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

Pharmacology and Beyond…

© Daniela M. White, MD 2011

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 BIO-

PSYCHO- SOCIAL

BIOLOGY Genetics; Biological response

ENVIRONMENT Life events

SOCIO- CULTURAL

Social support Customs values

COGNITIVE Appraisal Meaning

perception

BEHAVIOR Coping illness

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 Depression Based 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

A Proven

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

A Proven

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 Coil L

L

R

R

46

A Proven

Approach

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 BIO-

PSYCHO- SOCIAL

BIOLOGY Genetics; Biological response

ENVIRONMENT Life events

SOCIO- CULTURAL

Social support Customs values

COGNITIVE Appraisal Meaning

perception

BEHAVIOR Coping illness

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?