Download Assessment of Depression

Depression-Assessment
B. Anthony Lindsey, MD
Professor and Vice Chair
UNC Department of Psychiatry
SCOPE OF THE PROBLEM
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The Global Burden of Disease Study
reported unipolar depression as the
fourth leading cause of disability in the
world.
Projections for 2020 suggest that
unipolar major depression will be the
second leading cause of disability
worldwide.
Episode
*Major depression episode
*Major depression episode+
manic/mixed episode
*Manic/mixed episode
Type I
*Major depressive episode+
hypomanic episode
*Chronic subsyndromal
Disorder
depression
*Chronic fluctuations
between subsyndromal
disorder
depression & hypomania
Disorder
*Major depression disorder
*Bipolar disorder, Type I
*Bipolar disorder,
*Bipolar disorder, Type II
*Dysthymic
*Cyclothymic
“If I had __________, I’d
be depressed too.”
Definitions
• Mood - a person’s sustained emotional
state
• Affect – the outward manifestation of
a person’s feelings, tone, or mood
Major Depression
• Syndromal classification with
disturbances of mood, neurovegetative
and cognitive functioning
Major Depression
At least 5 of the following symptoms
present for at least 2 weeks (either #1
or #2 must be present):
1) depressed mood
2) anhedonia – loss of interest or
pleasure
3) change in appetite
4) sleep disturbance
Major Depression
5) psychomotor retardation or
agitation
6) decreased energy
7) feeling of worthlessness or
inappropriate
guilt
8) diminished ability to think or
concentrate
9) recurrent thoughts of death or
suicidal ideation
Major Depression
• Symptoms cause marked distress
and/or
impairment in social or occupational
functioning.
• No evidence of medical or substanceinduced etiology for the patient’s
symptoms.
• Symptoms are not due to a normal
reaction to the death of a loved one.
Bereavement and
Late Life Depression
• 25 – 35% of widows/widowers
meet diagnostic criteria for major
depressive disorder at 2 months.
• ~15% of widows/widowers meet
diagnostic criteria for major
depressive disorder at one year.
• This figure remains stable
throughout the second year.
Subtypes of Depression
• Atypical
 Reverse
neurovegetative
symptoms
 Mood reactivity
 Hypersensitivity to rejection
 MAO-I’s and SSRI’s are more
effective treatments
Subtypes of Depression
 Psychotic
(~10% of all MDD)
• Delusions common, may have
hallucinations
• Delusions usually mood
congruent
• Combined antidepressant and
antipsychotic therapy or ECT is
necessary
Subtypes of Depression
 Melancholic
• No mood reactivity
• Anhedonia
• Prominent neurovegetative
disturbance
• More likely to respond to
biological treatments
Subtypes of Depression
 Seasonal
• Onset in Fall, remission in
Spring
• Hypersomnia is typical
• Less responsive to medications
• A.M. light therapy (>2,500 lux)
is effective
Subtypes of Depression
 Catatonic
• Motoric immobility (catalepsy)
• Mutism
• Ecolalia or echopraxia
Epidemiology
Point prevalence

6 – 8% in women

3 – 4% in men
Lifetime prevalence

20% in women

10% in men
Epidemiology
Age of Onset

Throughout the life cycle, typically
from the mid 20’s through the 50’s
with a peak age of onset in the mid
30’s
Epidemiology
Genetics
 More prevalent in first degree relatives
3-5x the general population risk
 Concordance is greater in monozygotic
(~50%) than dizygotic (~15%) twins
 Increased prevalence of alcohol
dependence in relatives
Etiology
Original, clearly over simplistic
theories regarding
norepinephrine and serotonin


Deficiency states
States of excess
depression
mania
Problems with initial theories

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Inconsistent findings when studying
measures of these systems: MHPG (3
methoxy 4 hydroxyphenolglycol) and
5HIAA (5 hydroxy indoleacetic acid) in
the urine and CSF.
Treatments block monoamine uptake
acutely, however the positive effects
occur in 2-4 weeks.
Receptor theory more useful

Antidepressant treatment causes a
down regulation in central adrenergic
(beta) and serotonergic (5HT2)
receptors
– This change corresponds temporally to
the antidepressant response
Serotonin and Depression
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Decreased CSF levels of serotonin
metabolites
Decreased serotonin transporter
binding
Acute tryptophan depletion can cause
worsening in patients previously
responsive to SSRI’s
Gene-Environment
Interactions

Individuals who have one allele for a
“low efficiency” serotonin transporter
are more vulnerable to depression
after experiencing environmental
stressors (Kendler 2005, Caspi 2003,
Lenze 2005)
Neuroendocrine

Hyperactivity of HPA axis:
– Elevated cortisol
– Nonsuppression of cortisol following dexamethasone
– Hypersecretion of CRF



Blunting of TSH response to TRH
Blunting of serotonin mediated increase in
plasma prolactin
Blunting of the expected increase in plasma
growth hormone response to alpha-2
agonists
Functional Neuroimaging (PET,SPECT)
Decreased metabolic activity

Dorsal prefrontal cortex
– Anterolateral (concentration, cognitive
processing)
– Anterior cingulate (regulation of mood
and affect)

Subcortical
– Caudate (psychomotor changes)
Increased metabolic activity
Ventral
prefrontal cortex
Psychosocial

Risk Factors
– Poor social supports
– Early parental loss
– Early life trauma
– Female gender
– Chronic medical illness
– Introversion
Psychosocial


Cognitive Theory
– Patients have distorted
perceptions and thoughts of
themselves, the world around
them and the future
Possible to treat by restructuring
Secondary Causes of Depression
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Toxic
Endocrine
Vascular
Neurologic
Nutritional
Neoplastic
Traumatic
Infectious
Autoimmune
Depression – Differential
Diagnosis
Adjustment Disorder with depressed mood
– Maladaptive and excessive response to stress, difficulty functioning,
need support not medicines, resolve as stress resolves
Dysthymic Disorder
Bipolar Disorder
Other Psychotic Disorders – if psychotic subtype
Personality Disorders (cluster B) – Mood instability
with rapid changes is characteristic
Treatment
Biologic
 Tricyclic antidepressants
 Monoamine oxidase inhibitors
 Second generation antidepressants
– SSRI’s, Venlafaxine, duloxetine,
bupropion, mirtazapine

Electoconvulsive therapy
Treatment
Psychosocial Treatments
 Education
 Specific psychotherapies
 Vocational training
 Exercise
Treatment
When to Refer?
 Question regarding suicide risk
 Presence of psychotic symptoms
 Past history of mania
 Lack of response to adequate
medication trial
Treatment
Course
 One episode – 50% chance of
reoccurence
 Two episodes – 70% chance of
reoccurence
 Three or more episodes - >90%
chance of reoccurence
Dysthymic Disorder
Characteristics


Chronically depressed mood for most of the
day, more days than not, for at least two years.
Can be irritable mood in children and
adolescents for 1 year
While depressed, presence of at least two of
the following
–
–
–
–
–
–
Poor appetite or overeating
Sleep disturbance
Low energy or fatigue
Low self esteem
Poor concentration
Feelings of hopelessness
Dysthymic Disorder
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Never without depressive symptoms for
over 2 months
No evidence of an unequivocal Major
Depressive Episode during the first two
years of the disturbance (1 year in children
and adolescents)
No manic or hypomanic episodes
Not superimposed on a chronic psychotic
disorder
Not due to the direct physiologic affects of a
substance or a general medical condition
Epidemiology
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More prevalent in women, 4%
prevalence in women, 2% in men
Onset is usually in childhood,
adolescence or early adulthood
Often is a superimposed Major
Depression
High prevalence of substance abuse in
this group
Differential Diagnosis


Other mood disorders
Mood disorder due to a general
medical condition
Treatment


If no superimposed Major Depression
– Psychotherapy
Some evidence suggest
responsiveness to antidepressant
medication in some sub- groups
Course
Prognosis is not as good as Major
Depression in terms of total
symptomatic remission