STRESS DISORDERjP.TSD)
IYfSD is an anx.iety ruS<'rdt."r characterized by the persistent rccxpt!rienc,· uf ~l trmJllIll, eflm-Is to avoid I·ccollccting the trauma , and byperarousallTable 3-3).
Epidemiology
The prcvalence of PTSO h. e!)timated at 0.5% amOl1g men and 1.2% among women. ITS!) may occur at :lny age from childhood through adulthood and ma) begin hours, days, or even years after the initi"l trauma.
Etiology
The centra] etiologIC factor in IYfSD is the trauma There rna} be some neces.<,ary predisposition to PTSO because not all people who t:l(perienct" similar traumas develop the syndrome. Magnetic resonmKe
• TABLE 3-3
Posttraumatic Stress Disorder
Reexperience of the trauma Efforts to avoid recollection of the trauma Hyperarousal
unaging studies support a finding nf altered hirpt-c::ampa l volumc in VrSD.
Clinical Manifestations
History and Mental Status Examination
P~p le with PTSD have enduretl a traumatic even t (e.g.. combat, physical 3!>Sa lut, rape, explosion] tn which they experienced, witnessed, or were confronted with actual or polential death, serimlS ph)'sIcal injury, or a threat to physical integrity. The traumatic event is subsequently reexperienced through repetitive intrusive images or dreams or through recurrent illUSions, halluci nations. or flash b:lcb of the event. In an adaptive attempt, the.c patients make efforL~ to avoid recollections of the eve.nt, often through psychological mechanism~ (e.g., dissociation, numbing) or <I'-luaJ avoidance of circumstances that will evoke recall . 'J11ey also ~XPl:"ri+ tnce fa'lings ("I f detachme nt from others and exhibit evidence of autonomic hyperarousal (e.g., difficulty sleeping, exaggerated startle response).
Differential Diagnosis
Symptoms that resemblc PTSD ma}' be see.n in dep ression, CAD, panic disorder; OCD, and dissociative disorder. When sympt("lms resemble IYfSD, verify that there also :ue symptoms from alJ three categories; if not, consider one Qf the above diagnoses.
Management
Treatmcnt is \"ith 8 com bll1<ltion of symptom· dircacd psych("lnh~rmat.:o logic agent." and (lSY
dl("lt hcrapy (individual or group ). TCAs and MAO ls are the most commonly l L<,et! medications in P'ISl.), especially when there is a comorhid major depression. SSRls hav(' also been used. Psychotherapy is typically tailored to the natur(· of the t rauma, degree of coping skills. amI the support systems avai lable to the pa tient.
KEY POINTS
I. PTSD occurs in response to trauma . 2. PTSD is characterized by reexperience of the
trauma, efforts to avoid recalling the trauma. and hyperarousal.
3. It Is treated with medications directed at specific symptoms and with psychotherapy,
• OBSESSIVE-COMPULSIVE R!~QRI?-',,!l_ 5Q~I?) ___ ___ _________________ _
OCD is an anxiety disorder in which pal ients experience recurrent obsessions and compulsions tha t cau.se significant distress and occupy a significant portion of their live;.
Epidemiology
The lifetime prevalence orOCD is 2% to 3%. Typical onset of the disorder is be tween the late teens and ea rly l Us, hut one third ()f patients show symploms of oeD bcJorf' age l5.
Etiology
Behaviora l mtxlels of om d aim that obsessions and compulsions are p roduced and sustained through d ao;sic and operont conditioning. Interestingly, OCD is Sef'n more frequently after bru in inj ury or disease (t.g., ht'ad trauma, seizure wsordcrs, H untington's d isease), and t win studies show that monnzYb'Otic twins "have 3. higher concordance rate than dizygotic twins; thes!..' find ings support a b ic"llogic basis for the disorder. The neurotmnsmiller Sf'rotonin has been implicated as a mediator in obsessivc t.h inkin~ and compulsiv~ bt-haviors.
Clinical Manifestations
History and Mental Status Examination Pntknts w ith OCI) experience obs~ions and com~ pulsiC'lns. Ohst!l)!>iollS are recurrent intmsive ideas, thoughts. or i mag~ that ca use significant anx iety anJ distress; compu lsions are repetitive purposeful phys~ kal or men tal actions that are. genenllly performed in response to obsessions. Tlw compulsive "rituals" are meant to neutrnlil.e the obsessions, diminish anx icty, or Stl1n('how magically prevent a dreaded event or situat ion.
Chapter 3 I Anxiety Disorders . 19
D;fferen t;al Diagnosis It is important to distinguish the obsess.imzlll th ink~ ing of OeD from the delusUmal thinking of schizophren ia o r other psychotic disorders. Ohses.sions are usua lly unwanted. resisted. and recogniZL.J by patit:!nts as coming from their own thoughts, \vhereas delusions are generally regarded as distinct from patients' tho ughu. and are typicall y not resisted. For example, patienu with depres..<; ion often experience obsessive rum inations that can be distinguished from obsessio n<; becouS(' tlwy art' transient. not consideret.l lJl1\V"anl cd, ;'Incl not resisted.
Management
C lomipram ine and SSRls haw been shown to be q uite effective in treat ing OeD. Althou gh poorly studied, the beh:lVioural techniq ues o f systematiC" desensiti :totion , flood ing, and response Ilre\'e.ntio n have b~n used successfully to treat compulsive rituals. For example, someone who fcars contamina~ tion from an object will hold the object repeated ly in therapy while simultaneously being p revented lrom carrying out the ritual associated wlth thc d readed object.
ilIi KEY POINTS --J~ - -I. OCD is characterized by recurrent obsessions and
compulsions. 2 OCD causes distress and wastes time by com·
peillng pat ients to carry out various obsessions/compulsions/rituals.
3. lifetime prevalence is 2% to 3%, 4. It is treated with clomipramIne and SSRls. and
with systerT}<I tic. desensitizatiof], flood ing, and response prevention.
Personality disorders are coded on Axis n in the Ditl~ nustic (.md Statistical MatlUal of Metltal Disorders, 4th edition (OSM -IV) . Ten type.s of personality disorders are grouped into dusters based on similar overall characterist ics. There are three ret~ognized perS<.malitl' disorder clusters: odd and cn:cntric, (lramatil: and emotional, and anxious and fearful (Table 4-1 J.
DSM-JV general diagnostic criteria for personality disorders are outlined in Table 4-2. Criteria for individual personality ilisorders are disHlssed below. Personality d isorders frequently overlap in symptoms.
Paranoid Personality Disorder
People with paranoid personality disorder are distrustful and suspicious and anticipate hann and betrayaL
Epidemiology
Paranoid personality disorder has a lifetime prevalence of 0.5% to 2.5% of the general population. Relatives of chronic schizophrenics and patients with persecutory delusional disorders show an increased prevalence of paranoid personality disorder.
Etiology
Environmental precursors are unclear. Family studies suggest a link to delusional d isorder (paranoid type). There appears to be a sma ll increase in prevalence among relatives of schizophrenics.
Clinical Manifestations
History and Mental Status Examinati on People with para110id persona lity disorder are dis-
trustful, suspicious and see the 'world as ma levolent. They anticipate harm, betrayal, and deception . Not surprisingly, they are not forthcoming about themselves. They require emotional distance.
Diffe rential Diagnosis The key d istinction is to separate paranoia associated w ith psychotic disorders from paranoid perS<.l11ality disorder, especially because paranoia associated with psychotic disorders is generally responsive to antipsychotic medications.
Schizoid Personality Disorder
Individuals with schizoid personality disorder are emotionally detached and prefer to be left alone.
Epidemiology
Estimates of lifetime prevalence range as high as 7.5% or the general population, but becaus(:' people w ith sch i,.oid persona lily disorder are avoida nt of others, they are not commonly seen in clinical p ractice.
Etiology
There is some evidence to suggest increased prevalence o f schizoid personality disorder in relatives of persons with schizophrenia or schi,.otypal persona lity disorder. Un loving or neglectful parenting is hypothesized to p laya role_
Clinical Manifestations
History and Mental Status Exam ination These people are loners. They are aloof and detached and have profound difficulty experiencing or expressing emotion. Although they prefer to be left alone and generally do not seek relationships, they
~ not for s" l,el > ~ lie P"R "PGJI'I""" ! >
_lilly Disorden 1 CJasslfic:atloc1 of _1Iy Disorders
OusterS Cluster A (Dramadcl OusterC IOddlEccentrid Emotional) (AnxioUS/FearfuJ)
Paranoid Antisocial Avoidant Schizoid Borderline Depefident Schizotypal Histrionic Obsessive-
Narossistic compulsive
TABLE 4·2
General Diagnostic Crtteria for Personality Disorders
Personality disorder patients evidence an enduring pattem of lnner experienc~ and behavior, established by adolescence or early adulthood, that: 1. Deviates markedly from cultural expectations 2. Is inflexible and personally and socially pervasive 3. causes d istress 01' social or \NOI'k impairment 4. Is a stable pattern of experience and behavior of
OOg duration r stably unstable1 5. cannot be explained by another mental illness 6. 15 not caused by substance use or medical condition
NOTt: IndMduats with persoNI~ty ~ uMioli ly l'!\lI~ltllin intaet ,eaUty Iffiing. ~.Ihey may have lriI ......... psydlo(jc: syrnp«xm wtlen stressed b<t rMI (or ~l k>'>~ or fru'l1~tion. PerscNllity disorden lire different from. per1OnII6ty tl'1l~~ Ihat are typIrnfly IId<!p1:ive, ruitu,lIby ~co:pI:lIble, lind do not CIIU5@slgnificant dil.1rt!SS or imp<olr~,.
Soo,ce: DIagnOStic and ~t~tI§ticallT\llf)uat of mental dlso rders. 4lh ed. WolShington, DC: AmetlclIrl P<;yd1illtnc k;~ooation. 1994:327.
may maintai n an important bond with a family memher.
Diffe rentia l Diagnosis Schizoid p~rsona lity di<;ortler can be distingUished from avoidant personality di.<;order (see helm ... ) and social phobia by the fact that schizoid individuals Jo not desire re lationships. Avoidant and socially phobic persons desire and may seek relationships, but their anxiety handicaps t heir capacity to achieve rdatedness. Schizophrenia, aufi .... tic dismder, and Aspe.rger's disorder (~ less severe variant o f autism) are also differential d iagnosti c conditions.
Chapter 4 J Personality Disorders • 21
Schizotypal Personality Disorder
Individuals with schizotypal personali ty disorder have odd thooghts, affi:rts, percept ions, and beliefs.
Epidemiology
Lifetime preva lence is 3(~ of the general population.
Etiology
Studies d~onstrate interramilial aggregation of this disordt:r, especially among first-degree relatives of schizophrenics.
(Unicoi Manifestations
History and Mental Status Examination Schi ..... otypal personali ty disorder is best thuught of as s imilar to schizophren ia but less severe and without sustained psyc.hotic sYTnptoms. People with thiS" disorder have few relationships and demonstrate oddities of thought, affect, pcrception, and belief Many a r~ highJy d istrustful and often paranoid, which resul ts in a very constricted social world. The lifetime suicide rat~ among lhis population is 10%.
Differentia l Diag nosiS Sch,izoph.renia, delusional disorder. amI mQOO disorde r with psychosi.s are the major diITerential Ji agnose..
• CLUSTER B (DRAMATIC AND
~-'~'1°!!Q~I:\.l,L __ .
Antisocial Personality Disorder (ASP)
lndividuals with ASP repetitively uisregard thl' rules. and laws of society and ra rely experience remorse for their actions.
Epidemiology
Antisocial personality disofller is present in 3% of men and I % of women. About half h'H'e been arrt5te<i; about half of those in prison have AS P.
Etiology
ASP is more common among first-degree relatives of tho~ d iagnosed with AS P. In families of an individ\lal "'''1th ASP. men show higher ratt'S of ASP and substance abuse, whereas women have higher ra tes ('If somati7..ation disorder. A harsh, violent, and criminal t!11v1ronmenl alsll predisposes people to this disorder.
< I'>Ot for Bill e ! > < 118 .Iln.. npo,D:i!%I'I ! >
22 • Bluepnnw PsychIatry
Clinical Manifestations
History and Mental Status Examination fndividuah. with ASP di.,pby either a flagnmt or wellconcealed dlSregard for the ruJ~ and l av.·~ of sOCIety. They are exploitative, lie frequently, endanger Od leTh, are impulsiv{' and aggressive, and rarely experience ff'morse for the harm they Cal.L.,e others.. Alcoholism is a lrt'quenUy associated finding in this population_ Many individuals with ASP <l re indH1ed or jailed for their actions. Their Ijfctimc su icide rate j s 5%.
Diffe rential Diagnosis Bipolar disorder ami substance abuse disorder can prompt antiso< ial ht'havior., during th e al' ute illne,s that rcnut when the disorder j, control1ed. The anti social beha\'lOr of in{hidtlals \'lidl ASP, COIl Vt'l1'eiy, i ~ not state dt' pend('nt.
Borderline Personality Disorder
lndivi.duals with borderlme perSOnality disorder ~I.lffcr fnllll inst .. hili ty m relationships, self-image, affC( t , and impui':><' l.rm troL
Epidemiology
Liretime pl'1' \ alen(e is 1% lo 2% of the genCf:11 popula(ion.
Etiology
Gorderlme persoJl<l !ity di.~order is about five times as common among firs t-degret' reiatiVt's of boroerl int' patienLs.. In addition , thi!> disorder shO\\'~ inueased rates in familics of akoholi( ~ and families of individuab with ASP, as wel l a::. In famjli~ WJth mood ch::.ordl'rs. Pemales with borderline personality disorder frequent ly have ~u frered from sexual or physil al abuS<.' llr bOU1.
Clinical Manifestalions
History and Mental Status Examination Individuals with borde. line personality diS()rder tiuf fer from a legion of tiymploms. Their relationships arc infused with an~{'r, fl'3r of abandonment, and shifting ,dealiza tion and devaluation . Their selfimage is inchoatl, fragmented, aDd unstable with u;:mseque·nr unprediLtable changes in relationships, goals, ~nd vulul:::'. "["1lt;·y arc affcctJvcly unstabl t:' and rtactive, Wllh anger, dcprt'Ssl{)n, and pani~ prorntnent. "111CIt Impll!sivCl1CSS can result in many unsafe behavJOrs, Hldudulg drug usc, pron'lJ.scuily, gambling, and olher risk-taking bchilvior. "I'heir sdf-uestrtlctlvc urge, r€:.'.>uJt in II e£lucnl suicidal and parru:.uicidal
behavior (~ul...h a~ 5uperhdal cutting or buming or nonfatal ovcrdosl...'~ ill whu:h the i.ntent is not lethal). They also demons;t:ra te brief paranoia and dissodati \lC" symptoms. SUIcide attempts can be fi-nw ent befo re the age of30, and suicide rates approach 10% over a lifetime. TIle pnnnpal jntrapsychic defenses they lise are prll11ltive with gross denial, distortion, projection, and spHtul1g prominent. Patients rna}' have a broad range of comorbid illnesses, induding sub~tance abuse, mood disorders. and ea ting di.!iorders.
Differentia l Diagnosis Mood clison.ien. and behavior:ll changes due [0 a(.liv(' ~Ilhst."'int:e ~busc are the principal dirferential dlagnostic conside.ralioos. The diagn~tk dUl_"'5 are un~tab le rclation.~hjp~, unstable self-image/ unstable affect, and unstable or impulsive beh aviors.
Histrionic Personality Disorder
Indi\'iciurus with histrionir personality disordt'r have ext es..qve ~uperficja l emotionalily and a powerful need for attenLJoll .
Epidemiology
Ltfet.tme prevalenc{' is 2% to 3% of the general JX>pulation . In ( limLal St'tllngs, the diagnosis i.s most rrelj uently applied to women but may equally aff'"-"Ct men m the general population .
Etiology
There appears to be a fami lial link to somatiza tion disorder and to ASP.
Clinical Manifestations
History and Mental Status Examination Individuals with histrionic personal ity disorder are charanerizcO by their exc.essive and superfiLial emotionaiJtyand the.r profound need to be thc center or atten tion at all times.. T heatrical behavior dominates with li vely and dmmatlC c1o tJl ing, exaggerated emotional respon~c:s to seemingly insignifia mt events, and mappropriate flIrtatiolls and seductive behaVior acros.-. a Wide' vafl et)' of ClIcumstances. Despite thcir apparent pletho ra of emotion, the:.l' individ uals often have difficult), with intimacy, frequently bclievmg their rdationsbips are more intimate than they actuall y are. -
Differential Diagnosis Somatil'.atitm di~order is the principal dirrerenlial diagnostic clJn!,jdcratioll .
J nnt. f o r ...wet ;> " lie ,IlIIR rtpOj:\a"''' I ;.
Narcissistic Personality Disorder
Individuals with narcj!i.<;i<;l ic personaLty disorder appear arroganl and entiLled but suffer ITOm extremely low self~esteem.
Epidemiology
l.ifetime prevaLence is estimated al 1% jn the general population and 2% to 16% in clinjcal populations. Fifty to 75% of those with this diagnosis are men.
Etiology
The etiology of thj~ di!;order i ~ lUlk.llow n .
Clinical Manifestations
History and Menta l Status Examination People with narcissi ~1.ic personalit), disorder demonstrate an apparE:Jl tl y paradoxical combination of sc l f~tel1 teredness and worthlessness. l11ejr sense of se lf~importance is generally extravagant, and they demand attention and admiration. Conccnl or empathy fo r others is typically absent. They often appear arrogant, exploitative, and entitled. However. despite thei r inllated sense of self. below their brittll! facade lies low self· esteem and inlense envy of those whom they regard as more desirable, worthy, Or ablc.
Diffe rential Di agnosis The grandiosity of narci',sism can bc differen tiated from the grandiosit)' of bipolar disorder by the pres~ ence (If charJcteristic mood .'I)'mplorm, in bipolar di~order.
• CLUSTER C (ANXIOUS AND FEARFUL)
- - . ~ _ . ---- - " •• -_. - --.-- - - -- '---- p ' - - .
Avoidant Personality Disorder
Individuals with avoidant personality disorder desire relationships but avoid them becall.'>e of the anxiety produced b)' their scrtse of inadequary.
Epidemiology
Life time prevalence is 0.5% Lo 1 % of lhe general population and appean. to be of equal pre,,·aJenc(" in men and women.
Etiology
There ar€" no conclusive data. The pattern of avoidance may start in infanc)'.
Chapter 4 I Personality Disorders . 23
Clinical Manifestations
History and Mental Status Examination People with avoidan t persooalily disorder experience intense feelings of inadeq uacy. They are painfully sensitive to criticism, so m uch so that they are com~ pelled 1.0 avoid spending time with people. Their fears of rejection and humi liation are so powerful that to engage in a relationship they !>eek strong guar· anlL-'es of acceplance. 111e essence of this disorder is inadequacy, hypersensitivity to criticism. and con!i€~ quent social inhibition.
Diffe rential Diagnosis The major diagno~lic distinction is bet ween avoidan l pen;onality disorder and social phobia , generalized rype.
Dependent Personality Disorder
lndivid unls with dcpendent pcrsonalHy disorder are extremely needy, re lying on olhers for em olional support and decisiun making.
Epidemiology
Lifetime prevalence is 15% to 20%, 2('(, to 3% clinically.
Etiology
The etiology i.~ un known.
Clinical Manifestations
History and Mental Status Examination These people ycanl to be ca red f Of. Because of th eir e)..:treme dependence on others for I'motiol1al support and decision making, the~ live in great ili.1d contin ual fear of sepa ration from someone they depend on, ht!llce their !>ubmissive and clinging hehavims.
Differential Diagnosis People with dependent personality disorder are similar to individu<lls with border-line personalily dj!>~ order in their desire to avoid abandonment but du not exhibj l the impulsive behavior, unstable affect. and poor seLf~illlage of the borderline patient.
Obsessive-Compulsive Personality Disorder
' I'h~ individuals arc perfectionists vvho n:ql1ire a grea t deal of order and control.
< oot fOI" eaLe! > < lie .IVt" npo.n1lD! ! >
24 • Bh . .errint s Psychiatry
Epidemiology
The estimated p revalence is 1 % in the general population. Men arc diagno~ed v· ... ith obse<isivec:ompul:.ive pt':rsonality d isorder t wice as frequently as women.
Etiology
The et iology is unknown. bu t there may be an assodation wi,lh mood and anxiety d isorders..
Clinical Manifestations
History and Menta l Status Examination Ind ividua ls with obseSSive-compulsive personality d i!>ordcr arc pcrfe(:li onist s. T11ey require order and control in every dimcl'l~ jon of th eir lives. Their attention to mll1uliae freq uently impairs tl1eir ability to finish wh ;) t they star t or to maintain sight of their goals. T11ey are cold 311d rigid in relat ionships and m ake frequent moral judgm t.'nts; devotion to work often replaces i.ntimacy. They are serious and plodd ing; even rt.'CI'cation becomes a sober task.
Diffe re ntial Diagnosis O b!>e-'\.c;ive-compulsive perso nality disorder can be differen tiated I rom obsessive-compulsive dhorder (OCD) hased on symptom scvC'rity.
MANAGEM ENT
TIecau:.e persunali ty may have temperamen tal com ponents and i:o devclLlped uver a li retime of jntcraL"1:ing with the environment . per:;on ality disorders are gcncrally re:oistan t to treatment. In general, psydlOthcr:lPY is recummended for most personality disorder::;. Psychodynamically based therapies arc commonly used, although they m ust be modified to each individual and each disorder. C..ognitive, hehavioral, and f~Jllily therapies are also used to treat these
disorders. Em pirical stud ies validaGng the efficacy of various thera pies are gencraU}, lacking. Diale<:tical beha"ior Ihcrapy (OBY) was developed speci fically for the trt.'utment o f borderl ine personality disorder and has heen validated in em pirical studies. G roup therapy incorporating various p~-ychotherape.utic
modalities is also u!>oo. Pharmacotherapy is widely used in personality dis
(m.lcrs, although no specific medication has ken shown to treat any spl.'Cihc d isorder. lnstead, medications arc targeted at the various as!>OCiated sympto ms of pc.rSllllalily di!>orders. For example, mood slabill zer:. may be ust.'1.1 for mood in:.tability and impulsiveness. BcnJl;odiazepines are commonly used fo r anxiety, altho ugh the potenti al for abuse and dependence is too often overlooked. Beta-blockers are also used frequently. For depress.ion, obsessivecompulsive symptoms, and eat ing d isturbances, selective serotonin reuptakc inhibitors (SSRls) and other ant idepressants have been successfull y used . Psyc hotic or paranoid symptoms are oommonly treated with low-dose antipsychotics.
__ KEY POINTS II 1. Personality diSOl'ders are categorized into three
symptom clusters.. 2. Personality disorde rs consist of an enduring
patte m of experience and behavior. 3. They can produce transient ps.Ychotic symptoms
during stress. 4. They are treated with psychotherapy and medica
tions targeted at symptom relief. 5. Personality disorders are resistant to treatment 6. They may have genetic associations with Mis I
disorders.
Substance abuse is as conmlOn as it is costly to society. It is etiologic for many medical illnesses and is frequently comorbid with psychiatric illness. The Diagnostic and Staristical Mallllal 0/ Mental Dis()rd~, 4th edition (OSM-IV) defines substance abuse and dependence independent of the substance. I fence, alcohol abuse and dependence is defined by the same criteria as heroin abuse and dependence.TIlis chapter defines abuse and dependence and provides clinical descriptions of each substance-related disorder. The DSM-IV recognizes the different signs and symptoms associated with various drug addictions. We review the common suhstance-re1ated disorders in sequence.
• SUBSTANCE ABUSE --------------- --------- -- ------------------- -The OSr.,'l-IV defines substance abuse as a maladaptive pattern of substance use leading to clinically significant impairment or distress as manifestt.'(1 by one or more of the following:
• Failure to fulfill major role obligations at home, school, or work;
• Recurrent substance lise in situations in which it is physically hazanlous;
• Recurrent substance-related legal problems; • Recurrent substance usc despite persistent or
recurrent social or interpersonal problems caused or exacerbated by the effects of the substance.
• SUBSTANCE DEPENDENCE ---------------- ------------------------------Substance dependence is defined as a maladaptive pattern of substance lise leading to clinically signifi-
canL impairment or dist ress, as manifesLed by three or more of the following occurring at any time in a 12-month period:
I . Tolerance; 2. Withdrawal; 3. Repeated, unintended, excessive use; 4. Persistent failed efforts to cut down; 5. Excessive time spent trying to obtain the
substance; 6. Reduction in import,nt soci,l, occupational, or
recreational activities; 7. Continued use despite awareness that substullce
is t he cause of psychological or physical difficulties.
A lthough each substance dependence disorder has lU1i4ue features, these are considered the common features that define substance dependence. Each substance use disorder is discussed, with particular attenti on to their unique features.
• ALCOHOL-RELATED DISORDERS
Alcohol Intoxication
AJcoho! intoxication is defined by the presence of slurred speech, incoordination, unsteady gait, nystagmus, impairment in attention or memory, stupor or coma, and clinically significant maladaptive behavioral or psychological changes (inappropriate sexual or aggressive behavior, mood lability, im paired judgment, impaired social or occupational functioning) that develop during or shortly after alcohol ingestion.
The diagnosis of alcohol inloxication must be differentia ted from other medical or neurologic states that may mimic i.ntoxication, for example, diabetic
< not for sal .. ! ;> < HD ,IlllR npo,llllD'l ! ;>
26 • Blut:print6 Psychfauy
h.ypoglycemia; toxicity with various agents, including bUL not limited to ethylene glycol, lithium, and phenytoin; and intoxication with benzodiazepin~"S or barbiturates. The diagnosis of alcohol intoxication can be confirmed by serum toxkoJogic screening, including a blood alcohol level (I3AI .).
Alcohol Dependence
Alcohol abuse hecomes alcohol dependence when efrects on one's life become more global and tolerance and withdrawal symptoms develop. The alcoholicall y dependent paLient drinks larger amountS over longer periods of time than intended, spends a great deal of ti me attempting to obtain alcohol. and reduces parLidpation in or eliminates important social/ occupational, or recreational activiti es because of alcohol. In alcohol dependence, there also is a persistent desire or unsuccessful eAorts to cut dO\ .... n or control alcohol intake.
Epidemiology
The percent:?ge of Americalls v,·bo abuse alcohol .is thought to be high . Two thirds of Americans drink occasionally; I Z% arc heavy drinkers, drinking almost every day and becoming intoxicated several times a month. The EpidemiQlogical Catchment Area stlld~' found 3 lifetime prevalence of alcohol depcndmce of 14%. The male-female prevalence ratio for alcohol dependence is 4 ; 1 .
Etiology
The etiology of alcohol dependt."ll.ce is unknmvn. Adoplion studies and monozygotic twin studies demonstrate a partial genetic- basis, particularly for men ·..vith alcohobsm . Male alcoholic!> arc morc likely than female alcoholics to have a ramily history of alcoholism. Compared with control subjects, the relatives of alcohoLcs are more likely to have higher rates of depresSion and anti!'."Ocial personality disorder (ASP). Adoption stt1C\ies aho reveal that alcoholism i.~ multidetermined: genetics and environment (family rearing) both play a role_
Clinical Manifestations
History, PhYSical and Mental Status Examinations. and Laboratory Tests The alcohol-dependent patient may deny andlor minimize the extent of drinking, making the early diagnosis of alcoholism diffic.ult. TIle patient may present with anidel1t.s or falls, blackout~, motor vducle accidents, or after an Brrest for driving tmder
the influence. Becau~e denial is so prominent in the disorder, collateral information rrom family members is essenlia l to the diagnosis. Early physical find ing. ... that suggest alcoholism include acne rosacea, palmar erythema, and painless hepatomegaly (rrom fatty infiltration) .
Signs of more advanced alcoholism include cirrhosis, jaundice, ascites, testicular atrophy, gynecomastia, and Dupuytren 's contracture.. Cirrhosis can lead to complications including variceal bleeding, hepatocellular carcinoma, and hepatic encephalopaUly. Medical disorders with an increased incidence in alcohol-dependent patients include pneumonia, tuberculosis, cardiomyopathy, bypertel15ion, and gastrointestinal cancers (i.e., oral, esophageal, rectal, colon, pancreas, and liver).
There are also numerous neuropsychiatric complications of alcoholism . Wcrnickc-Korsakoff syndrome may develop in th e alcohol-dependent patient because of thiamine deficiency. TIU! Wernicke stage of th e syndrome consists of the triad of nyslagmus, ataxia, and mental conFusion. TIlese symptoms remil wit.h the injection of thiamine. (1 OOmg 1M). Without thiamine, Wernicke's encephalopathy may progress to Korsakoff's psychosis (antero~rade amnesia and confabulation), which is irreversible in two thirds or patients. Other neurops<ychiatric compli.cations of alcoholism include alcoholic hallucinosis, alcoholinduced dementia, pcripilL"1"a1 neuropathy, substanccinduced depression, !'lnd suidde. In the later stages of alcobolism, significant social and occupational impairment is likely: job loss and family estrangement are typical.
Various laboratory tests are helpful in making the diagno!>is. EALs quantitatively confirm alcohol in the serum. They can also provide a rough measure of rolcrancc.. In general/ the higher the BAL without significant signs ofintoxl,cation, the more tolerant the patient has become of the intoxicating effects of alcoho1. Alcohol-dependent patienls also develop elevated high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol, elevated mean C()rpuscular volume, elevated Sen1l11 glutamic-oxaloacetic transaminase, and elevated serum glutamic-pyruvic transaminase. cJ11irty percent of alcQhol-dependent patients, compared with 1 % of con trol subjects, have evidence of old rih rractu res on chest X ray.
Differential Diagnosis The diagnosis of alcohol dependence is usually dear after careful history, physical and mental
stahl" examination, and consultation \vith farnil}' or friends.
Management Management is specific to the clinical syndmme. AlcohoL intoxication is treated with supportive measures, including decrca~ing ext~..-nal stimuli and withdrawing the source of ale-ohol. Intensivc carl.' rna)' be required in cases of excessive alcohol intake complicated by respiratory compromise. All suspected or known alco ho l-dependent patients should receive orol vi.tamin supplementation with folate I rnglday and thiamine lOOmglday. If oral intake is not possib le, thiamine should he injected intramuscularly before any glucose is given (because glucose. deptl'tes thiamine stores).
Alcohol Withdrawal syndromes include the fo llOWing.
Minor Withdrawal ~The ~hakes" begin 12 to J 8 hours after cessation of dtinking and peak at 24 to 48 hours. Untreated, ul,complicated alcohol wit.hdrawal lasts 5 to 7 day~ It is characterized by t remors, nausea, vomiting. tachycardia, and hypertension . M;nor \~;thdrawal is lrcatcd with benzodiazepmes, such 3S ch lordiazepoxide (ljhri.um) or oxazepam (Serax) titraled to the degree of withdrawal signs. The benzodiazepine is then tapered ove!; a period. of days. 111C goals of treat ment are prevention of more secious complicatjons and patient comfort.
Major Withdrawal The risk of alcohoue seizurcs (~ rum fits,,) begins 7 to 36 hours after cessation of drinking and peaks between 24 and 48 hours. One to six generalized seizures are common but rarely lead to Slah.l" epilepticus. Akoholk seizures precede dc1.irium t remens ill 30% of cases. Seizures are treated acutely with iJ1tra· venous brnzooiazcpines. Prophylactic phenytoin (Dilantin) may he effective when admillistered during the high-risk period in patients with a h istory o f withdrawal seizures.
AlcoholiC" hallucinosis has an onset within 48 hours o f cessat ion of drinking and may last more than a week. rt is characlcrizl.-d b)' vivid, unpleasant auditory hallUcination s in the presence of a d ear sensa-rium. Alcoholic hallucinosis may be treated with" neuroleptic (e.g., halupt!ridol [Haldol] 2- 5mg t wice a day) . On rare occasions, cllCSC hallucinations become chronic.
Alcohol withdrawal deHrium (deljrium tremens) is a life-threatening condition manifested by dcliri,um
Chapter 5 I Substance--Related DiSOfdets • 27
(perceptual disturbanc~ confusion or disorientation , agitation), autonomic hypcrarousal ) and mild fever. It affects up to 5% ofho~pjtal.i zt'd patients vvith alcohol dependt."llce and typically begins 2 to 3 days after abrupt reduction .in o r cessation uf aJcohol intake, It is treated with intravenous bcnzudiazcpincs and supportive care. Treatment may need to occur in an intensive care unit, particu larly if there js ~i{!.nifi cant autonom.ic instability (e.g. , rapidly flucluating blood pressure). The syndrome t}'p icaUy lasts 3 da}'s but can persi~t fo r we.eks.
Alcohol Rehabilitation The. 1.wo goals of rehabilitatiun are subriety and treatment of comorbid psychopatholob'Y.
To have a la.o;ting recove ry, the patient must stop denying the illness and acct!pt the. cli<lb'11oois of alcohol dependence. A lcoho lics Allonymou.s (AA), a worldwide self-help group for recovering alcoholdependen l patients, has been shmm to be one of the most effective p rograms for achieving and majnlaJl1 ' ing sobriety. enle progmm invol\'cs daily tu weekly meetings tllat focus on 12 steps toward recovery. Members are expected to pursue the 12 steps with the assistance of a sponsor (preferably someone with several years of sobriety).
Alcohol appears to be a potent dcpressant, so treatment o f depress.ion should be geared to patients who remain dc-pre~ed after 2 to 4 weeks of sobriety. Anxiety is also common in withdrawing or newly sober paticnb and sbo uld be asses.ed after at leac;l 1 month of sobriety. lnpat"ient and residential rehahili. tation programs usc a team app roach aimed at focusing the patient on recovery. Group th erapy allows patient.!; to see the;r own prohlems mirwroo in and confronted by others. Family thcrapy allows the palienl to examine lhe role uf the family in alcoho lism.
Disulfiram (Antabusc) can be helpful in m"Lnlain ing sobriety in some patients.. It ac ts hy ililiibiting the second enzyme in the pathway o f alcohol metabolism, aldehyde dehydrogmase, so th[!t acet'l1debyde accumulatt.'S in the bloodstream, caus.ing flushing, nausea, vomiting, palpitations, and hypotension. In theory, di~ulfiram :;houl d inhibit drinking by making it physiologically llllp leasant: however, because the effects can bc fatal in rare cases, patients mu~t be committed to a~tinence and fully undl-"'fStand the danger o f d rinking while taking d isulfiram . TIle usual duse of disulfiram is 250mg daiJy.
Naitrexone (Rt'via) is an opiate antagoni~"t med· ication that has the strongest empirical support in
-< not foe sal e! ;> < HD ll)UI npolIant ! ;>
28 . Blueprint!> psychiatry
reducing alcohol intake among medications avaj,lable j,n the United States, f\laltrexone reduce~ both the amount of alcohol intake and the fTequcncy of alcohol intake. Naltrexone is usually dosed at SOmg per day, but higher doses may potentially be more effect ive. Unlike disulfiram, patients can continue taking naltrexone if they relapse to alcohol inLake. Naltrexone, as an opioid antagonist , may work in part by reducing the reinforcing high of alcohol ingestion.
rvlany studies have demonstrated benefits from rehabilitation programs, but nearly half of all treated alcohol-dependent patient.~ will rel apse, most commonly in the first 6 rnonths.
• KEY POINTS "}.
1. In alcohol dependence, denial and minimization are common.
2. Benzodiazepines are used in acute detoxification to prevent life-threatening complications of withdrawal.
3. Peak incidence of alcoholic seizures is within 14 to A8 hours.
4. Rehabilitation is aimed at abstinence and treating comorbid disorders.
5. Rehabilitation involves AA and group and family therapies.
6. Fifty percent of treated alcoholics will relapse. 7. Wernicke--Korsakoff syndrome is due to thiamine
deficiency. 8. Wernicke's triad consists of nystagmus, ataxia, and
mental confusion. 9. Korsakoff's symptoms are anterograde amnesia
and confabulation.
• SEDATIVE, HYPNOTIC, AND ANXIOLYTIC SUBSTANCE USE DISORDERS
Sedative, hypnotic; and anxiolytic drugs are widely used. They are all cross-tolerant with each other and with alcohoL Included in this c11.ss are barbiturates and benzodiazepines. Of these, the benzodiazepines are th e most widely prescribed and available.
Epidemiology
Approximately 15% of the general population is prescribed a benzodiazepine in a given year. Som e patients abu~e tlK"Se drugs.
Clinical Manifestations
History, Physical and Mental Status Examinations, and Laboratory Tests Sedative-hypnotic drug abuse and dependence are associated with syndromes of intoxication, withdrawal, and withdrawal delirium that resemhle those of alcohol.
Intoxication on ly can be distinguished from alcohol in toxication by the presence (or absence) of alcohol on the breath, or in the serum or u rine. Barbiturates, when taken orally, are much more Uke1y than benzodiazepil1cs to cause dinin illy significant respiratory com promise, Jntoxication can be confirmed through quantitative or qua litative serum or urine toxicologic analyses. Serum toxicologic screens can identify the presence of benzodia..:epines and barbiturates and their major metabolitcs.
WIthdrawal symptoms are listed in Table 5- 1. Withdrav .. al delirium (confusion, disorientation, and visual and somatic hallucinations) has an onset of 3 to 4 days after abstinence. Dependence requires the presence of three or more of the seven symptoms listed in Table 5-1.
Management
Treatmen t of sedati ve-h ypnotic withdrawal may be on an outpatient or inpatien t basis. Generally, inpatient detOxification is requi.roo when there is comorbid medical or psychiatric illness, prior treatment fai lures, or lack of support by family or friends. On an inpatient un~t, bmzodiazepines or barbiturates may be administered and tapered in a controlled manner. \.yithdrawal from short-acting substances is generall y more severe, whereas withdrawal From longer-acting substances is more prolonged .
TABLE 5-'
Signs and Symptoms of SC!c:1attve-Hypnotic Withdrawal
Minor Withdrawal
Restlessness Apprehension Anxiety
More Severe Withdrawal
(oarse tremors Weakness Vomiting Sweating Hyperreflexia Nausea Orthostatic hypotension Seizures
< ""t fo r /WIl e l ;> .. "'" I'JlR rtpOlI'l_ I >
\Vithdrawal from barbiturates is more dangerous than from benzodiazepines: it can (much more easily) lead to hyperpyrexia and death. Withdrawal is managed by scheduled dosing and tapering of a ben7.oWa:t.e pine o r barbiturate (diazepam o r pheno barhital) .
III patients w ho have been abusing alcohol and he.,zooia:t.epines or barbiturates, it ma y be necessary to perform a pen lobarbital challenge test- This test allows for the. quantification of tolerance to perform a controlled taper, thereby reduting the problems o f withd rawal.
Treatmen t of sedative-hypnotic dependence resembles that for alcohol dependence. After detoxification, the patie nt can enter a residential rehabilitation program or a day or evening treatment program. Referral to AA is appropriate becau..:;e the addiction issues and recovery process are similar. Families may be referred to AI-Anon, an AA focused famil y educat ion and support gro up.
KEY POINTS
1. Sedatives and hypnotic drt.J9S are cross-toferant with akohol.
2. They have intoxicating effects and tesutt in withdrawal states similar to alcohol.
3_ Tolerance can be measured by a pentobarbital chllilenge test.
4. Treatment resembles that for alcoholism.
• OPIOID USE DISORDERS
Opiates include morphin e, heroin, codeine, meperidine, and hydromc..1rp hune. Heruin is only available i1Jegall y in the United States. O piates are commonly used for pall1 controL
Epid emiology
O piate l L<;e and ahuse are relatively uncommon in the United States. lifetime prevalence in 1991 was 0_9% and point prevalence was less than 0 .1 %. although more recent surveys indicate opiate use and abuse has heen increas ing d uring the past decade. Many of those who use o piates recreationally hecume addicted. 'The ntmlher o f opiate addicts jn the United States is estimated at 500,000.
Chapter 5 J Substance-Related Disorders . 29
Clinical Ma nifest ations
History, Physical and Men tal Status Examinations. and l.aboratory Tests Most heroin and morphine users take o piates intravenously, whi,ch p roduces Bushing and an "intensely pleasurab le, d iffuse bodily sen.<;ation that rcsembles orga1>m. This initial "rush ~ is fo llowed by a sense uf well-being. Psychomotor retardation , drowsines~
in activity, and impaired concen tration ensue. Signs of intoxication occur immediately after the addict ~shoot!=; up" and include pupillaI)' constriction, respirdtory depression, slurred speech, hypotension, bradycardia, and hypothermia. Nausea, vomiting, and wnstipation are commo n after opiate use. Opiate use can he confirmed by urine o r serum toxicologic measurements.
Opiate abuse is defined by the criteri a for substance abuse noted above. In opiate dependence, tolerance to thc..' effects of o piates occurs. Addicts ~shoot up" three or more times per day.
\-\fi thdrawal symptoms usually begin 10 hours after the lac;t dose. Withdrawal from opjates can be highly uncomfortable but is rarely med ically complicated o r Ijfe-threatening. Withd rawal S}'ll1Ptoms are listed in Tabl,e 5-2.
Opiate addict.~ often have cnmorbid substance use disorders, antisoti~l l or borderline personality w sorders, and mood disorders. Opi.ate addicts are morc prone to cvmmit crimes because of the high COst of op iates. Opiate addic tion also is a5S<."lCiated \-\l ith high murtality rates fro m inadvertent overdoses, aCCidents, and suicide. Opiate addicts are also at higher risk of medica l problems beca use of poor nutrition and use of dirty needles. Common medical disorders include
TABLE 5-2
5ymjIIlJI ... 01 Opiate W\tIldrawal
Mikl Withdrawal
Dysphoric mood anxiety. and restlessness
Lacrimation or rhil10frhea Pupillary dilatation Piloerection Sweating Hypertension Tachycardia
"""" Diarrhea Insomnia Yawning
More Severe Withdrawal
Na..,.. Vomiting Muscle aches Seizures
(in mepetdine withdrawaf)
Abdominal cramps Hot and wid flashes Severe anxiety
< not foe sal e ! > < He llJlR npo.uant ! :>
30 • Blueprin1-6 Psychiatry
serum hepatitis, H IV infection, endoL.arrulis, pneumonia, and cel lulitis.
Differential Diagnosis
11,e diagnosis of opiate addict ion is usually obvious after a C'dfe.ful history and mental status and physical examinations.
Management
Patients addicted to opiates shou ld be Rradually withdrawn using meth adone. Methadone is a weak agonist of the inti opiate receptor and has a longer half-li fe (1 5 hours) than heroin or morphine. T hus, it causes relatively rcw into~cant Or withdrawal effects. Generally, the initial dose of methadone (typically 5- 20 01gJ is based un the profile of withdrawal symptoms. VVithdrawal from short-acting o piates lasts 7 to 10 days; withdrawal from longer-acting meperidine lasts 2 to 3 weeks.
CloniJine, a centrally acting alpha 2 receptor agonist th at decreases central noradrenergic output, can also be used for acute withdrawal syndromes. It is remarkably effective at treating the autonomic symptoms of withdrawa l but docs lillie to curh the drug craving. Risks of sedation and hypotension limit clonidine's usefllln C'!-" in outpatient settings. AddiLi,onal medicatiuns can b e llSeU to relieve uncumfortable symptoms of ,\vithdra\oval, such as dicyd o minc for abdominal cramping. prometh azine ror nausea, and quinine for muscle ames.
Rehahi.litation generall y involves referral to an intensive day treatmenL program and to Narcotics Anonymous, a 12-step program similar to AA. Methadone mainLenance, daily admini$lration or 60--100 mg of m ethadonf-' in guvernment-licensed methadone dinics/ is used widely for paLients with demonstrated physiologic dependence. l.ong-term administration of meth adone can aiJevi.ate drug hunger and minimize drug-seeking beh avior.
• KEY POINTS I 1. Recreational use.of opiates often leads to
addiction. 2 Opiate addicts are at increased risk of HIV/ pneu
monia. endocarditis, hepatitis, and cellulitis. J. High mortality occurs from accidental overdose,
suicide, and accidents. 4. Opiate withdrawal begins 10 hours after last dose. 5. Withdrawal is uncomfortable but not usually
medically complicated.
CENTRAL NERVOUS SYSTEM (CNS) STIMULANT USE DISORDERS
Cocaine ancl amphetamint.'S are readily available in the Uni ted States. The pattenlS of use and abuse or and dependence on cocaine and amphetamines are similar because both arc CNS stimulants with similar psychoactive and s-ympathominu'tic efh:'Cts.
1n the United States, cocaine is available in two rorms: as coca ine hydrochloride pOWdelj whi ch is typically .snorted, and as cocaine alkaloid crystal ("crack 'l , wh.ich is typicaUy ~rnoked. Cocaine has an extremely rapid on~et of action (\"" hen sno rtl_-.d or smoked) and a short half-life, rcquiri l'g frequent dosing to remain "high ."
In tlle United States, an amphetamin e (dextroam~ phetamineJ and metbylphenidate are available in p ill form by prescription ror th e treatment of obes~ty, narcolepsy, an d at1:enlion-deficitlhypcradivity diSor~
der. Various forms of amphetamine are used illicitly including a veTY pure form of methamphetamine, cruJeti cryslal meth amphetamine, whidl can be snorted o r smoked. Am phetamines have a longer half-life than cocaine and hence arc taken less rrequcn l1y.
Clinical Manifestations
Cocaine or amphetamine intoxication is characterized hy
1. Maladaptive behavioral ch augt.--s (e.g., e.uphoria or hypervigilanceJ;
2 . Tachycardia or bradyc.udia; 3. Pupillary diJatalion; 4. Hyper- or hypotension: 5 . Perspiralion or chill s; 6. Nallsea or vorrtiling; 7 . Weight loss; 8 . Psychomotor agitation or retardation; 9. Muscular \",'eaknC5s, respirator}' depression, chest
pain , cardiac dysrbyt.hmias; 10 . Confusion, seizures, dyskinesia, or coma.
Cocaine in toxicati,on can cause tactile hallucinat ions ("coke bugs''). Both cocaine and amphetamine intoxication can lead to agitat iun, impaired judgement, and transient psychosis (e,g., paranoia, visual hallucinatj,ons) Cocaine and amphetamine dep<,,":ndence is defined by the criteria outlined above for sub~tance
dependence, Withdrawal of cocaine or amp hetamines leads to
fatil:,'lle, depreSSion, nightmares, headache, profuse
nnt foc solei ;> '" "e PflR rtpQI\il:t:>l I :,
sweating. muscle cramps, and hunger. Withdra,,,al symptoms peak in 2 to 4 days.
Management
Withdrawal from amphetamines or other (CNS) st imulants i!> self-limited and usually does no t require inpatient detoxification . Psychosis from ampheta mine intoxication or withdrawal is generally selflimited, req uiring only observat ion in a safe envirunment. Antipsychotic medications can he used for agitation.
UltimaLely, the goal is rehabilitation. NarmLiCS Anonymou~, treatmenl of comorbid psychopath ol ogy, drugs to reduce craving, and family tJlcrapy are the essentia l featun:.'S of cocaine rehabilitation.
KEY POINTS
1. Cocaine and amphetamines ale CNS stimulants.. 2. CNS stimulants can cause transient psychosis (e.g ..
"coke bugs" or paranoia). 3. Withdrawal S)lmptoms (fatigue. depression, night
mares, etc.) peak In 2 to 4 days. 4. Withdrawal from CNS stimulants is self-limited
• CANNABIS AND MISCELLANEOUS SUBSTANCE USE DISORDERS
Cannabis
Cannabis is Widely used throughout tbe world in the forms of marijuana and hashish. TIle drug is usually smoked and causes a state of euphoria. Complications of cannahis include impaired judgement, pow concentration, and poor memory. Serious complica~
lions include de lirium and/or psychosis.
Club Drugs
C lub Drugs are a group of dnags classjfied by the National Institute on Dnag Ahuse (NIDA) according to their popula rity in dance cl ubs and other party venues. T hese d rugs are of a wide variety of chemi-
Chapter 5 I Substance-Related Disorders • 31
cal classes, but are linked hy their frequent use in sudal groups and the fact that tiley are commonly Laken together: BeC3tL<;e of their popularity and telldency for users to show up in emergency rooms, we review some of the more widely used C lub Drug." below.
Ecstasy (MDMA) - Ecstasy is a widely popular drug with mi.'I(<'-d. stimulant and balluc i.nogenic properties. Many users report a stimulant and euphoric effect, and MDMA appeani to specifically enhance tJu:" user's desire fOf intimacy with others.. As such, its use has been associated with an increased frequency of unsafe sexual activity. Acute use of MDMA has been associated with deaths from various cau.!ics' Long-term MDMA use appears to lead to a pe rmanent loss of fine-diametcr- sCfotonin axons throughout the brain_
Methamphetamine - Alw known as crystal or crank, methamphetam ine is a psychostimulant which is ne urotoxic to dopamine neuron::.. Methamphctam ine is often produced locally in small lahs and can thercfore \lary greatJy in p urity.
GHB - Gamma-hydroxybutyrnte is a compound used in lower doses hy bodybuilders and others seeking to gain muscle mass (GliB promotes the release of grO\\!th ho rmone). In higher doses, G HB is used to produce a hjgh, and is common among the club and party scene. G HB is easily Q\ierdosed, and can lead to death from respiratory arrest .
Kctamine - Also kno\,.rll as Special K, ketamine is <l dissociative anesthetic mostly used in veteri nary rnt.'Clicin e. It is used for jts hallUcinatory, di ssociative effect.
Rohypnol - Rohypnol is a benzodiazepine approved h'>f clinical lise in some countries ·ou tside. th e United Slales. Rohypnol produces classiC" bcnzodiazepine effects of sedat.ion. I lowcver, it has strong amnestic properties, and may be a frequent culprit in drugging o thers for the purpose of theft or sexual a~-alllt.
I.SD - I.)'sergic acid dieth ylamide is famous fo r its
hallUcinogeniC properties. Acute use can produce a highly euphonc rgood trip") o r a highly dysphoric ("bad trip~) hallucinato ry experience. I .ong-term LSD use can lead to psychosis 0[ hallucinogCll perl>j~ tiJ)g perception di~order.
Eat ing disorders are characterized by disturbances in eating behavior and an overconcern with lxxly image or size. Although eating disorders are classified into two discrete d iagnostic categories in the DiLlgnoStic (HId Statistical M(/mud of Mental Disorders, 4th edition (DSM-IV) , many s)'mptoms overlap. T he principal diagnostic distinction i:<; based on ideal body weight. When abnonnal eating behavior causes body weight to fall below a defined percentage of expected body weight, a diagnosis of anorexia nervosa is made. If ideal OOdy weight is maintained in the presence of abnonnal eating behaviOrs, a diagnosis of bulimia nervosa is made. Eating disorders likely lie along a continuum of disturbances in eating behavior and often are associated with mood disorders and other psychiatric illnesses (Table 6-1) .
• ANOREXIA NERVOSA ----------------------------------------------Anorexia nervosa is a severe eating disorder characterized by low body weight . Anorexia nervosa is d iagnosed when a person's oody weight falls below 85% of the ideal weight for that individual. The weight loss must be due to behavior directed at maintaining low weight or achieving a particular body image.
Epidemiology
The point p revalence of anorexia nervosa is betv,leen 0.5% and I % in women, and more th an 9Cflb of patients with anorexia nervosa are women. The prevalence in men is not d ear. Average age of onset is 17; onset is rare before puherty or after age 40. Anorexia nervosa is more common in indust rial societ ies and higher socioeconomic classes.
Etio logy
Eating disorders and their subtypes likely share many common ba<;es of origin. Psychological theories of anorexia nervosa remain speculative. Patient.;; \vith anorexia nervosa generally have a high fear of losing control, difficulty with self-esteem, and commonly display "all or none" thinking. Although it is not specific to eat ing disorders, past physical or sexual abuse may be a risk factor. Contemporary theories fOC,tlS on the need to cont rol one's hody.
Social theories propose that societal opinions, which equate low body weight with attractiveness, drive women to develop eating disorders. Although this fact may be responsible for some cases (e.g., anorexia nervosa is more common among dancers and models), historically anorexia nervosa has been present during periods when societal mores for beauty ,,"vere different .
Biologic, familial, and genetic data support a biologic and heritable basis for anorexia. Fam il}, studies reveal an increased incidence of mood disorders and anorexia nervosa in first-degree relatives of pat ients with anorexia nervosa. 'Iwin studies show higher concordance for monozygotic versus dizygotic twins. Neuroendocrine evidence supporting a biologic contribution to anorexia includes alterations in corticotropin-releasing factor, reduced central nerVOl1."i system norepinephrine metabolism, and that amenorrhea (caused by decreased luteinizing honnone and follicle-stimulating hormone release) sometimes precedes the onset of anorexia nervosa.
Anorexia NerYOsa
Restricting tYPe Binge eating/purging type
Clinical Manifestations
Bulimia Nervosa
Nonpurging lype. Purging type
History and Mental Status Examination DSM-IV criteria for tile diagnosis of anorexia nervosa include refusal to keep body weight at greater than 85% of ideal, all intense fear of weight gain, preoccupation with body size and shape, a disproportionate influence of body weight on personal worth, 2nd the denial of the medical r isks of low weight. Patients with anorexia nervosa generally do not have a loss of appetite; they refuse to eat o ut of fear of gaining weight. Amenorrhea is also a diagnostic criteria in postmenarchal females (delay of menarche mar occur in premenarchal girls). In some cases, amenorrhea precedes the development of anorexia nervosa; however, in most cases, it appears to be a consequence of starvation.
Individuals ·with anorexia nervosa commonly exercise intensely to lose weight and alter body shape. Some restrict food intake as a primary method oJ weight control; others u'le hinging and purging (use of taxatives, enemas, diuretics, or induced vomiting) to control weight.
The behavioral repe,rtoire -used to control body weight is used to further claSSify anorexia nervosa into tVo,'(l ·subtypes: restricting type and hinging! purging type. In the restricting type, the major methods of weight control are food restriction and exercise. In the hinging/purging type, food rest riction and exercise m~y be present, but binge eating and subsequent purging behaviors also are present.
TIle natural course of anorexia is not we.ll lmderstooo, but man y cases hecome c hronic. The long-term mortality of anorexia nervesa secondary to suicide or medical complications is greater than l m'O.
Differential Diagnosis
Conditions that can resemble anorexia should be ruled out. The.se include major depre.ssion with loss of appetite and weight, some psychotic disorders where nutrition may not be adequate, body dysmor-
Chapter 6 I EatIng Disorders . 33
phic disorder, anda variety of general medical (especially neuroendocrine) conditions. Anorexia nervosa is differentiated from bulimia nervosa by the presence of low weight il) the former.
Management
The management of anorexia nervosa is directed at the presenting symptoms. When medical complications are present, these must be carefully treated and followed. If ipecac use to induce vom iting is suspected, ipecac toxicity must be ruled out.
During starvation , psychotherapy is oflittle value hecause of the cognitive impairment produced by starvation. "Vhen patients are less medically ill, a therapeutic program including supervised meals; weight and electrolyte monitoring; psychoeducation about the illness, starvation, and nutrition; individual psychotherapy, and family thempy can begin . Psychopharmacology management often includes antidepressants, especially the selective serotonin reuptake inhibitors (SSRls) to treat comorbid depression. Psychopharmacologic t reatmen ts are used principally to treat any comorbid psych iatric illness and have little or no effect on the anorexia
per '"
KEY POINTS
1. Anorexia nervosa is a severe eating disorder characterized by low body weight.
2. It is diagnosed lTLore thim 90% of the time in women.
3", Anorexia l1ervosa can cause serious medical complications and has a g reater than 10% Ion g.-term mortality rate.
• BULIMIA NERVOSA
Bulimia nervosa is an eating disorder characterized by hinge eating with the maintenance of hod)' weigbt.
Epidemiology
The estimated point prevalence of bulimia nervosa is 1 % to 3 % of women. The male-female ratio is 1 : I O. TIlis Ulness occurs disproportionately among whites ill the United States:
< no t f <>r sale! > "'- He ll.llSl npoll!l7-M ! :>
34 • Blueprint!:> Psychiatry
Etiology
Many of tbe factors in the genesis of anorexia nervosa arc 'also implicated in bulimia nervosa . Familial and genetic studies support similar familial linkages in both disorders. Psychological theories for bulimia nervosa stress an addiction or obsessive-compulsive behavioral model Biologic, neurologic, and endocrine findings are less prominent in theories of causation of bulimia nervosa. Abnormal serotonin metaholism is tbought to play more of a role in bulimia nervosa than in anorexia nervosa.
Clinical Manifestations
History and Mental Status Examination
Bulimia nervosa is diagnosed in individuals ...... ho engage in binge eatiJlg and hehaviors designed to aVOid weight gain but who maintain their body weight. In addition, these are people whose selfevaluation is overly influenced by their body weight and shape.
Food binges fn bulimia nervosa may be precipitated by stress or altered mood states. Once a binge begins, the indiVidual typically feels out of control and continues to eat large quantities of food, often to the point of physical discomfort. Purging may follow and most often consists of vomiting, usually induced medlanically by stimulating the gag reflex or using ipecac. Other purging methods used to avoid weight gain include laxative and diuretic abuse and enemas. Bulimic individuals often exercise and restrict their food intake. A<; in anorexia nervosa, patients with buJirnia nervosa are overly concerned with bod}' image and are preoccupied with becoming rat. Bulimia nervosa is da.."5ified into two subtypes: nonpurging type or purging type [see Table £i. I ) according to w hether purging behavior is present.
Differential Diagnosis
Bulimia nervosa should be distinguished from the binge eating and purging suhtype of anorexia nervoS3. If hody weight is less than 85% of ideal/ a diagnosis of anorexia nervosa :is made . . Binge eating can occur in major depression and in borderline perscmality disorder, hut is not tied to a compulsion to reduce weight.
Management
The treatment for bulimia nervosa is similar to that for anorexia nervosa . Although medical complications of starvation are not present , other medical complications can require careful medical management and, at times, hospitalization. Psychotherapy focuses at first on achieving control of eating bchavior. Cognitive therapy may be useful in treating overconcern with body image. Self-esteem and inter~ personal relationships become the focus of therapy as the behavioral problems abatf'. Antidepressants, especially SSRls, arc more effective in the treatment of bulimia nervosa than in anorexia nervosa (including those patients who do not have comorbid depression) .
_ KEY POINTS II!!! 1. Bulimia nervosa is a severe eating disorder cllaf
acterized by binge eating and purging. 2. It is also characterized by maintenance of normal
body weight. 3. Bulimia nervosa is more common in women than
in men. 4. It can have serious medical complications.
MEDICAL COMPLICATIONS . ,.- .--- ---- -~------ --.- -------- _. ---_ ... -Eating disorders, when persistent, can have serious medical consequences. The lifetime mortality from anorexia nervosa is approximately 10%: it i<; unk nown for hulimia nervosa. Tahle 6-2 lists the common medical complications of eati ng disorders. The most serious of these, gastric or esophageal rupture, cardiomyopathy from ipecac toxicity, and cardiac arrhythmias secondary to electrolyte imbalance, can be fatal. Other complications parallel those of chroni(; medical ilInlO'ss, take a severe toll on the patient's overall functioning, and cause tremendous suffering and burden for their families. In addition to these medical complications, sect)ndary psychiatric alld neurologic sequela include cognitive dedine, metabolic encephalopathy, and severe mood disturbance, all with profound consequences fOJ;" patients alld their families.
TABLE 6-2
M _~.cI-"1IIsoodors
Behavior Medical Complication
Binge eating Gastric dilatation 01" rupture
Vomiting Esophageal rupture Parotiditis with hyperamylasemia H)'POkalemic. hypochloremic.
metabolic: alkalosis (with cardiac arrhythmias)
Ipecac toxicity (cardiac and skeletal myopathies)
laxative use ConstipatiOn (due to laxative dependence)
Metabolic acidosis Dehydration
Diuretic use Electrolyte abnormalities (with cardiac arrhythmias)
DehydratiOn
Starvation leukopenia, anemja Increased ventricularll:>rain ratio Hypotension, bradycardia Hypothermia Hypercholesterolemia Edema o..y skin. lanugo hair
Chapter 6 I Eating Disorders • 35
Many disorders seen in adults can occur in children. However, there is a group of disorders usually first diagnosed in children. Table 7-1 lists these disorders according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). This chapter reviews only the more common disorders.
Child psychiatric assessment requires attention to details of a child's stage of development, family structure and dynamics, and nonnative age-appropriate behavior. Consulting with parents and obtaining information from schools, teachers, and other involved parties (e.g., Department of Social Services/Youth Services) are essential to proper assessment .
Children, especially young children, usually express emotion in a more concrete (less abstract) way than adults. Consequently, dlild inte",'i{'\vs require more concrete queries (Do you feel like crying? instead of Are you sad?). Playing games, taking turns telling stories, and imaginative play are often used to gain insight into the child's emotional and interpersonal life. During play, observations are also made regarding activity level, motor skills, and verbal expression. Children are much more likely than adults to have comorbid mental disorders, making diagnosis and tTeatment more complicated.
The complexities of diagnosis in child psychiatry often require the use of psydlological testing. Tests of general intelligence include the Stanford-Binet Inte1iigence Scale (one of the first intelligence t ests developed. and often used in young children) and the \Vechsler Intelligence Scale for Children- Revised
(WISC-R). The WISC-R is the most \videly used intelligence test for assessing school-age children. It yields a verhal score, a perfonnance score, and a fullscale score (both verbal and performance) or intcl1igenee quotient (lQ).
There are many other tests and objective rating scales designed to measure behavior (e.g., impulsivcness, physical activity), perccptual-motor skills (by drawing people, placing pegs in appropriately shaped holes), and personality style (by describing what is happening in an ambiguous scene).
Because seizure activity or subtle electroencephalof:,'l"aph ic abnormalities are common in certain child psydliatric disorders, an electroencephalogram (EEG) may be vvarranted. The evaluation of mental retardation usually involves a search For possible causes.
• MENTAL RETARDATION
Patients with mental retardation have subnormal intelligence (as measured by IQ) combined vvith deficits in adapt ive functioning. IQ is defined as the mental age (as assessed using a WISC-R) divided by the chronologie age and multiplied hy 100. If mental age equals chronologie age, then the ratio equals one and the IQ is "100." An IQ of less than 70 is required for the diagnosis of mental retardation. Severity ranges from mild to profound and is hased on IQ (Table 7-2).
· no t ( e l: Slll " l ;. < II" ,IlJI1i npc~ :>
Chapter 7 I Disorders of Childhood and Adolescence • 37
TABLE 7-1
_~FlntDiagraalIn~ CIIMacd. Dr AdalIICIIG
Mental Retardation learning Disorders
Reading Disorder Mathematics Disorder Oi~der of Written ExpressH>n
Motor Skills Disorder Developmental Coordination Disorder
Communication Disord~ Expressive language Disorder Mixed ReceptivH;xpressive language Disorder Phonological Disorder StutterIng
Pervasive Developmental Disorders Autistic Disorder Rett's Disorder Childhood Disintegrative Disorder Asperger's Disorder
Attention·Deflcit and DisruptiVe Behavior Di<j()rder'i Attention·DefidtlHyperactivity Di~rder
Conduct Disorder Oppositional Defiant Disorder
Feeding and Eating Disorders of Infancy Of' Eafly Childhood
PIca Rumination Disorder Feeding Disorder of Infancy or Early Childhood
Tic Disorders Tourette's Disorder Chronic Motoror Vocal Tic Disorder Transient Tic Disorder
Elimination Disorders Encopresis Enuresis
Other Disorders of Infancy, Childhood. or Adolescence Separation Anxiety Disorder Selective Mutism Reactive Attachment Disorder of Infancy or
Early Childhood StereotypiC. Movement Disorder
Epidemiology
Mental retardation affects 1 % to 2% of the population and has 3 male-female ratio of 2 : 1. Milder forms of mental retardation occur more frequently in families with low socioeconomic status (SES); more severe forms of mental retardation are independent of SES. Most patients with mental retardation have mild or mocierClte fonns (see Table 7-2).
_ TABLE 7-2 -- l'e<centageof Total MR
OegreeofMR OQ Population
Mild 50-70 8'% _te 35- 50 1"'" s."",. 20-35 3--4%
Profound <20 1 -2~
Etiology
Mental retardation call be thought of as a fina l common pathway of a numher of childhood or perinatal disorders. The most common cause of mental retardation is Down syndromt! (trisomy 21) . Fragile X syndrome is the most common cause of heritable mental retardation . Inhorn errors of metabolism, perinatal or early childhood head injuries, maternal diabetes, suhstance abuse. toxemia, or rubella can all cause mental retardation. Overall, there are more than 500 genetic abnormalities associated with mental f'E'tardation. In 30% to 40% of patients with mental retardation, no dear etiology can be detennined.
Clinical Manifestations
History, Phys;cal and Mental Status Exam;nations. and Laboratory Tests Most mentally retarded children have physical malformations that identify them at birth as being at high risk for mental retardation (such as the characteristic facies of the child with Down syndrome). Infants can show signs of significantly subaverage intellectual functioning. Young children with mental retardat ion may be identified by parents or pedjatri~
dans after failw e to meet deveJopmental milestones in a number of functional areas (e.g .• delayed speech, sociaJ skills, or self·care skills capacity) or on scoring an lQ less than 70 on the Stanford-Binet (usuall}' only for "ery young children) or WISC-R (standard for school-age children) .
The onset of symptoms mm,1: be hefore age 18. The patient must have both an IQ less than or equal to 70 and concurren t deficit'> or impainnents in several areaS of adaptive functioning (e.g., communication, self-care. interpersonal skills). Laboratory
< not fmc SIll "t ;,. < ,to, AJ\JI nlX',IlU:>I ! >
38 • BIU/!:pn~ Psychiatry
findings may suggest metabolic or cluomosomal edala!,.,)'.
Differential Diagnosis
Attention-deficit/hyperactivity disorder (ADHD), learning disorders, depression, sth i;.:ophrenia, and seizure disorder can all rl'semble mental retardation, These disorders can also be comorbid conditions. Ch ildren suspected of having mental retardation should have a thorough medical and neurdogic evaluation , indudinf:: IQ testing, an EEG, and brain imaging (CT or MRI).
Management
Management depends on the degree of retardation, the course, alld the particular abilities of the child and the parents. Most children with mental retardation progress through normal milestones (standing. walking, talking. learning to recognize letters and numbers) in a similar pattern to normal children but at a slower rate. Growth and development occur in children with mental retardation. They can have developmental Spllrts, like norma l children, tbat could not have been predicted at an earlier age.
tn mild mental retardation, the child is typically considered educable. The child can usuaUy learn to read, write, and perform simple arithmetic. With family support and special education, most of these d liIdren will be able to li ve with thei r parel1ts. The long-term goal of treatmen t is to leadl the child to function in the wmmunity and to hold some type of job.
In moderate mental retardation. the child is typic.:aJly considered tfainablt'. With training, the child can learn to talk, to recognize his or her name and a few simple words, and to perform activities of daily living (bathing, dressing, handling small change) without assistance. The long-term goal of treatment is typkaHy to enable the child lo live and function in a supervised group home.
Children with severe (If proround mental retardation aJmost in variably require care in institutional settings, usually beginning very t:'.arly in lire. These forms of mental retardation are otten associated \vlth specific s}fndromes (e.g., Ta}·-Sachs disease] in which there is progressive physical deterioration leading to premature death_
.. KEY POINTS 411 1. Mental retardation is defined by 10 less than or
equal to 70 and functioning in .'!OJ)eCific areas. 2. It is more common in males (2 : 1). 3, It is most commonly caused by Down syndrome
(trisomy 21).
4. Mental retardation is managed in developmen-talty appropriate settings.
Leaming disorders are characterized by performance in a specific area of' leaming (e.g., reading. writing, arithmetic) substantially below the expectation of a child's ch ronologic age, measured intelligence, and age-appropriate edUc.1tion. The (DSM-IV) identifies three learning disorders: reading disorder, mathL .... nHl.tiUi disorder, and disoroer of written cxpr~sion.
Etiology
Specinc learning disorders often occur in families. They are presumed to result from fecru cerebral in,jury or from a nClImdc\'c1opmclltal defeo.
Epidemiology
Leaming disorders are relatively conunon. Reading diso~der affects 4% of school-age chi ldren and math· ematics disorder is estimated at 1 %. The incidence of disorder of mitten expression is not yet known. [,earning disorders are two to four times more common in boys than girls.
Clinical Manifestations
History, Mental Status Examination, and Laboratory Tests
Specific learning disorders are typically diagnosed after a child has exhihited difficllities in a specific academic area. Because reading and arithmetic are usuaUr not taught before the first grade. the diagnosis is seldom made in preschoolers. Some children may not be diagnosed until fourth or fifth grade, particuJ arly if they have a high IQ and can mask their deficits. TIle diagnosis of learning disorder is COIl -
Chapt'e r 7 I Disorders of Childhood and Adolescence. ' 39
finned through specific intelligencc and achievement testing. Children with learning disorders do not obtain achievement test scores consistent with their overa1J IQs.
Differential Diagnosis
It is important to establish that a low achievement SC(Ire is not due to some other factor such as lack of opportunity to learn, poor teaching, or Cllit ural factors (e.g., English as a second language). Physical factors (such as hearing or vision impairment) must also be nded out.
Finally, it is important to consider and test for more global disorders such a~ pervasive developmentaJ disorder, mental retardation, and communication disorders. It is n(lt uncommon ta find that several of these disorders coexist. A specific learning disorder diagnosis is made when the full clinical picture is not adequately explained by other comorbid conditions.
Management
Children with these disorders often need remedial education, especially if their d.iagnosis was made late. They also need to be taught learning strategies to overcome their particular deficits. Acceptable skills in the disordered area can often be achieved with steady supportive educational assistance, though patients may be affected hy these disorders through. out adulthood.
KEY POINTS
,. There are three types of learning disorder: mathematics, reading. and written expression.
2, They tend to be familial and are probably due to cerebral injury or maldevelopment.
3. Reading disorder is the most common and all three disorders occur mO(e in boys (2-4:1)~
4. The diagnosiS is confirmed through achievem.ent tests.
5. Physkal or social factors must be ruled out 6. Management involves remedial education and
learning strategies.
• AUTISTIC DISORDER .- -------- _.'--- --- . -- -- -- ----------- --------Autistic disorder is the most common of lhe pervasive developmental disorders of d lildhood onset. It is characterized by t he triad of impaired social interactions, impaired ability to communicate, and restricted repertoire of activities and interests.
Etiology
Auti~'tic disorder is Familial. C.renetic studies demonstrate incomplete penetrance r3b% concordance rate ion monozygotic twins], although a specific genetit: defect has not been discovered. A small pe rcentage of those with autistic disorder have a fragi le X chromosome, and a high rate of autism exists with tuberous sclerosis.
Epidemiology
Autistic disorder is rare. It occurs in two to fi ve children per 10,000 live births. The male-female sex ratio is 3-4: 1.
Clinical Manifestations
History, Menta/5tatus Examinationl and Laboratory Tests
Abnonnal development is usually first noted SOOn after hirth. Commonly, the first sign is jmpainnent in social in1eradions (failure to develop a social smile, facial expressions, or eye-t a-eye gaze). Older ch ildren OftE'Jl faiJ to develop nonverhal Forms of communication (e.g., body postures and gestures) and may seem to have no desire or to lack the skills to form friendships. There is also a lack of seekins to share elljoyment (i.e., not showing, sharing, or pointing uut objects they find i.nteresting). By definition, findings must he pr~nt before age 3.
Autistic disorder is also characterized by a marked impaimlt!nt in communication. There may he delay in or total lack of language development. 1110se children who do develop language show impairment in the ahility to initiate and sustain conversations and use repetitive or id iosyncrat ic language. Language may also be abnormal in pitch, intonation, rate, rhythm, or stress.
< n<lt for 3b. l.e ! :> < ~e .IUI1l npol<!IJ.M ! :>
40 • BllJeprinr.e Psychiatry
Finally, there are usuall}' restrictive, r~pt.."1.itivc, or st€r(."Otyped pattenls of beha\·ior, interests, or aL"1ivities. There may be an encompassing preoccupation with one or more stereotyped and restricted patterns of interest (e.g., amassing basebaU trivia) . an inflexible adherence to specific nonfunctional ro utines or ri tuals (e.g., eating the same meal in the same place at the same time each day), stereotyped or repetitive motor mannerisms (e.g., whole-body rocking), and a persistent preoccupation with the parts of objects (e.g., buttons) ,
Approxi.mately 25% of chi ldreo with autistic disorder have comorbid seizures; approximately 75(~ 1 havE' mental retardation (the moderate ty pe is most common) , EEGs and intelligence testi ng are typically part of the initi al evaluation . Rarely, specific special skills are present, e.g., calendar calculation_
Differential Diagnosis
11l(' diagnosis is usuall y clear after careful history, mental status examination, and developmental monitoring. However, childhood psychOSis, mental retardation (alone), laoguage di.-.orders, and congenital deafne"S or blindness must all be m led ouL
Management
Autistic disorder is a chronic lifelong di<;order with relativ~J), severe morhidity. Very few individuals with autism will ever live independently. O nce the diagnosis is made, parents should be infonned that their child has a neurode.velopmental disorder (not a behavioral d isorder that they might Feel responsible for creating) . They will have to learn bt-.havioral managcmt'nt t~dUlj<iUCS designed to reduce the rigid and stereotyped behaviors of ·the disorder and im prove social function in g. Many children ""ith autism require special education or specialized day programs for behavior management .
Autistic children with a comorbid seizure disorder are tn.'atcd with anticonvulsants. I .ow doses of nellrolcf'tics (e g_1 halop~ridol) and some mood stahilizers and antidepress<l nL<; have heen shown to help decrease aggressive or self-harming behaviors.
ATTENTION-DEFICIT I -'iy~!,~~g:lVJTX. RI.~C::!~.I?~~_ l~I?_IjP 1._._ ADHD is characterized by a persisten t and dysfunctional pattern of overacti vity, impulsiveness, inattention, and dist ractibility.
l~ KEY POINTS _
1. Autistic disorder is a rare pervasive devetopmeotat disorder characterized by impaired social interactions, impaired ability to communicate, .and re.tricted repertoire of activities and interests.
2. It Is fami lial and is associated with fragile X syn-drome and tuberous sclerosis.
3. The comot'bid seiZUre rate is 25~_ 4. The mental felardat ion rate Is 75%.. S. Autistic disorder is managed by behavioral tech
niques and neuroleptics.
Etiology
The disorder lUllS in families and cosegTegates with mood disorders, suhstance use disorders, learning disorders, and ant iSOCial personality disorder, Families with a child diagnoSt."o with ADHD are more li kely than t hose without ADHD offSpring to have family members with the above-mentioned. disorders.
'The et lolob'Y of tbe disorder is unknown, hut perinatal injury, maiJwtritiun , and substance exposure have all been implicated. Many children with ADHD have ahnonnalitics of slee p architecture (decreased rapid eye movement latency, increased delta latency), [EG, and soft n<.'urologic signs.
Epidemiology
·n 1E' preva lence of ADHD in school-age children is estimated to be 3% to 5%. The boy-girl ratio ranges from 4 : 1 in the gcm.'ral populatioll to 9 : 1 in clinical settings. Boys are much more likely than girls to be brought to medical attention.
Clinical Manifestations
History, Mental Status Examination, and Laboratory Tests
To meet criteria for ADHD, a child must evidence the onset of inattentive or hyperactive symptoms befor~ age 7; symptoms must also be. pre...;;ent in two or more settings (eg., school, home). Symptoms in only one setting suggest an environmental (lr psychodynamic cause.
Preschool-age children are usually brought ror eva luation when they are unmanageable at home.
Chapter 7 / Disorders of Childhood and Adol~ence . 41
Typica lly, they stay up late, wake up early, and spend most of their waking hours in various hyperactive and impulsive activities. Children with a great de~1 of hyperactivity may Hterall}, run about the house, cause damage, and wreak havoc.
When these children enter school, thEir difficulties with attention become more obvious. T hey appear to not filUmv directions, fo rget impurtant school supplies, fail lO complete homework or inclass assigmnents, and attem pt to blurt out answers to teachers' questions hefo re being called on. As a result of their inattention and hyperact i\,ity, these children often become known as "troublemakers." They fall behind their peers academically and socially.
Evaluation of the child in volves gathering a carefu l history from parent.'> and teachers (the latter usually through report cards and written reports). The chiJd's behavior with and without the parent is carefuJiy obselv ed dUring psychi atric assessment. Informal testing is carried ou l by baving the child attempt to complete a simple puzzle, writ(' the letters of the alphahet, distinguish right from left, and recognize letters traced on the palms [graphesth esia) . Physical eXamination, particularly focusing on 11t'.UroJogic fuoction, is imperative No specific laboratol)' or cognitive tests are helpful in making the diagnosis.
Differential Diagnos;s
It is important to dist inguish symptoms of ADHD from age-appropriate behaviors in active child rell (running ahout, being m.1isy, etc. ). Child ren can als(l appear inattentive if they have a low or a high IQ and the environm ent is overstim ulating or understimulating, respective ly. In either instance, IQ testing and careful evaluat ion of the school program will clarify the diagnosis.
Children with oppositional defiant disorder rna)' resist work or school tasks because of an unwiUingness to comply with others' demands but not out of difficulty in attention.
Children with other mental disorders [e.g., mood disorder, anxjety disorder) C.M exhihit inattention but typically not before age 7. The child's history of school adjustment is not usually characterized by teacher or parent reports of inattentive, disruptive behavior.
Symptoms that resemble ADHD can occur in children before age 7, hut the etiology is typically a side effect of a medication (e g., bronchodilators) or a psychotic Or pe rvasive developmental disorder;
these children 3re not considered to have ADH D. Of course. ADHD may be comorbid with any of the above disorders. A dual diagnosis is made only when it is needed to explain t he full clinical picture.
Management
T he man~ement of ADHD involves a combination of somatic and behavioral treatments. Most children with ADH D respond fa\'orahly to psychm.-timulaJlfs . Methylphenidate is the first-line agent, folJowed by o-ampbetamine. Cli nid ans try to use the small est effective dose and to restrict use to periods of greatest need (i. e., the school day) because psychostimulants have undesirabk long-term phys ical erfects (weight loss and in hibited body growth). Some child ren can be treated effectively with agents t hat raise nurepinephrine in the brain, such as hupropion (\¥ellbutrin) or atomoxetine (Strattera) a norepinephrine reupt ake inhihitor.
Behavioral management techniques include positive re inforcement, firm limit setting, and techniques for reducing stim ulat ion (e.g. , one playmate at a time; short, focused tasks).
KEY POINTS
1. AOHD disorder is characterized by inattentivenes!i and hyperactivity occurring in multi~e settlngs.
2. Symptom!i must begin before age 7. 3. AOHD is more common in boY!i (4: 1).
4. For a diagnosiS of ADHO, other causes of inattentivene!is or hyperactivity must be ruled out.
5. ADHO Is managed with p!iychostimulants and behavioral techniques.
• CONDUCT DISORDER AND OPPOSITIONAL DEFIANT DISORDER
Cond uct disorder is defined as a repet itive and persistent pattern of beha\'ior in which the basic rights of (Ithers or impo rtant age-appropriate SOcietal nonns or rules arc violated. I.)isordered behaviors indllde aggression toward people or an imals, destruct ion of property, deceitfulness, theft, Or serious vio-
-< not f or s ale ! > < He ll.II.R npo,llavo ! :>
42 • 51uerirint5 Psychiatry
lat~ons o f rules (school t ruilncy, runnIng away). Conduct disorder is the childhood equivalent 01 adult antisocial personality disorder (ASP) . It. is the most common dist1rder scen in outpatient psychiatric elinics and is frequently seen comorbidly ,,\lith ADHD or learning disorders. Adoption studies show a genetic predisposition, hut psychosocial b etors playa major role. Parental separation or divorce, parental substance abuse, severely poor or inconsistent parenting, and (lssociation with a delinquent peer group have been shown to have some rel(ltionship to the development of conduct disorder.
'TI-eatment invoJve~ individual and family ther<lpy. Some children may need to he remuved from the home and placed in foster C(lre. P(lren~ .. who retain custody ~lf a child \.'lith conduct disorder are taught limit setting, umsistency, (lnd other behilvioral techniques. Medications are used only to treat a cOm orbid ADHD or mood d isorder but not for the conduL1: disorder itself The long-term out,come depcnd~ Oil
the severity of the disorder and the degree and type of comorhidity. Twenty-five percent to 40% of children with mnduct disorder go un to have adu1t ASP.
Oppositional defiant diwrder is diagnosed in dUldren with annoyin& difficult, or disruptive bc.l1<l.vior when t.he rrequency of the hehavior signilicantly exceeds that of other dUldren his OJ her mental age (or that is le~s tolerated in the child·s particular culture).1t is a relatively new diagnosis that is meant to describe children with behavior prllhlems that do not meet criteria for full-blown conduct disorder. Management emphasizes individual and family counseling.
• KEY POINTS rJl
,. Conduct disorder is the childhood equivalent of ASP.
2. It is defined by observable measurable behaviors. 3. Conduct dIsorder is the most common diagnosis
in olltpatient child psydliatric dinics. 4. It is managed by limit .setting, consistency, and
behavioral techniques. 5, Oppositional defiant disorder Is a less severe form
of conduct disorder.
TOURETTE'S DISORDER ---~ ------~- ------- -.- ----- ---- ---- -------'I burette 's dis(Jrder is a rare disorder in which the child dc:rm.mstrates multiple invol untary motor <md vocal tics. A til: is a sudden , rapid , recurrent, nonrhythmic, stereotyped motor movement flf
vocalization.
Epidemiology
Tourette·s di<;ord£'r <!ffects 0.4% of the population. There is a 3 : 1 male-female ratio.
Etiology
Tourette's disorder is highly fam ilial ami appears to frequently co-occur with obsessive-compulsive disorder. Despite evidence of genetic transmission in som e families, no genE' ( or genes) h<!s yet been discovered tn explain the etiology of the disorder.
Clinical Manifestations
History, Mental5(atus and Physical Examinations The patient or family usually describes (In tJnset in childhood or early (ldolescence before age 18. VOC;;!! tics are usually loud grunts or harks but c<!n involve shouting words; the words are Sl)J,nctimes obscenities (coprolalia). The patient describes being aware of shouting the wllrds, being able to exert some control over them, hut being ovel\'1he1med by an tltlcontrollable urge to say them. Motor tics can involve fadaJ grimacing, tongue protrusion, blinkln g, snorting, (lr larger movemenL .. of' the extremities or whole body. Molor tics typically antedate vocal tics; harks or grunts typically a ntedate verbal shouts. The mot.ur tics are not painful.
Differential Diagnosis A careful neurologic evaluation should be performed to rule out other causes or tics. vVilson's disease and Huntington's di<;ease are the principal differentia.l diagnostic disordcrs. An EEG should be performed to rule out a seizure disordel: Careful evalua tion for other comorbid psychiatric illnesses shouJd be perfo rmed. Stimulants used to treat other psychiatric d isorders may unmask tics.
< <lot f ox s"lel :> < >Ie ,llftR npoJlS"''' I ;>
Chapter 7 I Disorders of Childhood and AdQI~cence • 43
Management
Treatment typically involves the use of low doses of high-potency neuroleptics such as haloperidol or pimo:dde. The dUld and h is or her family should receive education and supportive psychotherdPY aimed at minimizing the negative social consequcm:es (c.g., cmharra'\.<;mcnt, shame,. isolation) that occur with this d isorder.
KEY POINTS
1. Tourette's disorder is a tic disorder. 2. It Is rare and more common in males (3: 1). 3. When diagnosing l aurette's disorder, Wikon's and
Huntington's diseases must be ruled out. 4. It is treated with high-potency neuroleptics and
patlent/family support.
The cognitive disorders are delirium, dementia, and amnestic disorders. Table 8-1 lists the Diagnostic and Statistical Manual of MenIal Disorders, 4th edition, dassincation of cognitive disorders.
• DELIRIUM
Delirium is a reversible state of global cortical dysfunction characterized by alterations in attention and cognition and produced by a definable precipitant. Deliliwn is categorized by its etiology (see Table 8-1) as due to general medical conditions, substancerelated, or multifactorial in origin.
Etiology
Delirium is a syndrome \·"ith many causes. Most frequently, delirium is the result of a general medical condition; substance intoxication and \vithdrawal also are common causes. Structural central nervous system lesions can also lead to delirium. Table 8-2 lists common general medical and substance-related causes of delirium. Delirium is often multifactorial and may be produced by a combination of minor illnesses and minor metabolic derangements (e.g., mild anemia, mild hyponatremia, mild hypoxia, and urinary tract infection, especially in an elderly person). Common medical causes of delirium include metabolic abnormalities such as hyponatremia, hypoxia, hypercapnia, hypoglycemia, and hypercalcemia. Infectious illnesses, espccially urinary tra<.t infections, pneumonia, and meningitis, are often implicated. The common substance-induced causes of delirium are alcohol or benzodiazepine withdrawal and bem.odiazepine and anticholinergic drug
toxicity, although a greaLnumber of commonly used medications, prescribed and over the counter, can produce delirium. Other conditions predisposing to delirium include old age, fractures, and preexisting dementia .
Epidemiology
The t2xact prevalence in the general population is unkllOV\'l1 . Delirium occurs in 10% to 15% of general medical patients older than age 65 and is frequently seen JXlstsurgically and in intensive care units. Delirium is c.-qually common in males and females.
Clinical Manifestations
History and Mental Status Examination
History is critical in the diagnosis of delirium, particularly in regard to the time course of development of the delirium and to the prior existence of dementia or other psychiatric illness. Key features of delirium are
I . Disturbance of consciousness, especially attention and level of arollsel;
2. Alterations in cognition, especielly memory, orientation , languege, end perception;
3. Development over e period of hours to days; and 4. Presence of medical or substance-related
precipitants.
In addition, sleep-wake cycle disturbances and psychomotor agitetiun may occur. Delirium is often difI1cult to separate from dementie, in part because dementia is a risk factor for delirium (and thus they frequently co-occur) and in part becallse there is a great deel of symptom overlap, as outlined in
not t e l: 'lOuIel > < "" j:lJlR r!J>C',I\4lD1 I >
Delirium
General medical Subst~related
Multifactorial
TABLE 8-2
~""'I#DeII*
General Medical
tnfectiOU$ Urinary tract Infections Meningitis Pneunonia Sepsis
Metabolic Hyponatremia Hepatic encephalopathy Hypoxia Hypercarbia Hypoglycemia Fluid imbalance Uremia Hypercalcemia
Postsurgical H:,per/hypothyroidism IctaVpostictal Head trauma Miscellaneous
Fat emboli syndrome Thiamine defidency Anemia
Chapter B I Cognitive Disordefs . 45
Dementia Amnestic
AIzhei""'" type Vascular or;gin HIV-relared
General medical Substance-related
Head trauma-related \Parkinson'i-reiated Huntington's-related Pick's-related Creutzfeldt-Jakob-related General medical origin Substance-related Multifactorial
Substance-Related
IntDlCKation Akohol HallUCinogens Opioids Marijuana Stimulants Sedatives
Wrthdrawal Akohol Benzodiazep;nes Barbiturates
Medication-induced Anesthetics Anticholiner:gic:s Meperidine Antibiotics
TcxirlS Carbon monc:ucide Organophosphat~
deficits are generally more stable. In both conditions, there may be nocturnal worsening of sy mptoms with increased agitation and confusion ("sun4owning") .
TIle diagnosis of delirium is complicated by the [aLt that there are nO definitive tests fOT delirium. The workup for delirium ind udes a thorough history and mental statlL'i examination, a physical examination, and laboratory tE':"ts targeted at identifying general medical and substance-related causes. These should include uli nalysis, complete chemistry panel, Complete blood. count, and oxygen saturation . Additional workup might entail chest X ray, arterial blood g:Js (AHG), neuToim::lging, or electroencephalogram (EEG). EEG may reveal nonspedfic diffuse slOWing. The presence of a delirium is associated ""ith a I-year mortality rate of 40% to 50%.
Differential Diagnosis
Delirium should be differentiated from dementia (although both can be present at the same time), psychotil· or manic disorganization, and status complex partial epilepsy.
Management
Table 8-3. Key differentiating faLtors are the time (ourse of development of the mental status change (especially if the patient did not have a prim demcntia) and the prc.<;cncc l)f a likely precipitant for the mental status change. Individuals with delirium may also display periods of complete lucidity intersJX'rsro with periods of confusion, wherea<; in dementi~, the
11le treatment of delirium involves keeping the patient safe from harm while addressing the delirium. In the case of delirium due to a general medical ill ness, the underlying illness must be treated; in sub!;tancc·relatcd delirium, U"eatment involves J"cmoving the offending drug (either drugs of abuse or medications) or tJ,e appropriate replacement and tapering or a cross-reacting drug to m in imize withdrawal. Delirium in the elderly is frequently multifa<.1"orial
«: not f or sale ! " < He llJlR npollllDl ! ::;,.
46 • BhJtlpri r18 Psychiatry
, . TABLE 8-3
Delirium versus Oement~
Delirium Dementia
Hours to days Weeks to years Onset
Course/duration Fluctuates within a day. May last hours to weeks"
Stable within a day. May be permanent, reversible, or progressive over weeks to years
Impaired May be impaired Attention
Cognition Impaired memory,orientation,language Impaired memory. orientation, language, executive function
Perception
Sleep/wake
Hallucinations, delusions, misinterpretations
Disturbed, may have complete day/night reversal
Hallucinations, delusions
Disturbed, may have no pattern
Mood/emotion
Sundowning
Identified precipitant
labile affect
Frequent
likely precipitant Is present
labile affect; mood disturbances
Frequent
Identifiable precipitant not required
• OSMoN doe-< nol 'P"<ify a limit for t ..... duration for defirum; dfnlGlI ,,~~~ ""99"~t' rBoIution with in days to weeks.in most caS("i.
and requires correction of a multitude of medical conditions.
In 3ddition to addressing the cause of a delirium, oral , intramuscular, I.)r intravenous haloperidol is of gre2t use in treating 2gitation. LQw doses of shortacting bem.odinepines can be used ~pari ngl y- Providing the patient with a brightly lighted room with o rienting cues su ch as names, d ocks, and calendars is also useful.
It' KEY POINTS ,:;
1. Delirium is a disorder of attention and cognition. '2. 11 has an abrupt onset and a variable course. 3. It has an identifiable precipitant. 4. l-year mortality rate is greater than 40%.
DEMENTIA
Dementia is cilaracterlzed by the presence of memury impairment in the presence of other cognitive. defects. Dementia is categorized according to its etiology [see Table 8-1). It can arise as a rcsult of a specific disease, for example Al zheimer's d isease or HIV infection; a general medical condition; or a substance-related condition; o r it can h3ve multiple etiologies. The detinitivc cause may not be determined until autopsy.
Etiology
Generally, tile etiology of dementia is brain neuronal loss tllat may be due to neuronal degeneration or to cell death secondary to trauma, infarction, hypoxia, infcctit)n, or hydrocephalus. Table 8-1 lists the major discrete illnesses kJIo\ ... ·n to produce dementia. In additiun, there arc a large nlUllber of general medical, substance-related, <lnd multifactorial causes of dementia .
Epidemiology
The prevalence of dementi2 of all types is abo"ut 2% to 4% 2fter 2ge 65, llneasing with age to a prevalence of about 20% after age 85. Specific epidem iologic factors relating to di"ease-specihc causes of dementia are ICited in Table H-4.
Clinical Manifestations
History and Menta/Status Examination
Dementia L" diagnosed in the presence of multiple cognitive defects not better explained by 2nother diagnosis. TIle presence of memory loss is requiredj in addition, one or more cognitive defe<.ts in the categorie~ of aph2sia, aprdxia, agnosia, and disturbance in executive function must be present. Table 8-3 compares charat.teri."tics of dementia to those of delirium. Dementia often develops insidiously over the course of weeks to years (although it may be
Chapter B I Cognitive Disorders • 47
Alzheimer's Most common caUse of dementia, accounts for greater than 50% of all cases. Risk factClf'S are familiaL Down syndrome.. prior head trauma, increasing age. Clinically, It is a diagnosis of exclusion Post·mortem pathology reveals cortical atrophy, neurofibrillary tangles. amyloid plaques, granulovacuolar degeneration, k>ss of basal f~jn choJinergic nodei. Course is progressive. death occurs 8-10 years after onset.
Vascular Second most common cause of dementia. Risk factors are cardiovascular and ce,rebrovascular disease. Neuroimaging reveals multiple areas of neuronal damage. Neurological exam reveals focal findings. Course can be rapid onsetor more slowty progressive. Deficits are not reversible, but progress can be halted with appropriate treatment of vascular disease.
HIV Limited to those cases caused by direct action of HIV on the brain; associated illnesses, such as meningitis. lymphoma, toxoplasmosis producing dementia all! care,gorized under dementia due to general medIcal conditions. Primarily affects White matter and cortex.
Head trauma Most common among young males. Extent of dementia ts determined by degree of brilin damage. Deficits are stable unless there is repeated head trauma.
Palkinsoo~ Occurs in 10-60% of individuals with Paridnson's disease. The most likely pathological finding on autopsy is Uwy body disease. 8radyphren'a (slowed thinking) is common. Some indMduals a lso have pathology at autopsy consistent with Alzheimer's dementia.
Huntington's Risk ractors are familial, autosomal dominant on chrom.osome 4. Onset commonly in mid 30s, Emotional lability is prominent. Caudal'e atrophy is present on autopsy.
Pick's Onset at age 50-60. Frontal and lemporaj atrophy are prominent on neuroimaging. The dementia responds poor1y to psychotropic medicine.
Creutzfeldt-Jakob Ten percent of cases are familial. Onset age 40-60. Prion ts thougt'( to be agent of transmission. Clinical triad of dementia, myoclonus. and abnormal EEG. Rapidly progressive. Spongiform encephalopathy is present at autopsy.
abrupt after head trauma or vascular insult). individuals with dementia usually have a stahle presen· tali on over brief periods o f t ime, although they may also have nocturn al wor~ning of symptoms ("sun downing"]. Memory impairment is often greatest lo r short-tcnn memory. Recall u r names is freque ntly impaired, as is recognition of ramiliar ubjet.1:s. Exec· utivc functions of organi:7.at ion and planning may be lost. Paranoia, hallucinatiuns, and delusions arc o rten present. Eventually, ind ividuals with dementi a may hecome mute, incont inent, and bedridden.
Differential Diagnosis
Dementia shoul&be d ifferentiated From delirium. In add it ion , dementia should be differentiatc:d from those devd upmental disorders (such as mental retardatio n) with impaired cognition . Individ uals ·with major depression and psychusis can appear d emented; they warrant a diagnosi" o f dement ia only if their cognitive dehcits cannot be fu ll y attributed to the primary psychiat ric" illness.
A critical component of differential d iagnosis in dementia is to distinguish pscudodementia associ· ated with depression. Although there are many pred..<>e <.Titeria ror separating t he. two di.'tOrders, neurQpsychological test ing may be needed to make an accurate diagnosis. In pscududementia, maud symptOmS are prominent and patients may complain e).1:en:-ively o f memory impairment. They character· istkaUy give i don 't know" an~wcrs to mental st atus examination queries but may anS\ver correctly if pressL-d. Memory is inta<.1. with rehearsal in p5(.."Ududementia, but not in demcntia.
Management
Dementia from reverSible, o r treatable, causes sho uld be managed first by treating the underlying cause of the dementia; rehabiJitacion may be requ ired ror residual deficits. Reversible (or partially reversible) causes of dementia indude normal pres~re hydrocephalus; neurosyphilis; HIV infection ; and thiamine,
<: not f or s ale! " < He JllUI npoll""'" ! "
48 Bluepr'lnu. Psychiat ry
lolate, vitam in B12, and niacin deficiencies. Vascular dementias may not be reversible, but their progres,'. can be halted in some cascs. Nonreversible dementias arc usuall y managed by placing the patient in a safe cnvironment and by medications targeted at associated symptom s. Tacrine, an acetylcholinesterase inhibitor, has some ef1'icaq' in treating memory loss in dementia of the Ah·Jlcimer's type. r Iigh-potency antipsychot ics (in low doses) are used when agitation , paranoia, and hallucinations arc present. Lowdose bem.odiazepines and trazodone are often. used for anxiety, agitation . or insomnia.
I\" KEY POINTS o! 1. Dementia is a disorder of memory impairment
coupled with other cognitive defects. 1 . It has a gradual onset and progressive course. 3. It r(lay be caused by a variety of illnesses. 4. Dementia predisposes to delirium.
• AMNESTIC DISORDERS
Amnestic disorders are isolated disturbances o f memory without impairment of other cognitive functilms. 'TIley m ay be due to a gencral medical condition or substance related.
Etiology
Amnestic disorders are caused by general medical conditions or substance use. Common general mtC-dical conditions include head trauma, hypoxia, herpes simplex encephalitis, and posterior cerebral art""I)' infarction. Amnestic disorders often are associated with damage of the mammillary bodies. fornix, and hippocampus. Bibteral damage to these structures produces the most severe defi ci t.<;. Amnestic disorders due to substancecrela ted causes may be due to substance abuse, p rescribed or over-the-, counter medicetions, or ecddental exposure to toxins. Alcohol abuse is a leading cause or substellcerelated am nestic disordcr_ Persistent alu..lhol use may lead to thiamine deficiency and induce WernickeKorsakofr's syndrome_ If properly treated, the acute symptoms of ataxia, abnormal eye movements, and
confusion J,TIay resolve, leaving a residuaJ amnestic disorder called Korsakoff's psychosis (alcoholinduced persistent amnestic disorder).
Epidemiology
Individuals affected by a general medical condition or alo)holism are at risk for aIlmestic disorders.
Clinical Manifestations
History and Mental Status Examination
Amnestic disorders present as deficits in memoryl either in the inability to recall previously learned informatio n or the inability to retain new information. The cognitive defect must be limited to memory alo ne; if additional cognitive dclccts are present, a diagnosis of dementia or delirium should be consid ered. In addition to defect in memory. there must bc an identifiable cause fo r the amnestic disorder (i .e., the presence of a geneT<l1 medical condition or substance useJ .
Differential Diagnosis
Delirium and dementia arc the major d iHerential diagnostil~ considerations. Amnestic disorders arc distinguished from dissociative rusol·ders on the basis of etiology. By definition, amnestic disorders arc due to a general mcdical condition or substance.
Management
The general medical condition is treated \ ..... henever possible to prevent furthcr neurologic damage; in the case of a substance-related amnestic disorder, avoiding reexposure to the substance responsible for the amnest ic disorder is critical. Pharmacotherapy may be direct.ed at treating assodated anxiety or mood difficulties. Paticnts shou ld be placed in a safe, stru.ctured envimmnent. , \lith rrequent ml"lTlU1"y cues.
,"'! KEY POINTS '-II '1. Amnestic disorders are disorders in memory
alone. 2. They are caused by identffiable precipitants. 3. Amnestic disorders are reversible-in some cases.
Miscell aneous disorders docs not refer to any official Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSrvl- IV) classification but rather to psychiatric diagnoses not covered eisev-... here in this book. Generally, these diagnoses are either less common, less understood, or less frequently the focus of psychiatric practice than the d isorders previously covered. Although many o f these disorders are not uncommon, they seldom come to psychiatric attention for a variety of reasons (e.g., they may be treated by other medical specialists, patients may not mention them, or they may not be detected adequately). Table 9- ) lists the categoTies of disorders discussed in t his chapter.
• DISSOCIATIVE DISORDERS
Dissociat ive disorders are characterized by disturbances in the integration of mental functions. These disturbances are manifested by loss of memory for personal in form ation or identity, division of consciousness and personality into separate parts, and altered perception of the environment or sense of reality. Table 9-2 lists DSM-IV detined dissociative disorders.
Dissociativ~ Amnesia
In dissociative amnesia, an individual develops a temporary inability to recall im(.K)rtant personal informat ion. The amnesia is more extensive than forgetfulness and is not caused by another medical or psychiatric condition (e.g., head tnmma). The inability to rccall informati<.m may take several forms. In localized amnesia, in formation is lost for a speci tic time period (e.g. , a time associated with trawna). In selectiye amnesia, some information during a given
time period is retained but other information is lost. In gcncrnlizcd amnesia, personal information is lost for the crJtire life span. In continuous alllncsia, there is an inability to recall information from a single point in time to the present. In systematized an1llCSi:'l, particular categories of information arc lost to retrieval.
Dissociative amnesia is more common in people exposed to trauma, for example, exposure to battle or natural ois<lster.
Dissociative Fugue
Dissociative fugue is an amnestic disorder ch aracterized by an individual's sudden unexplained travel away from home, coupled with amnesia IiJr his or her identity. In this condition, patients do not appear mentally ill or otherwise impaired in any other mental function, including memory. In fact, patients are quite capable of negotiating the complcxitic.'S of travel and interaction with others. In rare cases, an individual will establish a completely new identity in the new home. Dissociative fugue is typically precipitated by a severe trauma or stressor and eventually remits without treatment.
Dissociative Identity Disorder
Dissociative identity disorder (formerly called multiple personality disorder) is a controvcn.:ial d iagnosis in psychiatry. The diagnosis of dissociative identity disorder requires the presence of two or more separate personalities (alters) that recurrently take control o f an individual's behavior. Individuals with this disorder often have amnesia for important personal information (also known as "losing time") . The various personalities (the average number by available surveys is seven di.stinct personalities) may be
«: not f o r sale ! ::> < He llJlR 1IpO.IlllD! ! ::;.
so • BlUe.pri l1 t5 PsychIatry
- TABLE 9-1
Miscellaneous Disorders
Dissociative disord~rs 5Omatoforrn disOfders Adjustment disorders Sexual and gender identity disorders Sleep disorderS" Factitious disorders/malingering
., TABLE 9-2
Dissociative Disorders
Dissociative amnesia
Dissociative fugue
Dissociative identity disorder
Depersonalization diSOf'der
Temporary inability to recall important personal information; more serious than simple forgetfulness
Amnesia for one's identity coupled with slidden unexplained travel away fTom home
Presence of two or more separate personalities that recurrently take control of a person's behavior
PerVasive sense of being detached from or- being outside of one's body
unaware Or cach other 's cxi'>tence and thus may be quite confused as to how they arrived at certain places or why they cannot recall personal cvcnts. At other timcs, one or more personaL ties may be av,r-are of the others, a condition known as coconsciousncss. Somc personalities may display conversion symptoms or self-mutil ating behavior. The altcrs may be of varying ages and different genders and demeanors.
Dissociative identity disorder is most common in fem ales and has a chronic course. Individuals with dissociative identity disorder are highly suggestible and easily ,hypn(ltized. Must report a childh(lod history of severe- physical or sexual abusc. Satanic or cult abuse report..~ are also common. [n many cases, these reports of abuse cannot be verihed , leading many clinicians to believe that individuals ,vith clissociative identity disorder may suffer frll111 memories o f events th at did not occur. \"Ihether these memories are truc or false, they cause a grc<lt deal of suffering.
Djs(lgreement over the very nature of dbsociative identity d isorder h(ls led to d ivergent treatment opin-
ions. Some clinicians believe th(lt ignoring the different personalities will cause them to recede; based on the notion that the easy suggestibility of these patients will lead to reinforcement of alters if they are discussed. Others believe that long-tenn psychotherapy, exploring- the various personalities and integrating them into a whole person, is the treatment of choice.
Depersonalization Disorder
Depersonalization disorder is characterized by "persistent or recurrent experienccs of feeling Jet,adled rr0111 and as if one is an olltside observer of one's mental processes or body" (DSM-IV). Individuals with this disorder may complain of a sense(l[ detachment, of feeling mech.mi'cal l..lr automated, and of absence. of affect or sensation. IndiViduals with depersonalization disorder arc easily hypnotized <md prone to dissociate.
SOMATOFORM DISORDERS . . ... - ------- - . _ ... -----Somatofoml disorders are dlaracterizcd by dJe presence or physical signs or symptoms without medical cause. In <ldclition. the.y (Ire not willfull y produced by the individual. The somatoform disorders are listed and defined in Table 9-3 (ldapted from DSM-IV).
Somatization Disorder
Somatization disorder is diagnosed when an individual has multiple medical complaints th(lt are not the resu lt of medical illness. The specific DSM-IV criteria are narrow and specific, requiring
• Pain in four different body sites or involving four different body functions;
• Two gastrointestinal symptoms (other than pain) ; • One scxual symptom (other than p ain) ; and • One pseudo neurologic symptom (other th an
pain).
In addition, some symptoms must have begun before age 30 and persisted for se veral years. Individuals with somatization disorder often have a history of complex medical and surgical treatments that may actually lead to iatrogenic complications of treatment. Patients , .... ·ith somatoform disorder frequently havc multiple phYSicians, m ake Frequent office and hospital visit.s, and may seek disability because of their conviction that thcy arc severc.ly and chronically medically ill.
< flOt: fOr :sA l el > < iii' ,IOJ!R nJ'O.l<"II:>! I >
Chapter 9/ Miscellaneous Disorders • 51
- TABLE 9 -3
Somatization disorder Chronic multiple medical complaints that include pain,gastrointestinal distuibance. sexual symptoms, and pseudoneurologk symptoms that are not due to a medical Illness.
Undifferentiated SOI'Tl<!toform disorder A X!ss ~ form of somatization disorder; involves fewer complaints and br'iefer course.
Conversion disorder Complaints involving sensory (such as numbness) and 'oduntary motor (such as paralysi5J function that are not due to neurologic dysfunction.
Pain disorder Pain is the major complaint. If medical causes are present, psychological factors have a major role in mediating the expression and impact or pain.
Hypochondriasis Preoa:upation with having a serious disease based on a misinterpretation of bodily function and sensation.
Body dysmorphic disorder Excessive concern with a perceived defect in appearance.
This disorder is more CI • .lmmon in remales (approximately 80% of cases), and its incidence is increased in first-degree relatives of those with somatiz ... tion disorder. F<lmilial and genetic !>wdies have also shown that male relatives of individuals with somatization disorder have an increased incidcncc of antisocial personality disorder (ASP) and substance abuse. Adoption studies suggest genetic influences in th is d isorder.
Various throries have been proposed to explain this disorder. Early psychoanalytic work focused on rcpn::ss(:d instincts as causative; more modern theorists propose that somati;o;ation symptoms may represent a means of nonverbal interpersonal communication. Bioklgic findings have revealed abnormal corlical function in somc individuals with this disorder.
• ADJUSTMENT DISORDERS
AccorcLng to LJSM-IV, adjustment disorders are symptoms (changes in emotional state or beluwiors) t.hat arise in response to an identified psychosodaJ stressor that is out o f proportion to what is expected in usual hwnan experience. Adjustment disorder is not diagnosed if the symptoms occurred in re>ponse to a psychosocial stressor so severe that an indi"id~ ual meets criteria for another axis I disorder (e.g., major depression) . Symptoms in response to bereavement do not meet criteria for the diagnosis of adjustment d isorder. Adjustment disorders occur within 3 months of the identifIed stressor and usually resolve .... -ithin 6 months, l1nlc..~ the stressor becomes chronic.
• SEXUAL AND GENDER IDENTITY DISORDERS
The DSM-I V classifies these disorders into se..xual dysfunctions, paraphilia, and gender identity disorders.
Sexual Dysfunctions
Sexual dysfunt~tions are sexual disorders associated with alterations in the sC),:ual response cyde (Table 9-4) or ... vith pain associated with sexual activity.111e spedfil~ sexual dysfunctions are defined in Table 9-5.
Paraphilias
Paraphilias include sexual disorders related to culturally unusual sexual activity (Table 9-6). A key {.Ti-
Desire Initial stage of sexual response;consists of sexual fantasies and the urge to have
""'-Excitement Consists of physiologic arousal and
feeling of sexual pleasure.
Orgasm Peaking selCual pleasure; usually associated with ejaculation in males.
ResolUtion Physiologic relaxation associated with sense of well-being. In males, there is Usually a refractory period for further excitement and orgasm.
< not foc "al .. ! :> < He llJUI npolI"'"'" ! ::>
52 • B1t:eprint6 Psychiatry
• TABLE 9·5
Sp&cific Sexual Dysfunctions
Sexual desire disorders Hypoactive sexual desire disorder Sexual aversion disorder
Sexual fantasy and desire for sexare very low or absent. Aversion to genital sexual contact with another person.
Sexual arousal disorders Female sexual arousal disorder Inadequate vaginal lubrication and inadequate engorgement of external
genitalia. Male erectile disorder Inability to attain or maintain an erection.
Orgasmic disorders Ferpale orgasmic disorder Male orgasmic disorder Premature ejaculation
Orgasm is absent or delayed. Sexual excitement phase IS nomlal. Orgasm is absent or delayed_ Sexual excitement phase is normal. Orgasm and ejaculation occur early and with minimal stimulation.
Sexual pain disorders Dyspareunia Vaginismus
Genital pain in association with sexual intercourse. Involul)tary co'1traction of extemal vaginal musculature as a result
of attempted penetration. Sexual dysfunction due to a general medical condition Substance-induced sexual dysfunction
TABLE 9·6
Paraphilias
Exhibitionism
Fetishism
Frotteurism
Pedophilia
Sexual masochism
.sexual sadism
Transvestic fetishism
Voyeurism
Sexual excitement is derived from exposing one's genitals to a stranger.
Nonliving objects are the focus of intense sexual arousal in fal)tasy or behavior.
Sexual excitement is derived by rubbing one's genitals against or by sexually touching a nonconsenting stranger.
Sexual excitement is derived from fantasy or behavior involving sex with prepubescent children.
Sexual excitement is derived from fantasy or behavior involving being the reCipient of humiliation, bondage, or pain.
Sexual excitement is derived from fantasy or behavior involving inflicting suffering/humiliation on another.
Sexual excitement (in heterosexual males) is derived from fantasy or behavior involving wearing women's clothing.
Sexual excitement is derived from fantasy or behavior involving the observation of unsuspecting individuals undreSSing, naked, or having sex.
tefion ror the diagnosis or a paraph ilia (as in all psychiatric disorders) is that the disorder must caus£' an individual to experience signi(lcant distress or impainnent in soda l or occu pational functioning. In other words, an indiVidual \vith unusual sexual practices who does not suffer signillcant d istress or impairment would not be diagnosed with a psychiatric illness.
Gender Identity Disorder
Gender identity disorder remains a controversial diagnosiS in psychiatry. Individuals \ ... ;th this disorder experience di.~tr('-',.~ and interpersonal impairment as a result or thdr desire to he a member or the opposite sex. Criteria ror the diagnosis require a pervasive cro.,,-,,-gendcr identification and persistent discomfort \ .... ith one's as.~igned sex. In addition, the diagnosis is made only in those individuals who do not have an
< not; r" c ,. .. h ol :> < '''' J:I}tJI "PO ......... I :>
intf1"sex condition (c.g., ambiguous gen italiA). Children with this disorder may engage in genderatypical play; adults may assume the societal role, dress, and behavior associated \vith the opposite sex. In addition, patients with gender identity disorder may seek sex reassignment .<:urgery and honnonal supplements. individuals with gender identity disorder appear to have the same range of sexual orientations as do persons wiLhout this disorder.
• SLEEP DISORDERS
Sleep disorders are illnesses rdated to alterations in the sleep-wake cycle (Table 9-7) and often have effect." on mood, cognitive, somatic, iJnd general performance. Table 9-8 outlines the OSM-IV classification or sleep disorders. Sleep disorders are categorized into primary and secondary sleep disord('fS.. Primary sleep disordeno are those disorders occurring as a direct resoJt of disturbances in the ~;le('p-wake cycle. They are divided into two cate-
TABLE 9-7
Nomapjd eye movement (NREM) Stage 0 Awake. Stage 1 Very light· sleep. transition from
wakefulness to sleep. Drowsy. Stage 2 Medium depth of sleep. occupies
Delta
Stage 3
Stage 4
REM
abollt half the night in adults. Serves as a transition stage between
rapid eye mavement (REM) and delta sleep. EEG demonstrates sleep spindles and k-complexes.
stow wave sk'ep, composed of stages 3 and 4. occupies 1 0--3~oftota l
sleep. Consists of a moderate amount of
delta wave activity; deeper sleep than stage 2,
Increased delta wave activity aver stage 3. Very deep stage af sleep.
Oteam sleep. EEG is active. mimicking that of the waking stage.
Depth of sleep is greater than stage 2 but probably less than deha,
• ~h 01 \Io!ep iI\ uwd ~ Is nOl II "'~ tf!fTll buI: ~Iy I~ It> ""'-"'! 01 arouwbiliry a.e.. how hatd ""'IOOJId it be 10 -....ken an indiYi6-uallmm iI poVtiaAar ~1"91!).~, the ea§e 01 arDl6ilbility ;~ due in patt to the typPcl ~ltll1lAu!. uml (e.g. flQh.e~ tt;oUI;h).
Chapter 9 I Miscellaneous Disorders - 53
gones: dyssomniao; and parasomnias. Secondary sleep di .<:orde.-s are a consequence of other mental disorders (e.g., depression) due to general medical c()nditions (e.g., somatic pain) or substance use (e.g., caffeine).
DY550mnias
Dys.<;mnnias a rc five primary sleep disorders consisting of disturbances in initialing and maintaining sleep, ff'€ling n~ted or refr('Jihed after sleep, or sleeping excessively. Table 9-9 defines the DSM-N determined key charact(' ri.~ t ics or each db;;order.
Parasomnias
Parasomnl.as are a tri ad or sleep disorders associated with complex behavioral events that occur during sleep or that arou.«! a person from .<:Ieep. The disorders are defined in Table 9-9.
A ractitious disorder i.~ one in which an individual willfu lly proouccs signs or symptoms of a medical or psychiatric iJl ncs." to assume Ule sick role and it .. 3."So
dated gratifications. This should be differentiated from somatoform dison.l~rs (which arc not Willful) and malingering, which is simply lying about signs or symptoms to obtain gains different from those obtained by assuming the sick role (e.g., to avoid th t· military or ror monetary gain) .
TABLE 9-8 ,...Sll._. Primary Sleep Disorders Secondary Sleep Disorders
Dyssomnias Primilry insomnia Primary hypersomniil Narcolepsy Breathing-related
sleep disorder Circadian rhythm
sleep disorder Pafasomnias
Nightmare diSOfder S\eep terror disorder Sftpwalking disorder
Sleep disorder related to anather mental disorder
Sleep disorder due to a general medical condition
Substance-induced sleep disorder
< not f or IIltl e ! :> < lie .Il.M llpO.Il.fL"DI ! :>
54 • Bh.ltlpru,w Psychiatry
• TABLE 9·9
Dyssomnias Primary insomnia
Primary hypersomnia
Narcolepsy
Breathing-related sleep disorder
Orcadian rhythm sleep disorder
Parasomnias Nightmare disorder
Sleep terror di~order
Sleepwalking diSOfder
Difficulty falling asleep Of staying asleep. or sleeping but feeling as if one has notrested during sleep.
Excess sleepiness. either sleeping too long at one setting or persistent daytime sleepiness not relieved by napping.
Sleep attacks during the daytime coupled with REM s~p intrusions or cataplexy (sudden, reversible bilateral loss of skeletal muscle tone). Daytime naps relieve sleepiness.
Abnormal breathing during sleep leads to sleep disruption and daytime sleepiness.
Sleep disturbance due to a mismalch between a person's intrinsic circadian rhythm and external sleep-WOlke demands.
Repeated episodes of scary dreams that wake a person from sleep, usually occur during REM sleep.
Repeated episodes of apparent terror during sleep; individuals may sit up, scream, or cry out and aPPE'ar el(tremely frightened. They do not uSUCIl1y awaken during the arrack. Occurs during delta sleep.
Recurrent sleepwalking, often coupled with other complex motor activity.
• SUICIDE ATTEMPTS
Epidemiology
Suicide is the eighth leading cause o f death in the United State. .. , Approximately 75 people commit suicide each day in the United States (25,000 per year) . Many more people attempt sui cide. The overall suicide rate has remained stable in the United States during the past 15 years. Although the rate of suicide in tccn-agcrs aged 15 to 19 is low compared with the genffal adult population, the rate cl teen suicide has risen dramatically in the last 50 years.
Risk Factors
Studies have demonstrated that the O\'crwhelming majority of people who commit suicide have a mental illness (most often a mood disorder or chronic alcoholism). The first-degree rdatives of people who have committed suicide are at a much higher risk of committing suicide themselves. Gay and lesbian youth have 2 to 3 times the rate of attefTIpted suicide compared to heterosexual adolescents. Suicide risk increases with age. In men, suicides peak after age' 45; in women, most suicidf'S occur after age 55. The elderly account for 25% of the suicides, although they represent only 1 ()4J6 of the population. Overall , men are more successful at completing suicide, perhaps because of their more lethal methods (shooting, hanging, jumping); women often overdose or attempt drowning. Married people have a lower ri~k of suicide than singles. Suicide is more common among higher social classes, whites, and certain professional groups (physicians, dentists, musicians, law enforcement officers, lawyers, and in<rurance agents). Biologic risk factors include low levels of 5-hydroxyindolcacctic acid in the cerebrospinal fluid of
patients who have committed suicide by violent mean!i. Among psychological risk factor.;, hopcles.~ness has been shown to be one of the most rel iable indicators of long-term suicide risk.
Clinical Manifestations
History and Mental Status Examination Most often , a suicide attempt is self-evident at pre.~entation, either because the patient or fami ly indicates that sllch an c,,·cnt has occurred or becau~c there is an acute medical or surgical emergency (i.e., overdose or wrist laceration). AJways obtain fu rther detaiL~ from the patient and any witnesses to provide a fuU history of the antecedents and the act itself. Occasionally, a patient will present to a physician io a more subtJe way, with nonspecil1c complaints. Careful inquiry may reveal that the patient has taken an overdose o f a medica tion with delaYf'd lethality (such as acetaminophen) .
Patients who have attempted suicide deserve thorough psychiatric evaluation. P.~ych iatric history and mental status examination should explicitly address depressive symptom~, such as suicidal thoughts, intent, and plans. The details of the suicide attempt arc critical to understanding the risk of a future suicide. Patients who carefully plat] the attempt, u<;c particularly violellt means, and isolate themselves so as not to be found alive arc at particularly hi gh risk of future .<;uicide completion.
Differential Diagnosis Patients who attempt suicidc most commonly ~Iffcr from depression, schizophrenia, alcoholism, or personality di~ordcr.; (or comorbidities of the above) . However, patients who do not meet criteria for any of tllCSC disorders can and do attempt or commit
56 • Bh.q.ori tltf.i Psychiatry
suicide, e.<;pecially if they have any of the ri.",k factors (e.g., hopelessness) .
Management
Su;ddal ideation should always be taken serio usly. Suicidal patien ts often ar{" fraught with ambivalence OVCT' whether to live or die, and intervention and effective treatment can be lifesaving. Most actively suicidal patients require hospitalization on a locked unit for their own sa fety. Potentially lethal items should be held securely by nursing staff, and the patient should be observed ca refully for the risk of elopement. Trea tment of the underlying disorder or distress derives from accu.rate diagnosis (an tidepressant'" or electroconvulsive therapy LECfJ for depression; antipsychotiC's and/or mood stabilizers for bipolar disorder, psychotic depression, or schizophrenia) .
Patients at lower risk o f suicide can often be managed as outpatient", if close follm,:-up is available, fami l}, members are supportive, and a treatment alliance exists. Frequent meetings with treatment providers, eliminating the means of suicide (firearms, potentially toxic prescription pills) , and enlisting spouses, partners, or other fami ly members are essent ial clements of outpatient treatment.
SPOUSAL ABUSE -_._- -.-~-.----- ---.---_._-_._-----_._---Abuse between SPOU~QS or partnt"Ts can take several forms: pbysica l, sexual, and emotiona1. Physical abme or battering is mO.~t Oftetl perpetrated by a male on a remal" partner, hut women do batter men and abuse also occurs in sa me-sex relationships.
Epidemiology
Spousal abuse' is a;timatC'd to occur in 2 to j 2 miliiOll V.s. households. Some St\ICl.ies estimate that nearly olle third of all women have been beaten b}, their husband at lea<;t once during their marriage. Many battcred ,vomen are eventually murdered by their spou<;es or boyfriend~,
Risk Factors
There is a strong association between alcohol abm;e and domestic violence. More than 50% of abusers, and many of the abll.~f'd, have a history or alcohol or other drug abusC'. As, children, most abusers lived in
, 'iolcnt homes where they either witnessed or \,\:ere themselves victims of battering. The victims of abuse, more often lhan not, are also products or viole.nt home;. Pregnant women are at elevated risk For spousal abuse, often directed at their abdomens.
Clinical Manifestations
History and Physical and Mental Status Examination Many victims of abuse are ff'luctant to report abusive episodes because they fear retaliation, believe. th l"}' are deserving of abuse, or do not believe that help will be effecti ve. Victims of abuse are often mis tre.ated in ways that prevent them from escaping the abusive rdationshi p. They are intimidated. maligned, coerced, and isolated by the abuser. Attempts to leave an ilbusive relationship rna}' be thwarted by fin ancial concerns, the \vdfare o( children, fear of being alone, or the threat of (urruN battering.
PatienL", may presen t in the company of their abuser (or the treatment o f "accidental" lacerations, rontu<;ions, fractures, or more severe trauma. Unless the patient is asked tactfully in the absence of the abuser, she or he is unlikely to reveal the true caUSe'
of inj uries. Physical examination should indude e.xamination
of the .c;k.i n for contusions (especially of the face and breasts) and a genital cxaminalion. The me.ntai st.'1tus examination should take into account the appropriateness o f the patient's and partner's reactions to the "accident."
Management
The goal of trea tment is to end the violence (i.e., both partners must agree to treatment) or to enable the victim to leave the relationship. Eithf'r opt ion is difJicult to achieve. Social agenCi es must be enlisted to aid in child protection and custody if the latter option is chosen.
Patients who refuse help should be told what emergency services are available and how to access them. Unfortunately, women arc most at risk for seriOlL'" injury or homicide when they attempt to leave the abusive relationship.
ELDER ABUSE ---- -~ -- ----"- --------- ---- -----_. __ .. -- -.----Approxi mately 10'N o f those older than 65 are abused. Victims Llsually live WltI1 their assailants, who
" rlo l; f o .- salet :> " Ole ,111m ~ I "
are often their d1i1dren. Mistreatment includes abuse and neglect and takes phy.~ ical, psychological, financial, and material fonns. The abuser may withhold food, clothing, or other nect5Si.ties or beat, sexually molest, or emotionally abuse the victim.
A5 with spousal abuse, the dder person is often
Chapter 10 I Special Clinical Settings • 57
reluctant to reveal the abuse. Clinicians should be alert to the signs of abuse. Treatment involves ap propriate medical and psychiatric services alld sodal a.nd legal services. Some states mandate reporting of elder abuse.
Antipsychotic medications are llsed commonly in medical and psychiatric practice. I\s a class, antipsychoties have in common their blockade of dopamine receptors and their potential for serious side effects ir u.",oo inappmpriatciy or without careful monitoring. The most commonly prescribed typical and atypical antipsychoties are listed in Table II - I . Their relative potenciC'S, relative side-effect profiles, and major adverse rea<..11ons also are described. Typical ::mtipsychotics (also called neumleptics for their tendency to caw;(' movement disorders) are generally equally effective, although they differ in side-effect profiles and potencies. Atypical anti psychotics (e.g.. risperidone and clozapine) have fewer extrapyramidal side effect~ at therapeutic doses compared to typkal antipsychntics. Clo:t::apine (and perhaps rispcridonc) arc more effective than typical antipsychotics for the treatment of refractory psychotic di.~orders.
• INDICATIONS
Antipsychotics generally are eff<.."Ctive in treating positive psychotic symptoms (e.g., hallucinations, bizarre behavior, delusions) regardless of diagnostic category Crabl£'" 11-2) . For example. hallucinations in schizophrenia, in Alzheimer 's disease, or secondary to cerebral toxicity or i.njury aU respond to antipsychoti(: medications. A ntipsycholics are thought to be less effective (With the exception of dozapine and possibly risperidone, olan:t:apine, and quetiapine) in treating negative psychotic symptoms (e.g. , amotivation, akinesia, affective blunting, social withdra\',ral) . In addition to their role in treating psychotic symptoms, antipsychotics are used to treat some rorms or nonpsychotic behavioral dyscontrol (e.g., organic
hrain syndromes, Alzheimer's, mental retardation), delirium, Tourette's syndrome, and transient psychotic symptoms as they appear in personality disorder patient~.
Mechanism of Action
The most prominent theory on the mechanism of action of antipsychotics is the dopamine hypothesis of schi:t.ophrcnia. This hypothesis purports that dopaminergic hyperactivity leads to psychosis. Evidence supporting a role for hyperdopaminergic states i.n schizophrenia (and presumably other psychotic states) is as follows: antipsychotic potency of traditional antipsychotics correlates highly with their potency or dopamine receptor blockade, individuals with schizophrenia have an increased nwnber or brain dopamine receptors, and dopamine agonist dru gs (e.g., amphetamine) can indllce or exacerbate exi.~ting psychosis.
The a<.tion mechanism of antipsychotics i.~ often much broader than simple dopamine blockade, which accounts ror the numerous side errecl~ and the find ing that their a<."tlon in the brain is not well correlated with regions thought to give rise to psychotic symptoms. In addition , newer drug<; such a.~ dozapinc and risperidone have prominent serotonin (5-hydroxytryptamin <..>-2 [5HT2D receptor blockade. It is unclear whether this serotonin blockade imparts anti psychotic efficacy or simply helps prevent o:trapyramidal side effe<.lS..
Typical Antipsychotics (Dopamine Antagonists)
The antipsychotic potency of typical antips),chotia. (and risperidone) correlates with their affinity ror the D2 receptor. Figure 11 - \ is a schf'matic diagram of the proposed brain pathways affc<"'1:Lod by typical an tipsy-
TABLE 111
Cemnmnly PrMcrIbed Andpsychotks
Orug Therapeutic Pottncy' ~atjve Hypotensive Anticholinergic EPI Other Adverse [)osaQe Range' Reactions
Typkal antlpsychotlcs (dopamine.antagonisls) Thioridazine (McUaril) 15O-BOOmg "" High High High low Pigmentary retil'lOpathy" Chlo!prornazine (Thorazine) lOO-<lOOmg 100 High High "'" l ow Perpl\enazlne (Trllafon) 8-32mg 10 "'W low low M'" Trifluoperazine (Slelazlne) 5-20mg I Mod low low High Thiothfllene (Navane) 5-30mg S low low low High Haloperidol (Haklol] S-30mg 1 l ow low "'W High Flupflenaline (Prollxln] 2-60mg 1 Mod low low High
Atypical anllpsychOllcs (sefOlonillldOp,lmlne antagonists) Ciozaplne(CIoZllrU) lSG-6OIlmg 100 High High High low Agranulocytosls Ovctlapine (Scroquel) lSo-SOOmg ISO High Moo Mod low Ziprasldone (Geodon) 4O-180 mg "'W "'W "'w "'W QT Inte.va l prolongation Aripipralole (Ability) lS-)Omg "'W "'W low "'W Oanmpine lZyprexa) lG-20mg " Mod Low "'" Low Rispefidone (Rlsperdal) Hlmg 1 Low Moo low low
, ~"""", ...... <:Iod "'~I" IWIlfl'l d~ _ Iowot '''"" \lie Iten!>MIc <:\osagI'_Ool"9l" ON ~.,..,. -. fDt gr .... rk pllle!n< ...... !of!l)01e """' ... taking 1nt1'fXtl"9 medlca!.lan. '" h ......... hrf ,""dial pfCb"'" .. Ad.~ fn>m M~ HY ..,d f<>lMnl SIt. .,. .... """~"' d St:N"",,.,..,,Ij·ln Ed. S<twrt:I>ftg AF.M ~ C8. .. rextbook '" psyd'Ic>PtwmOC"'''Ilf. 2"" td.J.rntrIc." I':Ij'thIoItic "',-,~ II iodlc.JlI'd ...... "'" miJilqrlm do .. ~Ifn" (I .... 100 mg '" thiool<btno io -..iYol"", 10 2 mg 01 ~11nd """"'" "'" be ..... Wd .. 1tt1 PI!it.oc)\ AI! ,~pQI ""'iI><),<ho!la .... ,""""'" 1<1 be -...~ 0'I'IiacI0w. Elfiaq for cIoo.pft;ond ~ 1 •• , lent ~ tc loG' >IV\' be "'~ 10 th •• 01 typ1<oI"'ij><)'tho>IIcs. • D.,. '" 1.,.1 u ol"', eYtt"1I. tIaW ' J>P«J¥fId ""I\' /or ~ J<Mt~ ... ModIfiICI . od "'I'IocI ..... by "",mll.1on fn>m IiyrNn Sf.,.".... GW, ROSl'IIbIUm Jf, Ko""booit of 1KJ<1IlM:tk: drug """- ott~ .... Phb:l.lplllo,lJpt>lr><on, WHII.m<.rId 1WkJn~ lOOO.
I
!
I •
, ! • i , I
~ i • ~
~ • , • > i a. ~ . , ~
, ~. •
• •
«: not 1'or " .. i e ! 0> < He ll.JlR npo,Il1iD'! ! :>
60 • Blt:cpritTth Psychiatry
• TABLE 11-2
Indications for Aotipsydlotic Drugs
Short-term use (<3 Mos.)
I
Effective Exacerbations of schizophrenia Acute mania Depression with_ psychotics features (combined
with antidepressant) Other acute psychoses (e.g schizophreniforrn
psychoses) Acute deliria and organic psychoses Drug-induced psychoses due to hallucinogens
and psychostimulants (not phencyclidine) Non-psychiatric uses: nausea and vomiting;
movement disorders PoSSibly effective
Brief use for episodes of severe dyscontrol or apparent psychosis in personality disorders
Long-term use Effective
Schizophrenia Tourettes syndrome Treatment-resistant brpolar disorder Huntington'S di5ease and other mo~ment
disorders Chronic organic psychoses
Possibly effective Paranoid disorders Childhood psychoses
Rep<ochxed by permission f,om Alii ..... GW, Rosenbaum; JF. H.llndboolc of [lSychiaric drug therapy, 4th edition. I'tllli!delphiil: Uppifl(;ott. Williilm~ ilnd Wilkln'i,.:'!OOO.
Froolal Cortex I
I Basal Ganglia I T Dopamine
I Umbic Sll1JClUreS I
chotics-. Dopamine-containing axons arismg from brain stem nuclei (the ventral tegmenta l area and substantia nigra) project to the basal ganglia, frontal cortex, and limbic areas. Typical antipsychotics block 0 1 receptors (as docs risperidone). Blockade of dopamine in the cortical and limbic areas results in reduction in psychotic symptoms, whereas b lockade or dopamine in the basal ganglia produces extrapyramidal side effects. Although antipsychotics, especially lower potency medications, may have. an initial sedative effect, their antipsychotic action is not immediate and takes several days to several weeks to peak..
Atypical Antipsychotics (Serotonin/Dopamine Antagonists) At present, in the United States fi\'e atypical antipsychotics arc marketed; others are likely to be a\'ailable soon. Antipsychotics are classified as atypical when they produce fewer movement side effects than typical anlipsychotics. In addition to dopamine receptor blockade, atypical antipsychotics block serotonin receptors of the 5HT 2. subtype. Figure 11 -2 dcpict.~ the similarities and differences of the serotonin and dopamine systems. Serotonin receptor blockade conveys some protection against e:ll:trapyramidal side effects and may impart antipsychotic efficacy. Rispcridone is similar to typical lletJroleptk--s in that it is a very potent blocker o f the Dz receptor. Clozapine, conversely, is a potellt blocker of the D4 receptor and has much less Dz affinity. The D1 receptor blockade may account for clozapine's broader therapeutic qualities.
V'fA Substantia Nigra
Figure 11·1 • Pathways affected by typical antipyschotics.
I Fronlal Cortex I Entire Cor1ex I -, :
I Basal Ganglia I , , , - T , , Dopamine , , , , ,
Serolonin j , ~- - -~- ~ -. -- ---- ------ --- . . -----
I Limbic StruchJteS I
Choice of Medication
Because all antipsychotics are considered cfficaciou~, choice or medication should be based on prior patient or fantily member response, side-effect profile (patient tolenmcel , and available form (i.e., elix ir or TM, or 1M depot availability). At present, dozapine is th e on ly medication clear ly shown to be superior in patients for whom typical antipsychotics have failed. Fluphenazine and haloperidol are available in depot preparHtions, which arc given intramuscularly every 2 tcJ 4 weeks.
Therapeutic Monitoring
Patients on antipsyehotics should be m onitored closely ror advcrse drug reactions. Particularly important are neurologic side. effecti; .~uch a.o; akathisia [rest· lessness), neuroleptic m ali gnant synd rome (NMS), and extrapyramidal symptoms (EPS). Patients taking antipsychotics that lower seiztlfe threshold should be carefully monitored for Seizure activity. Individuals taking c10zapine mmt have weekly white blood cell C(lunt~ to monitor for the development of agranulocytosis. Clozapine must be discontinu.ed immediately in patients: demonstrati.ng this potentially fa.tal reaction.
Blood Ic\'c1s havc generally bcen of Iittk usc in monitoring antipsychot ic efficacy, in part bpcauo;e &Orne medications have ma.ny active metabolites. Haloperidol levels have some utility in patients who have side effects at low doses or .. vho fail to respond to high doscs. Clozapi ne levels arc also frequently used. Noncompliance is oftell tbe cauf>(' or apparent therapeutic failure.
The durat ion o f therapy depends on the nature and .~everity of th e pati"nt 's il1nes.~. Many disorders, such as schi zophrenia, require maintenance antipsy-
VTA Substantia Nigra
Raphe Nuclei I
Chapte r 11 I Antipsychotics • 61
Figure. 11-2 • Pathways affected by atypical antipsychotic;.
dlOtic therapy. Because of lhe seriolls sequela associated with long-term antipsychotic usc, maintenance thcrapy should be used only after a careful risk-to-beneflt analysis with the patient and involH-d family.
Side Effects and Adverse Drug Reactions
Side effects of antjp.~ychotics arc a major considcration in physician prescribing. Patients who Catillot bear th e side effects o f medications arc noncompliant and suffer greater rates of relapse and recurrence. Certain sidf' effects such as sedation can be llsefu l to a patient with insomnia or scvere agitation but can also limit function ing. A comparison of side-eITect profiles for commonly lL<;ed antipsychotics is provided in Table II -I. Common side effects are described below. Further discussion of neurolOgic side effects is fnund in Chapter 16.
Anticholinergic Side Effects Low-potency antipsycholics have the greatest anticholinergic side effects such as dry mouth, constipation, urinary retention, and blurred vision. The anticholinergic properties, howe"\lu , counter th e EPS. [n some cases, anticholinergic delirium may occur, e:-;pecially in the elderly, those with org..'1nic brain syndromes, or patient.s on o ther anticholinergk agents.
Reduced Seizure Threshold Low-potenc"y typkal antipsycholio:; and dozapine are as~datcd with lo wering seizure threshold. Seizures resu lt ing from antipsychotic therapy arc t reated. by changing medicat ions, lowering the do,;e, or adding an antiseizure mf'dication.
< not foe s a.la! > < lie llJUI npolI"""" ! >
62 • Bluepril1te; Psychiatry
Hypotension
Orthostatic hypotension is particularly conunon \vilh low-potency agents and risperidone. The hypotensive effect of anti psychotics IS gt.'J1t..~ally due to alrha-receptor blockLtde.
Agranulocytosis
Agranu!ot..y tosis has been associated most conunonly with dozapine. Because of the potentia lly fatal nature of this adverse effect, cloza pine distribution is regulated and requires a \.veekly complete blood munt with differential to monitor for neutropenia .
Cardiac Side Effects Ziprasidone, low-potency anti psychotics (particlllarly thioridazineJ , and risperidone may cause Q T prolongation (v.lith risk of torsade de pointes). Nonspecific electrocardiographic changes may also occur with certain antipSYi..:hotic medications (particularly ·with clozapine and olanzapine).
Metabolic Effects
Although patients with psychotic disorders are known to have higher rates of obcsity and diabetes mellitus independent of medication ulerapy, stucUes. have incUcated that certain atypica l antipsychotic medications (particualarly olanzapine and d02.apine) are associated with high rates of weight gain , dys-
lipidc.:rnia, and may bc associated wit h adult-onset diabetes. All patients taking thcse medications should have regular metaboHc indices checked including lipid levels, fasting blood sugar, and blXly mass index.
Movement Disorders Movement disorders such as dystonia, EPS, akathisia, NMS, and tardive dyskinesia may occur and are discussed further in Chapter 16.
Other Side Effects
Skin and octJar pigmentation are common side effects of ncuroleptics, as is increased photosensiti\'~ ity. Thioridazine can causc pigmentary retinopathy at high doses. Increased prolactin le.vels (and sequela) may also occur. Quetiapine may ·increase the risk of dcveloping cataracts.
lIP KEY POINTS !Ii 1. Antipsychotics are used to treat the psychotic
symptoms of a wide range of disorders. 2. These drugs are equally effective but differ in
potency (with the exception of clozapin:e and poSSibly risperidone).
3. Antipsychotics can have serious side effects.
Antidepressants are used commonly in medical and psychiatric practice. As a class, antideprc:;sants have in common their ability to t reat major depressive illness. Most antidepressants are also effective in the treatment of pani c disorder and other anx iety db;()rdL"rs. Some: antidepressanL<; effe<..:tivdy treat obsessive-compulsive disorder (OCD) and a variety of other conditions (see indications below).
The mo..<;t commonly prescribed antidepres.~anL<; are listed in Table 12-1. Antidepressants are subdivided into groups hascd 011 structure or prominent functional activity: selective serotonin re uptake inhibitors (SSRls), tricyclic antidepressants (TeAs), monoamine oxidase inhihitors (MAOIs), and other antidepressant compounds with a variety of mechanisms of action . AntidepressanL~ are typically thought to act on either the serot(lnin or norepinephrine systems, or both. Choice of medications typically depends on diagnosis, history of response (in patient or relative), and the side-effect profile of the ffiL-dication. Antidepressant e ffects are typically not seen unt il 2 to 4 weeks i., to t reatment. Side effecL<; m u<;t be carefully monitored, especially for T CAs and MAOI s.
• INDICATIONS
Table 12-2 li sts the indications for antidepressants. The main indication for antidepressant medications is major depressive d isorder as defined hy the Diag· JUJsric alld Statistical MamUlI of Mental Disorders, 4th edition (DSM-IV) . Antideprc<;sants arc used in the treatment of all subtypes of depres.<; ion, including depressed phase of bipolar disorder, psychotic
depression (in combination with an antipsychotic medication), atypical depression, and seasonal depression (sec Chapter 2) . Antidepressant .. also arc indicated for the prevention of recurrent depress;ve episooes.
Antidepn'ssant medications may be effective' in the treatment of patient'; with dysthymi(: disorder, t.."5pedally when there are dear neurovegetative signs or a history of response to antidepressants.
Panic disorder with or without agoraphobia has hcen shown to respond to SSRls, MAO Is, T CAs, and high-potency benzodiazepines (alprazolam and clonazepam) .
OCD has neen shown to respond to the serotoninselective tricyclic clomipramine (Anafranil) and to SSRls at high dooSes (e.g., fluoxetine at 60-80mg/ day). Obsessions tend to be more responsive to pharmacotherapy than compulsions. Symptoms of OCD respond more slowly than symptoms of major depres.<;ion . Trials of 12 weeks or more arc needed before a medication can be ruled a failure for an OCD patient.
The binging and purging behavior of bulimia has been shown to respond to SSRls, TeAs, and MAOls in several open and controlled trials. Because SSRls have the most benign side-effect profile of these medications, they arc often the first-line p !>)I
chopharmamlogic treatment.
• MECHANISMS OF ACTION
Antidepressants are thought to exert the ir effects at particular subsets of neuronal synapses throughout the brain. Their major interaction is 'with th~
< not foe sal e ! > < He ~nR npo~~ ! >
64 • Blueprints Psychiatry
, TABLE 12-1
Commonly Prescribed Anttdepressants
Drug (Brand Name) Suggested Starting Dosage" Suggelited Maximum Dosage"
SSRls Fluoxetine (Prozac) Sertraline (Zoloft) Paroxetine (Paxil) Fluvoxamine (Luvox) Gtalopram (Celexa) Escitalopram (lexapro)
TCA> Nortriptyline (Pamelor) Imipramine (Tafranil) Desipr<lmine (Norpramin) Clomipramine (Anafrani1)
MAOls Tranylcypromine (Pamate) Phenelzine (Nardil)
5~20mg/day
2S-50 mg/day 1 0---20 mg/day 2S-S0mgqhs 20 mg/day 10mg/day
l D--25mg/day 10-50 mg/day 10-25 mg/day 25-50 mg/day
10-20 mg/day 15- 30mg/day
BOmg/day 200mg/day SOmg/day
300mgqhs 60mg/day 40mg/day
150mg/day 300mg/day 300mg/day 250mg/day
6Dmg/day 90mg/day
Other antidepressants Bupropion (Wellbutrin) Bupropion SR (Wellbutrin SA. Zyban) Nefazodone (Serzone) Venlafaxine (Effexor) Mirtazapine (Remeron)
75-100 mg/day 150mg/day 50- 100 mg bid 2Smgtid 1Smgqhs
150mgtid 200mgbid 600mg/day 125 mg tid 4S n'lg qils
400mgqhs Trazodone (Desyrel) SO m9qhs
*Geriatric paliftllS generally require lower~.
Modified from 51011 A, Psychopharnw:oIogy reference card 1.1996.
. TABLE 12-2
Common Indications for Antidepressant Usage
Effective Major depression (unipolar) Bipolar depression Prophylaxis against recurrence of major depression
(unipolar) Panic disorder Social phobia Depression with psychotic features in combination
with antips~chotlc Bulimia Neuropathic pain (tricyclic drugs) Enuresis (imipramine best studied) Obsessive-compulsive disorder (clomipramine and
SSRls) Atypical depression (SSRls or monoamine oxidase
inhibitors)
Probably effective Attention-deficit/hyperactivity disorder Cat<lplexy due to narcolepsy Dysthymia (chronic depression) Generalized anxiety disorder Organic mood disorders Posttraumatic stress disorder Pseudobulbar affect (pathological laughing or
crying)
Possibly effective School phobia Clnd separation anxiety Personality disorders
Re~ced by pem>i~siOI1 from Hyman SE,Arana GW, Ro,;enbaum JF. Hllndbook of ps~ilrtoc dl\lg therapy. 4th ed Philadelphia: Li ppincott Wdljams and Wilkin .. 2000.
Chapter 12 I Antidepressants, Eer, and PhotothelClPY - 6S
monoamine neurotransmitter systems (dopamine, norepinephrine, and serotonin). Dopamine, norepinephrine, and serotonin are rele2.'ied throughout t.he brain by nemons that originate in the ventra l brainstem, locus ccruk'lIs and the raphe nuclei, respectively. These neurotransmitters interact ,vith numel"Ous rft:epto r subtype; in the brain that are as,<;()ciated with the regulation o f glohal state fuO(,:· tions including appetite, mood states, arousa l, vigilanct!, attention, and sensory prm.:t!SSing.
SSRIs act by binding to presynaptic seroton in reuptake proteins, thereby inhibiting reuptake and ineTeasing thel£.~vcls (If '!'erotonin in the synapti<.: d eft, TCAs act by blocking presynaptic reuptake of bOlh serotonin and norepil1ephrine. MAOb at.:t by inhibit· ing the presynaptic enzyme (monoamine oxidru.t.D that catabolizcs nort'pinephrine, dopamine. and serotonin, thereby increa::.ing the It!vels o f these neur~ transmjtters pre!>ynapticaUy.
These immediate mechanisms o f ae"tion arc not sufficient to explain the delayed antidepressanl efft.,.cts (typically 2 to 4 weeks), Other wlknOwn mcchanisrns must playa role jn the successful psy· chopharrnacologi c treatment of depression.
• CHOICE OF MEDICATION
Many teXtbooks and artid ei assert that al l <!ntidepressants ha.ve roughly the !jamc efficacy in treating depression, Morc recent data looking at rates of remis:;ion 1)£ depression ind icate that venlafaxine and trit.:ydic antidI..1m:'ssant~ may he more effective tllan the SSRls at a<.:hieving depression remi ssion. The hi gher rates of remissjon are believed to be related to the c_ombincd actions (I f venlafaxine and TCAs on serotonin and noradrcncrgic ::.y,!,tems. Tht!:.t! d Tects may he ach ieved also by com binations of anti· dcprcs...ants such as bupropioo and SSRIs. This complicates medication doice, as before medication choice was ba<;ccl mainly (In symptom profile and diagnosis, prior patient response, side~effcct profi.l ~, and patient tolerance. Another factor to mosider \ .... hcn treating depression is remissjon ratC!i with a particular drug. More resean:h mu::.'t be done in this area to determine the rc.lative rates of depression remission, particularly in subt}'Pcs of patient.s -with depres.!.lon. SSRls, bupropion, venlafaxine, mirtazapine, and nefazadone are the most well tolercltcd anti· dep ressants and ar£.' generally thQught of a.s fi rst· linc agents for major depres~i(m . Compared with TCAs
and MAO Is, thcst! medications have very luw scda· tive, anti cholinergic, and o rthostatic hypotensive effects, These agents sho uld be considered fOT tlse especially in patients "';1th card iac conduction disease, const'ipation, glaucoma, or prostatic hypertrophf.
Among the t riq'Clil: antidepressants,. nbrtriptyiinc and desipramine have the least sedative, anticholinergic, and orthostatic hypotensive effccts. TIlt:)' can be used as first-line agt~nts in you nger, healthier people, especially if cost is a consideration (tricydics arc much le5::' expensive than SSRIs, bupropion, (lr
venlafa-xi l1e J, Because of the necessary diet rest rictions and the
risk of postural hypotension. the t-.1AO ls (phenelzine and tranykypromine) should be used most sclec· Lively. They can be quite e flective, however, and arc used in pat ients for w hom SSRls and triqrdio; have failed, jn patients with a concomitan t seizure disQrder (MAOh and SSRh. do not lower tht: seizure threshold), OJ" in those wi th atypical depressions or social phobia (MAOls or SSRls are most effective), High-dose SSRls and domipramine (despite its high sedative, anticholi ne rgic', and orthostatic hypotensive effects) arc the trt:!atments of choice for OeD .
• THERAPEUTIC MONITORING .. -. ---- -- - - --_. ---------- _. - _. _. --- _. -_.- --Approximately 50% of patients who meet DSM·IV criteria for major depression will recover with a single adequate trial (at' l ea,~t () weeks at a therapcu · tic do,~age) of an antidepressant. The most common reasons for failed trinls ar~ inadequate dose and inadequate trial length . Ho\,,rever, dosagl" and length of trial afC often limited by side effects (or no ncompliam:t!).
Pat ients on antidepressants should be monito red carefully for side effects or adverse drug reac..'tions (listed below]. Genera lly, antidepressant therapy of a tirst episode of unipolar depression should con· tinue for 6 months. Patients with recurrent or chronic depression require longer or perhaps lifelong maintenance treatment. Increasing the dose, augmentation w ith lithium or T3 (Cytomci), or a ('I1>)'chostimulant (e.g., methylphenidate), swit<.:hing aoridcpressanl!i, or addit ion of a second antidepressant is helpfu l in t reatinr: refractory deprcs.'iion. Patient.<; o n most TCAs require serum JE:\'cl measurements to determine appropri ate dosing.
< oot lor sale ! ;> < Ite ll1IA npo_ I :>
• SIDE EFFECTS AND ADVERSE DRUG REACTIONS
SSRls
Although specific SSRls have slightly different side~ cffel.:t profik"S, as a group their main side effects are nausea, headache, neuromuscular restlessness (resembling akathisia), insomnia or sedation, and delayed ejaculationlanorgasmia. SSRls combined with MAGh. m'e dangerous: a fatal serotonin syll ~ drorne may result.
TeAs
TCAs in many patients arc quite well tolerated but o\'eral\ arc less tolerated by patients for their side effects than the SSR ls, bupropion , or vcnlafaxine. The major side effects associated ' '''ith TeAs arc orthostatic hypotension , anticholinergic effects, cardiac toxicity, and scXl.tal dysfunction. Speci£c TeAs have relative degrees of each of these effects.
Orthostatic hypotension is the most common serious side etTect of the TCAs. Th is is partiCtllarly worrisome in elderl y pati ents, \\I·ho may be mme prone to fall s. Anticholinergic toxicity can be mild, incltlding dry mouth, constipation, blurred near vision, and urinary hesitancy, or more severe, with agitation, motor rcstlessocss, hal lucinations, delirium, and seizures.
Cardi ac toxicity may li m it thl;' usc ofTCAs in some patie.nts.. TCAs have quinidine~like cffects on the heart, potentially causing sinus ta chycardia; supraven-· tricuiar tachyarrhythtnias; ventricular tachycardia; ventricular fibri llat ion; prolongation of PR, QRS, and QT interva ls; bundle branch block; first-, sccond~, and third -dt-grcc heart b lock; or ST and T~wavlo' changes. Major complications from TeAs aJ"e rare in patients \,,;th normal hcarts. TeAs should be avoided in patients wit h {.undu(..ti.on system disease.
ScJ<uaJ dysfunction indudes irnpotenc.:e in men and decreased .St'.J..'l.1.31 arou~al in womcn_
MAOls
Patients who take MAOb are at risk for hypcradrcncrgic crises from thc ing~tion of sympathomimetic amines (sti(h as tyramine) that fail to he detoJ< ificd bccause of inhihition of the gastrointestinal monoami ne oxidase ~)'stem. Improper diet can lead to severe hypertensivc c'ises (tyramine n isisJ with
potential myocardi al infarctiQIl or stroke. Foods that must be a\'oidcd includc cured meats or fish, beer, red wine, all cheese except cottagc and creanl cheeses. and ovcrripe fruits. Many over-the-counter cold and pain remedies must also be avoided. Trea l~
mcnt of hypertensive crisis, if .'lc,'cre, may requ ire emergency medical attention, Including IV phentolamine (an alpha blocker) or continuous rv nitroprusside infusion.
MAOls caust.' a dosc~rclatcd orthostatic hypotension: tranylcypromine can cause insomnia and agitation; phenelzine can cause daytime somnolence.
Other Antidepressants
Veniafa)(inc (Effe)(OT, Effexor XRJ is a .serotonin and noradrenergit: reuptake inh ibitor with a hetter side effect profile than TeAs 0 ,- MAGis. A May 2002 meta~analysis of prior antidepressant trials suggcsted that venlafaxine and TCAs may have a greater remis~ion rate than SSRls. Further study is needed including morc hcad-to~hea.d comparison trials. Nefazod.{me (Serzone) and trn:t.(lCkme (Dc.!>yrd) arc sen..lto t 'i t' ~modulating antidepressants. Trazo(kme is prescribed rarely 3S a s(.l le antidepressant but is O rlCn
prescribed as an adjunct to an SSRI for sleep because it has strong sedative properties (at higher doses it servcs as an antidepressant) . In addition to sedation, trazodone <.:an 0 11 rarc ou:ac;ions induce priapism (prolonged, painful penile erec.:tion) that can ('auSt' permanen t damage. PatienLS mu.c;l he instructed to seck emergency treatment shou ld such an Cr C(:tl(ln
occur. t\'efazodone is similar to trazodone but is less sedating at therapeuti c doses. It appears to have n low rate of St'xual dysfunl .. "tion.
Rupropion (WeJlbutrin, Wellbutrin SR, Zyban) a ppl~ars to work by inhibiting t he uptake of dopami ne and norepinephrine. Bupropion has a low inddence of sexual ~ide ctTcc.:ts. In addition to Its
efficacy in treating major derres..c; ion~ bupTOpion has bCl.'1l shm'lm to be e.ffl..'(..tive in smoking ces.<>ation (marketed as Zyhan) and attention defidt disorder. Hupnlpion has a higher than average risk of seizures com pared ' \lith othto'l" antidepressants.: The risk of seizures is greatest above a daily dose of 4S0mg or after a single dose of greater than ISOmg (If
immediatc~releasc bupropion. Mirtazapine (RemeronJ is classified ~ a modula~
tor of norcpinephrine and scrotonin . It is quitE.' sedating 1n some Individuals, and has a low incidence of sel\ual dysfunction.
< nQt {vI[ ,..le ! .- < "" II"" npo_ !
Chapter 12 I Antidepressants. ECT. and Phototherapy • 67
Phototherapy
Phototherapy cQnsists l)f the I,xlOtrolled administ ration of b right light to t reat specific psychiatric illnesses.. Phototherapy is administered ll!!>ing !>'Peda ll ~. designed bright light boxes and has bL'Cn shown effective in the treatment of the seasonal subtype of major depression (aho kmJwn as seasonal affect ive d isorder). Phototherapy is also u5(..'(1 in the t reatment of the delayed sleep phase syndrome and jet tag. In the treatment of sea<;onal affective dismcicr, early morning bright light therapy is superior to evening light in mo!)t individuals. LiRht intensity of 2,500 to 10,()(X) lux is most t+fective. l .ight therapy can induce mlln ia in susceptible individuals.
Electroconvulsive Therapy (ECT)
ECf (formerly known as electri(: shock thera py) is one of the oldest and most effecti\'e treatments for major depression. Eel' also has somt: e ffic..:aty in refractory mania and in psychoses with prominent m(X)d components or catatonia. ECf appears to work via the induction of gdleralized seizure activity in the brain. The peripheral manifC1>tations of seizure activity are blocked by. the usc of paralytics, and memory for the event is b locked by the use of anesthetics and by sei7.ure activity. Modern ECf produces short-term memory loss and confusion. Ailateml ReT is more effa."tive than unilatcf".l1 ECT but produces more cognitive side effects.
KEY POINTS
1. Antidepressants have multiple Indkations including various forms of depressk>rl. anxiety disorders. bulimia, and OCD. among others.
2. Antidepressants act on ser<>tonergic and noradrenergic receptor systems.
3. Some antidepressants have been shown to be efficacious fOf particular disorders; for major depression, all approved antidepressants reduce symptoms to a significant degree. leAs and ven~ lafaxine may more frequently induce remission. Antidepressanls for depression are often chosen based on sld~effect profile and symptom constellation.
4. Some antidepressants. particularty TeAs. require monitOfing of serum levels.
5. The effects of antidepressants can be augmented by the addition of lithium" thyroid hormone. or psychostimulants.
6. Antidepressants have side effects that vary according to class.
The mood stabilizers most commonly used an' lithiwn, valproate, and carbamazepine. Table 13-3 list'> mooo stabilizers and their dosage and therapeutic levels. Other medications, such as calcium channel blockers, benzodiazepines, and ant ipsychotics, have some utility in refradory bipolar disorder.
• INDICATIONS
Mood stabilizers are indicated acutely (in conjunction with anti psychotics) for the treatment of mania. They are indicated for long-term maintenance PTOphylaxis against depression and mania in bipolar individuals. Anticonvulsant medications (valproate and carbamazepine) may also he useful in individuals baving seizure-related motxl instability. Mooo stahilizers are also used for treatment of impulsive behavior in individuals without bipolar disorders.
The choice of mood stabilizer is based on a patient's partku1ar psychiatric illness (i.e. , subtype of bipolar disorder) and other dinica1 factors such as side effel."ts, metaholic routes, patient tolerance, and a history of patient or first-del:,'Tee relative dmg responsiveness. Tab le 13-1 lists the major mood stabilizers and their most common indications. Some common and more serious siJe effects of mm.xl stabilizers are listed in Table 13-2.
The mechanism of action of mood stabilizers in bipolar illness is unclear. The range of neurotransmittel'S affected by the'>e medications and their disparate modes of action suggest that mania may be controlled by altering the function of several different neurotransmitter SystClTlS. Conversely, they may share a common mechanism of action that is yet to be elucidated.
• LITHIUM
Mechanism of Action
The mechanism of action of lithium in the treatment of mania is not well determined. Lithium alters at least two intracellular second messenger systems (the adenyl cyclase, cyclic AMP system, and the G protein-coupled phosphoinositide systems) and as an ion, can dircl.11y alter ion channel function. Be(~ause
norepinephrine and serotonin in the central nervous system (eNS) use G protein-coupled receptors as one of their mechanisms of action, their function is altered hy lithium. l.ithium also alters GARA (gamma-amino-butyri(~ add) metabolism.
Choice of Medication
Lithiwn is indicated as a first-line treatment for regular cycling hipolar disorder in individuals w ith normal renal function. Lithitun also is: used to augment other antidepressants in unipolar depression. Lithium is renally deared and can easily reach tox ic levels in persons with altered renal function (e.g., especially the e lderly). It is less effective in the treatment of the rapid cyding variant of bipolar disorder.
Therapeutic Monitoring
I.ithium levels should be monitored regularly until a stahle dosing regimen has been ohtained. Additional monitoring is neu'ssal)l in a patient with variable compliance or altered renal Function. In addition, patients should be warned about toxicity and be regularly assessed for side effects. Thyroid-stimulating hormone and creatinine should also be monitored at
nnt [ o r sal e l > < ,,,. ,IInR npo,lllllDl I >
Drug
lithium
VaJproate
Carbamazepine
tndlcations
AaJtemania long·term prophylaxis in bipolar
disorder Augmentation of antidepressant
medicatiOns Impulsedyscontrol
Acute~nia
Rapid--cyding bipolar disorder Mixed featllfe5 bipolar disorder Impulse dyscontrol
Acute mania Rapid--cyding bipolar disorder Ml){f!d features bipolar disorder Impulse dyscontrol
regular j." ervals to check thyroid and kidne)' funct ion, respectively.
Side Effects
Lithium has several minor but troublesome :.ide effects, including t remor, polyuria, gastrointestinal distress, minor memory problems, acne exacerbation, and v· ... eight gain. Approximately 5% of patients on long-term lithi um therapy develop hypothyroidism because the lithium intelf eres \v1th thyroid hormone production . At tOll ic levels, atallia, coarse tremor, e<mfusinl1, coma, sinus arrest, and death can occur. Lithi um has a narrow therapeu ti c wi ndO\,,~ and patients can bl'l'orne toxic at prescrihed doses, espt... ... cially if t hey undergo an ab rupt change in renal funct ion.
• VALPROATE
Mechanism of Action
The mech anism of action of valproate is UIOUght to
be due in part to augmentation o f GABA tunl1.ion in the eNS. Valproate increases GABA synthesis, decreases GABA breakdown, and enhances its postsynaptic efficacy.
Choice of Medication
Valproate is indicated in acute mania and in r.rophylaxis aga inst mania in bipolar d isorder (Tab le
Chapter 13 I Mood Stabilizers • 69
13- 1). It is more effect ive than lilhium for t he rapidl.ycling and mixed variants of bipo lar disorder. It may not pnwidc p rophylaxis against depression in hipolar disorder or augment antidepressants. It is used in treating impulse dysmnlmL
Therapeutic Monitoring
Valproate levels should be monitored regul arly until a stable blood level and dosing regimen have been obtaint...-d. Liver functilm tests should be checked a l
baseline and frcq 1.1ently during the first 6 montbs, espel"i ally because the idiosyncratic react ion of fatal hcpalotoxidty is most frequent. in this time frame.
Side Effect s
At lherapcuLic levt.'ls, valproate produces a variety of side effelts, induding sedation, mild tremor, mild ataxia, and gastrointest inal distress. lluombocytoperna and im paired platelet fum.::tion may also ocnlr. At toxic; levcLc;, co nfusit.m, coma, cardiac arrest, and death can OCl.l.lr. Valproate usage carries with it the risk of idiosyntr.luC but scriot.LC; side effects, Thest' include fatal he patotoxicity, fulminant pancreatitis and agranulocytosis..
• CARBAMAZEPINE
Mechanism of Action
The mechanism of at1.1on of carhamazcpine in bipolar ill ness is unknown. Carbamazepine blocks sodium channels in ne1.1ronS that have ju~t produced an action potential, blocking the neuron from repet· itive firing. In addition, carbamazepine decreases the amuunt of t ransmitter rdease at presynaptic terminals. Ca rhamazepi ne also appear:s to indifC'ctiy alter central GABA rKeptors .
Choice of Medication
Carbamazepine is generally considered to be 3
sccond"line drug (after lithium and va lproa.le) ror the treatment o f mania [fahle l3-I) . It is used in acute mania, p ro phylaxis agaim;t mania in bipolar d i5Qrder, and may be more effect ive than lithiu m in rapidcycling and mixed mania. Carbamazepine's efficacy in the prophylaxis and treatment of depression is not d ear. It is 31so used in treating impulse dysconrro l.
< not f OL sale I > < He ~R rrpo~~ I >
70 • Blueprints Psychiatry
TABLE 13-2
Drug
Lithium
Valproate
Carbamazepine
Side Effects
Side-Effect Profile
Therape~tic levels CNS: Endocrine: Cardiac: Renal: DermatologiC: GI: Hematologic: Other.
Toxic levels CNS: Cardiac:
Therapeutic levels CNS: Endocrine: Oermatologic Hepatic: GI:
Hematologic: Other.
Toxic levels CNS: Cardiac:
Idiosyncratic Hepatic Q, Hematologic
Therapeutic levels CNS: Oermatologic: Cardiac: Hematologic Q,
Toxic levels eNS: Cardiac Respiratory:
Idiosyncratic Hematologic
Carbamazcpinc, at therapeutic levels, produccs similar CNS side efft:~1:s to lithiwn and valproatt'_ Nausea, rash, and mild leukopenia are also common. At toxic levels, autonomic instability, atrioventricular blrn:k, resp iratory depression, and coma can occur. Carbamazepine has idiosyncratic side effects of agranulot~ytosis, pancytopt:nia, and aplastic anemia.
sedation, cognitive clouding, fine tremor abnormal TSH, clinical hypothyroidism T -wave change, sinus arrhythmia polyuria acne, psoriasis nausea, vomiting, dianflea benign leukocytoSis weight gain, fluid retention
ataxia, coarse tremor, confusion, seizure, coma, death sinus anest
somnolence, ataxia, tremor menstrual irregularitieS, thyroid abnormalities alopecia. rash mild transaminitis nausea, vomiting, indigestion thrombocytopenia, platelet dysfunction edema
ataxia, confusion, coma. death cardiac arrest
fatal hepatotoxicity pancreatitis agranulocytosis
ataxill, sedation, dizziness, diplopia
'''h decreased atrioventricular conduction benign leukopenia nau,""
somnolence, autonomic 1nstability, coma atrioventricular block respiratory depression
agranulocytosis, Pllncytopenia, aplastic anemia
Therapeutic Monitoring
Carbamazepine levels should be monitored regularly until a stahle dosing rebYjmen has heen ohtained. Patients should be carefully monitored for rash, signs of toxicity, or evidence of severe bone marrow suppression .
flot f o e ,",,J,e I :> < .... ",1m nPDA4;o:>1 I '"
Novel Mood Stabilizers
Several new agen t<; are being used as mlJ()l.\ stabilizers for bipo lar disordcl: I ,ike valproic add, they arc all FDA-approved anticonvulsants that arc now being studied for Ust' in treatment of acute manic episodes and for maintenance of bipolar disorder (see Table 1.3-3).
• LAMOTRIGINE
Mechanism of Action
The mechanism of action of lamotriginc in bipolar disorder is unknown. LatTIotrigine is approved by the I-,[)A for use 3 S an nntin.mvulsant and is u.s<--""Cl off-label in mood disorders. Lamotriginc in vitro has been shown to inhibit voltage-sensitive sodium channels. This effec t is believed to stabili ze neuronal membranes and modulate presynaptic excitatory ncurotmnsmittt.'f rclc3M'.
Choice of Medication
Allhough studies are stiU ongoing regarding the w.e of lamotrigine in bipolar disorder, it appears to have some an tidepressant as \ .... ell as mood stabilizing properties. Since its efficacy is not yet certain , it is currently only used after a patient has fai led or heen all ergic to more traditiona l therapie;.
Dosages are g~neralJy altert!d for the elderly, tho~ with rCl1aJ or other orga n impairment, or \..men comhined , .... ith interacting agents.
TABLE 13-3
Chapter 13 I Mood Stabilizers • 71
Therapeutic Monitoring
The development of serious allergic reactions to lamolrigine appears to be related to rapid dose escalation and/or d rug interactions. A clinically useful as..,ay for ~crum levels of lamotrigi ne L<i not available. Generally, this medication should on1}, be prescribed by a qualified p.<iychiatrist , neurologist, or other physician who is aware of the complex drug inteJ"actians that exist particlJlariy betvveen valproic acid and lamotri gi ne.
Side Effects
I .amotrigi nc can commonly cause ataxia, blurred vision, diplopia, di zzint!ss, nallSca, and vomiting. Severe, potentiall y li fe-threatening allergic rashes have been reported with the usc of lam{)trigine. The allergic rca r.:ti<'l0 can begin as a simple rash and lead to Stevens-Johnson syndrome.
• GABAPENTIN
Mechanism of Action
The m echanism of action o f gabapentin in bipolar disorder and in sei7.Ure disorders is unknown. Gabapentin inhibits induced seizures in fats and mice. Althl..JUgh it is stmcturally related to tJle neurotransmincr GABA, it has no bi.nding affinity to cl1e GABA receptor or to any other k11.own brain re(':l~ptors.
~~~~~~--------------------------------------------l
Drugs
lithium carbonate Valprokadd carbamazepine lamotrigine Gabapentin Oxcarbazepine
Starting [)(Isage
3OOmgbid-tid 250mgbid·ttd 100 mg bid-tid
25'-50mg qhsl 300mgqd 150mgbid
Therapeutk Dosage
900-1 SOO mgJday 1000-2500 mglday 600-1200 mglday 300-SOOmglday 900--'800 mg!day 600-1200mglciay
Therapeutic: Serum Concentration
O.6-UmEqIl 5O--120mglL 4-12mg/l
, Oowge$ ,~ ~Iy lowe<- few gerilllril:: patimu, patief1u taJjng In:efacting mediations, or JliIlienu with o !her medical po-obiems . • \lalproate wiI ~SIl \a~e ~ ""Yd, ne<:~illjng lowe!" dcMgn. AdalXed " om Stoll AL. P$yd1op/lMmarology referern:e urd, 1996 iWJd from PhysiQlln's desk l efl!l'tn(e,56tl1 eel 2002.
< n~t f or sal e l ~ < He ~nR npo~~ I >
72 • Blueprint5 Psychiatry
Choice of Medication
Studies indicate that gabapentin may be a useful adjunctive medication for mood stabilization and anxiolysis in bipolar disorder, but it appears to lack sufficient efficacy for use as monotherapy for bipolar disorder episode prophyla,xis. It is generally used as an adjlmct to more traditional agents such as lithium or valproic acid or to address particular target symptoms such as anxiety.
Therapeutic Monitoring
A similar dosage range is used for seizure and bipolar disorders, although the drug is not FDA approved for this use. The drug is excreted renally and unchanged.
There is no clinically available assay for serum gabapentin.
KEY POINTS
1. Mood stabilizers are indicMed for the treatmerlt of t>poIa, disofder.
2. ThEy work by unknown but likely varied mechanisms.
3. Efficacy varies according to the subtype of bipdar illness.
4. Mood stabilizers have serious fol(kltfes, so patients require regular monitoring.
The medications discussed in this chapter have anxiolysis in common. Although benzodiazepines have a wide variety of clinical applications (e.g., as preanesthetics, in the t reatment of status epileptic us, as muscle relaxants, and in the t reatment of insomnia) and other medications (e.g., antidepressants) are of utility in treating some forms of anxiety, the benzodiazepines are uniquely effective for the rapid relief of a broad spectrum of anxiety symptoms. Buspirone is a novel medication that, at present, is used primarily in the treatment of generalized anxiet y disorder; it does not appear to be effective in treating other t:ypes of anxiety (e.g., panic).
• INDICATIONS --------- -- ------------------ -- --------- --- ---Benzodiazepines
Benzodiazepines are among the most widely used drugs in all of medicine. In psychiatry they are used as the primary t reatment of a disorder or as adjunct treatment to other phannacologic agents. Benzodiazepines are used to treat a variety of anxiet:y disorders: panic disorder, generali zed anxiety disorder (GAD), anxiety associated with stressful life events (as in adjustment disorders with anxiety), and anxiety that complicates depression (see Chapter 3). In addition, benzodiazepines are used for the shortterm treatment of insomnia, for the treatment of alcohol withdrawal, for the agitat ion of mania, dementia, and psychotic disorders, and in the treatment of catatonia (Table 14-1).
Buspirone (Buspar)
Bu~pirone is used primarily for generalized anxiety disorder.
• MECHANISM OF ACTION
Benzodiazepines
Benzodiazepines appear to function as anxiolyt ics via their agonist action at the central nervous sy~tem (eNS) GABA ... (gamma-amino-butyric-acid) receptors (the GABAII, receptor complex regulates a chloride ion channel, CABAl! receptors appear to work by second messenger systems). GABA is a widespread inhibitory neurotransmitter with a complicated receptor st ructure, having multiple binding sites for GABA, benzodiazepines, and barbiturates. The mo~t likely mode of action of benzodiazepines in treating psychiatric illnesses is via their augmentation of GABA function in the limbic system . Because benzodiazepines are direct agonists at a rapidly responding ion channel, their mechanism of action is virtually instantaneous with their arrival in the CNS (in contrast to buspirone, see below).
Buspirone
Buspirone is a novel medication that appears to act as an anxiolytic via its action as an agonist at the serotonergic SHT 1u receptor. In addition , it has some D2 antagonist effects, although with unclear clinical signifi cance. Unlike the benzodiazepines, it does not work rapidly; a period of several weeks of sustained dosing is required to obtain symptomatic relief Bu~pirone has no GABA receptor affinity and is therefore not useful in treating benzodiazepine or alcohol withdrawal. It is not a sedative and is not useful in t reat ing in somnia.
< IlOt f or 5..1e l > < tie JlI!R npo~ I •
74 • Blueprints Psychiatry
TABLE 14-1
Anxiety disorders Generalized anx.iety disorder Panic disorder
Moc:xj disorders lerTlp:orary treatment of anxiety associated with
depressiol) Temporary treatment of insomnia associated with
depression Treatment d agitatiOn in acute mania Possible mood-stabRizing effect in bipolar disorder
Adjustment disorders Treatment of adjustment disorder with anxiety
Sleep disorders Short-term treatment d insomnia
Miscellaneous Treatment ofakathisia induced by neuro!eptics Agitation from psychosis or other G.n.1:SeS
Catatonia (espedally Iot'azepam) Alcohol Withdrawal
• CHOICE OF MEDICATION
Benzodiazepines
The selection of a benzodiazepine should be based on an understanding of potency, rate of onset, route of metabolism, effective half-life, and clinically proven effet..--riveness. Although all benzodiazepines appear to function by common mechanisms, the particular combination of the above factors land perhaps as yet unknown variations in affinity for receptor subtypes) produce varied clinical indications for different benzodiazepines. Table 14-2 illustrates the properties of some commonly \JSed bem:odiazepines and their common clinical uses.
Potency
The high-potency benzodiazepines ruprazolam and clonazepam are used in the treatment of panic disorder.
Rate of Onset
Fru,t-onset benzodiazepines, such as diazepam, may produce a "high" feeling and are potentially more addictive_ The fast-onset bem:odia7.epines fiura7.epam and triazolam are commonly used for insomnia, as is diazepam.
Route of Metabolism
All benzocliazepines listed, with the exception of !orazepam/ OXa7..epam, and temazepam, require oxidation as a step in their metabolism. Because the oxidative functions of the liver are impaired with liver disease (e.g., cirrhosis) or with a general decline in liver function (e.g., aging), benzodiazepines that require oxidation are more likely to accumulate to toxic levels in individuals with impaired liver function.
Elimination Half-Life
The elimination ha1f-life depicts the effective duration of al-"'1:ion of the metabolized medications. for medications with long elimination half-lives, toxicity can easily occur with repetitive dosing. In addition, toxicokJgy screens may remain positive for several days after the last dose of a long-acting benzodiazepine. Drugs with longer elimination half-lives offer less likelihood of interdose symptom rebound. For example, clonazepam is now favored over alprazolam in the treatment of panic because its longer elimination half-life provides better interdose control of panic symptoms. Medications with shorter elimination half-lives are useful for conditions sllch as insomnia because they are less likely to produce residual daytime sedation or grogginess.
Active Metabolites
Medications with active metabolites generally have a longer elimination half-life. Among the benzodiazepines, all but three drugs metabolized by conjugation (lorazepam, oxazepam, temazepam) and donazepam have active metabolites.
Buspirone
Buspirone is indicated for the treatment of GAD. Because of its long lag time to therapeutic effect, patients "'.lith severe anxiety symptoms may be unable to sustain a clinical trial. 8uspirone is favored as a treatment in individuals \vith a history' of substance or benz()diazepine abuse. In ge.neral, buspirone lacks the reliability of benzodiazepines in relieving anxiety but can be effective in some people.
• THERAPEUTIC MONITORING
Benzodiazepines
Henzocliazepine dosing is generally titrated to maximize symptom relief while minimizing side effects
TABLE 14-2
Pftquentf)' Used ~nes
0", O~. ..,. U5ual """,. Oo~ge Therilpeutk Equivalency ' mgl """go (!!!SI )' (!!!SI/dal)
Alpr.u:olam (Xanaxl , 0.25-1.0 11>-4.0
Chlordiazepo~ <0-100 5.0-25.0 15.1}-100.0 (Ubrlum)
Clonazepam 05-2.0 1.0-4.0 (KJonopinj
Diazepam {ValIum} 20 2.0- 10.0 4.0-40.0
Fluralepam 120 15.0-30.0 15.0-30.0 (Dalm_)
lorazepam (Atl ...... n) • 05-2.0 1<>-6.0
Ox"t.epam (5etaJoC) 60 10.0-30.0 30.0-120.0
Temazepam 60- 120 15-15.0 1.5- 30.0 (Restonl)
Trfawlam (Haldon) 0. 125-0.25 0. 125-0.5
'~gkdo<e,"",,""oItncy. •• t,. hwn. £IIrrinat1on tIOIf-illo in<:"-- aj l ..rn... ......... boIi_
00'" Metabolism Ellmlnatlon Ac;tlve Hill',Ufe" ."'.
Intermediate """" ... 6-20 y~
intermediate Oxidation 30-100 y~
Intermediate Oxidation 18-50 No
Fast Oxidation 30-100 y~
raS! Oxidation 50-160 y~
Intermediate Conjugation 10-20 No Slow CooJugatloo 8-12 No
Intemledlate Conjugation 0-20 No
Fast OxIdation 15-5 y~
C_ Uses In Psychiatry
Panic, an*ty
Alcohol detOl(ificatlon
Panlc.anJdely
Anxiety. Insomnia
insomnia
Anxiety. catatonia
Alcohol detoXification
lruomnia
Insomnia n ;0 ~ • • > , • o· ;r ,. •
, •
• • I
I
I •
• ! • ! , • ! I , ~ , ; ; ,
< [lot f or ~al .. l. > < .,,' .IlI!R (]JXI~
76 • Blueprints Psychiatry
and the potential for abuse. No routine monitoring is required; although serum drug levels can be obtained, they are not of great clinical use. Care must be taken in prescrihing benzodiazepines because of their ability to cause physiologic dependence. They cannot be discontinued abruptly due to the risk of a withdrawal syndrome that may include seizures.
Buspirone
No routine monitoring or drug levels are required when using buspirone.
• SIDE EFFECTS AND ADVERSE DRUG REACTIONS
Benzodiazepines
The major side eRects ofbenzodiazepines are related to the CNS. The primary side effect of benzodiazepines is sleepiness or a general groggy feeling. Although benzodiazepines are often used to treat agitation, they may produce d isinhibition (and therefore worsen agitation) in some patients (i.e. , the dderly). Benzodiazepines are minimally depressive to the respiratory system in healthy individuals but can lead to fatal carbon dioxide retention in patients with chronic obstructive pulmonary disease. In healthy individuals, death after overdose on
benzodiazepines alone is rare but does occur when benzodia~epines are taken with alcohol and other CNS depressant medications.
Buspirone
Buspirone does not tend to cause sedation, nor does it produce a significant withdrawal syndrome or dependence. The major side effects are dizziness/ nervousness, and nausea.
KEY POINTS
1. Anxiolytics include benzodiazepif)es and buspirone.
2. Benzodiazepines bind to GAB~ receptors and have a COI11JaratJvely rapk! o"set of action; buspirone binds to serotonin receptors and takes effe<t alter weeks 01 daily usage.
3. Benzodlazepines have a wide variety of uses, including arudolysis. alcohol detoxification. agitation, and insomnia.
4. ~jazepines produce physioklgic dependence and may manifest ill significant withdrawal syndrome.:
5. Buspirol"]e.uears only generalized anxiety, but does not cause physiologk dependence.
This chapter includes medications that are commonly used in psychiatric practice but that do not fall into the conventional categories of psychotherapeutic drugs. Many medications used in general medical practice have side effects such as sedation, stimuJation, or anxiolysis. Thes~ side effects are often exploited in psychiatry t o target specific symptoms (e.g., insomnia, anergia). Other drugs, such as p!>ychostimulants, have precise indications for p!>ychiatric usage. Many more medications than are discussed here are included in the psychiatric armamentarium.
• PSYCHOSTIMULANTS ----------- ------ -- -- -- ---------- -------------Psychostimulants are used in psychiatry to treat attention deficit disorder, narcolepsy, and some forms of depression (Table ] 5-1). The most commonly used psychostimulants are dextroamphetamine (Dexedrine), methylphenidate (Ritalin), and pemoline (Cylert). The mechanism of action of these medications appears to occur through their alterations of central nervous system (eNS) monoamine function. Their primary mechanism of action is thought to be facilitating endogenous neurotransmitter release (rather than acting as a direct agonist). Psychostimulants have the liabilities of inducing tolerance and psychological dependence, which mar lead to abuse. The side effects of these medications are due largely to their sympathomimetic actions and include tachycardia, inSOmnia, anxiety, hypertension, and diaphoresis. Weight loss may be an unwanted side effect in young children but a desirable one in overweight adults.
Medications with anticholinergic activity are commonly used in psychiatry to treat or provide prophylaxis for some types of neuroleptic-inJuced movement disorders (Table 15-1). Anticholinergics are generally used as first-line agents in the treatment of neuroleptic-induced parkinsonism and for acute dystonia; ther may also have some utility in treating akathisia but are best tried after beta blockers and lorazepam. The most commonly used anticholinergics are bem':tropine and trihexyphenidyl. In addition, diphenhydramine, an antihistamine that also possesses anticholiner!,ric properties, is frequently used to treat neuroleptic-induced movement disorden; and to pro\i'ide nonspecific sedation. These medications are CNS muscarinic antagonists. Side effects of anti.cholinergics, due to peripheral anticholinergic action, include blurry vision (due to cycloplegia), constipation, and urinary retention; their principal central side effects are sedation and delirium. Anticholinergic toxicity is a major cause of delirium, especially in individuals with dementia and HIV encephalopathy.
• BETA BLOCKERS
Beta blockers are used widely in general medicine. In psychiatry, they have a few specific indications (see Table 15-]). Beta blacken; likely alter behavior and mood states by altering both central and peripheral catecholamine function. For example, in anxiety, they may diminish central arousal; peripherally. they may reduce tachycardia, tremor, sweating, and hyperventilation. Common side effects of beta blockers include bradycardia, hypotension, asthma exacerb~-
<" IlOt f or " .. 1 .. 1 :. < tie IlI!R npo~ , •
78 • Blueprinw Psychiatry
Medkation
Psyc.hostimulants
Antkl101in.ergics
Beta blockers
Disulfuram Clonidine
Taoine
Thyroid hormones
Major Psychiatric. Uses
Treatment of-auention deficit disorder
Treatment of depres!tiOn in me elderly or medically ill
'rrealment d narcolepsy Augmentation of
antidepressants in refractOf)' depression
Treatment of neurolepticinduced parkinsonism
Treatment of neurolepticInduced dystonia
Treatment of impulsivity Treatment c:I performance
anxiety Treatment of akathisia Treatment of lithium-induced
tremor
Prevention d alcqhol ingestion Treatment of impulsivity Treatment ofTourette's
syndrome Treatment of opiate withdrawal Treatment of mild to moderate
memory loss in Alzheimer's disease
Augmentation of antidepressants in refractory depression
tion, and masked hypoglycemia in diabetics. Beta blockers may also produce depression -like syndromes charactetized by fatigue and depressed mood.
Disulfirnmis used to prevent alcohol ingestion through the fear of the consequences of ingesting alcohol while taking disulfiram (Table 15-1). Disulfiram blocks the oxidation of acetaldehyde, a step in the metabolism of alcohol. The bttildup of acetaldehyde produces a toxic reaction, making an individual who inge~'tS alcohol while taking dhulhram severely ill within 5 to 10 minutes. Symptoms include flushing, headache, ~"Weating, dry mouth, nausea, vomiting, and dizziness. In more severe reactions, chest
pain, dyspnea, hypotension, and l.'Onfusion occur. Fatal reactions, although rare, can occur. Disulfiram use should he restricted to carefully selected patients who are highly motivated and who fully understand the consequences of drinking alcohol while taking disulfiram. Side effects in the absence of alcohol ingestion include hepatiti.s, optic neuritis, and impotence.
• CLONIDINE
C10nidine is a eNS alphaz adrenoreceptor agonist. The alpha2 adrenoreceptor is a presynaptic autoreceptor that inhibits the release of CNS norepinephrine. Clonidine 's primary use in medicine is as an antihypertensive (Table 15- 1). In psychiatry, clonidine has been variously used. It is effective in decreasing autonomic symptoms associated with opiate withdrawal and in the treatment ofTourette's syndrome, and may be useful for impulsiveness and other forms of behavioral dyscontrol. Side effects include sedation, dizziness, and hypotension.
• COGNITIVE ENHANCERS
Donepe7.l1 (Aricept) and tacrine (Cognex) are reversible inhibitors of the enzyme acetyl-· cholinesterase and are used t o enhance cognition in patients with mild to moderat e dementia of the Alzheimer's type. Some of the cognitive deficits in Alzheimer's disease are due to loss of cholinergic neurons in the basal forebrain that project to the cerebra l cortex and hippocampus, \vhich results i.n a deficiency (Jf cholinergic neurotransmission . Hy inhibiting the enZyme that hydrolyzes synaptic acetylcholine, these drugs are thought to raise synaptic concentrations of acetylcholine in the remaining cholinergic neurons. Initially, these drugs reduce cognitive impairment; however, this effect wanes 'with the progressive loss of cholinergic neurons. Common side effects include gastrointestinal upset and other cholinomimetic effects incl uding bradycardia and increased gastric acid secretion . Tacrine can cause elevations in serum transaminase5.
• THYROID HORMONES
Thyroid hormones are used primarily in psychiatry to augment the effects of antidepressants (Table 15-
1). They also may be used as adjuncts in treating rapid cycl ing bipolar disorder. Although clinical hypothyroidism can mimic the symptoms of depression, some individuals without clinicaJ hypothyroidism may respond to thyroid augmentation. The theoretic basis for u<;ing thyroid hormones lies in the finding of altered hypothalamic-pituitary-adrenal axis functioning in depressed individua ls. Although there is dehate as to their relative efficacy, both TJ (tn ·jodo thyronine) and T4 (tetra-iodo thyronine) Cl"Q:<;S the blood brain barrier. T4 has been sbown to be of use in conjunction with lithium to improve c1inkal control of rapid cycling bipolar disorder. Side effects at low doses are minima l; when dosages result
Chapter 15 I Miscellaneous Medications • 79
in over-replacement, symptoms of hyperthyroidism emerge.
KEY POINTS
1. Miscellaneous medications are widely used,Of" treatment of symptoms and side effects.
2. They overtap with medications used In other medical PlCICtice.
3. They have side effects and efficacy' spedtlc to each medication and its target symptoms.
This chapter describes a group of major adverse reactions associated with use of psychiatric medications. Minor adverse reactions and side effects are outlined in the chapters on the respective medications. Although the adverse d rug reactions discussed below (with the exception of serotonin syndrome) are most commonl y produced by antipsychotic medications, they may occur in response to other medications. The major adverse drug reactions to antipsychotics, their risk factors, onset, and treatment are outlined in Table 16-1. Although the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, classifies dy~tonia, akathisia, extrapyramidal symptoms (EPS), neuroleptic malignant syndrome (NMS), and tardive dyskinesia <u; neurolepticinduced movement disorders, it is clear that akathisia can occur with the use of nonneuroleptic psychiatric medications.
• DYSTONIA
Dystonia is a neuroleptic-induced movement disorder characterized by muscle spasms. Dystonia commonly involves the musculature of the head and neck but may also include the extremities and trunk. Symptoms may range from a mild subjective sensation of increased muscle tension to a life-threatening syndrome of severe muscle tetany and laryngeal dystonia (laryngospasm) with airway compromise. The muscle spasms may lead to abnormal posturing of the head and neck \.o,'ith jaw muscle spasm. Spasm of the tongue leads to macroglossia and dysarthria; pharyngeal dy~tonia may produce impaired swallowing and drooling. Ocular muscle dystonia may produce oculogyric crisis.
Risk factors include use of high-potency antipsy-
chotics; young men are at increased risk. The condition usually develops early in drug therapy (within days).
Treatment of dystonia depends on the severity of the symptoms. In the absence of laryngospasm or severe patient discomfort, intramuscular (Itv1) anticholinergic medication (henztropine or diphenhydramine) can be used. In more severe cases or if laryngospasm is present, IV anticholinergic medication is used. Some cases may require intubation if respiratory distress is severe. Discontinuation of the precipitating antipsychotic is sometimes necessary; in other cases, the addition of anticholinergic medications on a standing basis prevents the recurrence of dystonia.
• AKATHISIA ----------------------------------------------Akathisia, a common side effect produced by antipsychotic medications, is also caused by serotonin reuptake inhibitors. Akathisia consists of a subjective sensation of inner restlessness or a strong desire to move one's body. Individuals with akathisia may appear anxious or agitated. They may pace or move about, unab1e to sit still. Akathisia can produce severe dysphoria and anxiety in patients and may drive them to become assaultive or to attempt suicide. It is important to accurately diagnose akathisia because if mistaken for agitation or worsening psychosis, antipsychotic dosage may be increased \"o'i th resultant worsening of the akathisia.
Risk factors for akathisia include a recent increase in medication dosing or the recent onset of medication use. Most cases occur within the first month of drug therapy but can occur anytime during treatment.
TABLE 161
OkonIer
Dystonia
Akathisia
EPS
NMS
Tardrve dyskinesia
Risk Factors
High-potency antipsychotics Young men
Recent increase/onset of medication dosing
High-potency antipsychotics Elderly
Prior episode of EPS
High.<Jose antipsyrnotics, rapid dose escalation, or 1M injection of antipsychotic5
Agitation, dehydration Prior episode of NMS
Elderly Long-term antipsychotic
treatment
""""Ie Afria m American Mood disorders
Chapter 16 I Major Adverse Drug Reactions • 81
Onset
First few days of therapy
First month of therapy
first few weeks of therapy
Usually within first few weeks; can occur at any point in antipsychotic therapy
Usually after years of u-eatment
T_t
IM/IV benztropine or diphenhydramine
Severe laryrl90spasm may require intubation
Propanolot,lorazepam (maybe anticholinergks)
Anticholinergic Lower antiJl§YChotic
dosage or change to lower-potency antipsychotic
Discontinue antipsychotic medkation
Supportive symptom management
Dantrolene, bromocriptine
May require intensive <are
lower dosage of antipsychotic
Change antipsychotics Change to clozaril
"The DSM-IV da5~ I'ofthe5e disorUeri defi~ tN;m M neurolepllc:..if1dO«d ~ disorders.The telll'l ne.JroIepricgeroerally ref~ 10 typic:;!1 «rtlps)'thotk~ b~Ql"'PtCf 11). Eor<:eprion~ indude ril;peridone.which 1~ ckmlfied liS ~n alypiQI ilntlps;ychoti( btJt DIn ~5e aM the above disorders; "SSRIs, wf1ich ttl! not net.lrolf!PI:~ drugs btJt can d l!ar!)' produce akathl:ila;and clozaril, which doe§ not appe;tr to produce dy5tooiil,al\athisia, EPS.or t ardive dyskinfl~ btJt may caus.e NMS.
Treatment consists of reducing the medication (if possible) or using either beta blockers (propanolol is commonly used) or benzodiazepines (especially lorazepam). Although there is some doubt 3 S to their efficacy, anticholinergics (diphenh}'dramine or benztropine) are abo used fretjuentJ}'.
• EXTRAPYRAMIDAL .s_'!'~.P.:rg_~~J~!'_~L. __ . ___________ ______ . EPS, also known as ncuroleptic-induced parkinson ism, consist of the development of the classic symptoms of Parkinson's disease but in response to
neuroleptic use. The mm.1. common symptoms are
rigidit}' and akinesia, which occur in as man}' as half of all patients receiving long-tenn neuroleptic therapy. A 3- to 6-Hz tremor rna}' be present in the head and face muscle.:s or tJ1e limbs. Akinesia or brad},ki nesia are manifested by decreased spontaneous movement and may be accompanied by drooling. Rigidity consists of the c1 as.<;ic parkinsonian "lead pipeH rigidity (rigidity that is present continuously throughout the passive range of motion of an extremity) or cogwheel rigidity (rigidity with a catch and release character).
Risk factors for the development of EPS include the usc of high-potency neuroleptics, increasing age, and a prior episode of EPS. EPS usually develops withi n the first few weeks of therapy.
< not f w "'<tl .. I .. :> < ke .. lIlSI ~ I ..,
82 • Blueprints Psychiatry
Treatment consists of reducing the dosage of antipsychotic (if possible) and adding anticholinergic medications to the regimen.
• NEUROLEPTIC MALIGNANT SYNDROME (NMS) - ---------- -------- --.- - --- -- -- ~ - ---------~---NMS i... an idiosyncrntic and potentially lifethreatening complication of antipsychotic drug use. Symptoms of NMS may develop graduaUy over a period of hours to days and can often overlap with symptom .. of genernl medical illness. The major clinical findings in patients with NMS are presented in Table 16-2. Many symptoms of NMS are nonspecific and overlap with symptoms common to other psy_. cltiatric and medical conditions. The diagnosis of NMS is also complicated by the waxing and waning nature of the clinical pil..ture.
Autonomic instabiJity coupled with motor abnormalities is essential to the diagnosis of NMS. Autonomic alterntions r..:an include cardiovas<.ular alterations with cardiar..: arrhythmia .. and labile blood pressure~ Low-grnde fever progressing to severe hyperthermia may also be present. Motor findings may overlap with other motor abnormalities in psy-
Autonomic Tachycardia. other cardiac arrhythmias Hypertension Hypotension Diaphoresis Fever progressing to hyperthermia
Mote' Rigidity/dystonia Akinesia Mutism Dysphagia
Bet)avloral Agitation Incontinence Delirium Seizures Coma
Laboratory Increased creatine kinase Abnormal liver function tests Increased white blood cell count
dUatric illness, for example, rigidity/dystonia can be confused with simple dystonia or with EPS. Mutism can be a sign of severe psychosis or catatonia alone, although this Joes OCLUf with NMS. Behavioral feahues such as agitation can also overlap with other psychiatric syndrome'i; however, the presence of delirium or seizures is a harbinger of more serious general medical illness (including drug withdray,ral) or NMS. Laboratory findings may reveal an increa .. ed r..:reatine kinase secondary to myonecrosis from sustained muscular rigidity. Liver enzymes may be elevated, but their relation to NMS is unclear. Leukocytosis is also often present.
Risk factors for the development of NMS (see Table 16-1) include the use of high-dose antipsywoties, rapid dose escalation, IM inje<.tion of antipsychoties, dehydration, agitation, or a prior history of NMS. Some factors may be. related to severity of illness (e.g., severely ill patients often have poor oral intake and become dehydrated, are more likely to be placed in restraints, and require 1M injection of an antipsychotic) rather than causative factors. Although NMS is most common during the first few weeh of antipsychotic drug therapy, it r..:an occur at any time during therapy.
Treatment of this potentially fatal disorder is "largely supportive. Specific interventions include discontinuation of antipsychotics (an option tha~ may take a long period of time in individuals treated with depot antipsychoties); dantrolene (a muscle relaxant) is used to treat rigidity and decrease myonecrosis; and bromocriptine (a dopamine agonist) is sometimes used to reverse dopamine blocking effects of antipsychotics. Symptom management including intensive r..:are with cardiac monitoring and intubation may be necessary. Symptoms ofNMS overlap with serotonin syndrome (Table 16-3). However, in NMS, muscular rigidity .and increased creatine kinase are prominent findings. In addition, serotonin syndrome develops in response to the use of multiple medications that affeLt. serotonin ftmction (especially monoamine oxidase inhibitors [MAOIs ]), whereas NMS develops in response to antipsychotic medications. In patients using both MAOIs and antipsydlOtics (e.g., refractory psychotic depression), the differential diagnosis r..:an be quite difficult. .
• TARDIVE DYSKINESIA (TD) ---~-~ - - -~ - - ~ -- -- ~ - ~ - -- ----- -- -- -- - ~ - - ~ ---~~-
TO is a movement disorder that develops with longtenn neuroleptic use; rarely, espedally in the elderly,
, TABLE 16-3
SKoeaIIIn 9)wIraa,. Autonomk;
Tachycardia Hypertension Diaphoresis Fever progressing ~ tlYperthermia
Mow Shivering M~1onus Tremor Hyperreflexia Oculomotor abnormalities
Behavioral Restlessness Agitation Delirium Coma
onset may not be. as delayed. TO consists of constant, involuntary, stereotyped choreoathetoid movements most frequently confined to the head and neck musculature. At times, the extremities and respiratory and oropharyngeal musculature' are also involved.
Risk factors include Jong-term treatment w ith neuroleptics, increasing age, female sex, and the presence of a mood disorder. Although TO is reversible in some ca.~, it tends to be permanent.
Treatment consist. .. of changing antipsychotics, lowering the dosage, or s\vitching to dozapine. Clo7.apine, which appears to work by a different mechanism from other antipsychotics, may reduce or eliminate the abnormal movements of TO.
• SEROTONIN SYNDROME
Serotonin syndrome can occur when multiple med~ kations that alter serotonin metabolism are used.
Chapter 16 I Major Adverse Drug Reactions - 83
Classically, this syndrome is produced when other serotonin-altering medications are used with MAOIs. This syndrome, which can be life-threatening, consists of symptoms outlined in Table l6-3. These include severe autonomic instability, motor abnormalities, and behavioral changes. The course of the disorder can become malignant and end in coma and death. A similar syndrome occurs when lv1AO[s are used with meperidine or dextromethorophan, and perhaps other opiates..
Serotonin syndrome has many similarities to NMS but may be distinguished in the follOWing ways.. Serotonin syndrome does not produce muscular rigidity or dystonia as does NMS. Further, NMS occurs during the use of antipsychotic medication; while serotonin syndrome occurs tlu-ough use: of MAOls or other serotonergic agents.
Risk factors for serotonin syndrome. other than combining MAOIs with other serotonin-altering medications, are not kn own,
Treatment for serotonin syndrome is largely su pportive and may require intensive care with cardiac monitoring and mechan ical ventilation. The offending medications shouJd be discontinued.
KEY POINTS
1. Major adverse drug reactions occur most commonly In psychiatry with use of anti psychotics and serotonin-altering medications.
2. Antipsychotks can cause dystonia, akathisia, fPS, NMS,andTD.
3. Seroton;n~altering medications can cause akathisia and serotonin syndrome.
4. All of the above adverse drug reactions Me
reversible, except for TD. whkh may be permanent.
There are a large number of competing theories influencing contemporary psychotherapeutic thinking. Psychotherapies derived from psychoanalytic, cognitive, and behavior theory are the most widely used. Cognitive and behavioral interventions have the strongest empirical verification; little empirical evidence supports the efficacy of analytic/dynamic therapies.
• PSYCHOANALYTIC! PSYCHODYNAMIC THEORY
The principal theorist responsible for launching psychoanalysis a<; a technique and psychodynamic theory in general is Sigmund Freud. Freud's theories proposed that unconscious motivations and early developmental influences were essential to understanding behavior. Freud's original theories have proven quite controversial and have led to the creation of various alternative or derivative theories.
Twentieth-Century Schools of Psychodynamic Psychology
There are three major rurentieth-century psychodynamic schools: drive psychology, ego psychology, and object relations theory.
Drive Psychology Drive psychology posits that infants have sexual (and other) drives. This theory proposes that sexual and aggressive instincts are present in each individual and that each individual passes sequentially through psychosexual developmental stages (oral, anal, phallic,
latency, and genital). Included in drive psychology is conflict theory, which proposes to explain how character and personality development are influenced by the interal."tion of drives \'lith the conscience and reality.
Ego Psychology Freud eventually developed a tripartite theory of the mind in which the psychic structure was composed of the id, ego, and superego. Under this theory, the id is the compartment of the mind containing the drives and instincts. The superego contains the sense of right and wrong, largely derived from parental and societal morality. The ego is responsible for adaptation to the environment and for the resolution of conflict. A major function of the ego is the reduction of anxiety. Ego defen<;es (Table 17- 1) are proposed as psychic mechanisms that protect the ego from anxiety. Some ego defenses (e.g., sublimation) are more functional to the individual than others (e.g., deni,,]).
Object Relations Theory Object relations theory (ubjects refers to important people in one's life) departs from drive theory in that the relation<;hip to an object is motivated by the primacy of the relation<;hip rather than the object being a means of satisfying a drive. Child observation furthered ohject relations theory, emphasizing concepts of attachment and separation.
The interpersonal school arose as an outgrowth of object relations theory. The interpersonal theorists emphasize that intrapsychic conflicts are less important than one's relationship to one's sense of self and to others. In other words, the relationships in a
Chapter 17 I Psychological Theories • 85
TABLE 17- 1
oan-lgoCs'p _Medleitisms
Oerual Feelings or ideas that are distressing to the ego are blocked by refusing to recognize evidence for their exmnce.
Projection Feelings or ideas that are distressing to the ego are attributed to others.
Regression Feelings or ideas that are distressing to the ego are reduced by behavioral retum to an &lI1ier development phase.
Repression
Reaction formation
Feelings or ideas that are distressing to the ego are relegated to the unconscious.
Feelings or ideas that are distressing to the ego are converted into their OpPOSites..
Displacement feelings or ideas that are distressing to the ego are redirected to a substitute that evokes a less Intense emotional response.
Ratlonallzittion feelings or Ideas that are distressing to the ego are dealt with by creating an acceptable alternative explanation.
Suppression Feelings o r Ideas that are distressing to the ego are not dealt with. but they remain components of conscious awareness.
Sublimation Feelings or ideas that are distressing to the ego are converted to those that are more acceptable.
Modified from Sadodt BJ, Sadcxk VA. U:lfwr~ ~ 0( psychiMry. 1th eel Phitadelphia: lippi~ W~lillfffl & Wilkins, 1999.
person's life are given primary importance in producing happiness or misery.
• ERIKSON'S LIFE CYCLE THEORY
Erik Erikson made major contributions to the concept of ego development. Erikson theorized that ego development persists throughout one's life. Erikson conceptualized that psychosocial events drive change, leading to a developmental crisis. According to Erikson 's model, individuals pa.<iS through a serio; ofUfe cycle stages (Table 17-2) . Each stage presents core conflicts produced by the interaction of developmental possibility with the external world. Individual progress and a.<iSociated ego development oCOJr with successful resolution of the developmental crisis inherent in each stage This model aUows for continued ego development until death .
• COGNITIVE THEORY
Cognitive theory recognizes the importance of the subjective experience of oneself, others, and the world . It posits that irrational beliefs and thoughts about oneself, the world, and one's future can lead to psychopathology.
In cognitive theory, thoughts or cognitions regarding an experience detennine the emotions that are evoked by the experience. For example, the perception of danger in a situation naturaUy leads to anxjety . When danger is truly present, anxiety can be adaptive, leading to hypervigilance and self-protection. When the situation is only perceived as dangerous (such as in fear of public speaking), the resulting anxiety ca.n be psycholoj,ricatJy paraly"~ing. A person may fcar public speaking because of an irrational fear that somethi ng disastrous will occur in public. A principal type of irrational belief is a cognitive distortion (Table I 7-3) .
• BEHAVIORAL THEORY
Behavioral theory posits that behaviors are fashionet.l through various forms of learning. including modeling. classical cond itioning, and operant conditioning (fable 17-4). A behaviorist might .propose that lhrougb operant conditioning, depressi.on is caused by a lack o f posi.tive reinforcement (as may occur after the death of a spouse) , resulting in a general lack of interest i.n behaviors that were once: pleasurable (or rcinforn .'d) .
86 • Bluepritrt;!'i Psychiatry
Trust versus mistrust Birth to 18mos.
Autonomy Ver5US shame 18 mos. to 3 yrs.
Initiative versus guilt 3-Syrs.
Industry versus inferiority S- 13yrs.
Identity versus role confusion 13- 21 yrs.
Intimacy versus isolation 21-40yrs.
Generativity versus stagnation 4O-60yrs.
Ego integrity versus despair 60 yrs. to death
The infant has many needs but does not have the power to have those needs met. The child is dependent on caretakers. If caretaking Is appropriate. a sense of trust and hope are created. If inappropriate or inadequate. mistrust develops.
The child is leaming about the use of language and control of bowel and bladder function and walking. As a resuJt.lt begins to choose to influence and explore the wortd If caretaking is appropriate, the child will develop a healthy balance between exerting Its autonomy and feeling shame over the consequences of exerting autonomy.
As the child develops increasing control of language and walking. he or she has increased initiative to explore the worId.The potential for action carries with it the risk of guilt at indulging forbidden wishes.
The child begins to develop a sense of self based on the things he or she creates. Caretaker influences are important in helping the child develop a sense of mastery and competence over creating.
Corresponds to adolescence. How one appears to others is important in this stage. There are conflicts between one's Identity and the need to gain acceptance.
The anxiety and vulnerability produced by intimacy are balanced against the loneliness produced by isolation.
If successful, the individual develops a positive view of his or her role in life and a sense of commitment to society at large. If unsuccessful, individuals move through life without concem for the greater v-.telfare.
An individual accepts his or her life course as appropriate and necessary. If this fails. the individual may regret or wish to relive some part of life, leading to despair.
Modified from Sadock 8J, SMhck VA. Compr~sr"e textbook d psychiatry. 7th ed. PhiI8deIphla: lippincott, W~liams & WIfldIlS, 1999.
, TABLE 17-3
..".. rtlClogoIIhe __
Arbitrary inference Drawing a specific conclusion without sufficient evidence
Dichotomous thinking A tendency to categorize experience as -all or none"
Overgeneralization Forming and applying a gene~ rondus1on based on an Isolated event
Magnlficationl minimization
Over- or undervaluing the significance of a particular event
Modified from Sadock 8J. 5a6ock VA.. Comprehensive textbook d ~Iry. 7th ed Phi18dl!1phla; Uppif1cott, Williams & W-~kins, 1999.
, TABLE 17-4
Modeling
Classical conditioning
Operant conditioning
A form of learning based on observing others and imitating their actions and responses
A foIm of-learning in which a neutral stimulus is repetltivey paired with a natural stimulus, with the result that the previously neutral stimulus alone becomes capable of eliciting the same response as the natural stimulus
A form of leaming in which environmental events (contingencies) influence the acquisition of new behaviors or the extinction of existing behaviors
Chapter 17 I Psychological Theories • 87
• COGNITIVE-BEHAVIORAL IJ:I_~~_~n! ~-'HI ______________ __ __ ________ _
Cognitive and behavioral t heories form part of the bases of CST. CRT involves the examination of cognitive distortions and the use of behaviornl techniques to treat L"Onunon disorders such as major depression.
KEY POINTS
1. Psychological theories are numerous, but those derived from psychoanalytic, cognitive, and behavioral theories are most widely used.
2. The psychoanalytic school emphasizes unconscious motivatoos and early Influences.
3. The cognitive school emphasizes subjective eJl:perience. beliefs, and thoughts.
4. The behavioral school emphasizes the Influence of learning.
S. The cognitive and behavioral schools have the greatest empirical support.
Legal issues affect all areas of medicine, including psychiatry. The laws that govern medical practice address physician duty, negligence, and malpractice as well as patient competence, consent, and right to refuse treatment. Previous court decisions, or precedents, are used as the standard by which a given action (or inaction) is judged. Practitioners should be aware of the pertinent laws of the state in which they practice in order to comply adequately with standanis of practice while respeding the rights and duties of their role. Reducing adverse events and legal claims in the health care system is known as risk management.
• MALPRACTICE ---- ------------------------------------------The legal definition of malpractice requires the presence of four elements: negligence, duty, direct causation, and damages. Negligence can be thought of as failure to perform some task with respect to the pati ent, falling short of the care that would be provided by the average practitioner (the standard of care) . Duty reflef...ts the law's recognition of the obligation of the physician to provide proper care to his or her patients. Direct causation requires that the negligence directly caused the alleged damages. Finally, damages (e.g., physical or emotional harm) must in fact be shown to have occurred. In short, maJpractice involves the negligence of a duty that directly causes damages. Malpractice claims in psychiatry principally involve suicides of patients in treatment, misdiagnosis, medication complications, false imprisonment (involuntary hospitalization or seclusion), and sexual rdation'> with patients.
• INFORMED CONSENT ------------------ ---------- ----- -------------Informed consent ha'> three components: information, competence, and consent. First, appropriate levels of information regarding a proposed treatment, including side effects, aJtemative treatment'>, and outcome without treatment, must be provided. Second, the patient must be competent (i.e., have the capacity to understand, reason, and make reasonable decisions regarding the risks and benefits of treatment). Third, the patient must give consent voluntarily. True emergency situations are an exception to
this rule; treatments necessary to stabilize a patient in an emergenf...Y can be given \vithout informed consent.
• INVOLUNTARY COMMITMENT ----------------------------------------------Commitments are generally judicially supported a(.1:ions that require persons to be hospitalized or treated against their wilL Although laws vary from state to state, commitment criteria lL'>ually require evidence that the patient is a danger to self, a danger to others or is unable to care for him- or herself Psychiatrist:' in most localities, have the right to temporarily involuntarily commit a patient if any ofthese criteria are met and a diagnosis of a mental disorder is provided (in other words, both a mental disorder and danger must exist). The duration of temporary commitment and the right" of the patient vary by jurisdiction. Patients who have been committed have a right to be treated, and unless they have been declared incompetent, they have the right to refuse treatment.
• THE TARASOFF DECISIONS: DUTY :r:<>_ W~!l_~_ 19!l_ !'!l~J:~q) .. _______ __ .. _ ..
'rarasoff vThe Board of Regents of the University of California (or simply, Tarasoff) wac; a landmark case that was heard twice in the California Supreme Court in 1976. Tarasoff I held that therapists have a duty to wam the potential victims of their patients. Tarasoff U held that therapists have a duty to take reasonable steps to protel..t potential victims of their patients. In most localities, this means that the ther· apist should take reasonable a<..uon to protect a third party if a patient has specifically identified the third party and a risk of serious harm seems imminent .
• M'NAGHTEN RUlE:THE INSANITY DEFENSE
Named after a mentally ill man (M'Naghten) who attempted to as.<;assinate the prime minister of England in 1843, this rule forms the basis of the insanity defense. According to the M 'Naghten rule, a
Chapter 18 I l egal Issues • 89
person is not held responsible for a criminal act if at the time of the act he or she suffered from mental illness or mental retardation and did not understand the nature of the act or realii'..e that it was wrong. In more recent history, the appropriate use of the insanity defense ha.c; been calleJ into question. Some legal theorists argue for the designation "guilty but insane" to indicate culpability but at the same time re(.'Ognize the presence of a mental illneos (and presumably the need for treatment).
KEY POINTS
1" Malpractice COnsists of negligence, duty, direct causation, and damages.
2. The Tarasoff decision led to an expe<tation that therapists aDd doctors take reasooabte action to protea persons whom their patitmts ha\le specifically threatened.
3. The MrNaghten rule is the basis of the insanity defense.
@ "24 ~ /111ft _.-, at sd*'4lI. ' _ seIIIS .......... ", 1~sh.I"'d6."" rIgon.HI --........... -.. _--"'."'_ "'" ..... It. _ bJ _ He hod _.-..,cae_hthtdboon·· 'dog .... 1NsgJa • .,.-•• ,-..:hoIItmerlr .. , ...... ,,_ cae _ • wac _ at ().2. 'IIIe _ IIoeIy
.........-_It..-.has_~c &. ..........
b. 0100 ...... Co CIcapIrie d. Que\IojIIne e. TNaiIltazMe
2. A 19 )'IIIHJId..-,ptlllllbforagynecologk.erem-___ ............ _ ~ sod 1aooIy.
F ....... Inqo*y..- ............. has lode "'_ Bdtof ~nt ~ UMI aaIvfdII.. trouble (()I~ ~end has __ "'111 and eoting _ ............ She .. 'NIl urd Me "mptorM begin I'I'\Cft thin 2 """""'_Sht .............. -._. __ ~_ ... lwdlnlc_ .... hor~_ ~ _ • TSH _ • """"" __ was
_ .. lA.5IIe _....-*""'" "'" '" 1 to 2_"..-. '1tIo __ II<oIycbgnaolslE .. ~-b. MIP' deIlIIIII ra. .... c. _ ........ duo ... --'_""_ d. __ di_
e. IbmII bela...,..
@ nne weNrIW begin .. fluel •• for .. epIsoded .21 .. Di\,.studI8ItisblaughtlOlhe .... 9I'!lCJ1DOm bJher"""""' .... ~ 1 __ .... .-.
began ocmg ~ at hor don" .... )'. 5ht began ~ up II nIgIW ~ on 1*>l«Is"" _ ..... ..... 1Iod of her dosses end "...... ClOlIy getting 2 to 3 hauls 0/ oIeepper nlght.reported ~ r_,,", was
opo;oIot1g _1IIIidII< _ 1ept , .... ,~III ",._ret ...., ~ .... FII _ "'" OA. She Hood ropId1y
'"'"' adIed, aIJItii- ",skins to IearfuI ~ don. She _Old _ -.g flit "'" _ -.. and said ........ hod boon ~ ... _ .. as ... ...-. '1tIo cIrrgr ...... ""'_ h:
.. --b. lIpoIor ......... c.~ d.~ __ .. _IIne~_er
4. An 15 -'*' Mood -. of • local ~ Is -.gtrt In bJ her son for • ...- ..... to .... "'"'care pwvwtdeL He ,.m tNtlhe Is pre.gle$IMfy mote
lorvetfuIand "00._ ...--.i&llrglimat " • '9 her InDnIY _ ~ to put her In • rvsing _She has no prIor.-.y of _Of ..... brO'w.a_ '""'" She hn no '-'wa: HrV risk facton. _ b.famIIy.-y of .... , ...... In on oIder-... Qn ..... the peIIent is *till ........ engeging.She _ """"""" of del _ ... her ....... -..
_ end _ .,... "'" ".",.. '" """"" _prIIIarI-.buI ___ ofpollllcol _ .... ponIes_JO-"prIor.She __ ....
., caMncedtt:.t .... son Is out to~ her money and
put .... _" buI_ -IIIIY-.... 'MJUId support .. <onduIIIIn.NewoIcltbI ex;;wn is non__CTocan_and_curor ..... _ _ for ___ ...",.". liN .... Is ~ ____ B",endnlodnlew�s ... nonnoL
5enrnr IFI1 .. '-""' '1tIo _11oeIy dlognoois h: .. YaKualrden'ea b.TonIory~ c. MajDrdap.asIun 4. AIzhNner\ denlenGa .. ~-
<! rmt em, " . l e I :. "" "I! .IIJUI opo_ t >
5. A 39-ytM-okt man vtsm; a new primary care p~dan for a first visit at the urging d his mocha He denies symptoms of depresslon except for ocasionallow mood. His father died v..f1en he was tA and he has lived with his mother since that time. He works itS a computer pr0-
grammer and says that he has many acquaJr1tances but few friends and no romantic relationships. His ~ had to convtnce him to go to the appointment bec;Juse
he had trout:ate deddlng to see a physician. His mother accompanies him on the visit and relays that she often decides things for him I:>ecause he has "neyer been able to think for 1iimseH".~ He says,"Peopte think rm too dingy. The truth is I just want people to care about me. ~ When you speak wttn him alone. he appears to have a nannal intellKt. no magicaC or odd thinking. and a stable sense of self but I'e\'eaIs a desperate rear then his mother wiN abandon him. He denies any setf-destrucUve or;mputsive behaviors. The most likely d~J105ls is:
.. - penonality-b. Depondent penonaIJty dhonler c. Sdllzotwal p."""aIity disorder d. Narcissistic petlOOality disorder .. Sdllroldper>onallty_
6. A 77-year-old female with a history of mild AlzheHner's dementia Is evalUlfted In the EWforconfusiOn.Her family reports that she was cst her baseIne until this morning when .he become 1n0SHlng1y _ted. 00 ""
recognizing fa'l'IIy ~ ... had known the day before.ln addition. she repeatedfy~ned ofhearJlg voices down the ~ when there was onty a televklon. On examination, she is initially pleasant and alert. She Is oriented to penon, but is comnncect that she is In an army borr.ru and _ )OU and the other _I _ are military pda. She can speI the word world forward but not backwaIds. Later In the interview she seems distracted and then doles off. I..aboRtory resuks reveal normal flncftng5 except fct' a mJId anem .. tncre.sed wac with ",,"",oed PMNs and band rorm.. UrlnalyO • .....,. no blood. 50-100 wee pel' HPF. gross bacturIa.The most hkely diagnosis Is: a. Worsening dementla b. Delirium Co ~ disorder d M.;o. dep<eooNe_ e. Meningftls
7. A :z3..year-old male who is in psycflcpharmacological and psychotherapy tn!tatment with you for major depression a'Ssociated with a ~ romantic breaIc."UP states that he would like to kiN the new boVfrtend d hiS ex. He has no history of vidence. but has spoken at Ie:ngth of his rage. humlHation, and powerlessness in ~d to the breakup. He teUs you the intended victim's name and address. .
QuestIons • 91
saying that e-mything will be fine once his rival Is out d the pic:Wre. You are very concemed and offer the patient an iIlpadent admission; in addition. you teU him you beIeve )'OU need to warn the intended victim and the poke. The patient refuses an admisskln and refuses-tD alkwi you to contact any 00bide patttes, stadng that you are t)ls therapist, and are thefefore t:>omd by corilden-tiaIIity laws. You fear that you wM110se your I6cense if you dfsclost the contents of the session. The patient then storms from your office., yelPng that)'OlJ can't be trusted. You "","Id: .. No<IIy the police and tt.e .. tended _m of your ~'s staterl.ents.
b. Request: a case consultation from the hOSpital ethicist. c. Attempt: to contaCt yow piJtlent's. family 50 they can
coovioce him to cool down. d . .. ...... the """"'""""'Ity of tt.e ...... py __ e. Consider raising the patient's medicadon dosage at
the ne><t meeting.
8. A 53-year-old male Is broUght to the EW ~ the police after he was found wandering In ttaffic. He is ~Ied. agItatod. and conMed. On phyolcol exa",.-n he !>os vitat signs fA blood pres5U'e 2001110. '-rt rate at 124, respirations 22.. temperature lOl"F. He has prominem dllmd pupils. 5)1T1melrical hypenefiexia, acne rosacea. palmar erythema. and tender hepatcmegaly. On mental status examination he is orlentrd only to person. He has difficufty paying atrentIon to )OUt questions,. at times appNrtng to focus on the inteMew but at other times commenting on bugs crawling on the walts. He cannot provide any useful histoly. He has iIltetTnjttellt epiSodes of out of control bet\:iMor.ewntually requiring resnints by the EW ...rI. laboratory .....,. ..,.,., mild pancytOpenIa on CBC with an inaeasecl MeV: electrolytes ate
normal vMh eM exception of reduced mag~um; IIvef functions show InQeased Rver enzymes witt! deaei!I5ed albumin. Urine and 5e(Um toxtcotogy screens are neg&
..... Head cr k negative. LP b nonnaI. Th. ""'" likely cIagnoskl< 8. Dementia b. Sdll"""""",,, c. Opiate withdrawal d Coalnewtthdrawal e. Alcohol withdrawal
9. A 2(}.year-oid femaJe colege student comes to the emet"
geo<y room complaining of brI<! episodes of"fluttering" in her dlest and chronic lightheadedness. sa.. has a benign medkaI history iIfld takes no medicatloo5. On physical e}G!WTl, her skin is pale,. her heart rate is 54, and her blood pressure Is 88150. When .she rekictantly partJally ctsrobes for further examinatiOn, you note an emac"iated body. She weigh! 78 pounds and stands
5' fI'. When )IOU CCJmIIII!iftt an her low' body WI!Ight. she &tfthe.Iy SUtIS, -rm. rat «M.·She says chit me hu been .-wng "" 3 to 4 I\aurs per day ..... bogio .... mIIege 2,.... _ ShI! ,_"""" to __ per_ which wcaunts conlfJ~She has not bed
her paIod In '4 .-ShI! denies dopos_ meed ..... _ ","" .her _ body In-. _ .. Nave Intact MSOIIIklg. She denies tIIngIng or purgi1g 1>0_. Tho..--..-Is:
.. ....".. ---- /lOI1IUI!Ik>g '"'" b. "'--'*'!Ie~,"", c. -. ..... dtI;_'"'" d. AnoI'I!'JIiI nencsa...estritdi*o ~ .. bady~-
G ""8S~ __ • .-yaf~_ _dell ...... lsbnJughttr.m.loaInunlnghometo ... II!IheIVIIltYmomciuetolnor • 'II IewIId~ ~On_.her'-Is __ ""_ and her pupils ... _Hor blood _ Is ,_
heart f'III:e" 99,respinIImy rMt is 16.and body ~ .... ,,!I!I.6'f. ShI! Is _to place lind _ ....... ",-ofblunyvision, __ .-.....In hor _ lite nunIng '-.-_ IhIt ... ~"'-_tgly"fllaladond",", ............ ITlII!fIadIons helle been tried ro deer.'1! the agitation. The~_.....,ber"" ..... _shehas betomelhlsccnfused ........ laIC 24 houos.SIte ... not __ "'I fOIls and .... pIIysbI -... IndudIngfIAI........".....ondr.nso.coplc_ Is 011 ............... Tho noootllloely dIognosis Is: &. YtbnanIng demee d:ta ' b._ c. eeo.- Iooo!moni1age d. AntktiORnergk:: delirium .. ~*-
I'. A 64 year-aId WtIIND fs SHft"'" 0UCpIUtt1l medir:aI cINe 2 months after an acIn'1is.on for a tvA. HIt I.nhIM ~IIS d right fadaI and arm J*esIs haw! now "'_ compIo!4I!Iy. _. tho _pIoIno 0I1eeIing • ... her ........... ·SIle .. _ ",..-to~!IOt>!I
to .... herdoughOer end _""'-' once. _ but
"'"' she ....... boon In 4 -.. Far INs; she """'"' feoIIng"lorribly guiIly.·SIoe .... _!hot. man _ she was dodnu Just pIor to 1100.- .... been coDog .... ........ not _ "b.-She_'just don't ...... ...,...,. ............ _· __ W ........ _ ~ sod. SIlo begins ~ .... _ ........... lind _ ... doosn't~._ ....... _feft 1hIs __ .""'hIstooy_~_ ... wIII1In ........ 1ImIts though .......... ., fool .... ' am just ~ _. She has lost IS -. from _ait poclf. __ most IIIotIydlogrOOlls"
a. Mood diiDrder '*- to a geaaiaI medal CDIIJdltton b. _.,.....,...aoy_ ~ 5omaStaIdeI1 clsontlil d. SocIal phoI>Ia e. o,.II1otl*-
'2. "_.,I __ f>II<NoVk-.Ho_ .... he was In goad~_ und · ... _ __ -.,.. wIII_1Ioo __ 01
ndtip/o_1n -. be _ ...... ..._ eland ...... boa ,",,-.Ioa 01_ during ... ~Ho .... ~p/IysiatI~_ hIs~but ...... _"" ....... ~IS_hls ..... doorge he __ ~1osInp h1sjobond lois home.Hohas __ fmn_lor...".
""'" '0,.... ......... hoIp 01-.. CBf ano/ M. ,."........-ICOioty.,.. .... , ... _ .. -heohh diooI>II!y _ 01 .. ~ '" ""'" duo '" _ .......- 01 coo __ 1nCIIIdIn!I _ .... __ Ihot_fllm"""'''''"''' He-. ... ,..II ................. .., .... lIg" ... _ ond _ he..- "'"'1'''''''''' II> _ IOI!WS """,",01_ ond anN/Iy _ ....... _
log WIlt '"-io. nw_liIooIy.dIeg-a is: .. IJIssoc:IatIve 1dorIIIIy _IDIDJ
b. -1InIOiIIIY-(GAD) c. ....... ""' __
. d. CDnoPox />IrdII apIIepsy e. _ ...... -.1PISDl
n. "27 ___ .... Is brought '" 1Ioe EW Il¥'" load poIat bealulll! 1M has been I .. 51(lag her neighbors. .... 1omiIv-1hot1Iy __ '"'" _ '-I "" ... , ..... TIoo pcb _Ihot ... ___ ___ C3IIedbeawso .... _bongIng ...
oil her noigH>on' """" '"'" "'''''.19 In 110&..Upon _g .... ".,..... - !he poIce found ... place1p1>o1llllor ..., ___ rutting goobogo .... food In the ._ 11>0 _ ..... _ond ____ .... __
___ ond """""""" In ... /IWtng ....... III WINd ... OIl 1I1e· .... _1110 ..... nt's famIIy_ !hat lor ... paot _ Of so "'" has seemodlnaeo5trtgly _d1soociodng ___ fomIyltlMtiOs ond gMng
"".~job ... ~--In __ .... lad IIbrupdy ended • Ionct""" ___ Ior ... poniallar ........ On _ __ ",,110& __ ,, __
-.g ............ oId/rty--.SIoo_WIrI ond guaNecl.Her _Is _In __ ..., prod_SIooII _""" __ "",has been defending htrRI agaiIJ5I aliens who WiWft to U&e
he, as. __ SIoo lid .... !hot "'" began pIc/Iing up 011 /oiddeIo.......-in toer......u at __
'" .. .at fw sal,,' > <: .... _ q>CI_ I >
Ing an ..... """I*Kl< """- IrwohIIng tho CIA. She SUIteS tNt she WI: her job to rncritorttwse hidden vans__ ond _ .... holboon -.g In her _ ...... _ ttwy _ .... b ... III -... She ended her __ ... _ she flit _ "'"
aliens MXIId hamo tho poopIo she awed __ She
denies subance use or any medaII S),II"""S. 5M ....... _ .he .... boon eoIIng .... _ng ...... and that her mood b good. She __ ng'-" Dllgnostlc 'esUog. -.cling dnog !ICft!<tI, CB(, _'1isIr)' po"""" _ MIl ...... normal TIle __ II<IIy diagnosis Is: .. Schizopt.renla
II. BiI><>IM--c. Major depoe""," d. __
e. _ penoNIIty dIso_
1 .. An 1&yMr-oid man is seen Ina prisoncl~baroutlne physJaoI ........ He_ ~ _ he is")81 for.....-.ng two ~ In I' botd.ed robbery artdl'f'L When you ask lIIm_hls __ ~he_ .............
am!5t5 .xt some mnvictions b theft. ~ drunk driving. Mld rape. PenIII records iIIlCIkiIII! iii pa'Sistenl:
_ d lying ond""" wtoilo n"",._ ond.hot he exh_ no ....... wtooncought br __ Hehas ...... _ psydoIotricaIly __ ond de ...... onr episodes d_--,,,fIuctuolIng mood He _ no grondIosItY. __ """"'" Of ps)ChatIc
syml"""'''FoomiIylolslooyis ~for _ dependence in his father and mother and 1m" no history of bipolar _ . He _ ........ hat h~ """'" ond subsequent foster plIr«ItS cftRn beat him with SIrIpS or boards when he was a child. He was knocked ~ sdous on sewraI occatioIl5 but has no hIstDfy of seizures and dentes nightmares Of' flashbacks from the abuse. He has had sulddaf idNtion but has net made SUicide ......... Of """ ..... _ tile most IiIo!Iy diagnosis is: & Conduct dlsotder b..............- ...... disooder(PnO) c. Cydathymk_ d. 1Iipo'-_ .. AnmOOaI penconaIIty _ode (ASP)
1s.. A 33-year-cJd male Is ",edfol' asubstanceabuseeval_alter he wasanested forcfrimg __ 1I!d. He Is A!Iuc1ant. but ....... he must c.."..... _ the _to_",... ........ IegoI~He state'S that alcohol is not really a problem fof hkn. MKi that he an control his oinking SIl)'ing. ... can quit when-fttII!I' I want to.. He does admit 10 two prior drunIen drMng ........... __ 1>0 __ fJOm two dIf·
_ .jobs lor·sneIIItog .... _·but bel ..... he ....
Quesdons • 93
oaIIy flood - 'Ik - - "jerI<s.' .. .rec:8'It fOI'I\Intk: rNdonship .., endfd becw.... he _ too nouch. He ...... thai he -..,-, drink doIy. cxoIy __ .r.wtlmes. _ .... me<e.....aycn _ndL,,"_no_d ___
_ .... no prior ..... """ ., ....... lois _ d __ TIle __ Ilely~1s:
& Nard ' II( penonaIty cftsarder b.AIaoIooIdepoo_ c. AnIIsodaI pel SOI_ dtsordI!r tA5PJ d. __
e, AIcohd ... o:btIm
(ii) A 23-)1Yr-old\llMlln <OI'1'leS to an emergency room afIer being found unconsdoul with an empty botde of l-mg -. d Iot_" br her body. SIlo Is .... _ arrMoI .. tho Ell but __ or<! has. ""'*"" tooy_dlO' __ d .... ood __ d
9011!0. She Is ~ g;w.n IV.- _ no efIoct. ___ ._ot._ ... I\lmed-
_ .. gM!n,wIokh....,..In_~Ht!r boIfdend ... _ "'" _ ""'" _ -,,",lor. Iew_ and _ she .... geaing • ...uy_reaIIy .oon: A lew hours_Ill tho _he __ he told her thIr he didn't war'f to move .. with her. She _ wIsIbIy _ and heIolt.Aftartl>o ......... ",... -._ begIn"' __ her. She ooIays that she has
been in this 5ItuItton befDre and -c.rft beAewe'" tNt it Is haolperoIng IgiIn. 5/01! _ a ..... d _ rolit-.... _ both men ond _Eodo_ _1lII'kIy"f1llng1n_·wI1Io."peofoct"penonlollowed br. period In _ the ................... her. Two)'Nn ago. she dwell! .d to jump out of • window _ her bOyfriend _ up with her. SIlo has been in poychotI1enopy""",_ time and .... oocentIy been prescribed Iora:o:epano lor • __ : DurIng the
intel..tew. she Is Intemlltlently tearful but her speech is normal ., raa. and prosody. She 8lIIhIb;ts no deIuIkJnld _ and denies aodIIory .... uciNo-.. T10e IV ___ ""' __ Is_y:
a.~ II. ThIamIne c._ d. FUnuenil e. Danpam
17. A 41-year-old man Is seen in an ou1pati!lIIt P5)d1iabist's _ "'"' ..... >9 0/ Iong-<tandIng feelings 0/ __ low self esteell .. and low ~ that he has ecperIanced mostclthe~forman,.)'M"S.."hesneverb@en ~ MW!r made ill suicide MtellifJtf and M\I8
t.n affected enough ~ the symptoms to SlOp ~ Of to limit his adIw _ life. He oeaorotIy got __
While he 1Iolnks that his • ...-.os """'....- to
<_ ~w..t >'1 _"'~' )
.. • .. " ..... II'IItcHdl)'
'* __ ...... _ •. " ...... , .... _ 67"., .. Wid .... dwRe. n. MOIt-..y .... -... & Mllard. Ella, b.Sd*'*~ ......... c.~,*""'_ cI. In". ' .... ...,1IIIIOnW eo ArlI 3 =_ ... _ ... dIP Hndmoad
ta,"~-GId ... It .... 7 ...... .-...-
...... cIk*_ r ...... ....,'-'~q.I&· SIIe_~ ... __ 04_doII _ _ ",,*,"11 :lA_.,- M .... 1JIrIh .. ...-t .. r.r_dII __ ... ..-........ _ • ~ ....., ..... He fIiIId 10 ,. ~ ... .v.tizn ...... .,tiId .... _,... ,~ ... cWt .... .,..c 7 ~ 110 __ "' .... ..... .. _-'* .. ""'-...... _-_ ... .,. .... tn ............... lIladdlllDl\. .. -_ ................ " .. -... _ ... -----.. ....,---_",NiI.I, .III_lho_ ............ A_ Rt. all aod_scl ....... u. .. _-cI. :.u .. .-ctt ... ..
&~---.. ... tI. " .... oId ... I5 •• I2I1f .... ewd.-=-••
t ,7' ........... (aI.71d_r.s" .. IC ..
<1I0I0_ ... ____ - ... -._ sa"*,, fill' u.w. & ....... mel ..., __ .. It .. <I_III _ .... _
, 'RvI ""'''II ~_Ip--,:.''''''''."" _ 1II_ho""" __ ..... _ .. ... • .,." ...... '"'It ............ _"" ... _ IIIrc a' .... £II ... ~CDI'Ian .... hM _ __ ., .,..,_ ... _ ..... <1 .11 ...
"'J11 - .... 5 0' .... ,......,..". .. = .. ~ __ .., .. _ ... 1011_ -_ ... _ ... _ ... -. ..... ,'" .... d... In .. M NlI.lIJIdr.,1 to _._NljiIfd_"' ................... m <1I0I0 __ • ____ '"'10 .......... .., ICLS 7&!l1lma! .. eMIle _ ...... 1, .. _. - ... __ ....... ....., ... *-...... "'" •.• ~H od 011_" __ "'" __ be .... _ ... It..-...r _ ___ ......, ....... iW ....... __ n. _"",_<1_""",,10: ........... f~ .... II. "'"" .. _ Co c:.dIIcMI$1I p_ el. oprc. 0111'" .. _--.g
·r . p" •• ~M ...... pV >
20. A 41)leL'dd fent*.mrpa;_ ..... ClUB ~ hrr .......,-~--.r- ... __ that.JIII up .. bMI U'Id wwc. ar aII5 M'" __ .,"", fIUIIa""" ... - _ ...... dwIag ..... ·Kt_Iftd .. nat..., .. GCeic.a. Hor ___ ...... __ loucI!l ShI
__ Mho ............... ."._ n._ a..1 "IE .. SIIsp .......... b. NstcalF,. c. n ' ..... n MIll ... onter d. ...., ....... IIw
.. 51.ph"". IIKwdlr
2'1. A,"". oIdlnll'l ..... CIIII'OW'dSCIII.~ ..... _1MIng •• __ ..... _Ht_,-nGFlllwiIh. PI)'dMt .+da" not Cllhndtl Jpei"Med III!ItIIpin ... ~ 25l1li an "'" __ _ JIDU to 1M ...... a.a .. he .... been~ II ........_ .... _Nl_""'ftndNin ....... ... _,Ht ... )IiIU_bo_ ..... _ .... ... ""to '--., .. 1IooI_0Iha_ ...... ... Isnot ......... INiNINIClfOlllrr ......... adthe _oIII ....... ho_·~ ... 1II\IdIOIk ........wNdI .... td,&.tI.N -.ell" .. '" .... ...,..,.to;..WCII ....... at IIst.\13111 ...... .. ___ --... It_" ...... 0II1s __ " _ "'" _ ..... __ ...
:12, A 15,... ... _1t ....... "' ... ,........... _ beca«. hII piIII8 _._ S_I! d Icy ,. bet ... ...,_tiIot ...... _ ..... -.uy-.g_ ... ........... CIDIWi dw.,..t.5 b ~ ... ~- .. - ..... " ...... poND If _ ....., _*II _...,,_ --, ... US •• ___ ........... ...
...... · ... " F ............... -...-... ... ....... _ ...... __ Nl_n. __ dsnl..." ...... , ..... Ns ... r .. ..,. ....... he ..... . pOtce:rlJl-ve_ bale ... ~ .. thrt __ ", __ -.a_cAIoIiIt·HoIt
--'* -""' ... - .... _''''" _..,_IJr .. ___ r.: a. Mdt"",. 1~.CfI II. 5cI1IIIopIiiiri Co $4*-WC." d. 'b.ftnI"s ...... .. CDnIU2 cIJcMIIr
~ A __ wanan"'" he< gynewlogbt rho' .... "" ne¥eI' had in orgasm during sexual interccuse. She reports that she ~ an active libido and masturbates to _ """,,",'!y. s.. _,hat she and her pa ...... are commftted to each other and that tNy are affection_ She says !hat when !hey'" ~ she becomes __ with ongo_t or the .-s ".... and
vaginol_ but""""'" her ........ anemprs to enter her vagina she feels ~dlsgusted"' and "loses an Interest.· Her vagina does not prevent-entry and entry Is not painful. She deries other ps)'CNatric or medical pr0blems. _. "'" ocknowIedges. hIoto<y at ""_ secuaI ....... The most IibIy dIognosis Is: a. Female orgasmic disorder b. vaginismus c. HypoactNe sexual desire disorder d5exual_d_ e . Female sexual arousal cIsorder
4 A ~""d IemaIeWlth no prio< psy<hioUtcOlmedl<al history is brought to the EW by II friend because she fett that she was hIWlg a heart at1ZKk. The padent has no known risk factors few coronary artery diwase. She ..".,.. ....... or dlfficutry bruthIng. chest tIgh"""" and MUSea. She is agitated, pacing, and very concerned _ .... mlghtbe~On~ ........... btKhyprue. tachytatdk. and flushed but Is otherwise f'IOfTMl. DIogncstlc testing. ;"dud;ng an EJ<li, pobe. O>dmetry. erythrocyte sedimer'ltation (ate. cardiac: ~ drug screen, and TSH, shows no abnormaltties:.1he most likely dlegnoiis fortNs padent is:
-
a. U ..... bIe angina b. Genenltad._ dlscnler (GAO) Co PanIc_ d MojOl depresol\le If_ e. AkchoIIntodcMion
25. A 29-year-old rM~ aNfive wt1ting professor k eva1u-ated b)' his primary care prcMder in lall!! Decerober be<ause hoi "" ..... _'"9 _ngIy 'Oed,o_<. ond derftssed lor the past 2 months. He _ tho! he has lett like thb ..... ~be<thtough -..ory or the past 5 ___ """""9 to _~ .....
MamI. AorIde. ~ reports that he feels as f he awt't get out of bed In the mornings. his stopped pertkjpatlng in sports or social acttv\tk!S, and is Melif'Q Increasingly If"""""" WIth poor conc.entradcn and an Inability 10 wuk.He_ ....... __ portlcIJIoflylor
carI>ohyd<otes. and "" go"ed 10 .... "", In the past month. He is quite concerned thai he rs now '"too lilY" to perform iWlY aeetiYe worlc. His physical examlnatlon Is normal with 1fle exception that he is about lS pounds
.... - bcx!y_'.OIagno$tk to>tin!J IndudIngCllC, ele<t<oIyre panel, and TSH b nonnaI. The most likely d8gnosls at this poW is:
Questions • 9S
o. I\dj",~ If_ with depr...ed mood b. Mood disorder due to a general medical condition c. MoJc<dop ....... _
d . Dysthymic disorder e. SchImpIuenIa
® A4~ male who". "'""'" ~n addkt ond" now maFnlalned on mechadone at 80 mg/day is admitted to the surgery service following an automobile accident tn which he sustJined a tlbia/flbula fracture requiring open rmuction with internal fucatk:ln Because fA his history d heroin dependence the intern orders ketorolie (ToradoQ Instead of the routine paUent-<Olltroiled onat_ (PCAJ pump, but does _ on orde< at oxy
codone/a<:etamlnophen (Percocet) at 1 tablet p.o. every 6 hours as needed for breakthrough pan. The patient: is also given his 80 mg mainll'nance dosage or methadone. Despite the maximum dose ofToradoI and use of the presaibed Percocet. the patient cornplu'lS of sewere pain.
steting that the Percocet "isn't touching the pain." On examination. the __ " ..... _ pulse " 1211. blood pressure 1801100, respirations 3CVmirute. The best intervention .. pfftefIt is to: a. Tete the petient you win add meperidine b. Telt the padent he is drug seeking and needs to stick
with the prescribed regimen c. Oreaease the Pefmcet because the patient is likely to
"""'" It d Switch the petient toa fICA pumpand titrate the dose
to pain A!!IIef e. TetI the patient he shouidn't be ., paln becauw he is
"",eWIng" lot" or ........
71. A 47"')N1'-dd ~Ie with a 3O-)'eiJf' history of heavy akohot dependence is ewtuated in the EW alter "tripping- on the stairs and hitt\ng her heed. She Is dlshewled. has a btoOdy nose,lInd reeks of alcoholOri mental status exanWlation. she Is inhlally i~ and uncooperative. She Is admitted to the hospital for detoxffication. Aft« iii successful detoxif1c.adon you conduct a more thorough mental status exarnJnation. The patient reports that she is In a good mood end has no compfalnn. She S8'J'S she thinks she wII stiJy lIWIIy from lIIcohol this time. She Is jovial. but does not appear to remember yot.I'
name orhaving met)'Oll before.This has hoappened twice today.The most Ukely diagnosis I. a. Anxiety Osofder IS EpiWroIhemotoma c.. AlcohoHnduced penistlng amnestic disorder d AlzheJrner'I dementia e. Alcohol wlthcbwal deUrlum
21. A 41 ~H)Jd man with a 21-yeat·history of bipolar disorder comes to 1h! EW with ataxia" C(MIfSe tremor or his upper ectremitles, confusion, and clianhea. He reports .
that he has been "'~ "graM _beause _Is ... hoi_and 1hoo he "gets no _at_because ""~-..... - ... -__ 40rnv ... dII)I __ 3I1Ornv em. _'''ogondllOOmgem.-.g.--.n 300mgeach InOIIIing and 400"'9 am evenIng.u.a.... 25019 -".-og. ond 100_" • 019 mHo _ ~ iiIIOd"ny -.tt dNgs. On ............ , "" heart,.. is 100 and reguIar~bIood pessure is 98160. leo
pblltUly rate is 14 and 1I!Ii'lIMittft is 98.1"F. The most
..... --'" .. IJINum 10iddIy b. ~ aoooIdIy e. _ .. taddty d ea __ pInoo aoooIdIy
e. llioIoporidoI aoooIdIy
H. A~ __ Is_In"'£W_hor _ -.ght hor In _ she __ ... night "do-..tolng-."l1oe ___ .... _
has been dopoeued lor a very long lime. ond _ "'" hoi been o.ndoogaIng .............. She __ dot _ toos been Ii$og she -*I be _ GII_ ond_IIIt_-.IMng.The ___ ....
toos been pnogoosIi uoIy """" dope&J cIuiioog Iho _ -.. 5he .................. 01 losing .... job _
monm ago dw to D.IIItac:b.. but she b ele.-es they let her go beause .... '"""" poofoomlng __ In -.. 3
-. OSIO"'''-alon!tOenn """""'" tOIoCIonohIp oIS,....._.graMdooIoI_and_One _poiarlO_-'she __ hor~ ___ ... had_ ... ....", ___ being _ and _ .... would _10 ....... . 5he lows Nornalg_butwon'lbe_lDaIbd living Iheoe II1II' looog«.5he ....... _ ....... ,.._
owly dopoeued lor at Ieost one """'" and has hod _ ~ syn..-os 01 dop1!sIIon. In addIIion,. she reports a pIIlb.rKI __ of ... 'ledaniIt.and __ ""'.1yIng In bed_-.g ... _ hg. She nom tNt. W Is hop ~1e:1S about the fuIure. and ....... _. -... ... wll.,...leeIbener. 5he Is vague wtoen cIIoocttv __ ...... 1UiddioIIIy ...... ....... oho __ oIONjor~butyou ... concened _ ... --. _ 0151<. The __ "'-""
..... 0I5I<._""_1n this _ Is:
a. Major ciepressloo b.~_ c. lou d • romantic re&atIonshtp d Loss 01 hor Job e. Hcpekssness
® A ' __ boy_nolooown_ordnoglUwy praenb ~ the emergef1l:y room appearing mnfused. As you are e.nInIng him ho _ you ..... your __
'It,.... oj, , .. ~;., .t. 1IIoe.1s~·lIsbo""ill)arIs~for_ The boy ...... 1iIoIIr ......,. a.~
t b. GHB e.1SO d_ .,-
51. A'" """ _ to be 10 hIoo mid .... Is I>ocough'" thteYi by. __ "", pIIIIent-tumOosIOn __ ......... _11 ...... _ porIoroj
<yonaMo,-",cyonoIIo.and_......,...oI 3-51r'nh4e.19 is UII tJPDIIl5Ive eapt ........... 11> ~_nob.TIIe ___ thtp IO."1OY __ .. ,_" 10 _· .... 110 _ any.ideo 01_ k might hiM _ or the modo! of~.No _ .-_ ..... COl'" pooIIoo .... 1oocI!< 1100.
"'dnoglhopllllent~_ .. Aba"," : •• b._ e. CocoIne d _ .. ,.., ......
U. A '7"}'1OH1d ... _ Il1o ptnoory are .tJeaue .. .-ws..ewOfdedIibaulNsbel11 b1hey ccmpIaIn ",. ... Is.~In .... I8I ....... IIIdng_ cIUoIng sholl.1Ay In the noamIngand MquentIy ~ Inglorogporlodsof_1n honctwoIIoIngll1n>ugloM .... _ ... ...,~ ... _ ........ _ ..... gotrldd .. .... _ ..... loocI!<and IIooothohollD_ .... thoy .... oIgoroe_ho_Hls ___ doy ..t cIoIippo!d;The __ l1ooIvcloogo_lorthis _is: a. 0IIseuM! c~_(OCIlI b. __
c. Ga .. u,.,d __ tGADI d IIody dysmorpIoK _
.. NMdsUIdc pmoIlIIIty ......
JL It »~ mediDrI SIUdent: II teen WI a tat psy___ b ..... ..t-.gsol __
_wlthlllo_iopol • ..-_ ... iDIIIOIIOIc rei dailshIp. 1he ..... 1PIst eveIuIIas the patient thor· ~ and finds ... _oar 01 iNjor cIIp_ or ....,.dIsorder.1he .... eKpIlste5 II IongomIditg ,. ......... and IOrIllnlk:cRiltatiol\butr-.thM w.._ ........ _ooIslho~ _ "" ....... sIoouId ..... repaiIIIw. or tIoange P5)iChoIM:f11P'14 tD dru 110p • betIro5exuII CIfIMtadon. 1110 dwopist: a. Shedd fiad cu whedls 1M SUldll'ltWMb toc::hange b. .. ptapOIIng ...... :ce-b.sec' IA5ltlient lTocxIIIIIIy C. __ tho_to,--""thenpy_
"'"""'"
d. Should send the srudent to ___ JndI.-
.tduaI ...... py e. Is PIOposing an l81P0WfI end eIhicaIIy questionable b~
34.. An 18-yar-01d college nudent is brought to the MlEf·
gene)' ""'"' by .... _ poIi<e due to a..tIng. dis
!Urbanct an campus. On .....- he "'" oucIiI<>ry ha~ ogItation. ond rapid, Incohen!nt speech. The length 01 lime ..... he has had the .... puxns Is unknown. Substance abuse tistory b: unknawn.1he most III<eIy diagnosis ;" .. Sch--." cIt...b. Winter depession Co Generalized anxiety dtIorder (GADI d. AtypIcal doj>n!ssIon e. Obsessive compulsive clsordrr (OCO)
)s. /. 29-)'ear~ Itwestn"ent banker is brought to the emergency room by his tMiness partners beaIu1e d IncmsIng_Theparlnen.-that .... poIienIhasbeen working _ .......J the _ far the _ ....... '"
meet II crtdcaf deadline. On exam the patient Is U!n5e,.
tremulous. ~ hypeNigiar>t. _rdk. and hypertenSive. His urine drug screen is positive for .....,....",Ines.The poIienI """""ntIy ........ to _ about: II bottle d .. rinown type of I.IpI)RfS cUing Ihe pa5l week. The most ~ agent for trHang this con· dtdon wr:dd be. a. Buspirone b. SenroIIne
c. Flu"""'" d. Oextroamp/!eta"""" e. OIanzapine
l6. The mother of I 27-year-old ~ female Is c0n
tacted (aft .. obtaining permission from the poIienIl p<iO< to inltiatlng treatment. You etepIain to the mother that . p5)Ch0sts I.s present and that Inidation d an antipsychotic medication Is the appmpriote -. The
"""""' says that she Is waried about Ion!ttenn side effects because her uncle was IIeated with stelazirlr for many ~ and now has strange..sIow movements of his upper body and _Of the_ng antlpsychotics. whkh has .... hlgheot ..... 01 causing.....row dysIdneslal .. HoJoperidoI b. Rlspeiidone c. CIozapIne d.~ e. OIanaplne
37. A 5hUr-oid male padent: suft'els sudden death due 10 a presumed can:Mac anhythrrhassodated with TCA to3ddty. The pMjent had been (not too carefuU~ evablted at
Questions • 97
an EW for ~ of confusion only a Jew hours __ but had been dlsdwged.AIthough theeliN
aI 5Cenario was suggestive d anticbolinergic intoJdcit
tiDr\ often .sodRd with antichoIlnergk: properties of some ilnddeptes:sants. the EW ~n failed to check II triqdIc.....,."...... ...... The pa ...... wVe decides ",suetheEWphysIc ... ondthe_far __
pracdce In the ute tJI her husband. A legal eenll!tlt that ....-.~ 01_..........."",
.. The """"""II< !loti> h ApI<hy c. Benofkence d. 0I0e<t causation e. Intention
.sa. You prescribe an SSRl-da55 antidepressant for a pWent suffering from major depn!ssion requJring an Inpatient psychialb1c ~ssIon. Two days 1;t1et' ttl!! pIrIient appears n1OI1<edIy _00 and k _ the coorido<, The
nursing stall Is '"'Y concemed, suggesting the patient rrey need ad<IUonaI sedation. On your exam the ptIIHent I, agitated and _ bcxrodng he. legs up and -. during yow interview, and she can't focus on the CO~ wrsadon. She rdes that she doesn't know what is hap_but ......... just an'! sit "'~ feeling like she has to mcwe her legs around. The most Iikt'Iy dliIIgno5is is: a. Neurdepdc: malignant syndrome h __ _
c. Generalized.ruddy disorder (GAO)
d Serotonin syndrome e. Caf'fane mtoxkadon
J9. A l~year~ is diagnosed with OCD after 5e"o'WoII)8I"5 of symptoms consming d intrusive thoughtS that he had harmed someone and chronic obsessions about deanD· ness. He Is nearly disabled by arodety. During a famUy 1_. his parents a<k you W ...... dtd _Ing wrong _ raising theV child. You explain thot. """'"'Y to older Idas. contemporary theories for the origins 01 . <XD Include genedc. neurochemical, and subtle brUl injury buch as foCtowIng mechanical brain Irjwy and some forms d enc:ephaIH1s). You explain that this c0ndi
tion " ..... .-_ rneckaOOns '""" the SSIlI cJass 01 ontldepressants and ~. The most
useful loon 01 ~ "" OCD;" .. lnterpe ...... _
h~mlc_ c. Ps)<hoonalysls d. Cognit_ ....... ps)<hotherapy .. -poychothe-
40. A 38-year~ man has a history or bipdar tIsorder that began 81 age 19 wtth a manic episode. Since then he has had ........, manic epsodes and ....... __
Ie • """"""'" Psychiatry
.,,_ but net mote INn lour episodes per _. He
tnIIde one unsuccessfuf suicide attempt by overdose at _ 24 dontng a paniadaIty ....... clop ...... _.
The most appropriate malnrenance therapy for this pademis: a. AlDcetine
b.~". ~ PhenytoIn d. Uthilml carbonate e. aono..pam
". A 53-yoar-old ....... d"_tolh.1npadent P'JOChIolrk: .... for .... tmentolblpolardlscrtler Is _1yIng"!he hallway. On exam. he is consdous, but I, t'Onfused and dysarIhric. The _ note ..,.. he has been progIOSIIveIy _ and confused for .... past 24 hours. He_' _Il10 _ ... trying to kII rne," Upon_ his chart.. you note Ihat he was admitted one week prior and le5UIred on Ns UIWII dose of ~dueto • low ~ l"hrft dIIrs ago. he developed an ..... fifto
pfttofy "lfection and was heated with an antibiotk.l:f1s last ~e 1M was ) days ago. You alnduct a 1hon>ugh p/IysIcaI_.- 01 systemS 10 ....... _
S<lfthattheoodentcld "",..-. syncq>aIepilOdeand ... ,.,.. _ when he fel. The..-1I<eIy diagnosis Is: • . MalIngering b. DomentIa ~ Drug toxIclty dProgm .......... ~I_
.. --~ @ A 24 ~ woman who IIws with her parents sees,
you for a>nouIbdon boca".. her psji<I1cIherop. ~ that she may need • ~ She rwpons !hat sinai good .. ting from college and "'" _ 01 her f_3 __ 0g0shohas_~ __
dent wtth Iow~. poor iiippi!dte.poor (QIiCetlb.tIon,
and feelings 01-""'" She .... ...- had rodng thoughts or _ ~ 01 monIa and ..... fomlly hisU>ry 01 uripoIar rIepe5sIon \'au d_ her with major depression. Of !he ~ !he best _
treatment would be: .. Ilu$pIrooe ~ b. CitlIIopram thetopy c. Pht:hn~ therapy
d za.7 d.erapy e. i~therapy
U. AJleI .,.-otd man prl5entS in your prfmary care cftnk: with his partner. HIs partner tells you that the man has beoome foogetful oocentiy. He has been .. __ _ .. 01 ... lifo but he has a fOmIIy ~ 01 Alzhelne's dei,1efltia. His hither developed AIzheImer's kl his 70s and an aunt developed It '" her 60s. Nt8
testing for ether cause 01 dementli, )<IU suspect
AlzheImer's demenua. The best medcadon tmerwntlon would.,.. .. [)opirrft _1IagOniSt ilelkadons h Acet)!IchoInestI!Iee inhibitor mecIcMions
~_""""'Inh_"""""'" d. GAIA antagOnist ne:lcatlons e. GASA agontIl medications
44. A 22-year-old INn 'htaoleCentlyW. fnd frgm his job 81 an auto mechar* pesa lIS In the en IetgeIIC)' room ~ pIoIring 010 C<lrIIpDcy ogoInst him ..... __ •
pIac •. ....., he Mt begin. It> eopIain "'" _ h sound. like possible _ place horusment. You Ihlnk about Nferrtng him to alrowyer when he_you thot
his boss b In"'~ from Jupbet' and that his ~ -... ... !he ... "",,,,,~ ... _ ""'"" you .... hOntodesa;be!he ... _ ....are,he_lIyelalJo. ...... rkNy_""'Y_!he ....... !he_ and '-lloey conspired II> ...... _ ..... 0II0er "-these W1USUiI btIm, ,. appears normal In tenTI5 crI ..... and body _.The ..-1IIoeIy"",,- olseN. ophI'eIlia In thIi pMktnt is: .. -b.Ca_
~~ d...--e. ResIdual
45. A~ .......... _rr1~_5dolq>t_ pnnoid type, stabs hb: frfeIId In the abdomen witt! a __ he_ ..... ""' __ ~_
... nc:arrooIaI. .... _Is ........ ...- but""' ......
Your potioni ... been oecunemIy """'"""'" """ medications and _____ shcr1Iy ... !he
__ .. found to be _01_ -. reoIIty.Ho .... yoa , woo trying to _ iIoe world ...... tyrInnk;aI
_ " ,. "'" _ .... .,.- pIeod5 "'" guilty to chorge5 01_ murdo< bf ....... rr11n5erity. The ___ the podent-rnentaII\' II .. the
time rr1 ........... butaogues_the-"'" 01 mental UIness ........ not 1Uftic ..... for Ihe __ -.... The _ " ~ The ............. 01 !he Insanity deer,. that nut edsl in addition to th! peence d a ........ _-a. HIving taken ~ for 1he mentallineH b. CornrnInIng!he crIrne wIIh • high likelihood 01 being
aught c. An InabfIty to ~ thet the act was wrong d The preserocerrl_ or-. e. BeIng ~ bf!he vIcdm
.06. A 56 _ old man _ alorogstondlng hbwry 01_ depefdeftte .. brought into the ~ room by
ambu~nce after having a sertes of SQizures whHe at: home. HIs wIfe..oct tI1at her Mband had been drinking daily but had recenttythrown out aU Clfthe ak:ohoI in the house and tdd her tNt he was stopping"coId turkey.You beUeve tI)It the seizures may have been due to __ K Iile podEnt did have. withd ......
sebure. he most likely quit dmking how many hours prim w his admission? a. 2-6 b. 6-12 c. 12- 24 d 24-12 e. 72- 144
47. A 48-year-okt woman With alcohol dependence presents in the emergency room alter being found down cutsme her home in a ~ state. 'too team from the ernergenc:y recotd that she has frequentty pteSerlted in the past with ak:oho4 IntQldca1;ion. While evaIuadng her she exhibits WiOOng and waning disorientation and then suddenly becomes hypoten:sNe. She Is b'fInsferred to the leU _ belng irntialy medically ".bHI,.d with • preltminary d\agnosIs- of alcohol 'withdrJJMII delirium. After severctt days In the KU. her delirium and autonomic instability resolve. but the nursing staff report that she is stili *acting ~:On eJ(am the patient is noted to haW! nystagmus. ataxia. and anterograde amnesia. She CCNerS this memory defidt fairI'j wetl in c:asuat conversa-tlon,but It is dear that she is confabulating durtng a great dl!aI of the intefview. The most 'libIy dagnosis for this patient is! .
a. Ifwtemicke's encephalopathy I> 1<oBaIu>II' psycho>Is c. Wemicke..fCorsakoff syndrome d SubdtmIII hematoma e. Epidural hematoma
48. A 23-year--okl woman is brougtlt to the EW by the ~Ia! who sa)' she was creeting a ~ in a local shopping moll.The woman ls agitated ,-,arrivoIand speak. ing rapidly. She tells you !hat .. the )'ClUng men in the mali were laughing at her and that they al wanted to hurt her. After ~ mlnutes of discussion. she begInS
Questions • 99
to act strzIngely towards you and asks you to Ietwe her alone.A nursetetlsyou a few minutes after you leave her side that she dlinks)lOU are laughing at her too and that you might h.irt her. She appei!1f5 to Mve paranoia and you begin to try to determine if she has a primary mental disorder or if the condition is due to the effects Clf a sub-stance or a general medical condition. If the condition Is due to a sumtance. whk::h c:I the ro.lowing is most Mke4y to produce these symptoms? .. Am_ I> IlenzodiazepIne ~ Op;ates d Nicotine e. Caffeine
49. A 57...year-()kj woman had a ceiebrovasc:ular acddent two months ago that resulted in left l4'per extremity pilrtiaI hemiparesis. Her son brought her to your dink: because he WitS concemed that she seemed Jethargic for the past month. The patient reveals that she feels hopeless about her lite situation and is having troubk! with earty morning awakening. SInce the condition may have been precipitated by the (VA. the best course of action woukt be to:
a Begin treatment WIth buspirone b. Begin treatr'nent with Iorazepam Co BegIn treatment with sertraline d. BegIn treatment ¥lith litNum e. Begin treatment wtth valpfoic acid
50. You are asked to see II 27-seven-year--old man who was admitted to the psychetric unit In the hospital 2 days ago. The nurse reports to )IOU that the patient has developed a hand trefnOr that looks Ike he Is roiling a ~M. He also tefts you that the patient k walking very stiffly and
appearS to be having troubte mttlating his rno.oements. Whkh of the folloYAng medications would be most likely to naveo caused the condition abow? a. Lol"ilZ$ilm
b. BeJutrop"" Co Thioridazine d 00zaPne: e. Haloperidol
t. < The~"" ....... ~~",,_ tunls1Ic lI"tiofi. AIIhoustI mIny ........ s can caR
~ .. ~dtioojIIne ...........
~ rIIk d ...... ~ for "'" """"' __ chg_It .... ""'....,~ __
~~W8C-"
2." This petient pIESeMS wtch. cOII .... tian d ~ ct... ..... tA .. rl __ mood.aMlgii.lriIMdoI .... poor
OlI ...... adorl. and dIIitwbIIKes of" ..., .... ltw hyponormIo"" • .......,--. .. _._ .... at)IIIaI ~ d """'" depoo_. The swn_~ _ __ "" "'" _ ~ 2 ___ """
n • den 01 a,mpIIImIls lIDO sewI't tnd too suddIn '" 0nIII ...... _"" ............... _.....-2_ d len'''' ___ ......... WhIle. gI!!Mr.II ......
COIl.on 0DUId ".c,zllally be 1he au. dIllY W6I_1t deiwt dOl'li. ... ,.. .. racA.~-...... 1Rd1he Iockd_""~~._auoed_· ondory cIepo ..... _ ""''-- ...... -.ce. _ mood _cleo shadd ..... be ... _ In ftr~_.uiOi""bul the ,-.......... cI moder-
... -~ .. ..-y ....... """*Y-OIW d ............. det Tho fact ............... 6 _prIor ....... ..-d .. " __ ......... ka may have been. pNdpbnt. bW this corn , 1b1 d symptoms is mote severf; ..... normal baeaven.ettto
Sod _ .... ~ __ be~_bipoIor_ "ClIIIiiiIJih~lsd .. __ __ -.M.In_ ....... Ihe_"" _cl_lhe ___ .. _hod an_d~_.In""_d • dopo ...... "'-..-._ .... P¥I""'< ._ •• that Ire .... aQd bI eM 0NIt tA ldIIlopI.er4 the oooanI<swn_ •• _~not .. _~ ..
_ .. ___ "" .. _6.-... _at-_""~1toe .. _deou __ s ... '" • suddIft cNnge In bit ...... not a pel .... ......,. d .....-...,-_ ...... _--_._--....-,,_. ... d Tho ___ I>1"-""_'_~dao ..... lIa.-oAo9-...... , ..... _-__ "* fadonforAllhttn.n ................. ca ...... ClUlld .............. ced .. .,..,w.ory fJldefraCli. "-' ........... andprlorloajod _Tho _ .... otok _of _ ogaand fIomiIy '-Y d cIeo._11IY _1S.-y1n .. -.gof ... _obIc-. and • ...".,aooe HIt __ • .., b_ """'" of cIeo._ """ II _ dofio:IMcy. ~ arc!
--~ ... - .... .-.g"" appo ........ A I'lClllIIoaI ...... e. .. iIiiIduI&. ftC)
plDrtlllllory~cMdIc wallrar •• c .PC .......... noC.-.. d._ ........ __ 1Iht SIeCa.d I'WIQStQJt.I'NWlCMRddll ........ _essIan eM .... ..., mel • ., 1napIIn._ however." PItienI: hllIIOOIher¥'...".toJl4'PlDrtacllgna4soldlpuesdllA The p1 1ft wonIIII .... her son ....,. be PIfaI'" bUt ~fttodng __ --... ...s-. skInI.ls COfIImOft In demende.
" .. I'eopIe _ "'" ___ '" .. .....s "" ..., -. ...... - .. -""~-00IIIIcI01jI.n.y _ ... be_.~~ ___ "''''_ of_~_ ... _""'cIopend.Caoo_<d '" ..... _ 1000_ pcnonoIIr _ ...." ..... . ___ ..... of ..................... I0Il. -.lIoiIpodont_not ......... _ofspooch, """9W.-..and ___ ~.,... ...-or __ lshe ... ___ _
-~-...
lob
Dementia al'd deIrtum shOw • great dP.aI of symptom
~anddoo._~. otsk"""' ..... deIirium. Thb.-m has ....... ydowkopod _ . The ..... """'" of_
k _ In ""'"' a.ou .. '" doysl. and " -......... by _ aognItlon. Including --.", In _
(heortng __ mbpen:eMng.-.. .......... a. mI"'-Y ........ neII •• _ ..- (InobIIity to ""'" _ bad<wardsl. and aIUnd ~ d arousal (a&ert to dazing in a brW time periodJ.HalIudnBtIons lsuch iii heiftlg wMasJ are c~ _"of.pS)<hotlc_.buttNs_~_mIo
~ we nat typical of ~ Mojo< ~ itIont wotAd not account for the ~ dittuIbed sensortum and cognitive clouding. pII'1ktJlatfy with sud\ an IQ.Ite tfme couno. The _ ~ of _
nud\aI rigidity. phoooonoo~ '" _localizing sIgno--<Ioes not suPf)Ort the ctiegnoIis 01 meningitis. in tN, indMdLaI.
7 ••
The Tarasoft """ _ by the CaIIomia ,.",..... Coon. estaNtsh.:t thZII: the confidI'ndaIity of a psychccherapeutic. sesskln must be violated when In IdenIIied tt*tI party Is at otskoflrnmlnerotharm.ln_thIsNingestallfishedthat ""' __ ----_to_the _.-. from a paOio!on _funher._ of the pollee In thIs ___ lndude.n_ ..... irMlIurary c.ommi1ment' of (he patient: to a psychiatric h0spital WhIle the st:andwds for tr ..... oh, ..... ry con ••• bl'lent vary Aorn ..... to 51 .... they geneoally __ ..... the potiont must have a mentalliness. iiInd that the patient is at rbk of ""'.fwm orol_ng ........... to ..... ..-I ....... ... The dIniaoI evidence points to • histtory 01 d\oonk: '-lI aIcDhoI use In this patient. The physical sam fwldings of poImoor orythemo and ..". """"'" suggest 1ong-....cfUog _ ~: the enlooged ......... I ..... __ an ._ fatty or __ . The __ _
sIgno h!<per._and dllaO!d """'" all...,. to ..-..mk ........ producodby __ TheCBC ....... ..,.
dooce 01 aIcchoHncluced bone ......- _ won. megaIobIastk anemia due to foIIte deficielq. Additional metabok findings aJIJW'i1OIl in ~It lndiYkIuaI. Include ~ and akohcHroducerI _this IrodMduoI b _and N • ..., hoIIu_indicating .... ho has _ the ..- ...... compIIcotIon 01_ Mthd.- mtjor _ with alcohol w1thdrawaI deIIrUn (c:teIrium b1!nIens).
•• d
Answers • 101
further f1Iines the dagnosls to the A!5'tricti11Q type. Although patIonuwith ................ d_Ix>dylmage.potiems with Ix>dy dysmorpNc dI_ do ............... woIght
""'and .........
10. d
The patient pteents \VittI dassic symptoms d an anticholinergic delirium: dry mouIh., mild hover, constipation. urinary ,ateiltlOr'i. blun'ed vkkln, confusion, wv::I agltiltion. The acute change In the patient's menUil statUS Is not oonsI5tent with a
prior aourse "'slowly poogoessho de" ... otla.l'sao-......tIa Is a term used to describe patients who dewtop apparent ~ _ItS In the setting of deprossIon. AItIo<ougI1 • cerebral hemorYhage woukf likely ~use an acute mental _us dlonge In on I!Ide1y pmon. the pad'" _Id likely have neuroklgk abnormalities and/or a history of head -. 11 ••
There is a high rate of depression post<VA; this patient _low mOO4aMedonio.foetingsofgulltpoor_ and weight loss for more than the minimum R!ql.Rd 2 weeks. "T1i! syI"IlI)toms are sewre enough and are nor the Iong-<twodIng _lew! symptom. 01 dysIhymIc: _.
_ she hasn't been "'YtIng'" g_1doen Of ~ ......_ phooe calls. thl ..... Idon<e Is pan of the depns.skin. not M'l indiatfon d.an avoidBr«. personality disorder or sodII phob6e. She has realistic concerns about her appa~ wetgt1t loss. unlike a person with somatization dilolder who would gener.ny haw concems about her body that have no boskln_
12 ••
PTSD "characterbed by wllMssing Of experiencing tr.uma wIth ..... itant sympton. <*-(1) _'ng tho trau .... (2) attempts to avoid recoIJecdon$. of the traumatic rxperIence. and (3) penisbttll autononic h)'perarousal. Use 01 alcohol Of
other drugs to bIod< the.,... ...... 01 PTSO is aommcn and akohol dependence Is fooquentIy dIagnco.ed .. _ Ind • vIduaIs. GAO Is not assodiiled with the experienc@c:AtralmA An Indhllcbl with GAD might _ to """" from ....,. nomic hyperIrou .. ,. but does .......... the ___ 01
trauma, flashbacks. or avddance present in PTSO. Major ~ ~ CD-OCOJrs with PTSO. but the sympIDms ~ to Nth diagnasK an be separatI!d with • C3n!f1.1 ~. C<ompIex _ epilepsy can pre ..... with -.r. ...... that may __ but the additional ~ and hlstofy required 10 diagnose PT5D are not
poesonl
The faiiunl to m ...... """" than _ of IdeaIIx>dy w<IgIot 1),. combined with tIoo _ seIHmog ........ the dIognosjs A_of KIoIr<opIvenIa requl ... a gre ..... than 6-month ..- neMOSa. The lade of bingo eating and/or ptMglng period of positive and nego_ symptoms oI"",dtosi. coo>
bftd wfth sodII Md ~ deeerionlllon. BIgoIar" crder requhlihe pilJ al'lCe cI ..... one __ cI .... and utUIIy ........ of cydos of.- .... dope ' ''\ '"'" _ Is ""m." .. , In ... -* pi.- of I>IpoIa: _ but ""'.,...._ ......... _of ........ _ and speed\,d .. c:ased~"'" !alad ~eItJ,. ..... dlpqalon....,bellDOd ladwilllpt)d'lalls..bAa.pIIdra'It does ........... -.:. of -... mojor .... ' ~. __ con Iood to pt)d'laIIs..epeoBly,,-, hoi: --. ..... __ of ___ be __ >Old .........., ___ Ioodtothe
... cI .... lOdII ... oca,..lIoi.r dysfundiaR ~
--by "'" patient,
14: •
_podonI"'_.~_oflogoontdis""" fof ....... ""'_of~"d ... _f*ayof_ negIect« .... ls nat ...:am ..... DeIpIe" NPOrt fA. __ .-...ofPTSDIs .... madt..-_ .. ~ __ of .... _ _ .. _ ... ,_of ... _ .. _of_ _ and lad< of poIof """ "alb .... __ I>IpoIa: _dol "'" qdc"",,*, ..... doI ....... _ PIdenI: """ ..... been dilgnmld wfth c:cnduct ...... In -----1**'_ ... ...-~I>SP, ,s, d A~_ ... __ .. cIognooed_
.. lIdwIduIIt.. su'c_~ .... paired abety tID flllfillmojor __ .. _.,......pd>Ie ......... ofMb: _In~ ___ .... _ 1egoI..-,m..- to • ___ -,
fR:Im • MInd or ,.,.., member woukt be oidI:aI in INs podonI'$ <Me to,..ery _ ... f*ayls _ and to .... out IkahoI dIpIndence. DenIal t5 • ClM'IIRqI d , _ MIICbanIsm ................ they~mIriI' .... ar ....... _dledogoooof_IOO_:Ihe-,._oecI Is_to_on __ dllgrakof..-,
Ity _dot, """' .. no _"" cUIng'" ~ .. _ .. SUI)pQft I ~ of aIcoh::I .... ...., I.e.. odor ~ *ohaL skITecI tpeech. "lLOOicl:_rIonr lrr\lIfIed)odgu: ... II'Id so en).
'L.,l. ...... _ ............... oA:a ................ . and can hnrnecllelt, ... the IfI:Ias d ba-I pOt Inlocbeloi .. NakIa:II. Is .. aplite JE<OtpD .......... ........ Is • 8 vbI~ neIIher has IDI e8act an be • a:III!!Pftil.·. ~ -........ d~shcIrt«tII.g ......... and dlaepam.a be:~wouId boIhWQnlB'l ~ dazepi:. Iitt'Cllklldc:n.
17a C _.,-.. ... __ ~ __ de! .. _
_of.,...._2,...._He ............ "" _fof.mojor.,. ' ...... __ .. _ ....
...._of-__ - .... ""-... .......,_ .. ...-",-....---~II!I .. ftIOd ... ~ the IDwIewl ~ .,.... ....... -IAl •• t stressor tIN -...w ... ............ -_ .. _ ... sIgr/Ii<anII}<--IL. _cHldclbl>lays .. _ .... _a_r.r-. ~ll)In ...... IOIIII ..... _(1)""'_ -"'O'.an:I CIJ .. !Clt)tjlld behI*«I11 ___ 1bed*l ........ ......,.-... of._ .......... ·_. oogaIna ",,_ .. _ ........ _ for_ plnnla.Capdurt cIIaIdat IJ. bIN lac' dIa .... .... • __ Iht"'*lIgIOsof_ ... _ .... _
............... _" ..... _ .. "' ... of ASP ~UClult5 ........ , cWdt ...... 1s c,.· I II' ~. pet ...... I111 ..... ' .... rce·in.'-two.m cue .. *'P (JudI. KhDaI_ haM.. 11:.,.. ...... f"""_ a.r ...,a&tMllIolnwNdldmn: • ICI~ ..-r " dor __ be __ SopM-, ""*'YdsordIr llda FtWik d bf-.llCy ..... ad btl' ___ (sudo.ayIngl ___ ....
I pMaIry c:agI_
w, c T10e podonI_'~ ___ of -. ~. IaldcliMld.1CA. ......... .,.... moremecJ+! ........ PldCJfMdIlKlIhDw&~d~"""""" Gy mouolo and sIght_ ~and Iow9ada _lCAs ... Qf " ............ "'" """" ...... --... .....,.. .. _~and __ _
CClftwaor ...
a. T10eI iii goMolrG _ of..., _ - • ""'" pMedto,,,-._:e. _lsthlrlnthebmer.. .. 1XftDI'i ~ -.. __ and .. o4GI*- __ doe permn ........ p' .. Sleep W'IOr ch»der tpIsodIs octU' ... dlbwae~nU:tI2 ............. oczur .......... ,..z •• .tIIt:~""",a ~.,'.4t .. thltrB.llts-. .. aaacblnd·~ (00"""' ..... -.-... of ___ Iii ~ ........ -~dooIng ..~...- ... t ___ ....., __ ..
.. ....... ca,dmella4l: ... SleepJ !Idngdswo dar"._ .. _._ ..... _ ........ >11 pooiIIoIIand __ «"" ____ -ac __ ""'"
21. c
This patient exhtbtls tt-.e daHk: symproms d ~ II common side effect or antlpsydKItic medicatlons. PzItitnts wtthm;,"""-.e><NbitaQi ___ _
They "",,'ly"-" on lnn«1eeting of ............ (often k:IcaIIzed to the legs). tt is important to dlstinguish akathtsia """' restlessness and ag_ due to __ """""" Of arudety. Other rTIO'f'ement cIsorders. such as. dystona (muscle spasm). tardilo<e dyskinesia (slow, Involuntary muscle I1'IOWnlents) Of Parldnsonism (piIkofflng tft!n'IOr. festinating galt. masked fades) should Itworys be ruled out In pat6ents t.Mdng neuroleptics. Patients with neutdeptjc malignant syndrome can present with agitation or l'I'IQ(or ~Ity, but the absenceof fever ahd a normal serum CPK make this dIagnosfs un~ke4y.
22. d
Tourette.'s disorder is char.actemed by involuntary VOUI!.nd motor des. Sometimes the vocal tics are grum:s or barks, but they c.1n develop into word tia. TOUfette's disorder is mote common tn)'OUng males (3:1 ~ ratio) and ortSef Is usuodly In late adolescence. Adolescent ~Iian is an anecd(Uilenn for teenage beha\tior but does noI explain vocal and motor lics. SchIzophrenia is nat I/kefy becaus.e this )'OOI"Q
man does not have psychotk syrnpIDrn5. Substance abuse can produce a behavioral change in an indMdual. but vocal and moror tics are no[ dassk:.Conduct disorder is d'~ when a child consislentty vioiates the tmic r1ghts d other5 and tgnores societal rules and norms. A chikt suspected of having Toutette's disorder mould have a GWd'uI mediall and neut~icaI evaluation. Wi$Of1's disease i¥1d Huntington's disease need to be ruled out. and an EEG should be per-fonned to assess for seizure disorder.
23. d
The patient has sexual desn and Is physiOlogIcally capable of arousal and orgasm. Although she Is CM"tse to genital c:ontact. the contact is neither painful IlOf prevented by vaginal contrac:.tkln as it 'WOuk! be In vaginismus. Sexual aversion is of unclear etiology. Many. tI'Iough not an. patients report a chikthood history d sexual abJ5e. Treatment is ...... gh c ........... therapy.
24. c
Panic: disorder typically occurs more ofren in remaIes and has an onset in the earty lOs. A person with myocardial isdlemia might present with slmil<v symptoms. but this diseaY! wotJd be Lrlilkely in a padem with no cardiac risk factors and normal laboratory tests. GAO presents with chronic worry that pervades rNef'J aspt'ct dllfe and psychomotor symptoms d r~t
Iessness, easy fatigue. Impaired colIU!ntllli'iof\ IrriIabAity, muscle tension, and steep difficulty. Major ~on mao,o have associated symptoms of i!N'\l(jety, but requWes 1tle pre$-
Answers • 10)
era d depressed mood 01' anhedonia in conjunction wtth ne~ symptoms. Alcohol ~n may __ of"9-"'-~I.but
-.. _ ...... i.""", IhIy In _ .... "'Y.In __
tion. other phvsIcai stgM « alcohol imoxIaJtion are usually preen1.and a urine: drug screen woufd ~ alcohol
n . c This )'OlrIg man has had 2 months' dlndon of depressed mood ..... neu_tM! _ of deoe_"""'llY, decreased Interest tn Ufe.lrooeaud appetitE! Vro'ith weight gain. d!sturbed steep. and impaired concentmIon An adjustment dborder 15 unMkety In an individual who reports no sttesson. and would not be diagnosed if symplOms meet: o1terla for majof depression I!\IeI'I In the preence of a precipilating event T'here Is no evidence to suggest a genet;!l1 medical. concltion as causative: of this patient's pf'd_ms; however. this sIIouId IIways be consideo<d. In "'" _~ \I1yn>I<I_ .nd anemia and elec1roIyIe saeen nAe out ammon .. _hemotolog1c.and "-_""""'offollgue.Dyothymic disorde, requires that mood and ~ symptoms are presencfor 2)'eimand tNt· they be less ~
thai> """" ~ "" majoo _ Tho paderot does _ ~ 0S)'Chcdc _ ...,....... .....
schlzop'"''''''
;16.d
OpIate-dependent patients. whether on methadone malnte"""'" ",_chronic opiates.wtI __ toIonnce
to the effec:ts of opiatrs added for pain ~. As a resuk. they wII_. higMfdole of pal1H1!1 .... ng __ than ...... oplatMepondont potIe ... Whole cInJg-...tung _lor ~ common among indMduals with substance abuse d'iSOI'ders" thl. potiec1t d""i¥ oI>Joctlwly __ ~gns of pal.,. related sympathetic activetlon induding diaphoresis and ekovated vital signs. He--atso h" 8 severe 1n)wy,1iket)' to produce: a great dHI of path. The patlent may attempt to D'oIefU$e the PeA pump, but wHI display signs of OWfSeda:tion, euphoria. and vftaI sign depression. all of which c:an be objectively monItooed.
21. c
ThIs pati@nt has 8 kmg history of alcoholism and disp&ays amnesia fOr recent events. Atthouql amciety <:an Interfere with memory. the patient does not appear af'IICiou5. EpkbaI hemorrhage m6ght cause a declining ~ of consciousness Of focal nt'UrOIogkaI defect 6n lN$ ptItient M 'MIUId not produce focal memory deft!cts..AIzhekner's dementia is.sodolEd with memooy loss, but ........ oddltional cognltI¥e ImpainnenU and is more canmon in an oIdet age group. Thi5 patient 15 at risk for akchol wid'IdnIIwaI deWriI.«n but does not show r.idenc:e d douded sensorium or atttf'ltioo disturbance.
.. r" t f or p u, J ;> ". p.AII ~ • ;>
:za.. SinceIld1lum;,oonaII!I_ .......... __ be_
by staes '" deIIjdnoIIon _ ..... InsoAIidenqc. 5igrIs '" _b»ddty.lnclud-.gc:oano_.~_1ftd
_ .. _In'" po1IonLAId>ough """"""'" """"'Y can -.ty ..... In _ and "'""""'" ~ b not assodated with coarse tremor or ~ CIrbamazePne kNIIs an! allo not as Millitl,*, to levels of dehyIhIon. Fk.ocedne can cause nausea. hHdKhe..ft!5111i1oes1.InsornnIa.and ~ It Is g ...... ...- ..... In .........
HoIaperidoI.-Ity "'" ...... """-~-. and at high ....... level$. or Pf<>IongatIan end ~ tonade de pol .....
a. Among aM the tacton Iisted.hoIIeI!IIllttSS has been shown to be one '" the ..... _ ~ '" Iong-tenn suicide mil. Major dept.SIIer. and '"""' mood ~ end ....,. stana! abuse dIson:Iars ~ atso risk factors for !IUkJde.
JO.< ThIs padon po ...... _ ........ _ ~ Irwot.IIng the _ 01 aI>jeas In the _ field. _Is.
common f'Incftng In LSD "1It«1r~ .. RohypnaI Is a potent -'-PIne "'- Is not "'-' to ...... _ Alcohol eM produce __ (usually ~ during
cur~ IIIc:dlaI wfthdnIwtI. Tbjs is unIIreIy: in this aBe as the ~ boy his no __ ..... hIstooy. FmIy. herein_not cause-.. :11 •• ~ 01..-. -.nan;y prcduce prcIaund _
lory depreSor .. Bet .. "zepIne alone or alcohol akIIIe ~ uAIIoeIy to produce'" magniaade aI • ....-. cIopoouIon bur might do so finge5lod In~ __ ~ Cocaine doe. not produce ..... ...., dopI_.1<eIonft is • _ .... ___ "'- pooduces little ..... ....,
deptosoIon. .... The patient cIsPays Din tDlll with gmM a1d c:IeIrlINs and cornpuIsioe WIIhIna _loB to ....". the genus. WhlethepoOlontllkelyhls......,_gto ... _ ... he_notdlsplaf_~_po,* _ GAO CM be ruled out due Ia 1ht fact 1hat his .-udety is not pervosMond",..tllepoOlont_ .. ~_ \en Body dysmorphk disorder con be Nod aut _ .... __ not hove. _ body ",-,_
persoNIty _eM be Nod out OS the ___ not
_.nlblt arrcgonce C<JUIlI<d _low self ..........
- • ___ a.paou ~ SoW (p>oot'. W ;>
31..
sexual OIIei.bitioll is a CatnpWJc GJNEPI ft!qUirIng much furdw .... n.._ariglraol __ ............. 0I.~ ___ ~""._1Obo _"_~_..-ttyor __ _ lars. sud1 IS howPc .... ~ __ pattdoglzed bv the _..........."._ ",lOSing _tNIdo!ncle_ homasatuIII oMIilliltlON were as normal as hetemseKuaI _100 ... ~ .... __ """' the DSM (I)IagnosIIc oro! __ at _ ~denlin
1Wl._~_""",,-,,-con
potentiIIy COft\'St ",,1ncIvWuII's'hcnosexual odIw'ItItIDn to hetaQsexuaI Ofierltadon. 8ecaUil ttwe is no sdecl1lftc eYidena! to support thII deIm..nd bea:t:ae ~ ther.1py 1s ...... ~domogIng.the""IO!riaon~_ teCOI,.;1!I Ids that ethkaI dwIphts refrain from aU8I11P'S to -.go .. - ...... _ .
14.. Thb..-.._, .. _~.,,_and_. IJnIII funher hloOory Is _ or ........ ..- .. -...c!.the",-Is ___ be • ...-__ oIodo1lopt •• ___ .... penIoIfar tIIe,.quloed 6 _ ... __ the _ for odoIloptorenIa.
.~be • ..- ...... -~ ....... In. pokd -. ~ bipolar _ ...... -dis" ..... n.. ~ '""II _ be ~ (e.g. ~ ___ AIIhoI9> ~ ..... GADcon __ , ..... "' ....... -.. 1hey.e..., not 19" 7 d and do ROt ~adIcry haIu---",tI1uught--.. --~ and"",*" d,puIM'.-." _ ..... _ 01 _ _1Rae_ ~ """ _ sleep.
Tholl- """"""",01 ~-..g.-OCDhove~bIe_ancI""""""'"
"'0 QlanI8pine is an atypc;JI anIips)chodc: thII: is used In the _ <i P¥l"*01.., <llalDgy.lluspftJnels-.oed b GAO but Is In''ctM In PI)dtosIL 5ertRIIne Is iII1 SSIU """ CIOUId be .- In c:urojun<2ian ..... an ~ to _. mojor deptoaIon wIIh __ -.... bur ~ .... -__ In~anclmIght_.monIcej>loode.
fIurNaIrif Is • "lK'4arll.~ a!t!!IJlU' ar48gOi .ht that Is _ In _,.,. -". ~ Is. ~doot _____ , ..
and _ "- .,." ..... """""'" _ In oIoIs potfont's p5J<IIosis. .... IWoporIdoIIs theonl)/ noun>IejlIic",typkoI~on IIoIs list. N ........... any • """" h/ghef ohk '" QUSing
tardive dyskinesia than do w newer, atypKaJ anrIps)dtodcs such as risperidone.alanzaplne.d ........ ____
37. d
The components of medical malpfact:ice include duty. neglgence. direct causation, .nd ct.mages. HI the ottJer options
... not part of the 1egaI_ ""..-<01 m--.NameIy. mat there must haOJe been is duty on the- physidarfs pan to prov~ Pf'opef care to the patient. There must haw been negl6gence on the physidan's partin falfWlg to meet' the standard 01 are in such drcumstances. Direct causation means ,hat the _ negllgef>C1! must ...... boer> the dl"'" cause of the aIeged damages. Damages means that the pattent must have SlIfenKt some bad outcome because of the physician's behavior. Beneficence refeB to a component. of ethical decision making.
3&b
Akalhbla Is most commoriy """'" by antips)<hotlc mediations. ".rtlcuIany typbl .. ~ (_
tics). AkatIlisia produced by drugs In the 55R1 class b less UkeIy, but these mecUartiDh5 an! 50 widely used and are ~ ""bed by so many no~lalriC ~ that "'" important skfe effK1 may be mhdagnosed. AbIhisia js profowlCIy distressing to some pat~and in some atSeS leads to attempted or successful suidde. It Is easlty treaUlble by remcMng the c«ending agent in most CASeS. Add'mg betablodteJS and benmdlazeplnes is also hefpfiJl
19. d
lnterpersonal psychotherapy is usefU in treating depressiot\ parUcutarIy YtN!n relationship issues are a key compcnent of the "...,.... depression. Psychodynamic.
psychoonlllytlc. .... supportlw """""""''''' ha"" not been demonstnlted to be as effective as cognltl~behiMoral psychotherapy fDf the t~atment 01 oeo. nor for ruany other conditions.
oo.d DespIte the emergence c:I it variety of new mood st.abIlzefs, lithium remains the most empirically growlded trNtment fur blpoIard_without rapid ""ling _Fl..."....;no, an antidepr6Wlt of the 5SRI dass.. Is generally c0n
traindicated in individuals with bipolar dIsordef. as most anddeprHsants CM' Inaea5e the lilrellhood of a manic epsode.LamotJ1gine is an antHeIzure rnedlcadon wtth mood stillbilzlng Pfoperties also. Lamotriglne requires further study, but early ft!pOfb indkate that It may treat bath the depressive and the manic phases of bipcMr disorder. Phenyt'Oin ts an anti-selzure medication that has not been shoYIn to be effectlve In treating bi~ diiorder. Clonazepam is e klng-acting benzodlazepine that mil)' have IAefuI
Answers • 105
prOperde5 in adjunctive treatment 01 acute mania. but Is not
an e:stabttshed treiItn'ent for ~ therapy kl bipolar -41. c The best elCplanation fof It\e patient's condition · at the momenr Is drug IOXIcky due to etewted carbatnazepine __ The"...,.. displays """"" __ """"""" with catbomazepIne I<»ddty. The _ to _ the dIa~.
resb with the 5eqUenc:2 01 ewnts. The padent HkeIy was noncom"',.", with his mediations as on .....,.....,. leading to reduced IeYets of mood stabiftzet and • maniC: break. Upon adminlon. he was restllrted at his usual OUtpatient doses; which presumably provide • ,hera_ '*"9 1_ when tlIken 115 scheduled. Then, an aotlbiotk is added. We are not
provided with the name 01 the drug. but It is impOnant to remember that some antibiodcs. such as macrolide antibiodes, may inhibit the metaboIlsm d medk::ations metaboltzed by the her'!; c:ytod'If'ome p4S0 enzyme system.
41b
Man)' medklldons can be used to treat depression.. Neitbef busPra Ie nor reserpine would be used (0 trNt depteSSion. _~ ... onxloIytIc_hasl_-',",~ RHc:rpine depletes central a.:R~ neurons d n0repinephrine and can. In fact. ... "'" ~ Uthium Is often used in conjmction with antidepresslnts as an augmenradon strategy In severe depession.but W'OUkt nat generally be a fl'st-llne U-tment unaess a bipolar depression is suspec1led. OtoIqlr.Im and phenelzine ... baCh __ an<Idept..
santi. fioweYef. phenelzine II monoamine Okidase inhibitor with ~danget"", side _is not .fim.IIne ..... · mI!nt. Cltalopr." Is safe. wel-t:oIerated.and considered along wkh other SSRis to be a first·Une treatment: for depress6Qn.
41. b
MII!IrT\Of)' ImpaInnent '" AlzheImer's dementia ts thought tD be secondary to loss of basal forebrain cholinergIC neu-CXlS. 1\CetyIct1oI __ or m-..oons Inducing tacrino (Cognex) and donepozU (ArIcept) I""""" synaptic acetytchoIIne conc.enb'aIion. AnUchoIineryiC medications CsudI as tow-potenc)' antlpsychatia and dlpheMydramtne ~ should be avoided .. __ dementia.
Dopamine antagonist medkations are frequently used for tr8ting psychodc syq:Jtom5 (svch as pdnOIa. haltudM...... and agItationl In dementia. _ r.upI2II<e InhtbibJrs are used to treat depression and are frequendy used In depfesslon co«curmg wtd"I dementia. GAM antagonist mediations (e.g.. fturftaZl!nll) are used in the treatment of iICUte be!nzodiolzeplne overdose; GA8A agonist medicati0f\5 (e.g., benzodlazepineos. barbiturates) may be used for agitation in dement\a but mey worsen memory cMfficultles.
106 • "''''''''"'' PsycI1iatty .... Catatoni: schtzophn!Na ~t6 the presence of catatonic ''''''''''"'' _ and WIO!I ~~ DIsooganIzod _ ph""" requires the ,......." of dbooganI>ed spe<d1 .... _and _na .. aIfea. __
",...... is diagnosed .....,.-.. are ..... .- fat ."Mf .... ---schtzophn!Na "diagnosed--paden! ...., fatmerIy had prominent .,..-""'_ of schizo. phrenla now has only residual negalNe symptoms or minor positive ~ptoms.
45. c
Taking ~ fat. _ i~ taking a "'" of beIog caught. a'kt havfng haIIucinattons rw defulions are faacn _Ibd ...... the _condItian but ....... port of ... insanity defense. BeIng proyok:ed by the vk1Im is Rot a C~ pcnent of "'" imanIty .w.n... ThoInsorHty _ ;, _ known as the M'Naghten rUe Cnitmed for a rTJei Italy II man who attempted to ~ a British prime mlnlsler).
46.d
Mi'lor atcohoI wIttldoIwIJ begins as eas1y as 8 few hour's aftef the ~st drIot<. Major ok!J/IaI wIIhd'- begins somewhat later. AkohoI withdlawal seizUres occur betweeA 6 .-,d 4a hours after cessation of akohoIlntake. Akddic hallucinosis (com;st;ng primarily of audl1Dry ha_ willi a clear sensoriurri) oaur wtthin 48 hours after cessatJon of alcohol Intake. AkohoI withdrawal delrtum is ~ by CDn"
fusion and f1aIIudnatIoN, """'""""' .",.,.o"K"al. and mild _. and has onset 48 to n ............. last akohoI
Intake.
47. c Wemicke-f(Qrsakoff S)'fldrome is a set10us and usuaIy in'eversibIe compI_ of heavy _ use .,......t by thi
amine deficiency with assodiIted hemorrhagic ptaretlon In ... mommlllory txxte.. __ ~ is the
eady ... go of 0.. cnndItiOI1 and a>mIsts of ~ nystagmus. and atalda. Prompt treatment with th\amfne
reJ!IeIion ~ or -~ may -' • pogo ....... to -. P>}dloIiJ (~ am ... 1a and oonIabuIaIIon~ ""'" the lui Wemic~ 5)'1"1Cin:wne is e5IiIbfishecL It ts irmersllle In about two thirds of.,....... .... _ and OIlIer "'*""""'" ~ .. II>ougIrt to be ~ teIo!<od t<> dopamIn. _ In .... _1n_1D __ ~"","pO\1Int eIIectJ at dopamineogIc __ ()pi-. and __
&<Ph"; _ on>du<» poIOr1(lId ~ ~ use. but .... ~ psyct.-_ during _ .... Nkx>_ and _ .. -"""""'" _ but _
prodllce ".....,....
49. c An arttIdepIessant is the mosr approp ... treatment for major depe5sIon...., fI k may ..... -. caW!d by. evA.
liINum would only be ~ in tills case for augmentatio<l of ... antIdopessao< in the case of • partlaI _ Valproic acid -'Id be .-W ~dlscrd« or _...,.,,.-.. __ susp!<ted. _ and ~ mIgIlt be used ad]unctIwIy __ for ..... '" but would __ -
ally be fifst..fine t:reatr'T.nt.
50..
The patient ... ___ """""" 0 drug-
Indua!d condition resembling ..... """" disease. The "'pill rdIIng"""""1< _"9 OOltoand-cuIly;-.g -ment5 .e at symptoms of hrkinMln's. Since the cIsease is due to law areb"; _ ........ drugs that bIod< dopamine .-... most IiI\RIy 10 "";C the _. Neither Ioruepamor betiZ1rqlir. bkxk dopamine rec:EJ)tOr1. Alti10ugh 0._ .. end _pine boIh block dopamine
"""""'" they are law _ ~ """ or/y weakly block dopamine leceptors and 1ft Bs li1c:elyto cause __ ....,...""""""- __ • prlk!nt dopamine
bIod<er. ~ most ll<ely to cause tile syndrome.
Andreasen NC, Black DW. lntnxluctury textbook ur psychiatry. 3rd ed. Washington, DC: American Psychiatric Publishing, ZOO!.
&ldessarini RJ. Chemotherapy in psychiatry: principles and practice. Cambridge, MA: I larY"dfd Ulliversity Press, 1985.
(""..ursini RJ, Wedding D. Current psychotherapies. 6th eJ. Belmont, 0\: Wadsworth, zorn Da\·ison GC, Neale J M. Abnormal psymulq,,}'. 8th ffl. New Yurk: Juhn Wiley & Sun.~ Z(XX).
Diagnostic and statistical manllal or mental disorders. 4th eel. \Vashington, DC: American Psychiatric ASSOCiation, 1994.
Iiales RE, YUllofsky sc. Textbook of d inical psychiatry. 4111 cd. Washington, DC: American Psychiatric Publishing, 2003 .
I lyman SE, AranOl GW, Ro.<;cnballm JF. Handbook of psychiatric drug thCf"llpy. 4th ro. Philadelphia: lippincott, Williams afld Wilkins, 2000.
Physicians desk referencf'_ 56th ed. MUlltvale, NJ: Medical Econumic<;, 2002.
Saduck B.f, Sadock VA. Comprehensive textbook of psychiatry. 7th cd. Philadelphia: lippincott, Williams and Wilkins, 1999.
Victor M, Roppcr All. Adam's and victor's principles of neurology. 7th cd. New York: :rvkGraw-llill. 2001 .
Note: Page numbers with anfindicate figures; thOSf' with a t indicate tables.
Abilify. See AJipiprazoie Ahu<;('
child, 93, 95, 103 dill-I, 56-57 spousal, 56
Acetaminophen poisoning, 55
Acetylcholinesterase inhibitors, ] 05
Adjustment disurders, 5 1, 74t
Adolescents mental disurders of, 36-43, 37. suicide attempts by, 55
Adrenocorticotropic hormune (ACfH), 31
Mea definitiun of, 8 pseudobulbar, 64t
Agoraphohia, 14-]6,63
Agranulocytosis clozapine and, 591, 6 ]-62 valproate and, 6'9, 70t
AIDS. Sf!e HIV disease
Akathisia, 6J, 66, 74t , 80-8 1 beta blockers fur, 77, 78t case study on, 94, 97,103,105 risks for, 81.
Alcohol abu<;(', 26--28. See alro Substance abuse; Withdrawal syndromes amnesia and, 48 ocnzoola"£pines with, 29 ca'>C studics on, 9 1, 93, 98- 99, 101 ,
105-106 delirium and, 44, 45t dependence ami, 26--28 disulfiram fur, 27, 78 management of, 27-29, 74t, 75t mental retardation and, 37 personality disorders and, 22 spousal abu<;c and, 56 \Iojemicke-Korsakuff syndrome and,
3t, 26-27, 48, 99, 103,106
Alcoholic Anunymous (AA), 27-29
Alcohol intoxicatiun, 25- 27, 103
Alogia, 2t
Alprazolam dosages fur, 75t for panic disorder, fi3 for social phobia, 17
Alzheimer's di.o;ea<;e, 3t, 47t. See also Dementia antipsychotics for, 58 case studies on, 90, 91, 98, 100,
101, 105 management of, 48, 78, 105
Amenorrhea, 33
Amnesia alcohol-related, 48, 103 dissociative, 49, SOt types uf, 49
Amphetamines, 77. See also PsychC6tirnulants ahusr of, 30-3 1 for ADHD, 41 paranoia and, 99 psychotic episode fmm, I, 3t, 58 withdrawal from, 30-3 1
Anafmnil. See Clumipramine
Anemia, 44, 45t
Anhedonia, 4
Anorexia IlcrV()!;a, 32- 33 . See also Eating di~order.;
case study on, 91-92, 101
Anurgasmia, 52t, 95, 103
Antabuse. See DL<;ulfiram
Antibiotics, 45t, 105
Antichulinergics, 77. See al.ro specific drugs, e.g. , Beta blockers arrhythmias and, 94, 102 delirium and, 3t, 44, 45t, 61, 77,
92, 101 dementia and, 105 indicatiun.~ for, 78t, 80
AntiCOllvu!sants, 26--27 . See also specific dru~ e.g., Carbamazcpine
Antidepressants, 63--{j6, 64t. Sre also specific types, e.g., Tricyclic antidepressants for autism, 27
cost of; 65 dosages for, 64t fur eating disorders, 33- 34 indications tor, 63, 64t, 65 mania am1, II mf'Chanisms uf actiun, 63- 65 munitoring of, 65 for persunality disorders, 24 psychostirnulants with, 78t psychotherapy Wi th, 10 for schizoaffective disorder, 4 side effCL"ts uf, 65-66 t J1T>CS of, 10
Antipsychotics, 1 ~2, 58 -62. See also specifIC drugs, e.g., Iialopcridul atypical, 58, 59t, 61 f for autism, 40 dooages fur, 591 efficacy of, 59t indication.<; fur, 58, 6Ot, 61 for mania, 11-12 mechanism uf action, 58-60, 6Of;
61f munituring of, 61 fur persunality disorders, 24 fur schiwaffa:tivc disorder, 4 side effects of, 59t, 61-62, 80-83 for tic disorders, 42
Antisocial personality disorder (ASP), 2]-22, 26 case study on, 93, 102 condlJ(:t disorder and, 42 management of, 24 somatization disorder and, 5 1
Anxiety henzooiazepines for, 7St defined, 14 generalized, 17- 18 separnt ion, 16, 37t, 64t, 102
Anxiet)' disorders, 14-1 9. See a/so Gf'llt'ralizf'd anxiety disorder antidepressants for, 63 types of, 1St
Anxiol)'tics, 73- 76, 75t. See aLm specific lypeS, e.g , Benzodiazepincs d{)!;ages for; 75t
.. f\l>t [ or " al .. ! >« .... ",II" aptrnar .. f ..
indicati{lIL~ for, 7]- 74, 74t m~hanim1 of action, 73 monit£)ring or, 74-76 side clfccts 01, 76
A pnea, sleep, S3t, 54t, 102
Ariccpt. See DlInr.pC7;ll
Ariplpraz(llc; 59t
ArrhythmiilS eat ing disunk-ni and, 34 TCAs and, 9 4 , 102
Asperg(';!"'.c; diso.. ..... der, 2 1, 37t
A b,·an. &e Lor.lZepam
AtomoKet ine, 41
Atl<lchment di5()J"dcr, rcacti\"f:, 371 A ttcnti()]l-dditit /hY I'X""r.lCtivily di~OIJcr
rADH01, 37t, 40-4 1, 102 a ntidepr~nto; for, 64t, GG curuluct dison:\cr with, 42 managcIT)Cnt lIf. 41, 78t
Aut~tic disorder; 21, 37t, 39 40 GiS£' stufly on, 94 , 102
A~oidant Pl=lInality Jison:Ier, 23- 24
Barbitllfates, 28-29, 102
B~!H1 1 ganglia, 601-; 611" tkhavioral thempy, 15,85, 87t, lOS
for ADHO, 41 tor autism, 40 {i iait'rtiGlI , 24
Benadryl. 5re Dip1lenhydraminc
BGlzoo,azepines abuse of. 28 for alcohol \\ithdrawal, 27. 7St , 91 ,
101 duh clrup and, 3 1 for delirium, 4fl FlI r d emcrl tia. 48 d(I!>ago- for, 7St hGAD, 18 half. lifI- of, 74, 75t indication.~ fUf, 73- 74. 74t for mani3, 11 - 12 mechanism of action, 73 O\'crdo!;e of. 9] , 102 for panic disurrkr, 14, J 5, 6J for personality (uSQrlw.r~, 24 side effPtls uf, 76 ..... ithdrnwaJ fmm, 28- 29, 44, 45t ,
76 Bcnztropme, 77, 80
Ht-ta blockers, 77-78 for akathisia, 77, 78t for ('.AD, 18 indication.<; fOfj 78t , 8 1 for personality dison.lN"S, 24 side effects of; 77- 78 for social pholm, 17
Bmb>eing, 33-34, 63
Bipolar dlsordm, 10-13 . Sre also DeprcssKlll; ManiA antidcpres:c;al1t.~ for, C,4t, 105 3.l1tipsyl.:llOtil's end, (lOt"
ASP and, 22 case l>·tudif'!; on, 95 96,117-98,
104, 105 lamotri&inc fue, 11 - 12, lOS maml&emml of. 11 - 13,68--72,
69t- 7 It,79 r:lpid cy..:ling, 13 sdultoaffecti\'f', 4 ~uidde and. 12. 13 tre:ltmE'l1t-J"t"'iist:I1l I, 60t
Body d~morrh , c dl.c;orclfor. Slt
Borderline p{,fWnality JiwrJer, 22 bipolar disorder ver.ms, 11 l)'d othymia and, 13 csting disorder With, 34 man3gcmcnt or, 24 p!>ychotic ('piwde With, 6
Bru in tumor; 3t
Brp.IIthinA-rclatcd sleep dL~order, 53t, 54t, 102
Brid" PS)·l.:hotk Jl~orJer, 6-7
Bromu(;ripline, 82
B\llimia nCI"VOS3, 3:\-34, 63_5«- a.L;n Eating dborders
Buprcpion for ADHD, 41 dU53go for, 64t side effn:ls of; 66 for smoking cessntion, 66 SSR I With, 65
Buspar. Sec Buspirone
Buspirone, 104, JOS fur GAD, 18,73--74 mechanism of al1.Ion, 73 side cHfi1.S 01; 76
CannabL\ 3 1, 451
Carnam81.cpin<,,69- 70 dosages for, 7 J t
for mania, 12 side cffirt~ ()( 7Ut, 104. IUS
Carbon ciisulfide pOi:sonil1)l , Jt Carbon 11"K11loxide poironitlg, 45t
CatarKlS, 62
utatonia Jepf('&~rOn lmd, 13 loraY.cp301 for,74t schl:.:ophrcni ll and , 2, 3t
Olexa. ~ Citmopr.lln
Cerebrovascular accident (CVA) dementia after; 47t, 48
Inde)( 109
J("'pr~:m (trIer, 92, 99, rOl , 106 psychu tic cptsoJc after, 3t
C hildhood disin tegrative disorder, 37t
Childrr.n abuse Cl( Y3, 95, 103 antip.c;ydlOtic.~ for, fI(lt
lTIPJ1 lal dj~rriffS of, 36-4], 37t
Ollordia7.cpuxide, 27, 7St
C hlorpromaZirx", 591
Cirrhtl:.i\ 26
Cita lupram, 64t, 105
Clomlpl""oImlnc, 63, G4t, 65
Clnna7.r"plllll, 63 , 751
C IOIIi (line, 3D, 78, 8]
C lozapin(', 58 ca..~ study on, 90, 100 indiutiOl"l:!O for. 61 ITlrc hanism (1f action, 60 side effects of; S9t, 6 1--62
CI07.Brii. Se¥! Clol'.3pinc
Oub dru)lS. 3 1
C(II:aioc. See also Substa!lcE' abuse uhn~uf, 31 dopamine anci, I psych(1tic episode from, 3t l'o'ilhd(3Wai f .. om, 30-3 1
CoIUlCX. ~ Tacrine
Cogrnti\"C'- lxhaviOlai thcr:apy (CBTJ, 87. 51¥. I~Lw Bt-hav;oral thf'.OIPY J« OClJ, 105 lor panic uiMJrdct-, I S
Cogllilivc J isorJers, 44-48. See {J.so sptYific types, e.g., DCIllCIltia l yp('S of, 4St
Cognitiv(" f'nhall(;etX, 48, 78, 105
Cuj:;niti\·r theory, 8, SS, 871
C"'() IMut1l\('l\.1, involuntary, 88
CosnrnUIl1cl<liun d isurlle J"$, 37t. ]~
Competence, 88
Compulsions. 19, 63. See also Obsess., Co-
comp ulsive disorder
Condit iuning. 87t
Conduct disorder, 37t, 4 1 ..... ,'2
Consent, informed, 88
Conv('T"sion t\isurder, S it
Cvprolnli ll,42
Cro:utJeltlt-Jakob disease, 47t
Cushmg.·" ~YJldrome, 3t
C)cluthyml(" tlisonlcr, 1 2~ 1 3
Cyicrt. Set> Pemoline
D .. lmane. Sec AurnzcpaRl
DnntTolrnt'", 82
110 . Blueprints Psychiatry
Deliritlm, 44- 46 ant icllOlinergics 3nd, 44, 45t, 61,
77,92, W I antfpsychotics for, 60t C31L<;CS of, 45t demcntia vpmLS, 45--46, 46t, 91,
10 1 manilgement of. 45--46
Delirium tremens, 27
OehlSi01~ 5- 6 ant ipsychot jcs tOr, 58 demenilll with. 46t ob~ion.~ wrsus, 19 sch.i7.0phrcnia and, ! 2, 3[ types of, 6t
Of'ITIf'ntia, '16-48. See (ILl() spf'Cific types. e.g. , Alzh~mer's disease a!colwl-induccd, 2fi delirillm I-wruS, 45-46, 46t , 91 ,
101 psychotic f'Pisode with, 3t
Dependence, 25, 7K See olso Substrulce abllS(' alcohul, 26-28
lkpetulent pcrsofl3lity disOrder, 23 case study on. 9 1, 100 m:magemcnt of, 24
DepersoT1aliz3tion dioor-der, 5U
Dcpr~ion. See (J.5CJ Major depressi\'e disOrdcr; Mood disorders alcoholism and, 27 antipsychotic<. fur, OOt: atypi(:3l, 13,63, 64t, 65 bipolar diSOrder l'I?nU.!, I I causc:s of. 8 dement ia 311d, 47 <louhle, 10 hyputhyruidism ~Ild, 79 managemrnt of; 9- 10 postpar\llm,o, 13 psydlOlic, I . 3 t , 10,63,82 srnizuaffective disorder ..... ith, 4 S('a~ona l, 13, 63 , h7 sLeep disturbances in, 9, 53 anerstfOke, 92, 99, 10 1, 106 substance abuse a.no, 20 ~lIbtypes of. 13 suj<;ide and, 9t., 10 , 55-Sn
D~I\SitiZatilln, s)'!'tf'matic, 15 17, 19
Desipramirte,64t
Dcsyrct See Tr.u.oJonc
lJc\'e loplllffit:ll disorder.;, 37t
Dc:xtroamphetamilli'_!lel' Amphet3minC!';
Diabetes mellltw;, 62
Dia[ectical beh,.vior thmp)' (DB'I). 24
Di3zcpam, 102 dosages for, 75t for withdrawal, Z9
Dicydominf', 30
Digit31is toxicity, 31
Dipllf!Tlhyor.;rnille, 77, SO, 105
Dison\P.I' of wri tten expression, 37t, 38--39
Di~ociativ(' fugue., 49, 50t
Di!'SCICiative identity disorete.-, 49- 50, SOt
Di&ulfiram, 27, 78
Dillrr.ti(,:~, 34, 35t
Dunellenl, 78, 105
Dop:'lrrune amphetamines and, 31, 106 antagonists 01; 58 -no, 00f, 6 1f.
195-- 106 antideprCliSants and, u5 psycho.<;i." and. I, 3t, 58
Down syndrome. 37
Drive psychology, 84
Duty to warn, 89
Dyspareunia,52t
Dyssomrrias, 53t, 54t
Dy~hymic di!iOTder; 10 :l.'l tfllcprcssants for, u3, 64l c:u;c study Oil, 93----,94, 102 depression IJeT.qJ.S, 9t
Dystonia, G2, 80, 81 t
Eating disorders, 32- 34 case stuoy 011, 9 1- 92, [OJ da<;.~ification of, 331 of early childhood, 37t managcmeflt of, 33-34, 63, O4t medical complkations with, 34, 3 5t
Echolil lia, 13
Ecstasy, 31
EHexor. See Venlf1I'axine
Ego defenses, 84, 85t
EjaCl.ll1ltion, prematufC, 52t
Elde.rly abuse of; 56-57 antidepressant~ and, 10, 64l benzodia7(~pincs 8M, 76 delirium jll, 44-46 demtlltia in, 46--4 7 lithiuIll aoJ , 68 movement di~ordcrs in , 81 t , 82-83 psydHJ.~tirnulants ~nd, 78t suicide among. 55 TCA"al1d,66
Electroconvulsive therapy fECT), 56, S7 indiClt ion ... fur, 10 111ania and, 11
Ei<X'tfolytc imlmlances, 34
Elimination di50rde~ 37t, 64t
J'.ncephalopathy cirrhosis With, 26
del irium from, 31, 45t elating disorders and, 34
Enuresis, 37t , 64t
Epidural hemorrhage, 103
En.-ctile disorder, 521
Erikson, Erik, 85, 86"t
Erotllmanic ddIL~ion, tit
1-o:<;Cltalopram, 64t
Ethylellt glycol poisoning, 2fi Exhibitionism, 52t
Exposure therJPY, 15-16 Extrapyramidal symptoms (EI-'S), 58----62,
59t,8 1-82 case stuoi~ (In, 94, 99, 1m, lOG mOnitoring fo(, 61 risks I:Or, 81 t
I'aditious disorders, 53
t"at emboli syndromt.'. 45t
Feeding disorders, 37t
Fctidlism, 52t
FlOoding thl'rapy, In-P, 19
F1uma7.f'ni l, 102 Fluuxctine, 63
dosagcs for, 64t side ef1f.cts of, 90, I no, JCl4-1 05
Huphctl3Zille, 59t, 6 1 Flur~zepam, 75t
nn\,OJ(amjJlf'~ ()4 t
I''o\atl'_ deficimcy, 48
Fragile X syndrome, 37, 39
Freno, Sigmund, 84
Ftotteurism, 52t
Fugu(>~ dissociative, 4Y, sOt
G~bapcntin, 71- 72 dOS'Jgcs for, 71t fo( GAD, 18 for mania, 11-1 2 for soc..ial pl:!obia, 17
Gamma-amitlO blltyriC acid tGABAI bern:ooiaze,pin co; lIno, 73, 105 gahapt'Jlti f1 and, 71 moo<.! stabili1.crs and, 68- 69 pan ic disorder and, 14
Garnma-hydrmrybutyrate (GHB), 3'
Gender identity disorder, 52 53
Generalized anxiety Ji~order (GAOl, 17-18,04t , IQ:l_See also Anxiety buspironc for, 18, 73- 74
Gcodon. See Ziprasidone
Ghu:;ocorticoids, 3t
Gnmdiosc ddusion, tit
I-Iattion. See TrW-olam
HaldoL Sl>e H31opcridol
Ilallucinat ions a1..ohol wi thdrnwal and, 27, 106 ~ntip£ydlOtics for, 58 ca~e study un, 96, 104 delirium wi th. 46t sch.izoplueni:l and, 1- 2, 31 st imulant-induced, 30
, IaUucinogem: allti~) chotics and, 60t ~I irium from, 3t. 4St
Halopen dol for ~lcobolic h~ llucinu.;js, 27 fOl-autism, 40 for delirium, 46 monitoring 01; .6 1 fur psychosj,,- G I side eftect.~ d, 59t, 97, 104- 106 for tic d isoJ'"ders, 42
, la~hish. Setf unllabh.
Head trauma delirium 91l('f", 4St ckn)(,llti:l after-/ 47t ITI {';tlta\ ret3nlatiOIl and,]7 OeD Bnd, 19 .<.eh i zophrcJ\i~ and, 4
I Idplessne;os, lean lPd, 8
l·k patoccUular C9fcmoma, 26 1·lerom. 5ef.> O piate;
HippUCBIllPus, 18 Il istfiollif JX'SSOll.3.li ty disorder, 22, 24
, !IV dll,ease dementia with, 3t, 4 7t, 1 7 substance abuse and, 30
Ilum~xuality, 55--56, 96-97, I (l.1
Il untJl1gton's di.<;eaM' antipsychotics for, 60t (\ementia an( ~ 47t psychotic cpisode With, 3t tk disordt-n; ,kr,n,$, 4 2, J 03
H}drQl:c phallL,\ 4 7
1-I~·dromorphonc, 29
H)'pt'racti\'It}. Sec Attention-Jeficit/h}'peractivit)' diMlrocr
Hyp(~f"C!llcf'm i a, 3t., 44 , 4St
HypO'"~lycem i B, 3t
I lypersomnia, 53t, 54t
I lypnotKs. Sec &ooul"t.-hypnot ic dru",
I lypoC'Jlcerma, 3 t
Hypochondri9.'ii!i, 5 1 t I I}'pt)glycemia, 3t, 2ti, 44 , 45l
Hypomania, III( 12 I I),ponatremia, 44, 4Sl
Identity roSOl"l.b d issociat i\,{', 49-50, 501: !;l'ndrr, 52-53
Imipramine,64t
Immigr.mL~, 5
Lm putencc, 52t, 66 InfurmcO consent, f:!f:! Insani ty ddCu!.c, 89, 98, J06
msomnia. See Sleep d;~
Inu·J li~en~ quotient (IQ), ]6, 3 71
Interpenonal theory, 84-85 1n\"Uluntary (ommitmCtlt, HH
Ipct'ac toxicity, 33- 34/ ]5t
Isoniazid,31
Jcalou!;y, Gt
KetarnilW',3 1, 104
KJonipin. &to Oona7.r:pam
Korsakoff's j>!;ycho.Qs, 26
l.alTlotrir;Tne, 7 1 rorb,pobrJi~r<kr. 11- 12,105 dosage!' fiJr, 71 t
LcarncJ hclp!cssll~ 8 Leanung disorders, 37t , 38-39, 42
Legal is.<ruf'S, 8R-89, 97, 98, lOS, IU6
Lc\'Ol!{lpa, 3t
LexaprO. Set.- Esdtalopram
LiruiunL ~ Chlordiazepoxide
Li thium, 121 68-69 antiJepres&mts with, 1U, 65, 68 cilM' study 01l,97-98, 105 dosages for, 71 t side effects of, 69, 70t tuxid ty from, 26, 69, 78t, 104
Lornzepam, 741, 8 It rlosages for, 7St ovcrdot;c of, 93, 102
Luvox. Sro FlIII·o):amine LysergiL: acid JiMhylamklc n SO), ]1 ,
%, 104
Major depre!otSive di5order. 8--10, Sre (Iiso Deprcs.siOil C"JSt'". stlld icl. l~ l, 90, 95, 96, ] (X),
103, 104 t:rite."i a for, 91 eating di:.ordl'..B with, 33-]4 management of, 9-10, 63----67, 641 PTSD aod, 18 n"Cunent, 9f ~OijffC'l.:ti l'e disor-dO'" with, 4
Ma~crin8, 53
Malpractice, 88, 97, lOS
Index 111
Mania, 11- 12, 1 J l Set- cJ.ro Bipolar cl ,SOrdCN; ~ntipsychotics for, 60t r:ntcria for, l it m~"aJ;eml'fl t of, 11- 12,68-72.
69t- 7 lt photothm.py and, f 1, 61
MMiju:"ma, 3 1. 45t
Mao;oclul">l1), 52t
MathcmOitics disorder, 371, 38-39
I\-'IDMA. See Ec.~ta .. y
Me1.mcholic depression. 13
Mcllnnl. Scr. Thiuridazill{!
Memory fa lse, 50 impaired,46--49 loos o~, 48--49, sOt, IOJ
Menlflg itis, 44, 45'-
Mf'ntal r<>umation, 36--]8, ]7t antip!>)'chotics ror, 58 m:lnl\gcmct"l t ol ] 8
Meperidine, Z9, 45t
McubolJc uisunkf"!; un t ip!')'chll[iC.~ ~nd, 62 t1diri lJll1 and. 3t, 44, 45t inb(ltn,37
Mct.hadOJle, 30, 95, 103
Methamphetamine. &e Ampi-telaillines
Mf' thohcxital, 102
Methylphenid!te, 3D, 77 for ADH D, 4 1 an\ideprewnts with. 65
Migration psydtuo;i .... 5
MirtH1)1pin", 65 lk"6agcs for, 64 t side. ~t1; of, 66
M'N:lghtf'1l rule, 89,106
MOl!oomult' oxicla<;e inhibitors (MAOls). 10
choil..'t" of, 65, 105 d~gcs Kw. &it rnE'Chanism of :ll"tion, 65 fur p-.mit: disorder, IS, G3 fur PTSD, 18 ~{If. eflects of, 66, 82- 83 for S\.)(:;a l phubia, 17 withdr;l ..... al from, 3\
Mood rlisonlrrs. See ai«J :;pec;fir rypes, t'.1I., Mania from mctlical condition, 91, I I , 13,
92, 101 st:hi7.oafTf'Cti\'C, 4 seasonal, 13,63,66 substancf'- indllcoo. 9t, II , 13, 90,
100 types of. 8 , 9t Unipolar, 8- 10
'12 ' Blueprlrt.9 Psychiatry
Mood ruhi lizCf'!\ nR-72, 70t See abo specific: druJt$. t.f!, . lithium C.1SC study on, 97-98, 105 indications for; 68, 691
Morphine See Opiates
Motor ~kill~ Jisnm~, 37t
MovC'mcnt di.~ord crs. 37t , fiOt , 77, 80-83. See also spmfic typt>s, e.g., Tardin' dyskinf'!;.i a Caso:' study on, 94, 103
Mult ipJ(, p(,lsonali l y d i~nrdPf. Su OiSSI)Ciatille ideot ity di.<.Qrde r
Muti:orn, 37t , H2
Naln,xno(', 102
NaltTf!xcme,. 27- 28
NSlcissistk peI'SOflality d isof'dt'f, 13-24
Narcoll'p~y, 53t, 54 t, 102 an tido:pressallL~ for, 641 p~)'(hm;limulanu for, 7St
NarcOl ia; Ano nymolls. 30--31
Nard i!. .'in phcnt' t1.ine
Na\·ane. See Thiothixene
Nefazodoot; 65, {j6
(to!>a~ for, 64t
Neg tigeoCC', 8, 97, 105
N I' UTOIf'ptics.. s~ AlI tip:o; ~dlOliQ\
N£.ltfOkptlc mallgoant syndrom C' (N f\,ISJ, 6 1-62. 8 11, 82, IOJ
Niacin dehcien<:y, 31, 48
Nightmar($, 53t , 541, 102
NOf'cpincphrlo t; H, 4 1. f-iS
NOfprumin.. See Of'5lprn mi l1 l"
Nortriptyline. 641
Obc~ity, 62
0htect re la t jons IhCOl)', 84-}\5
O bsc-ssiolls, 19
Oh~"""i \lf:-COmpLl l:sh"C dif;Ordcr (OCD), 19 cac;e study on, %, I ()4 management of, 19,65,97, lOS o~i\'e-cornpulsil'e personaUty
dison't!r rlC1')U~. 24 panic a ttacJ.: venr,-~, 15 SSRls for, 63 tic; With, 42
Ob,c;c:;sil'C'-Compu lsi I'C pcn;onalily diroruff, 23- 24
O Janzapine, 58, 104 ~Jc cffcr:ts of, 59t, 62
OPI;,Jtc~, 29--30, ~ also Sllb;tanccabuse case sludi~'S on. 95. 96, 103, 10-1 Jel irium from. 45t
methadone and, 30. 95, 103 ovpm Ofir of; % , 104 vJithiJra\\'iil from, 29 .... 1(). 29t, 7f!
Oppositicmal defiant Ji.~ordr.r. 3 7t, 42
Organophosphate poisoning, 451
Or~mic dj~()!'derli, 52t , 95 , 103
Oxa7.l"pam, 27, 75t
Oxeamazppinc, 71 t
Paill disorder, 5 I t
Pnmf'lc.. See NontiPlyline
P-.mjc, attack. 14-15 criteria tor, 15f GAD IJl'.'73'US, 17
Pallie di~l)fd t'r; 14-- 15 .3nlidcprc:.&mts fot. 63 case stndy on, 95, 1(1.1 managcrm::nt o~ I 5, 74, 7<1 t
F".l.ranoia antipsychotics lOr, 60t delusional diS()l"d~ with,S, 61 schizophrcrua aoo, 3 t. 98, IOfi &iml1 lalll-induu:d,30
Paralloid pen;(lnality disord er, 20, 102 ddll. .... ooal di~llrdcr and, 5 managt" lTlent of, 24
Pnrnphili8!;, 5 1-52, 52t
ParasolTUlia.<;. 53t, 54t
ParkInsonism. 5ffl t-:xtrapYI"alT1iJaI symptoms
Parkin~on '5 disca!;!:, 471
P-"rnate. St>e Trnnylcypromi.nc
"'''TOXemIC', 641 P-dXil _ See ParID:ctulC
Pl.oOophilia, 5 21
Pd lagra. Slie Niacin deficiency
Pemoline, 77
Pr ntohamital chaUP.flgl' l('St, 29
Pcrph['flazinr,59t
l'cnion3Iit}' d isordt:n, 20--24. See aiS(l specific types, e~, Schi7.oid fWl'sonalit}' disorder an tipsycholiCs 10.-, 58, 1-iOl. eriten/! ror, 2 1 t cyc\otll ),mia and, 13 fIWlagcmcnl 01; 24, 641 5umtanc~ 3bu.~ and, 22,29 types ul; 20, 2 1t
PE' r\'3.~i \le dpvelopmental di~der.;, :t IL
Phencyclidine ( PC P), 31, GOt
Ph~lldzille. 65, 105 dosall"'" f('l r ~ 64t .~ i de Pfff'CL~ ('I f, 66
PI1NlOOarhital, 2!I
PhenytOin, 26-27
Phobia drfinition of; 15 school, 64t social, I5-17.2 I , 64t,65 specific. 16
Pho nolO£icai diSOl-(1eI, 371
Phototh~rllp y, 11, 67
Pica,37t
Pid,'s d i!iC3SC, 31, 47t
Pim07.iclc,42
PIlL'llmOilia, delirium and, 44. 451
Poisoning acctll.minophen, 55 carbamazl'pinc>, I U5 d elirium from, 3 1, 451 digital is, 3t eth),lm t' gly<::ol 26 inlm:ic"t illll 'o'I/'1:nj .~ 2(, ipt'c~, 33-34, 35t tithillm, 26, fi!l , 7Rt, 104 mood stabilizer. 26, fi9- 7fl, 70t organophU"ph!ltc. 451 phenytoin, 26
Porphyria, 3t
Poo;tpanum depression, 6, 13
i'oMlr.l tlm ali(; SlJo$S disonlcr ('''rsO), 18 (a.~r study nn. 92, 101 rnanagE'lllt'nt ('If, I H, 641
Premat ure rjaclliation, 521
l'Tiapisln, 66 ProlixilJ . &e Fluphemmn('
Promctha:tilJe, 30
Propanolol, 8 h
Prozae.. SH Fiuoxet itlt:
PM"UOObl11bar aileel, 64 t
Psclldoocm entia, A7
Pseud~p8rkinsonislTI, 106
P.<:}'chnanaly.;;iS, 84-85. S5t
/,:o;y(hotc>gic alll~ting, )6, 3 7t
Psychologkal theories, 8 4 · 87
Psy<ha;u. Set! also Psychoti.: di<;ordc,· alypical, 3 t drfinilion of, 1 d'1l rr~ion and, 1,31 JfU~ for, 58, 60t KorsakoWs, 26 migroMIl. 5 PL'Tsonality d isorde rs ;,Jod, 2 1 t sch izoaf'Fel: live d isorder and 4 stimulant-inJu« '(),3O '
P~}"<hosocial therapy, 2-4
P1iych()li; limlilants, 77 abu.sf' of. 30--3 1 fOr ADllD, 41 311tidrptT"",-<;3nts With. 10, 65 anl ips)'Chot jC$ lind, llOt
caw :>llldy on, 97, 104 delirium from, I , 3t, 45t, 58 im:l ic;atim ..... ror, 7Ht lrumia anJ, II paranoia and, 99 tic: disor-den; (lnd, 42 withdrawal from, 30- 3 I
I'sychot ic dison:lcr .. w (lLIlJ P5ychosjs bnd; 6 7 I..auses of, 3t typl'!i of, 2t
l\J,.ging, 33--34, fl.l
QUt'"tiapinc: for schizophn:nia. 58 .sid .. effats of, 5~\, fJ2
Rapid cycling, 13
Reactive attachmf'fll clL<;OJ"dpr, 371
Read ing UL'iQIl.kr, 37t , 38-39
Rcmcron. See M irta:.!apiof'
Re>Cfpinc, 105
Ilf'_"JHIOS-C prCI'elltion therapy, 19
Rc:storil Sre TCITUl"Zepam
Ret inopathy, pigmentar y, 591, 62
R I'll· s disorder, 371
Hc,·ia. Su Naitrcxot)('
Rispc,.dal. See Rispcridonc. Rispeid one, 58
mechanism of action, 60 side effi.cts o r. 59 t, (;2
IHtalin .. w t.·1P.thylphf:.nidatc
Roo)'PTlo1! 3 1
Rubella, 3 7
Rumination di~ {"II"tWr, 37t
Sadl~m, '521
Schi2.oaffet."livc rlisonlcr, ~, ! 1, 104
Schizoid pt!n;onali ty d isorder, 20- 2 i , 24
Schi1-Ophf('.nia, 1- 4 case studies on, 92-93, !:.IS,
101- 102. I(IIJ diagnosi\ of. 2, 31 dopamine hypothesis fOl, 1, 58 Ill;magem ent uf, 2-4, 58, GOt, 61 prodrome of, 2 schizoaffi.cli\" f' disorder IIt'm<S, -4 .scllizopllTt!llifnnn JiM"lru."'T" l~lL,", 5 subtypes of, 2, 3t sll icide and, 2 !<)'m p l.orr15 01; 1- 2, 2t, 97, IIH
SchiZophreniform di1oOn!eT, 31, 5 antilJl'iych otics fOl", 60t case study on, 97, 104
Schi7.otypil l persOflll lity di~rdcr, 2 1 mana,i!;cment of, 24 J"1'>}·cho t ic. episode with, 6
School p hohl3, 64 t
SCOIsnn al afft. .. -ril"(' uisorucr, 13,63, Gl Sedative-hypnotic. elrugs
abuse of, 2H dd.iJ ium [rom, 45t w ithJra.....-,,1 from, :l1", 28-29, 28t
ScizllrCI> al. ohol withdrnwal, 27 ant idepre;.o,;ants and, 65, 66 an t ip~)'dlOt.ics and, 61 aut ism and, 40 do;lirium from, 3t, 45 t from meperidine, 29t mood ~tabili~ ITS <lnd, 68 o eD and, 19 tit disord ers ;\Ild, 4 2
Sd c("l.h·e St.'f<.lt rn.l.in rf'tlpblkp inhibitors (SSR I ~), 10 ahllhisia from, 97, 105 bupropiOO With, 1)5 choic f" of. fi5, 105 dQ;agcs 10.; 641 rOT ("aling disordf"rs, ] ], (>3 t'"fficacy 01; 65 ~1AOIs With, 66, H2-{j] mechani~m of IKtinn, 6') ror QCI), (j:l rOT p~nic disorder, 15,63 lor personality disor-dtm>, 24 lor 1''1'51>, 1 H side effects oj, 66. 80, 83 fOr SQri rol phobia, 17
Separauon an)(kl)" 16, 3 7t, 64t , Hl2
5crax. ~t' O)(azepam
Seroquel. S«- Qu .... tiar ine-
SerOlOrtln. Su alit) Sf'If"ctivc serot onin r~lIptak(' inhihitOTs
.antiucprl'!iSanL~ Ilnil, 6:; Ilntip~;ychot ic~ alld, 58, 60, 61 f blllimi3 3nJ, 34 depr~'iinll and, H OCl) "'lid, IY
Scmtonin $yndrome, Gli, 62-83 Sertralinl',64 t
Ser7.one. S«: Nera"l.nJClnf'
S~ l"l'3~gnmC'nt ~ utgc ry, 53
St'xllal dy!;hmction, 5 1-52,521 al 1tidt'pl"f'WlnL~ li nd, (if i ca.~ .nudy Oil, ~JS, 103
Sexually rnnsmith.·d dir.Nlseli (51Th), 3t, 47
Sexl.I.3l ori...,tatioTl, 55-56, 96-97, 104
Sexual response,5 l t
Sleep dlsordel ~ 53 ADI ID and, 40 brcathinl!J-rcktcd, 53t, 54l, 102 depression and , 9 rn.an ~gl'fl1cn t or. 7St
P'TSD and, 18 typt$ (If. 53 t, 54t
Slecp st"ages, 53t
Inde)( 113
SkC'p t C'rTCl1" disordCl", 53t , 54t, 94, 102
Smoking <:es.sa tion, G6
Sonl"il'ly, 27
SodHI phobia, 15-17 allt idcpres);(lIlL~ for, M t, 65 !;Ch izoid personality disordcr l!Cr.SU S,
21
Somatiz ation JiMnJer-, 50-51 , Sit pcnionality t:Ii.~'1I""ders aou, 2 1- 22
Somatofon n disrn-der~, 50-5 1, S ll, 53
S))l.'t:."t.<h <lisorg;lnizm, Z, 3t povcrty of, 2t
Spnmal abuSC", 56
Standford-Binet Intel ligt:ncc Scale, 3G-37
Starvation .. 33-34, 35t
Stelazine. See '(iinllopcrazinc
Sto:rl·orypic behavior aut ism lind, 40 Iks 31lU, 42
S t~vpn ~·Joht1~on syndrome, 7 1
Sti lllll.J ~nts. Set> psycho:.timulants
Stl"3ttera. See Atomoxf'linp.
S tr('lkC'. See Ce-rt'-hrovasculru- lIcckk-nt
StuttC'ring, 371
Slibnanoc ahu....;c. Ser a/slJ spedji£ tyfJt'~, P..', A kohol ;:obllsc ASP and. 22 , 26 case stlldy 01"1 , 93, 102 conduct di.~ortkr anu, 42 de~nilkm of. 25 dchrium with, 3 t, 45t mental rf'l>! rJaUon and, 37 p ain mcdic3tiol1s and, 9 5, 1m pCJ"$Onalily d isorders and, 22, 2!J I;l;l,i"l.ophrcnia With, 4 somatizllt iOfl diS<:!r"do?r anJ, 5 I spousal abuse lmu, 56 ~uk.id o:- and, 2.{)
S\lhsblllll' dl'fK'.Jldenc:e, 25
S\lhs~ntill nigrd, 6Of, 6! f Suicide::, 55- 56
bipolar disorder and, 12, 13 CAS(' st udy on, 93 , 102 dcp rt>S!lion alld , £It , 10 malpractice d ailns and, 88 mana~emmt of, 56 pt."'fsonali ty cli.~ordC'J"!i and, 2 1- 22 rL-.h fOl", 55, 1(}4 schl7.ophl"C'Tlin and, 2 SlIbr.talX"e abuse and, 29
SundownillS, 45, 46r, 47
114 Blueprint!!> PsychIatry
Syphilis, 3t, 47
S~'~l t!mic Illpus erytherna lo~w; (StEl, 31
T;lCriru:, 48, 78, 105
Tarnsoff decisions, 89, 9 1, 101
Tardi\'e i:ly~lullcia (1D), 41, HIt, 82- H3, \04- 105 _ See aLllJ MOVf'_m~nt
disordcrs
Tay-Sachs diseasc, 38
Ttt/l;lzepam, 751
Thiamin Mciency, 3t, 26-27 delirium and, 451 d~m~ntia and, 47-48
11lioridazine, 591.; 62
ThiQthixelw/ 591.
Thor.uinf'_ See ChlorpTl)ma:dne
Thyroid &~ordt'rs dP.p~{)n and, 79 psychotic episode with, 31
' lltyroid hormones, 10, 65 , 78-7~1, 7St
TiCI;, Sre Tourelte 's diSOTder
Tofranil , See Imipramine
Tour~tte's disorder; 37t, 42-43 antipsymotics for, 58, 60t C<lse study on, 94, 103 clonid ine for, 78t
' Ioxicity, Sre Poisoning
Tnln~·"exti~m, 52t
Trnnylcypromin~, 05 dno;:age!i for, 641 side cffect.'l of, 66
1i<t:wdo[le ror dementia, 48
dosages 10,., G41 hlde eff~ct.~ o[ fi{i
l j-iazo]arn , 75t
' Irkydic anlidepre;.,'O<IIlt.~ (TCAs). 10 c1loice of, 65 dosages. for, fi4t clficacy of. tiS mechanism of actiOll, 65 monit oring of, 65 (or neuropathic pain, O4t for OeD, 63 ror palljC disorder, 15', 63 for lY rSP, 18 ~id~ rffects of, Ofi, 94, 102
Trifluoperazine, 59t
Trihexyphenid~·I , 77
' iHlafon .. w PPfphf':f\azi l\t'
1nsomy 2 1, 37
Twclvc-stcp ptO~rams. 27- 3 1
Unipolar depres.~ion, 8 10. SiX' 0/50
Bipnlar disorders
urinary tract in{cctions, 44, 45l
Vagjnismu~ 52!, 103
Valium. See Diazepam
Valproate, 12, fi9 do.-;ag~s lor, 7 1 \. skl~ eff{'cts or, 69, 70t
Venlafaxine dosages ror, 64t efficacy of, 65 sid.: effects of, 66
Vitamill 13 ., deficiency, 3t, 48
Vomiting, 33- 34, (;3
Vop~urism, 5Zt
Warn, duty to, 89
Wpcl l~l ~r (ntd ligence Scale for Chi ldl'f!n- H~'isoo. (WISC-R), 3&--37, 37t
\Vellhutrin. &e Bupropion
Wemjd~-Korsakofl' syndrbm e, 3t , 26-27 amnf':'iia with, 4H, Ir13 (~~1lifh on, 99, 1(16 dciirium with, 45t
Wilson's disease psychotic episode With, 3t t ic disorders 11t!m1S, 42, 103
Withdrawal :.yndromes, 31, 2G-29 alcohol, 27, 7St , 9 1, 9H-99, 101,
l ex; balbi1t1rate,2..Q benzooiaze'pine, 28---29, 44, '1St, 76 ca:ainc, 30- 3 1 dciirium in, 3t, 44, 45t opiate, 29-30, 29t , 78 sedative-hypnotic, 31, 28-29, 28t st imulant, 30-3 1
Wri tten expreso;ion. Jisordt'f, 37t , 38---39
Xan~x . See Alprazolam
Ziprasidone, 59t, 61 Zoloft. See Sffiraline
Zyban. Set> l-\upmpioll
Zyprexa. See Olanzapint'
. --- .... --' . --MYCAH,n