Mood Disorders (Depression) Flashcards
1
Q
Outline the criteria for MDD. Differentiate from PDD.
A
MDD:
- A. 5 or more of the following:
- Depressed mood most of the day, nearly every day, indicating through self-report.
- Anhedonia.
- Significant weight loss/gain (5% in a month).
- Recurrent hypersomnia/insomnia.
- Psychomotor agitation or retardation (not self-report).
- Fatigue.
- Feelings of worthlessness or excessive/inappropriate guilt.
- Diminished thinking/concentrating ability.
- Recurrent thoughts of death, suicide ideation, suicide plans, or attempts.
The hallmark of PDD, introduced in the DSM-5, is its chronicity:
- A. Depressed mood most of the day, more days than not, for 2 years.
- B. (depression symptoms).
- C. During the 2-year period, the individual has never been without A and B for more than 2 months at a time.
- D. Never a manic or hypomanic episode.
Much poorer outcomes than MDD, average duration is 4-5 years, but can persist for 20 years or more. Double depression- the coexistence of MDD and PDD is termed “double depression”.
2
Q
What is the reason that the 2-month grief exclusion was dropped in the DSM-5 and why is this problematic?
A
- It was dropped due to no exclusion for other types of loss (expected to be expanded, but was instead dropped entirely).
- It’s problematic because normal grief patterns may be misdiagnosed, increasing false-positives, unnecessary resources on treatment, potential stigmatisation, and inflated prevalence rates. In DSM-IV, people experiencing MD symptoms following bereavement were not at an elevated risk of depression recurrence of later MD in the same way that people who have MD episodes under other conditions are.
3
Q
Outline the comorbidity of depression. What is the problem of co-morbid anxiety?
A
- 51% of those w/ MDD have lifetime anxiety (Kessler et al. 1996). Anxiety can delay recovery, increase risk of relapse, disability, and suicide attempts (Hirschfeld, 2001).
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4
Q
How long is an average depressive epsiode if left untreated? What factors influence the length? Evaluate the extent to which depression is a recurrent disorder? What is remission defined as? What is the difference between recurrance and relapse?
A
- If left untreated, the average length of a depressive episode is 6-9 months.
- In a sample of untreated women, predictors of increased length included financial difficulties, severe life stressors, and high genetic risk.
- In approximately 10-20% of people with MDD, symptoms do not remit for over 2 years, in which case PDD is diagnosed.
- Remit is defined as at least 2 largely asymptomatic months.
- Recurrence is distinguished from relapse.
- Relapse refers to the return of symptoms within a fairly short period of time, i.e. the underlying depressive episode has not yet run its course.
- Recurrence is defined as a new, distinct period of depression. Recurrence rates are estimated to be 40-50%, with evidence suggesting that the probability of recurrence increases with the number of prior episodes and also when the person has comorbid disorders.
5
Q
What are the five specifiers for a major depressive episode?
A
- Melancholic features: Three of the following: Early morning awakening, depression worse in the morning, marked psychomotor agitation/retardation, loss of appetite or weight, excessive guilt, qualitatively different depressed mood.
- Psychotic features: Delusions or hallucinations (usually mood congruent); feelings of guilt and worthlessness common.
- Atypical features: Mood reactivity- brightens to positive events; 2-4 of the following symptoms: weight gain/increase in appetite, hypersomnia, leaden paralysis, being acutely sensitive to interpersonal rejection.
- Catatonic features: A range of psychomotor symptoms from catalepsy to extensive psychomotor activity, as well as mutism and rigidity.
- Seasonal pattern: At least two or more episodes in past 2 years that have occurred at the same time (usually autumn or winter), and full remission at the same time (usually spring). No other non-seasonal episodes in the same 2 year period.
6
Q
Outline and evaluate genetic influences on depression.
A
Family Studies:
- Mood disorder prevalence is 2-3x higher among blood relatives of those diagnosed with unipolar depression.
Twin studies:
- Suggested a moderate genetic contribution to unipolar depression. The MZ co-twin of a twin with UD is ~2x as likely to develop major depression as a DZ co-twin. Averaging results suggests about 31-42% of the variance in liability to MD is due to genetic influences. Estimate is substantially higher (70-80%) for more severe, early-onset, or recurrent depressions.
- However, even more variation is due to non-shared environmental influences than to genetic factors in more forms of MD.
Serotonin Transporter Gene
- The serotonin transporter gene has also been implicated in depression. Caspi et al (2003) tested 847 people from NZ followed from birth to 26 years of age. Those with the ss phenotype were twice as likely to develop MDD following four or more stressful life events as those with the ll alleles. Moreover, those experiencing severe maltreatment as a child were also 2x to develop MDD than those with ll + maltreatment and those with ss without maltreatment. This is strongly indicative of a diathesis-stress model.
7
Q
Outline and evaluate the neurochemical factors in depression.
A
Monoamine theory
- Once popular, has now been all but disproved entirely. However, no compelling alternative has been proposed.
- For one thing, serotonin system dysfunction cannot be the sole cause of depression; antidepressants usually bring serotonin levels up to normal very quickly, but it often takes at least two to four weeks before mood improves significantly.
- Intensive investigation has failed to find convincing evidence of a primary dysfunction of a specific monoamine system in patients with major depressive disorders.
- The antidepressants that do not act through the monoamine system, such as tianeptine and opipramol, have been known for a long time.
- Experiments with pharmacological agents that cause depletion of monoamines have shown that this depletion does not cause depression in healthy people nor does it worsen the symptoms in depressed patients.
Reduced Dopaminergic Activity
- More recently, reduced dopaminergic activity has been implicated in depression in at least some forms, particularly atypical depression and bipolar depression. Such belief is congruent with the theory that dopamine is responsible in pleasure and reward.
8
Q
Outline and evaluate abnormalities of hormonal and immune systems in depression.
A
Hypothalamic-Pituitary-Adrenal Axis
- Majority of hormonal research has focused on the HPA axis, particularly on cortisol. Elevated cortisol is harmful to an organism, promoting hypertension, heart disease, and obesity.
- In 20-40% of depressive outpatients, and 60-80% of severe inpatients, there are elevated cortisol levels.
- This may be because dexamethasone, a potent suppressor of plasma cortisol, fails entirely or fails to sustain its suppression in about 45% of patients w/ serious depression.
- Chronic elevated cortisol also results in hippocampal cell death, which may explain memory impairments in those w/ depression.
HPA Evaluation
- However, chronic elevated cortisol also found in other psychiatric illnesses.
Hypothalamic-Pituitary-Thyroid Axis
- People with hyperthyroidism often become depressed.
- In addition, 20-30% of patients with depression and normal thyroid levels still show axis dysregulation.
9
Q
Outline and evaluate neurophysiological and neuroanatomical influences on depression.
A
- Damage to the left, but not right, anterior prefrontal cortex often leads to depression. A number of EEG and PET neuroimaging studies have supported this.
- Left frontal asymmetry in never-depressed individuals predicted onset of major and minor depressive episodes over a 3-year period. This is thought to be related to symptoms of reduced positive affect and approach behaviours to rewarding stimuli, and increased right-side activity is thought to underlie increased anxiety symptoms and increased negative affect associated with hypervigilance.
- The orbital prefrontal cortex shows decreased volume in individuals with recurrent depression (associated with responsivity to reward).
- The anterior cingulate cortex shows decreased volume and abnormally low levels of activation in depressed patients, suggesting impaired selective attention, self-regulation, and adaptability.
- Amygdala shows increased activation, which may be related to biased attention.
10
Q
What is the role of stressful live events in causing depression?
A
- Severely stressful life events often serve as precipitating factors for unipolar depression, especially for young female adults. Most of these life events concern loss of a loved one, serious threats to important close relationships or to one’s occupation, or severe economic or serious health problems.
- Humiliating experiences are also precipitating factors, as well as the stress of being a caregiver to a spouse with a debilitating disease such as AD.
- People with depression may also generate their own stressful life events through poor interpersonal problem solving and poor functioning (e.g. forgetting to pay bills), which perpetuates the disorder.
- However, care should be taken in that depressed people are likely to view the precipitating events as more stressful than they actually were so their own perceptions of stress may result from the cognitive symptoms of the disorder, rather than cause their disorder.
11
Q
How can personality/cognitive diatheses precipitate depression?
A
Neuroticism
- Neuroticism is a vulnerability factor for depression, as highly neurotic people experience a wide range of negative moods, not just sadness.
- It is also associated with worse prognosis.
Introversion
- Limited evidence that high introversion may also serve as a vulnerability factor (whether alone or w/ neuroticism).
Cognitive Diathesis
- The cognitive diathesis focuses on particular negative patterns of thinking that make people who are prone to depression more likely to become depressed when faced with one or more stressful life events.
12
Q
How can early adversity act as a diathesis for depression?
A
Early adversity increases an individual’s sensitivity to stress in adulthood, creating both short- and long-term vulnerability. Long term effects may be mediated by biological and psychological variables.
However
Certain individuals will remain resilient and stress-inoculated.
13
Q
Outline Beck’s cognitive theory of depression.
A
- Cognitive symptoms of depression often precede and cause the affective symptoms (rather than vice versa).
- It is a diathesis-stress model in which negative cognitions are central.
- Underlying dysfunctional beliefs, known as depressogenic schemas (rigid, extreme, and counterproductive schemas) predispose an individual to depression.
- These are thought to develop during childhood and adolescence as a function of negative experiences with parents and significant others- this is the underlying diathesis.
- Dysfunctional beliefs may lie dormant for several years until activate by stressors or depressed mood, which fuels the current thinking pattern.
- This creates a pattern of negative automatic thoughts, involving unpleasant, pessimistic predictions.
- These pessimistic predictions focus on three themes termed the negative cognitive triad:
- Negative thoughts about the self.
- Negative thoughts about others and the world.
- Negative thoughts about the future. -
- These pessimistic predictions focus on three themes termed the negative cognitive triad:
- This triad is maintained by a variety of negative cognitive biases, such as:
- Dichotomous/all-or-nothing reasoning.
- Selective abstraction (focus on negative details, to the neglect of other elements).
- Arbitrary inference (jumping to conclusions based on minimal or no evidence).
14
Q
Evaluate Beck’s Cognitive Theory
A
- Has generated very effective cognitive therapies.
- Helps to explain many prominent characteristics of depression.
- Research has suggested that stressors are not necessary to activate depressogenic schemas or dysfunctional beliefs that lie dormant between episodes.
- As well as considerable evidence for dysfunctional beliefs and NATs, also considerable evidence for certain cognitive biases.
- Depressed people have better or biased recall of negative information and negative autobiographical memories.
Evaluating the causal aspects of Beck’s Theory
- More mixed results. Causal hypotheses usually tested with a prospective study design, i.e. those without depression tested for cognitive vulnerability at Time 1, and then followed for a set amount of time, at which point they are tested again.
- Only some studies have found that dysfunctional beliefs at Time 1, in interaction with stressful live events, predict depression at Time 2. Some of these used inadequate study designs.
- Several more recent studies with more adequate designs have found more supportive evidence. Lewisohn et al (2001) assessed 1500 adolescents for dysfunctional beliefs or attitudes, and then measured stressful life events a year later.
- Those who started with high dysfunctional beliefs and who experienced high stress were more likely to develop major depression.
15
Q
Outline and evaluate the learned helplessness and hopelessness theory of depression.
A
- Seligman et al noted that laboratory dogs exposed to uncontrollable shocks later acted in a passive and helpless manner when placed in a situation where they could control the shocks. Those exposed to equal amounts of controllable shocks had no trouble learning to control them.
- “When animals or humans find that they have no control over aversive events, they may learn that they are helpless, which makes them unmotivated to try and respond in the future. Instead they exhibit passivity and depressive symptoms. They are also slow to earn that any response they do make is effective, which may parallel the negative cognitive set in human depression.”
