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Antidepressants and Treatment of Mood Disorders

This document provides an overview of antidepressants and the treatment of mood disorders. It begins with definitions of depression and mood disorders according to DSM-IV criteria. It then discusses the epidemiology of mood disorders, neurobiological theories of depression, and psychosocial risk factors. The remainder of the document outlines various treatment approaches for mood disorders including pharmacotherapy with antidepressants such as SSRIs, psychotherapy, and other somatic therapies.

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Fuad Hadi
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42 views

Antidepressants and Treatment of Mood Disorders

This document provides an overview of antidepressants and the treatment of mood disorders. It begins with definitions of depression and mood disorders according to DSM-IV criteria. It then discusses the epidemiology of mood disorders, neurobiological theories of depression, and psychosocial risk factors. The remainder of the document outlines various treatment approaches for mood disorders including pharmacotherapy with antidepressants such as SSRIs, psychotherapy, and other somatic therapies.

Uploaded by

Fuad Hadi
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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Antidepressants and Treatment of

Mood Disorders
Anita S. Kablinger M.D.
Associate Professor
Departments of Psychiatry and
Pharmacology

Outline of Lecture

Definitions
DSM-IV diagnoses and criteria
Epidemiology
Neurobiology
Psychosocial theories
Treatments

Definitions
Depression can refer to many things and
mean different things to different people
Symptom versus syndrome
However, for a clinical depression
consistent with DSM-IV, this must lead to
functional impairment

DSM-IV Diagnostic Categories


Major Depression
Dysthymia
Depressive Disorder
NOS
Bipolar Disorder, Type
I or II
Cyclothymia

Bipolar Disorder NOS


Mood Disorder
secondary to GMC
Substance-Induced
Mood Disorder
Adjustment Disorder
(separate
classification)

Epidemiology
Depression is the most common cause of
disability in the world
U.S. costs approximate 43$ billion per year
for mood disorders
Lifetime prevalence rates: (according to
NCS), 21-24% for women and 12-15% for
men

Major Depressive Disorder


(MDD)
>2 week period of
change in behavior
with 5 of the following:

*depressed mood
*anhedonia
appetite disturbance
sleep disturbance
psychomotor
disturbance

fatigue or loss of
energy
worthlessness or guilt
impaired concentration
suicidal thoughts

* 1/5 symptoms must


be these
Rule out physical
cause

Time Course of MDD


Often lasts for a year without treatment
Chances increase by 50% for another
episode after current episode (i.e. high
relapse and recurrence rates)
Many go on to experience chronic
depression (but may be a result of
inadequate treatment)

Heritability of Mood Disorders


Genetic factors very important
RR of MDD is 2-5x greater in relatives of
depressed patients than controls
First degree relatives of Bipolar patients are
24x more likely to develop BAD than general
population
Twin and adoption studies help to understand
and define this illness

Psychosocial Theories of
Depression
Risk factors include:

recent stressors
poor social support system
history of early parental loss
gender
family history of depression
negative cognitive style

Theories of Depression
NE and DA broken down to variety of products through
MAO and COMT
5HT is broken down by MAO to 5-HIAA
Major mechanism for terminating signal is neuronal reuptake
Monoaminergic Theories
Reserpine (early antihypertensive)
Iproniazid (used to treat TB)
Imipramine (originally studied as an antipsychotic)
Drugs enhancing noradrenergic functioning were
antidepressants (eg. stimulants)

Indoleamine Hypothesis of
Depression
Serotonin is functionally deficient in
depression
Decreased brain 5-HT and CSF 5-HIAA in
many depressed patients
Antidepressants tend to increase central
serotonin transmission
Depressed patients show reduction in 5-HT
reuptake sites
Blunted neuroendocrine challenges

Neurotransmitter Hypothesis of
Mood Disorders
Led to catecholamine hypothesis
NE in depression and in mania
5-HT production or reuptake in depression

Flaws: depression or mania not reliably


produced and clinical response exceeds
mechanism of action of drug

Neurobiology of Mood Disorders


Neuroendocrine abnormalities: reflect central
neurotransmitter dysfunction
hyperactivity of HPA: increased cortisol,
nonsuppression of cortisol in DST
blunting of TSH release following TRH infusion
blunting of GH release with alpha-2 adrenergic
agonism and serotonin-mediated increases in
prolactin

Other Alterations in Depression

CRH
acetylcholine activity
GABA levels
Excessive glucocorticoid activity in psychotic
depression
Hippocampal volume loss

Neurobiology of Mood Disorders


Sleep abnormalities: usually found in
endogenous depression

prolonged sleep latency


shortened REM latency and change in timing
increased wakefulness
decreased arousal threshold
early morning awakening
reduced stage 3 and 4 sleep

Kindling-Sensitization
Hypothesis of Mood Disorders
Suggests that repeated exposure to stress
and/or neurochemical changes during
depressed episode sensitize brain regions
responsible for affect
Repeated episodes may permanently alter
systems within the CNS
Leads to shorter well periods, increased
frequency and severity of illness

Treatments

Pharmacotherapy
Psychotherapy
Social interventions
ECT
TMS
VNS

Which Medication?

Safety
Tolerability
Efficacy
Payment
Simplicity

Available Types of
Pharmacotherapy

Tricyclic antidepressants (TCA)


MAOIs
SSRIs
SNRIs
Atypical antidepressants
Mood stabilizers
Antipsychotics

General Treatment Rules


Often takes 4-6 weeks for response
Monitor for response versus remission
Vegetative symptoms tend to improve first,
cognitive symptoms take longer
SSRIs are the first line of treatment for most
MDDs
Address biopsychosocial needs and maintain
meds for 6-12 months

Tricyclic Antidepressants
Available for more than 30 years
Cheap but not clean
Act by NE and/or 5 HT presynaptic
reuptake inhibition
Side effects include anticholinergic effects,
orthostasis, slowing of cardiac conduction
Secondary better than tertiary compounds

Selective Serotonin
Reuptake Inhibitors

Produce response rates close to 70%


Safer and better tolerated than TCAs
Given once daily
Starting and therapeutic doses often similar
Most common side effects include GI symptoms,
HA, insomnia, anxiety, and sexual dysfunction
Five available in the U.S.

Novel or Atypical
Antidepressants
Bupropion (NE and DA reuptake inhibition)
Trazodone (5 HT2 alpha-ANT)
Venlafaxine and Duloxetine (NE and 5 HT
reuptake blockers SNRIs)
Mirtazapine (presynaptic alpha 2 ANT and
5 HT2 and 5 HT3 ANT)

Psychotherapy in Depression

Supportive
Insight-oriented
Interpersonal
Cognitive-behavioral
Psychodynamic
Individual, group or family

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