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    Organic,

    including

    symptomatic,

    mental disorders

    FOO - F09AGUS HARDJANA SAIMAN dr,Sp.KJ

    padjadjaran university

    maranatha christian university

    immanuel christian teaching hospital

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    Overview

    This block (F00-F09) in ICD X and the PPDGJ III classification are :

    F00. Dementia in Alzheimer's disease

    F0l . Vascular dementia

    F02. Dementia in other diseases classified elsewhere

    F03. Unspecified dementia

    F04. Organic amnesic syndrome, not induced by alcohol and otherpsychoactive substancesF05. Delirium, not induced by alcohol and other psychoactive

    substances

    F06. Other mental disorders due to brain damage and dysfunction

    and to physical diseaseF07.Personality and behavioural disorders due to brain disease,damage and dysfunction

    F09 Unspecified organic or symptomatic mental disorder

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    Historically: the field of neurology - organic disorders

    psychiatry - functional disordersTraditionally: - organic brain disorders -

    - "nonorganic"

    -"symptomatic".

    That distiction is also antiquated, since basic neuroscience can

    identify structural correlates of functional abnormalities at the levelof genes and other molecules.

    The division between structural and functional rests solely on which

    biological level is arbitrarily chosen as the cutoff po int .

    An accurate approach is to accept the ideas that each biological

    d isorder,including mental illness, has a structural pathology at somelevel or assortment of levels and that structural abnormal ity is

    reflected as a disorder of func t ion or regulat ion.

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    DELIRIUM the hallmark symptom of delirium is an impairment of

    consciousness, usually seen in association with global impairmentsof cognitive functions.

    DEMENTIA is a syndrome due to disease of the brain, usually of a

    chronic or progressive nature, in which there is disturbance of

    multiple higher cortical functions, including memory, thinking,

    orientation, comprehension, calculation, learning capacity, language,

    and judgement.

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    I.DELIRIUM

    - an imp airment of consc iousness, a sudden onset (hours or

    days) a br ief and f luctu at ing cou rse, and a rapid im prov ement

    - Delir ium is a synd rome, no t a disease. to have many

    causes,central and systemic,acute confus ional state, acute

    bra in synd romes, metabol ic encephalopathy, toxic p sychosis,

    and acute brain fai lure.- (l ) the cl in ical need to ident i fy and treat the under lying cause

    and

    - (2) the need to avert the developm ent of delir ium related

    compl icat ions.

    Such compl icat ions inc lude accidenta l in jury b ecause of thepat ients cloud ed consc iousness or impaired coord inat ion or

    the unnecessary use of restraints.

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    EPIDEMIOLOGY

    Del i rium is a common disorder .

    - Ab out 10 to 15 percent of pat ients o n general surgical wards

    and

    15 to 25 percent of p at ients on general medical wards

    About 30 percent of p at ient in surgic al intensive care units andcardiac intensive care un its and

    40 to 50 percent of pat ients wh o are recover ing from surg ery for

    hip fractu res have an episo de of del ir ium .

    -The causes of po stop erat ive del i r ium in clude stress of su rgery,

    pos toperat ive pain, insom nia, pain medicat ion, electroly teimbalances, infect ion, fever, and b lood loss .

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    EPIDEMIOLOGY

    - Ad vanced age is a major r isk factor for th e developm ent of

    delir ium.

    About 30 to 40 percent of hospita l ized pat ients more than 65

    years o ld have an episode of del i r ium.- Other predisp os ing factors for the development of deli r ium

    are young age (that is, child ren), preexist ing b rain damage , a

    histo ry of del i r ium , alcoh ol d ependence, diabetes, cancer,

    sensory imp airment and malnutr i t ion.

    -The presence of del ir ium is a bad pro gno st ic sig n.

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    ETIOLOGY

    The major causes of del i r ium :

    central nervous system diseasesys temic disease (for example, cardiac fai lure), and either

    intoxicat ion or w ithdrawal from ph armacological or toxic agents .

    When evaluat ing a del i r ious pat ient, the cl in ic ian shou ld assum e that any

    drug the patient has taken may be causatively relevant to the del ir ium .

    Pathophys io logical mechanisms have been sugested

    for del ir iumneurotransmit ter hyp othesized to b e involved in del ir ium is acetylcho l ine,

    and neuroanatom ical area is the reticular formation.

    In part icular, the deli r ium associated with alcohol w ithdrawal has been

    associated w ith hypeact iv i ty of the locus ceruleus and i ts noradrenergic

    neurons.

    Other neurotransm itters that have been imp licated are serotonin and

    glutamate.

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    DIAGNOSIS

    It may occu r at any age but is m ost common after the age of 60 years.

    The del i r ious state is transient and o f f luctuat ing intensi ty; m ost c asesrecover wit hin 4 weeks o r less.

    However, del ir ium last ing, with f luctuat ions, for up to 6 months is n ot

    uncommon

    A d eli r ious s tate may be su per imposed on, or pro gress into,dementia.

    Diagno st ic g uidel ines

    For a def in i te diagno sis, symp toms, mi ld or severe, shou ld be present

    in each one of the fol lowing areas:

    (a) impairment of cons cious ness and attent ion

    (b) global disturb ance of cogn i t ion(c) psyc hom otor disturb ances hypo or hyperact iv i ty

    (d) distu rbance of the sleep - wake cyd e

    (e) emotio nal dist urb ances, e.g. depressio n, anxiety or fear,

    irr i tabi l i ty, euphoria, apathy, or wondering perplexity.

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    DIAGNOSIS

    Includes:

    acute brain syndrom eacute con fusion al s tate (nonalcoho l ic)

    acute infect ive psychos is

    acute organic react ion

    acute psycho-organic synd rome

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    Different ial d iagnosis :

    Dement ia (FOO - F03),

    acute and trans ient psy chotic disord ers (F23. -),

    acute states in schizop hrenia (F20. -)

    mood [affect ive] diso rders (F30 - F39)

    Del i rium, induced b y alcohol and other psy choact ive

    sub stances, should be cod ed in the appropr ia te sect ion

    (Flx.4).

    F05.0 Del i r ium, not su per imposed on dementia, so desc r ibed

    This code shou ld be used for deli r ium that is no t

    super imposed Upon pre-exist ing dementia.

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    Different ial d iagnosis :

    F05.1 Del ir ium , superimposed on dementia

    This co de should be used for cond i t ions meet ing

    the above cr i ter ia bu t develop ing in the cou rse of adementia (FOO - F03).

    F05.8 Other delir ium

    Includes: del ir ium of m ixed or ig in

    subacute confus ional state or del i r ium

    F05.9 Delir ium , unspecif ied

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    COURSE AND PROGNOSIS

    Altho ugh the onset of del ir ium is usual ly sudden, prod romalsymptom s (for examp le, rest lessness and fearfu lness) may occur in

    the days preceding th e onset of f lor id sym ptom s.

    After the identi f ication and th e removal of the causative facto rs, the

    symptom s of del ir ium usual ly recede over a three-to-seven-day

    period,

    The older a patient is and the longer the patient h as been del ir ious,

    the long er it takes for the del ir ium to resolve. that is remembered

    only vaguely.

    The occurrence of del i r ium is asso ciated w ith a high m ortal ity rate inthe next year, prim ari ly because of the serious n ature of the

    associated medical con di t ions that lead to del i r ium .

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    TREATMENTThe pr imary goal is to treat the under ly ing condi t ion

    that is causing the del ir ium .

    The other important goal of treatment is the provis ionof ph ysical . senso ry, and environmental support .

    Usually,deler ious patients are helped by having a

    fr iend or a relat ive in the room or b y the presence of a

    regu lar sitt er.

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    TREATMENT

    Pharmacological Treatment

    Treatment are psy chos is and in somnia.

    The drug of ch oice for psy cho sis is haloper ido l (Haldol) a

    butyrop henone ant ipsy cho t ic drug;

    Phenothiazines should be avoided del i r ious pat ients , because

    thos e drugs are assoc iated sign i f icant ant icho l inergic effect

    Insomnia is best treated with either benzodiazepines w ith short

    half- l ives or w ith hydro xy zine (Vistar i l), 100 mg.

    Benzodiazepines w ith long half l ives and barbi turates shou ld beavoided un less they are being used aspart of the treatment for

    the under lying diso rder ( for example, alcoho l w ithdrawal).

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    II.DEMENTIA

    Dementia is a syndrom e due to disease of the brain, usual ly of a

    ch ronic o r progress ive nature,

    Disturbance of mu l t ip le higher cor t ica l funct ions, includ ing

    memory , think ing, or ientat ion, com prehension , calculat ion,

    learning capacity, language, and judgement.

    This syn drom e occ urs in A lzheimer 's disease, in

    cerebro vascu lar disease, and in oth er condit io ns p r imar i ly or

    secondar i ly affect ing the brain.

    Dementia produ ces an appreciable decl ine in in tellectu al

    func t ionin g, and usual ly some inter ference w ith personal

    act iv i t ies of d aily l iv ing , suc h as w ashing, dressing , eat ing,

    personal hygiene, excretory and toi let act iv i t ies. i tsel f w i l l

    depend largely on the soc ial and c ultural sett ing in which th e

    patient l ives.

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    EPIDEMIOLOGY

    Dementia is essential ly a disease of the aged.

    Of Am ericans over the age of 65, about 5 p ercent h ave severedementia, and 15 percen t have mild d ementia.

    50 to 60 percent have dementia of th e Alzheimer 's ty pe

    Alzheimer 's typ e occupy mo re than 50 percent of n urs ing h ome

    beds.

    The second m ost common typ e of dement ia is vascular dement ia-

    account for 15 to 30 percent of all dementia cases.

    Other dementia 1 to 5 percen t of all

    By the year 2030 an est imated 20 percent of the- popu lat ion wi l l b e

    more than 65 years o ld. Thus, the current annual cos t of $15 bi l l ion

    for car ing fo r dementia pat ients

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    ETIOLOGY

    Dementia has many causes;

    Dementia of the Alzheimer's Type

    Alo is Alzheimer in 1907,

    Senile plaques,

    Am yloid precursor protein.

    Neurotransmitt er abno rmali t ies.

    Other po tential causes.

    Vascu lar Dementia

    Binswanger'sdisease.

    Pick's Disease

    Creutzfeldt-Jakob Disease

    Hunt ingto n's DiseaseParkin son 's Disease

    HIV-Related Dementia

    Head Traum a-Related Dementia

    Dementia can be a sequela of h ead tr auma,

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    A lzheimer's disease

    Is a primary degenerative cerebral disease

    It is usual ly insid iou s in on set and develops s lowly ,per iod canbe as sho rt as 2 or 3 years,

    The onset can be in mid dle adul t l i fe (Alzheimer 's disease ofpresenile onset), high er in later l i fe (Alzheimer's disease of

    seni le o nset).

    There are characteristic changes in the brain:a marked reduct ion in the pop ulat ion of neurons

    appearance of neurof ibr i l lary tangles

    neur i t ic (argentophi l ) plaques, which c onsis t largely of amy loid

    and granulovacu olar bodies.

    Neurochemical :a marked reduct ion in the enzyme chol ineacety l -t ransferase, and in other n eurotransmit ters and

    neuromodulators.

    Dementia in Alzheimer's disease is at present irreversible.

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    Figure 10-4. Microscopic brain section showing pyramidal cell layer of hippocampuswith numerous triangular intraneuronal neurofibrillary tangles [ ] and several senileplaques [ ] (Bielschowsky stain; original magnification x190). Figure provided by Dr.H. V. Vinters, Section of Neuropathology, UCLA Medical Center, Los Angeles, CA,from Vinters et al. 1988. Used with permission.

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    F01. Vascu lar dementia

    Vascular (form erly arter iosc lerot ic) dementia wh ich in cludes

    mult i infarct dementia, histo ry of TIA w ith br ief imp airment of

    con scio usness, f leet ing pareses, or v isual loss.

    Diagno st ic guidel ines

    The presence of a dementia

    Impairment of cogn i t ive funct ion and focal neuro logical signs.

    Insig ht and judgement m ay be relat ively wel l preserved.

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    F01. Vascu lar dementia

    An abrupt on set or a stepw ise deter iorat ion, conf i rmation

    can be provided only by c omputer ized axial tomography or

    neurop athological exam inat ion.

    As soc iated features are: hypertens ion, carot id b rui t ,

    emotio nal labi l ity w ith transient depressive mood , weepingor explos ive laugh ter, and transient episo des of clo uded

    cons ciousn ess or del ir ium, of ten provoked by fur ther

    infarct ion.

    Person ali ty is bel ieved to be relat ively wel l preserved, butpersonali ty changes may be evident

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    Figure 10-7. T2-weighted magnetic resonance imaging of a patient withvascular dementia shows extensive white-matter hyperintensities. Figureprovided by Dr. Bruce L. Miller, UCLA Harbor Medical Center, LosAngeles, CA. Used with permission.

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    Different ial diagnos is.

    Consider: delir ium (F05. -); oth er dement ia, part icular ly in

    Alzheimer's d isease (FOO. -); mood [affectiv e] diso rders (F30 -F39); m ild o r moderate mental retardatio n (F70 - F71); su bdural

    haemor rhage (traumatic (S06.5), no nt raum atic (162.0)).

    F0l .0 Vascu lar dementia of acute onset

    Usually develops rapid ly af ter a suc cession o f strok es fromcerebrov ascular throm bos is, embo l ism , or haemorrhage.

    F0l .1 Mufti- infarct dementia

    This is more gradual in onset than the acute form

    F0l .2 Subc ort ic al vascular dementia

    h istory of hyper tension and in CT foci of ischaemic destruct ion

    in the deep white matter of th e cerebral hemispheres

    F0l .3 Mixed cort ical and sub cort ic al vascu lar dementia

    F0l .8 . Other vasc ular dementia

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    F02.8 Dement ia in other specif ied diseases classif ied elsewhere

    Inclu des dementia in:

    Carbonmonox ide pois on ing (T58)

    cereb ral lipid os is (E75. -)epilepsy (G40. -)

    general paralys is o f the insane (A52. 1)

    hepato lenticu lar degeneration (Wilso n's disease) (E83 .0)

    hy perc alcaem ia (E83 .5)

    hypo thy roid ism , acqu ired (E00. -, E02)

    into xic ations (T36 - T65)

    mult ip le sc lerosis (G35)

    neuro syph il is (A52. 1)

    niacin deficienc y pellagra] 52)

    po lyarter i t is nodosa (M30.0)

    sy stemic lupu s erythematosus (M32. -)trypano som iasis (Afr ican B56. -, American B57. -)

    vitam in B 12 deficiency ,E53.8)

    F03.Unspecif ied dement ia

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    CLINICAL FEATURES

    Memory ImpairmentOrientat ion

    Language Impairment

    Personal ity Changes

    Psychosis.Other Impairments

    Psychiatr ic.

    Neurological .

    Catastroph ic react ion .

    Sundowner synd rome.

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    DIFFERENTIAL DIAGNOSIS

    dep ress ive di so rder (F30 - F39),del ir ium (F05); m ild o r moderate mental retardation (F70 -

    F71);

    iatrogenic mental diso rders due to medication (F06. -).

    Dementia of the Alzheimer 's Type versus Vascular

    Dementia

    Vascu lar Dementia versus Trans ient Ischemic Attack

    Del i r ium

    Depression

    Fact i t ious Disorder

    SchizophreniaNormal Ag ing

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    COURSE AND PROGNOSIS

    The class ic cou rse of dementia is an ons et in

    the patient 50s o r 60s, with g radual

    deterioration o ver 5 to 10 yearsleading

    eventually to death.

    The age of onset and rapidi ty o f deter iorat ionvary among dif ferent types of dementia

    Psycho socia l Factors

    TREATMENT

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    TREATMENT

    Some cases of d ementia are regarded as treatable

    The general treatment approach

    prov ide supp ort ive medical care,

    emotional su ppo rt for the pat ients and their fami l ies,

    the maintenance of the patient 's phy sical health, .

    symptom atic treatment

    Part icular attent ion m ust be pro vided to caretakers

    and fami ly members

    When the d iagnosis o f vascular dementia is made,

    r isk factors

    Pharmaco logic al Treatments

    Current ly avai lable treatments psyc hoact ive drugs

    Tetrahyd roam inoacridine (Tacrine)

    Psychodynam ic Factors

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    III. AMNESTIC DISORDERS

    single symptom of a memory disorder that causes sigcant impairment insocial or occupational functioning.

    EPIDEMIOLOGY

    Amnesia is most commonly found in alcohol use disorders and head injury.

    ETIOLOGY

    Thiamine deficiency. Hypo-glycemia, hypoxia (including carbon monoxide

    poisoning), and herpes simplex encephalitis ,tumors, cerebrovasculardiseases, surgical procedures, or multiple sclerosis plaques General insults

    to the brain-for example, seizures, electroconvulsive therapy (ECT), and

    head trauma-.

    Many drugs benzodiazepines triazolam (Halcion),

    CLINICAL FEATURES AND SUBTYPES

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    CLINICAL FEATURES AND SUBTYPES

    (anterograde amnesia - retrograde amnesia).

    Short term memory and recent memory are usually impaired.

    Memory for overlearned information the such as childhoodexperiences,

    Cerebrovascular Diseases.

    Multiple Sclerosis

    Korsakoff's Syndrome

    Alcoholic Blackouts

    Electroconvulsive Therapy

    Head Injury

    Transient Global Amnesia

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    DIFFERENTIAL DIAGNOSIS.

    Dementia and Delirium

    Normal Aging

    Dissociative Disorders

    Factitious Disorders

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    COURSE AND PROGNOSIS

    The specific cause of the amnestic disorder

    determines the course and the prognosis for a

    patient.

    Transient amnestic disorder with full recovery is

    common in temporal lobe epilepsy,ECT, the intake ofsuch drugs as benzodiazepines and barbiturate , and

    resuscitation from cardiac arrest.

    Permanent amnestic syndromes may follow a head

    trauma,carbon monoxide poisoning. a cerebralinfarction, subarrachnoid hemorrhage, and herpes

    simplex encephalitis.

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    F06.Other mental disorders due to brain damage and

    dysfunction and to physical disease

    The decision to classify a clinical syndrome here is supported bythefollowing:

    (a)evidence of cerebral disease, damage or dysfunction, or of systemic

    physical disease,

    (b)a temporal relationship (weeks or a few months) between the

    development of the underlying disease and the onset of themental

    syndrome;

    (c)recovery from the mental disorder following removal or improvement of

    the underlying presumed cause;

    (d)absence of evidence to suggest an alternative cause of the mental

    syndrome (such as a strong family history or precipitating stress).

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    EPILEPSY

    GENERAL SEIZURE.ABSENCES (PETIT MAL).

    Partial seizures.

    SymptomsPreictal symptoms.

    Ictal symptoms.

    Interictal Symptoms

    PERSONALITY DISTURBANCES.

    PSYCHOTIC SYMPTOMS.

    VIOLENCE.

    MOOD DISORDER SYMPTOMS.

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    IMMUNE DISORDERS

    AIDS.

    Systemic Lupus Erythematosus

    ENDOCRINE DISORDERS

    Thyriod Disorders

    Parathyroid Disorders

    Adrenal Disorders

    (Addison's disease). (Cushing's syndrome)

    Pituitary Disorders

    Sheehan's syndrome.

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    terim k sih

    t s

    perh ti n

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