Transcript Diagnostic Criteria

Chapter 8:
Major Depressive
Disorder
Lorie A. Ritschel
Charles F. Gillespie
Eiríkur Ö. Arnarson
W. Edward Craighead
Terminology
 Depression is a term used to describe symptoms
and behaviors, not a diagnostic label
 Biology, emotions, behaviors, and cognitions
contribute to the etiology and maintenance of
depression
 Major depressive disorder (MDD) is a mood
disorder characterized by one or more major
depressive episodes (MDE) without a history of
manic, mixed, or hypomanic episodes, and not due
to a medical condition, medication, or substance
Diagnostic Criteria for MDE
 DSM-5 includes nine symptoms
 Five (or more) must be present during the same 2-
week period AND cause clinically significant
distress or impairment AND may not be attributable
to physiological effects of a substance or medical
condition
 Symptoms must include either:
 Depressed mood most of the day, nearly every day
(dysphoria)
 Loss of interest or pleasure in all, or almost all, activities
most of the day, nearly every day (anhedonia)
Diagnostic Criteria (cont.)
 In addition to dysphoria or anhedonia, must also
experience at least four additional symptoms nearly
every day:
 Significant weight loss or gain, or decrease or increase in
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appetite
Insomnia or hypersomnia
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings or worthlessness or excessive inappropriate guilt
Diminished ability to think or concentrate, or indecisiveness
Recurrent thoughts of death or suicidal ideation (with or
without a specific plan)
DSM-5 Criteria for Major
Depressive Disorder (MDD)
 DSM-5 includes nine symptoms
 Five (or more) must be present during the same 2-
week period AND cause clinically significant
distress or impairment
 Symptoms must include either:
 Depressed mood most of the day, nearly every day
(dysphoria)
 Loss of interest or pleasure in all, or almost all, activities
most of the day day, nearly every day (anhedonia)
Diagnostic Criteria for MDD
(cont.)
 In addition to dysphoria or anhedonia, must also meet
at least four additional symptoms nearly every day
(i.e. a total of 5 of 7 symptoms):
 Significant weight loss or gain, or decrease or increase in
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appetite
Insomnia or hypersomnia
Psychomotor agitation or retardation
Fatigue or loss of energy
Feelings or worthlessness or excessive inappropriate guilt
Diminished ability to think or concentrate, or indecisiveness
Recurrent thoughts of death or suicidal ideation (with or
without a specific plan)
Specifiers for MDD
 Single or recurrent episode
 Mild (2), Moderate (3), Moderate-Severe (4 or 5)
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or Severe (4 or more with motor agitation)
With psychotic features (mood-congruent or incongruent)
In partial or in full remission
With catatonia
Following used as descriptors:
with anxious distress
with mixed features
with melancholic features
with atypical features
with peripartum onset
with seasonal pattern
NOTE: Premenstrual Dysphoric Disorder promoted from DSM-IV Appendix
Dysruptive Mood Dysregulation Disorder (initial age btw 6 and 18)
DSM-5 Diagnostic Criteria
for Bipolar Disorders
 Bipolar I (BD-I)
 Criteria met for at least 1 manic episode
 Not better explained by a schizophrenia spectrum
disorder (e.g., schizophrenia)
 Bipolar II (BD-II)
 Criteria met for at least 1 hypomanic episode AND 1
depressive episode
 Criteria never met for manic episode
 Not better explained by schizophrenia spectrum disorder
DSM-5 Criteria: Manic and
Hypomanic Episodes
 Manic episode- notably different elated, expansive, or irritable mood
and increased activity/energy with ≥3 (≥4 if only irritable) of the
following lasting for at least 1 week and causing significant distress or
impairment:
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Inflated self-esteem (grandiosity)
Decreased need for sleep
Racing thoughts or flight of ideas
More talkative/pressured speech
Activities with potential for painful consequences
Increased goal-directed activity
Distractibility
 Hypomanic episode- Same symptom criteria, but…
 Shorter (4 days instead of one week)
 Not severe enough to cause marked impairment in functioning (no
psychotic features and no hospitalization)
DSM-5 Criteria: Depressive
Episodes in Bipolar Disorder
 Depressive Episode: total of ≥ 5 of the following 9
symptoms for 2 weeks or longer with significant
distress and/or decline in functioning
 Intense sadness and/or loss of interest must be present
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and other options are:
Insomnia or hypersomnia
Psychomotor agitation or retardation,
Changes in weight or appetite
Loss of energy
Difficulty concentrating or making decisions
Feelings of worthlessness or guilt
Suicidal ideation or behavior
Specifiers for Bipolar Disorders
 Type of current (or most recent) episode
 Severity: mild, moderate, moderate-severe, severe
 With psychotic features: mood congruent or incongruent
 In partial or in full remission
 With catatonia
 As descriptors:
With anxious distress
With mixed features
With rapid cycling
With melancholic features
With atypical features
With peripartum onset
With seasonal pattern
Bipolar Diagnosis: Related
Conditions
Other Specified Bipolar and Related Disorder:
Patients with brief and recurrent manic or hypomanic
phases that fall short of the duration criteria or too few
symptoms (subthreshold variants)
 Cyclothymia
2 or more years of switching between hypomanic and
depressive symptoms that do not meet the full DSM-5
criteria for a hypomanic or a major depressive episode
Prevalence of MDD
 Lifetime prevalence rates of approximately 17%
(Kessler, Chiu, Demler, & Walters, 2005)
 Twice as prevalent for women (20%-25% lifetime)
compared to men (9%-12% lifetime)
 Peak age of onset for first episode of MDD is
between 15 and 19 years of age (Fergusson et al.,
2005)
 Probability of a second episode is 50%.
 Probability of recurrence of MDD is greater among those
who have their first episode earlier in life (Lewinsohn,
Rohde, Seeley, Klein, & Gotlib, 2003)
Behavioral Models of MDD
 Behavioral principles
 Positive reinforcement: increasing behavior by providing a
pleasant stimulus
 Negative reinforcement: increasing behavior by the removal of
an unpleasant stimulus
 Ferster (1965, 1966, 1973), Lewinsohn (1974), Skinner
(1953): depression is related to a reduction in
behaviors that elicit positive reinforcement from the
environment
 This is due to a low rate of positive reinforcement for behavior
and…
 Withdrawal in the presence of anxiety (negative reinforcement)
Behavioral Deficits in MDD
 Anhedonia and amotivation (Beck, Rush, Shaw, & Emery, 1979)
 Anhedonia: loss of interest in activities that previously brought pleasure
 Amotivation: loss of desire to continue to attempt these activities
 Depressed individuals hold a belief that they cannot complete a task and
will not derive satisfaction from having completed one
 Avoidance (Dimidjian et al., 2007)
 Avoidance: passive, short-term strategy of isolation in order to minimize
distress
 Functions as a negative reinforcer, by minimizing distress (e.g., takes
away the annoyance of having to go to work), but also reduces the
opportunity to encounter positive reinforcement in the environment (e.g.,
friendly interactions)
 Treatment targets: Increase activity to increase likelihood of
experiencing positive reinforcement and block avoidance
strategies to decrease negative reinforcement
Cognitive Models of MDD
 Beck (1976): Thoughts of depressed individuals are
distorted in a negative way due to negative selfstatements (negative automatic thoughts), informationprocessing deficits (cognitive errors), and enduring
negative cognitive patterns (schemas/core beliefs)
 Automatic thoughts: Negative responses to prompting
events, including negative views of self (“I’m unlikable”), world
(“I don’t fit in”), and future (“I’ll never have friends”)
 Cognitive errors: Perceptual processing errors that screen
out positive information and bias negative or neutral
information in a negative way
 Core beliefs: Stable negative beliefs about self, world, and
future shaped by developmental influences and life
experiences that organize how one interprets information from
the environment
Cognitive Models of MDD (cont.)
 Seligman (1975) and Abramson et al. (1989) learned
helplessness theory: individuals become depressed
because they view their situations as futile and
themselves as unable to bring about changes in these
situations
 People give up trying when they have determined that a
situation is terrible and not likely to change no matter what
they do
 This happens because attributional styles for negative events
are internal (“I am so stupid”), global (“I am always terrible at
everything”), and stable (“I will be alone for the rest of my life”)
 Hopelessness: Combination of negative events and a negative
cognitive style
Cognitive Deficits in MDD
 Individuals with depression:
 Have a negative cognitive style, which affects the way
they think, perceive, and remember information.
 Interpret and recall information and events with a
negative bias
 Engage in repetitive focus on bad feelings and
experiences from the past and to disengage attention
from thought content (rumination)
 Show referential attention negative stimuli.
 Treatment targets: Increase attention to positive
stimuli, decrease rumination, and increase active
problem-solving strategies
Biology of MDD
 Depression is a heritable, complex genetic disorder passed down
through families, additive and multiplicative models of genetic risk
studied
 Candidate gene association studies have evaluated candidate
genes hypothesized to predict differences in risk for MDD
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Serotonin transporter gene (5-HTTLPR)
Brain-derived neurotrophic factor gene (BDNF)
Glucocorticoid receptor chaperone protein gene (FKBP5)
Type 1 corticotrophin-releasing hormone receptor gene (CRHR1)
Methodological issues: failed replications, design issues limit conclusions
 Genome-wide association studies (GWASs) are better
methodologically (e.g., strict significance level, atheoretical, entire
genome may be investigated) and have identified candidate genes
that may influence MDD
 Studies using intermediate phenotypes to investigate specific
depression symptom components (e.g., anhedonia)
Biology of MDD (cont.)
 Neurochemistry of Depression
 Monoamine hypothesis: MDD caused by a deficiency in the
CNS concentration or reception function of the
neurotransmitters norepinephrine (NE) or serotonin (5-HT)
• Deficiencies in 5-HT or NE signaling play a role in depression and
suicide
• Treatment: medications that increase the extracellular level of 5-HT
(e.g., selective serotonin reuptake inhibitors) and NE (e.g., tricyclic
antidepressants) by inhibiting the reuptake of 5-HT and NE are
efficacious in treating MDD
 A genetic polymorphism chronic exposure to stress may
decrease the expression related to brain-derived
neurotrophic factor (BDNF), a neurotransmitter that plays a
role in the regulation of neuronal survival, differentiation, and
function. which negatively impacts hippocampal function,
episodic memory, and HPA-axis function
Biology of MDD (cont.)
 Neuroendocrinology of Depression
 The Hypothalamic-Pituitary-Adrenal (HPA) Axis is a
feedback loop responsible for responding to stressors through
the release and inhibition of the stress hormone cortisol
• Dysregulation of the HPA axis (e.g., high amounts of cortisol in the
bloodstream, excessive cortisol secretion and insufficient cortisol
suppression) is a state marker of depression
• Early life exposure to stressors and elevated cortisol may have a
persistent effect on later HPA axis dysregulation
 Psychoneuroimmunology of Depression
 Concurrent secretion of cortisol and pro-inflammatory
cytokines act in a feedback loop to stimulate and terminate the
inflammatory response to acute stress
• HPA axis dysregulation and systemic inflammation may play a role in
the etiology of depression due to the body's inability to regulate
physiological reactions to psychosocial stress
Biology of MDD (cont.)
 Brain anatomy and brain function
 In a circuit-based view of brain function, multiple brain regions
play an integrated role in the regulation of physiology and
behavior
 Hippocampus: plays a central role in the regulation of HPA axis
activity and explicit memory
• Hippocampal atrophy has been associated with exposure to traumatic
stress and prolonged exposure to stress hormones, and reduced
hippocampal volume has been associated with risk for a lifetime
duration of depression
 Subgenual cingulate: Plays a role in the regulation of negative
states by coordinating projections to brain areas including the
hypothalamus, amygdala, and frontal cortex
• Treatment targets: Subgenual cingulate is a target for deep brain
stimulation for patients with treatment-resistant depression (Mayberg et
al., 2005)
Integrative Model of MDD
 Diathesis-stress model:
 Individual predisposition (diathesis) may be biological and/or
psychological
 Predisposition is activated by environmental factors (acute or
prolonged stress)
 Dynamic and transactional process:
 Developmental: External environment influences an individual,
individual likewise impacts the environment
 Interactive: Emotions may be regulated by the limbic system
(neurobiology) or the cortex (cognitions)
 Intervention in one domain (e.g., neurobiology,
cognitions, emotion, behaviors) will indirectly affect the
other domains
Assessment of Depression
 Clinical interviews:
 SCID – Semistructured interview of current and lifetime Axis I
disorders based on DSM criteria
 LIFE – Semistructured interview to assess the longitudinal course of
Axis I symptoms and disorders
 Self-report measures:
 BDI-II – Intensity of current cognitive and somatic symptoms of
depression
 CES-D – Screening measure for the general population (not for
diagnosis or symptom severity)
 Clinical rating scales:
 HAM-D – Most common measure of depression change in research,
measures intensity of depression and change of levels of depression
over time
 QIDS – Symptom severity across the nine DSM symptom domains
Psychological Treatment of MDD
 Generally effective for treating MDD and equally
efficacious as antidepressant medications
 Behavior Therapy
 Focused on decreasing unpleasant events, decreasing
avoidance-based strategies, and increasing pleasant
events in order to increase opportunities for positive
reinforcement from the environment
 Cognitive Behavior Therapy
 Focused on recognizing and correcting cognitive errors,
changing underlying core beliefs, and preventing future
depressive episodes
Somatic Treatment of MDD
 Somatic treatments include electroconvulsive therapy, transcranial
magnetic stimulation, magnetic seizure therapy, deep brain stimulation,
and antidepressant medications.
 Most antidepressants work by directly altering monoamine (serotonin
and norepinephrine) neurotransmitter activity, specifically altering
synaptic concentrations of monoamines.
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Monoamine oxidase inhibitors (MAOIs)
Tricyclic antidepressants (TCAs)
Selective serotonin reuptake inhibitors (SSRIs)
Dual serotonin and norepinephrine reuptake inhibitors (SNRIs)
Atypical antidepressants (e.g., buproprion)
Augmenting medications (antipsychotic medications, thyroid agents, antianxiety
medications)
 Most medications have significant side-effect profiles, some have
treatment-emergent symptoms (e.g., suicidal ideation).
 Even among efficacious psychological and psychiatric treatments, more
work is needed to determine which patients will respond best to which
treatment.