Alternative Therapy Treatments for Depression and Anxiety
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Transcript of Alternative Therapy Treatments for Depression and Anxiety
Pharmacology and
Beyond…
MOOD DISORDERS
© Daniela M. White, MD, 2011
GOALS OF THIS PRESENTATION
Create familiarity with the use of
psychometric scales to help in the differential
diagnosis of mood disorders
Formulate an integrative treatment, tailored
to the individual needs of the patient
Provide understanding of the principles of
newer treatments of depression (i.e.TMS)
STYLE OF THIS PRESENTATION
Created with the clinical approach in
mind as a collection of clinical “pearls”
Suggests an open approach to a
variety of treatment modalities
Open to discussion and questions, best
at the end of it
MOOD DISORDERS by DSM-IV TR
MAJOR DEPRESSIVE DISORDER
DYSTHYMIA
BIPOLAR DISORDERS
CYCLOTHYMIA
MOOD DISORDERS DUE TO A GENERAL
MEDICAL CONDITION
AND LAST BUT NOT LEAST…
MOOD DISORDER NOS.
When nothing else fits, a diagnosis of mood
disorder nos. is appropriate
Very helpful for the child and adolescent
patients with ‘severe disturbance of
temperament’ (a possible future diagnosis in
DSM –V)
MAJOR DEPRESSIVE DISORDER
ESSENTIALS OF DIAGNOSIS
Sleep changes
Interest (loss of)
Guilt (worthlessness, regret)
Energy loss or fatigue
Concentration difficulties
Appetite changes
Psychomotor retardation or agitation
Suicidality
DIFFERENTIAL DIAGNOSIS
CLINICAL INTERVIEW
PSYCHOMETRIC SCALES (PHQ-9 or QIDS-SR; MDQ;)
BASELINE BLOOD TESTS: METABOLIC PANEL, CBC WITH DIFF, TFT’S, TESTOSTERONE LEVEL,VITAMINS LEVELS, LIPID PROFILE
RULE OUT BIPOLAR DISORDER
PHQ-9 AND QIDS-SR
Psychometric scales for depression
Help the patient to have an objective sense
of their depression
Help us to evaluate the response to the
treatment
Very useful for legal depositions
PHQ-9 AND QIDS-SR
PHQ-9 is a patient health questionnaire,
comprising 9 questions.
Scoring helps differentiating between
different degrees of severity of the
depression
QIDS-SR – quick inventory of depressive
symptoms, also allowing scoring and
differentiating the degrees of depression
REMEMBER….IT’S NOT A BIPOLAR DISORDER IF ….
THERE IS NO HISTORY OF A MANIC OR
HYPOMANIC EPISODE…
MDQ is a very handy tool for reviewing the
manic/hypomanic symptoms
MDQ
Mood Disorder Questionnaire
Screening for bipolarity, especially sensitive for Bipolar I
13 items, reviewing symptoms of mania
7 items answered with yes , happening within the same period of time
Level of severity – moderate
Developed by Hirschfeld, MD
ONE MANIC OR HYPOMANIC EPISODE
Changes the diagnosis to a Bipolar
Disorder
Changes the treatment
Changes the outcome
WHEN IN DOUBT:
ITS BETTER TO BE SAFE THEN SORRY
Is safer to err on the side of bipolar disorder (esp. in
children and adolescents when the criteria are less
well defined)
In doing so, explain your rationale to the caregivers
Finding the right medication can be a balancing act
(unipolar vs. bipolar depression, side effects vs.
therapeutic effects)
BIO-PSYCHO-SOCIAL
ASSESSMENT
FORMULATION
TREATMENT
BIO-PSYCHO-SOCIAL MODEL
Represents factors that
we need to be aware of
in order to make an
accurate diagnosis and
treatment BEHAVIOR
Coping illness
COGNITIVE
Appraisal
Meaning
perception
SOCIO-
CULTURAL
Social support
Customs
values
ENVIRONMENT
Life events
BIOLOGY
Genetics;
Biological
response
BIO-
PSYCHO-
SOCIAL
BIOLOGY OF DEPRESSION
• Genetic predisposition (suggested by the
familial nature of the depression or mood
disorder)
• Medical conditions: low vitamin D, low B12,
hypothyroidism, autoimmune disorders; low
testosterone, blood dyscresias ( anemia)
BIOLOGY OF DEPRESSION
Depletion of monoamine levels;
Abnormalities of intracellular signal
transmission and/or gene expression;
Other neurotransmitters (GABA, glycine etc);
Hormones (thyroid and adrenal hormones);
Neuropeptides (CRH,endorphines,substance
P)
NEUROENDOCRINE FACTORS
Abnormalities of the HPA axis (hypothalamic-
pituitary-adrenal axis) : increased cortisol,
increased ACTH
Most depressed patients are euthyroid; some
have subclinical hypothyroidism ( more
association with cognitive impairment)
BDNF( brain derived neurotropic factor)
levels are decreased with stress
BRAIN IMAGING
Decreased left prefrontal cortex (PFC) blood
flow and metabolism
Basal ganglia abnormalities
Increased amygdala activity
Abnormalities in hippocampus
NEURAL MODEL
Dysfunction of the DLPFC, limbic and striatal systems impair the modulation of the amygdala/hippocampal structures
Neuroimaging is not cost effective for the clinical practice, at this point (not used for diagnosis purposes)
PSYCHOLOGY OF DEPRESSION
Psychoanalytic and psychodynamic theories
(depression as a result of loss, anger turned
against self …)
Behavioral and cognitive theories ( cognitive
distortions and misrepresentation of life
events)
SOCIAL-ENVIRONMENTAL FACTORS ASSOCIATED WITH DEPRESSION
Life events ( death, divorce, loss of loved one, loss of career, change in career, job conflicts...)
Evaluate social network ( let’s not forget the social media…FB, twitter)
Evaluate spiritual or religious life, belief system
Family life, living situation, family diagram, family conflicts…
Military service
Hobbies, extracurricular activities
Exercise, nutrition, sleep habits
WHAT FOLLOWS NEXT?
How do we formulate treatment?
Following the same guidelines of the bio-
psycho-social model…towards an integrative
approach in psychiatry
INTEGRATIVE TREATMENT
Pharmacological (SSRI, SNRI, NRI, SSRI+ 5HT1 partial agonist, SSRI+ 5HT2 antagonism)
Biological treatments (TMS, light therapy)
Psychological treatment (various forms of therapy)
CAM (complementary and alternative medicine) including:
-Meditation for stress management (yoga)
-Dietary guidelines, exercise, nutritional supplements
-Botanical remedies
-Bibliotherapy ( effective treatment for mild moderate)
PHARMACOLOGICAL TREATMENT
Antidepressants (SSRI, SNRI, NRI,
SSRI+5HT1 partial agonists)
Check for a family history of a good response
to a particular antidepressant
What worked before will work again
Some patients are sensitive to the difference
between brands and different generics
PHARMACOLOGICAL TREATMENT
Always optimize one medication before switching the
class or augmenting
Discuss side effects ( patient education is very
helpful to increase compliance)
Take into account patient’s financial concerns
(increases compliance)
Discontinue medications that do not work to avoid
unnecessary polypharmacy
More doses, less compliance
SSRIs
All of them in generic forms, including Lexapro;
Mostly helpful in depression with anxiety, obsessive features;
Less desirable for lethargic forms of depression;
Increased crave for carbohydrates, possible weight gain and sexual side effects;
SSRI’s continue..
Risk of SSRI induced apathy ( patients are not depressed anymore, just blah..)
Risk of SIADH – rare, but possible especially with polypharmacy
Possible drug-drug interactions with fluoxetine, paroxetine, less with escitalopram
Prozac FDA approved for child/adolescent depression
SSRI’S continues
Sertraline FDA approved for OCD in children and
adolescent patients
Lexapro approved for GAD and depression in 10-13
years old
Discuss with patients and the families the black box
warning ( suicide risk under age 24)
MDD could end with suicide, as an outcome to the
lack of medical intervention
SNRI-Cymbalta, Effexor, Pristiq
Think about them like the broad range antibiotic…work on serotonin and norepinephrine
Cymbalta has equal action on both S and NE from a lower dose
Effexor and Pristiq tend to act more on NE as the dose escalates, at lower doses acts like SSRI (more or less)
Less apathy because of the NE component
Less sexual side effects because of NE component (especially with women)
SNRI continue
Risk of HTN with Pristiq, Effexor, less with
Cymbalta
Less discontinuation syndrome with
Cymbalta, because of the longer half-life time
Warnings for the Serotonin syndrome from
the pharmacies and manufacturers
NRI –wellbutrin, aplenzin and generics
Great antidepressants, but not antianxiety
medications
Rarely useful in anxious depressed patients,
could increase the anxiety levels
No sexual side effects, no weight gain
Help with the SSRI induced apathy, because
of the NE component.
TRAZODONE AND VIIBRYD
Practically weight neutral and not causing sexual side effects
Viibryd works as SSRI and partial 5HT1 agonist
Trazodone works as a SSRI and 5HT2 antagonism( SARI=serotonin antagonist-reuptake inhibition)
Oleptro (Trazodone –ER) helps with sleep, the formulation allows qhs dosing, less next day drowsiness then Trazodone-IR
Viibryd: absorption is increased with food ( also nausea, a main side effect is mitigated when given with food)
MIRTAZEPINE
Antagonism of pre-synaptic alpha2-receptors
Helps the depression associated with anxiety
Main side effects are weight gain and sedation; no sexual side effects
Has antiemetic properties
Could cause granulocitopenia (pay attention to increase frequency of sore throat complaints)
MOST COMMOM STRATEGIES
Augmentation with atypical antipsychotics
(Abilify, Seroquel, Zyprexa)
Weight gain a possible side effect, as well as
next day sedation; akathisia possible with
Abilify
Fairly rapid response, within two weeks
separation on MADRAS scales from placebo
Continue…
Thyroid, lithium augmentation ( needs TFT’s monitoring, and li levels)
Lithium shown as having antisuicidal properties, even at lower doses 300-600 mg/day
Lamictal augmentation, not as popular
Folate (Deplin) supplementation enhances the response to antidepressants
Buspar augmentation suggested by STAR -D
Pindolol augmentation also noted to increase the rate of response to antidepressants
QUESTIONS?
Best Practices Treatment Guideline for DepressionBased on 2010 APA practice guidelines and NeuroStar TMS Therapy® indication for use.
Adapted from: Practice Guideline for the Treatment of Patients with Major Depressive Disorder, 3rd Edition, APA (2010)
39
Unmet
Medical
Needs
BIOLOGICAL TREATMENTS
TMS – the new kid on the
block
Light therapy
Transcranial Magnetic Stimulation (TMS)
The treatment coil produces MRI-strength magnetic field pulses.
Magnetic field pulses pass unimpeded through the cranium for 2-3 cm. and induce a small electric current.
Induced electric currents stimulate the firing of nearby neurons, causing the release of neurotransmitters and clinical effects.
Faraday (1839) Experimental Research in Electricity. Vol 1; Barker (1991) J Clin Neurophysiol; Barker (1985) Lancet
41
AProven
Approach
TMS
Requires a Neurostar
Device
Chair
Computer system
TMS
Refer back to the APA 2010 guidelines
FDA clearance since 2008 for depressed
patients who failed between 1-4 trials of
antidepressants
Indicated before the atypical augmentation
Delivers treatment locally, therefore it has no
systemic side effects
Treating the Brain as an Electrochemical Target
Major brain regions known to be
involved in mood regulation
Amygdala
Ventromedial
Prefrontal Cortex
Prefrontal
Cortex
Anterior Cingulate Gyrus
Brain activity can be altered:
• Chemically (eg, via
drugs) or,
• Electrically (eg, via
TMS)
– Drug action is anatomically
diffuse and systemic
– TMS is focused, non-
invasive and non-systemic
Pizzigalli (2011) Neuropsychopharmacology
44
AProven
Approach
TMS
One of the four types of neuromodulation
Other neuromodulation treatments: DBS,
VNS, ECT
The only one that is not invasive
The patient is awake while receiving
treatment
Activation of fronto-cingulate brain circuit following a course of TMS applied
to the left dorsolateral prefrontal cortex in patients with Major Depression
Targeted Effects on Mood Circuits in Brain
Kito (2008) J Neuropsychiatry Clin Neurosci
TMS CoilL
L
R
R
46
AProven
Approach
TMS
Moving magnetic field creates electrical
currents that penetrate thru DLPFC and
reach hippocampal structures, targeting the
amygdala
Locally depolarizes neurons and creates
changes in the neurotransmitters at the
postsynaptic levels
LIGHT THERAPY
Usually used to treat Seasonal Affective Disorder with specially build lamps
Parameters for use are 7000 lx intensity at 20 inches exposure, about 60 minutes, in the morning after arousal
Has been used in the treatment for unipolar depression in special population (pregnant and elderly patients)
Shows improvement compared to the placebo studies using blue or red light exposure
COMORBID MEDICAL PROBLEMS
Need to be addressed accordingly
Refer to a PCP and establish a good
connection to help coordinate treatment
(adequate treatment of HTN, obesity,
diabetes, anemia, low testosterone levels)
Refer to a specialist for endocrine problems
(hypothyroidism, adrenal insufficiency,
hypogonadism)
CAM
Complementary and Alternative Medicine
Used in addition to conventional medicine
Represents a diverse set of therapies
Most commonly represented by the dietary
supplements
Also includes: acupuncture, hypnosis,
homeopathy, ayurveda yoga, meditation etc
NUTRITION
• SPECIAL DIETS?
• FOOD PREFERANCES
(CARBOHYDRATES CRAVINGS)?
• EMOTIONAL EATING?
• NUMBER OF MEALS PER DAY?
• SNACKS?
NUTRITION- the minimum we could do
Ask about the number of meals and snacks per day
Ask about food preferences
Ask about illnesses that could require special diets
or expose patients to certain nutritional deficits
(malabsorption of B12, Folic acid)
Ask patients to keep a journal of their daily intake, of
food and beverages (include water, soda and alcohol
intake) for 3-5 days
NUTRITION-the minimum we could do
DIABETES patients could have hypoglycemic episodes that could cause palpitation and diaphoresis, irritability
ALCOHOL dependent patient could have B12, folic acid malabsorption – contributing to the depressive symptoms, lack of energy
Folic acid deficiency reduces the response to antidepressant ( less substrate for their action)
NUTRITION - supplements
If deficient in folic acid or B12, supplement with folic acid (OTC) or Deplin ( metfolate)
B12 injections and the nasal spray have a better absorption rate that the oral tablets
Sometimes blood levels are irrelevant, and a lot of physicians supplement based on the history of poor/inadequate nutrition
Encourage a balance diet, sometimes calculating the baseline metabolic rate help the patient to establish goals ( there are apps for that)
Vit D. deficiency-supplement with vit D
EXERCISE
Ask patient if exercise is part of their daily or weekly
routine
Ask details about what the exercise involves
Playing drums, picking up the mail, or walking the
dog doesn’t count as physical exercise
The minimum they could do is walking with a speed
of 2 per 30 minutes, 4-5 times per week
EXERCISE-common chores examples
Washing and waxing a car for 45-60 min
Washing windows or floors for 45-60 min
Gardening for 30-45 min
Wheeling self in wheelchair for 30-40 min
Raking leaves for 30 min
Stair walking for 15 minutes
etc
EXERCISE-AT WORK
Stand instead of sitting when talking on the
phone
Take the stairs instead of the elevators
Walk down the hall to talk to somebody then
calling on the phone
Schedule exercise time and treat it like a
business appointment
EXERCISE – overcoming barriers
Ask about physical exercise at every
appointment
Discuss benefits of exercise for depression
(augmentation value to antidepressants)
Recommend exercise as a prescription
Encourage patient to increase physical
activity daily
EXERCISE – possible mechanisms
Elevations of endorphins in CNS
Changes in Serotonin and Norepinephrine
Increased levels of BDNF (Brain Derived Neurotrophic Factor)
Reduction of serum cortisol
Elevation of body temperature
Improved self-esteem
Distraction from daily stress
Induction of a relaxed state via biofeedback
YOGA
Can reduce depressive symptoms and
induce remission
Questionable application in older or less
fitted patients ( since the patients in the
studies were young and relatively fit)
No safety issues or adverse events
MEDITATION
Is a complex mental process that involves changes in cognition, sensory perception, emotions, hormones and autonomic activity.
Likely affects different neurotransmitters systems, including dopamine, serotonin, glutamate.
The overall understanding of the biological mechanism in terms of the effects on body and brain is still limited.
MEDITATION
attempts to reach a subjective state characterized by
a sense of no space, no time, no thought (i.e.
thevada)
attempts to focus attention on a particular image,
object, phrase, or word (tibetan buddhism)
focuses on whatever thought and feelings enter the
mind (mindfulness meditation)
etc
GOALS of MEDITATION
• Used in psychiatric and medical practices for
stress management
• Depression relapse prevention programs
• Pain treatment
• Eating disorders
• etc
St. John’s wort
Hypericum perforatum)
Induces significantly higher remission rates than placebo in mild to moderate depression
900-1500 mg/day
Can affect blood levels of medications metabolized by Cyt P450
Mostly recommended for depressed patients who can’t tolerate SSRIs
SAMe
Metabolite involved in biosynthesis of norepinephrine, serotonin, dopamine
Shows greater efficacy then placebo
800-1600 mg/d
Can be used as an adjunctive treatment for incomplete response to standard treatment
Can be used as a complementary treatment to speed the onset of antidepressants
PUFA-polyunsaturated fatty acids
Most commonly known Omega 3 (EPA and DHA)
come from fish oil
Most sources of Omega 6 come from cooking oil
The ratio between Omega 6 and Omega 3 is
currently greater then 10:1 when “ man has evolved
on a diet ratio of 1:1”
The change in ratio has been linked with a lot of
health problems, including emotional problems
OMEGA 3-Dietary Recommendations
Two servings of fatty fish each week
One caps of most supplements has 180 mg of EPA
and 120 mg of DHA
3 capsules per day are needed to reduce cardiac
risk (900 mg )
Patients with cardiovascular disease have a higher
incidence of depression
Depression studies used higher doses ( 1800-9000
mg of n-3)
HYPNOSIS
Is a social interaction in which one person,
designated the subject , responds to suggestions
offered by another person, designated the hypnotist,
for experiences involving alterations in perceptions,
memory and voluntary action.
Depends upon the dissociation from normal thought
process and awareness, and a relative shift towards
the unconscious process.
HYPNOSIS
Is rarely a therapy in itself but rather a
vehicle for therapy when the unconscious
mind would otherwise get in the way.
The hypnotist is guiding the patient to self-
hypnosis.
Patient’s ability to do so depends on the
relationship he has with the hypnotist.
HYPNOSIS APPLICATIONS
Ego strengthening
Anxiety
Depression
Stress reduction
Public speaking fear
etc
PSYCHOTHERAPY
Interpersonal psychotherapy- addresses
interpersonal loses, social isolation, role
transitions and disputes, deficits in social
skills
Cognitive therapy- helps patients recognize
and correct erroneous beliefs and
maladaptive behaviors
PSYCHOTHERAPY
Marital and family therapy- reduces the risk
of relapse in depressed patients who also
have marital problems
Selection of the specific therapy is based on
the patients needs and strengths
QUESTIONS?
MOOD DISORDERS by DSM-IV TR
MAJOR DEPRESSIVE DISORDER
DYSTHYMIA
BIPOLAR DISORDERS
CYCLOTHYMIA
MOOD DISORDERS DUE TO A GENERAL
MEDICAL CONDITION
BIPOLAR DISORDERS
I – episodes of mania cycling with depressive episodes
II- episodes of hypomania cycling with depressive episodes
Cyclothymia- hypomania cycling with less severe episodes of depression
MANIA WITHOUT DEPRESSION IS VERY RARE
MANIC EPISODE
Inflated self esteem/grandiosity
Decreased need for sleep
Talkativeness
Flight of ideas
Distractibility
Increased goal directed activity/agitation
Engaging in high risk activities
MDQ
Mood Disorder Questionnaire
Screening for bipolarity, especially sensitive for Bipolar I
13 items, reviewing symptoms of mania
7 items answered with yes , happening within the same period of time
Level of severity – moderate
Developed by Hirschfeld, MD
BIO-PSYCHO-SOCIAL MODEL
Represents factors that
we need to be aware of
in order to make an
accurate diagnosis and
treatment BEHAVIOR
Coping illness
COGNITIVE
Appraisal
Meaning
perception
SOCIO-
CULTURAL
Social support
Customs
values
ENVIRONMENT
Life events
BIOLOGY
Genetics;
Biological
response
BIO-
PSYCHO-
SOCIAL
BIOLOGICAL FACTORS
BP has a strong genetic association, more
then 2/3 of patients show family history of
affective disorder
Neurotransmitters theories conceptualized
depression and mania as two opposing poles
i.e.: less NE/S available in depression, more
NE/S present in mania ( antidepressants
increasing the levels of NE/S induce mania)
BIOLOGICAL FACTORS
Abnormalities in electrolyte distribution in
affective disorders ( retention of sodium
during intracellularly during depression)
The activity of sodium/potassium-activated
ATP-ase is lower in the depressive phases
Lithium responders are reported to have
lower erythrocyte Na/K ATPase
PSYCHOSOCIAL THEORIES
Same as in depression
More stressful life events precede earlier
episodes
Early episodes increase the vulnerability for
future episodes
Kindling- repeated episodes increase the
severity and duration of the illness
PHARMACOTHERAPY of BIPOLAR DISORDER
Treatment of acute mania
Treatment of acute bipolar depression
Maintenance treatment of bipolar disorder
ACUTE MANIA
MOOD STABILIZERS
Typical (lithium carbonate, valproate,
carbamazepine)
Atypical antipsychotics (all of them
approved by FDA for antimanic
properties except LATUDA (lurasidone)
MOOD STABILIZERS
First line-atypicals Easier to use (no need for frequent monitoring of blood
levels) and faster response
Less likelihood of toxicity (vs. lithium or carbamazepine)
Safer in overdose
Adverse effects include weight gain and possibility of
metabolic syndrome (need monitoring of weight, lipid
panel, VS)
All, but one FDA approved, for mania treatment
One approved for both mania and depression (Seroquel)
MOOD STABILIZERS
Traditional mood stabilizers tend to be added on to
atypicals if failure to respond exist
LITHIUM levels need to be 0.6-1.2 mEq/L ( varies
slightly with the laboratory used)
High potential of toxicity (with NSAIDS, dehydration
and low salt–diet)
Monitor for side effects and the appearance of new
ones during the treatment (signs of toxicity)
Still very reliable and the cheapest on the market
MOOD STABILIZERS
VALPROATE-750-2500 MG/DAY Rapid oral loading at 15-20 mg /kg
Faster response then lithium
Risk of liver toxicity, need to check LFT
For women in child age bearing age, supplement with high doses of folic acid ( preventive of neural tubal defects)
Blood levels btw 50-120ug/ml
Increases levels of other medication by enzyme inhibition
MOOD STABILIZERS
CARBAMAZEPINE Approved for mania in 2004
600-1800 mg /day
Blood levels of 4-12 ug/mL
Add high doses of folic acid for women with child bearing potential
Potential of blood dyscrasias ( check CBC)
Weight neutral is a great benefit
Decreases levels of other medications by enzymes induction
BIPOLAR DEPRESSION
Most antidepressants do not work, work for a short
period of time or induce mania
Best treatment is a mood stabilizer (i.e.lithium, or
atypicals with that indication-Seroquel, or Symbiax)
A combination of two mood stabilizers if one fails to
induce response/remission
An antidepressant could be added as a third line
Lamictal or Ziprazidone low doses could also work (
not FDA approved)
OTHER TREATMENTS
TMS, Light therapy, ECT
All the other treatments discussed in the MDD
treatment
Therapy including the education about the
disorder
MAINTENANCE TREATMENT OF BIPOLAR DISORDER
Prevention of recurrent episodes is the
greatest challenge
Kindling will make future episodes more
severe and more difficult to treat ( rapid
cycling occurs later in the disorder
FDA Approved Agents for BD
AGENT MANIA MAINTENANCE
Aripiprazol Yes (2004) No
Carbamazepine XR Yes (2004) No
Divalproex Yes (1996) No
Lamotrigine No Yes (2003)
Lithium Yes (1970) Yes (1974)
Olanzepine Yes (2000) Yes (2004)
Risperidone Yes (2003) No
Asenapine Yes (2009) No
Quetiapine Yes (2004) No
Ziprazidone Yes (2004) No
PRINCIPLES OF BD TREATMENT
Maintain dual focus: short term and prophylaxis
Mania as medical emergency: treat first, chemistries later
Load lithium and valproate; titrate lamotrigine
Retain lithium in treatment for antisuicidal and neuroprotective properties
Educate patient about the illness
Use regular visits
Contract with patient as needed for suicide and substance use avoidance
DYSTHYMIA
Depressed mood most of the day and present almost continuously
“ill humored” – term introduced in 1980
Used to be called-”depressive neurosis”
Pts. complain that they have always been depressed (early onset)
Low-grade chronicity for about 2 years
5-6 % in general population
BIO-PSYCHOSOCIAL MODEL
Biological Factors: similar to depression
Psychosocial Factors:– Personality and ego development culminating
with difficulties adapting in adolescence
– Early interpersonal disappointment leads to ambivalent love relationship as an adult
– Disparity between actual and fantasized situations lead to diminished self-esteem
– etc.
TREATMENT
Psychotherapy is considered the treatment of choice
Medications such as an NRI (bupropion) and SNRI
(venlafaxine, duloxetine) are effective treatments
Exercise, healthy diet
Meditation
Supplements such as PUFA and Vit B12, folic acid
(for documented deficiencies)
CYCLOTHYMIC DISORDER
A mild form of Bipolar Disorder II
Has episodes of hypomania and mild
depression
Mostly agreed over a biological origin of the
disorder
Some psychiatrists believe it’s just the result
of a chaotic life
TREATMENT
Biological therapies
– Mood stabilizers as the first line
– Caution with antidepressant since the high risk of
inducing a manic episode (40-50 % conversion)
– Same guidelines for the dosing of mood
stabilizers
TREATMENT
Psychosocial therapies Increasing the awareness about the disorder
Family and group therapy to repair the damage caused by the disorder
CAM Exercise
Dietary supplementation (PUFA)
Bibliotherapy (i.e. An Unquiet Mind)
Meditation
etc
MOOD DISORDER NOS
A very common diagnosis for children and adolescent psychiatry
Anytime there are difficulties in distinguishing between depression and mania and doesn't meet criteria for other diagnosis (different then the mixed episode when depressive and hypomanic symptoms coexist)
Use mood stabilizers as the first line treatment
QUESTIONS?