Mood Disorders - Anx-Dep Overlap, MDD, DD

Question 1

Describe the overlap between axniety and depression

Answer 1

anxiety and depression share common symptoms

anxiety and depressive symptoms commonly co-occur

child and adult ratings of anxiety sx’s and depressive sx’s demonstrate a high degree of overlap

clinician ratings are typically better at differentiating depression from anxiety in adults as opposed to kids

anxiety disorders are commonly comorbid with depressive disorders

anxiety d/o and depressive d/o are commonly cormobid with other disorders (e.g. personality disorders)

there is a sequential relationship between anixety and depression

differential comorbidity between depression and specific anxiety disorders

pure depression is less common that n pure anixety

Question 2

which anixety d/o’s are most commonly comorbid with depression

Answer 2

OCD, PTSD, and PDA

Question 3

which anixety disorder is the least comorbid with depression?

Answer 3

SP

Question 4

Who do you make sense of the OCD PTSD and PDA rates of comorbidity?

Answer 4

Alloy’s helplessness/hopelessness model

OCD PTSD and PDA perhaps assocaited with certain rather than uncertain helplessness

Question 5

What are three theories we can turn to to understand the overlap between anxiety and depression?

Answer 5

tripartite model (watson)

helplessness/hopelessness model (alloy et al.)

rumination model (nolen-hoeksema et al.)

Question 6

describe Clark and Watson’s (1991) Tripartite model (of comobrbidity)

Answer 6

conceptualizes the overlap as being underlain by common and specific generalized vulnerabilities (factors)

the general distress factor (high NA)

• common to anxiety and depression
• accounts for the shared symptoms: anxious/depressed mood, insomnia, poor concentration

low PA factor (anhedonia)

• lack of interest, loss of energy
• specific to depression

the anxious arousal factor

• dry mouth, rapid heart beat, and dizziness
• specific to anxety

Question 7

What was Alloy et al. (1999) rationale for proposing her Helplessness/hopelessness model of depression?

Answer 7

theory needs to account for:

• the seq relationship between anxiety and depression
• differential comorbidity of depression with specific anxiety disorders
• relative lack of pure depression vs. pure anxiety

Question 8

describe Alloy et al.’s (1999) Helplessness/Hopelessness model of depression

Answer 8

her theory proposes that depressive/anxiety syndromes are determined by:

• helplessness expectancies
• negative-outcome expectancies
• the certainty of these expectancies

helplessness represents a vulnerability to stressors

failure (or success) to cope with stressors contributes to to the relative certainty-uncertainty of negative-outcomes expectancies
- a pessimistic attributional style contributes to certainty/development of depression

hopelessness represents a subset of helplessness (i.e. certain helplessness) - specific to depression

Question 9

using Alloy et al’s (1999) model, describe the “equations” that lead to pure anxiety, comorbid anxiety and depression, and hopelessness depression

Answer 9

uncertain helplessness + uncertain negative-outcome expectancies = pure anxiety

certain helplessness + uncertain negative-outcome expectancies = cormorbid anxiety and depression

certain helplessness + certain negative-outcome expectancies = hopelessness depression

Question 10

Nolen-Hoeksema got interested in talking about __________ b/c it it ________________?

Answer 10

rumination; is common to both depression and anxiety

Question 11

define rumination (and differentiate from worry)

Answer 11

thinking in a repetitive and passive way about one’s negative emotions focusing on their symptoms of distress AND the meaning of their distress

Question 12

We read a study by N-H for class; he was studying the relationship between rumination and the onset of depressive episodes: what was his rationale for conducting that study (i.e. what did the previous research say)

Answer 12

rumination predicted depressive episodes

rumination themes often reflect uncertainty about managing/controlling one’s environment

rumination appears to contribute to hopelessness about the future and negative self-evaluations

Question 13

What were the results of N-H’s study?

Answer 13

Rumination predicted depressive episodes, including the initial onset

rumination predicted anxiety symptoms as well as it predicted depressive symptoms

P’s that had mixed anx-dep were also higher on rumination than P’s with either anxiety or depression alone

Question 14

Sum up the three models – what do they contribute to your understanding of the relationship between anxiety and depression?

Answer 14

Clark and Watson’s (1991) Tripartite model - contribute to my understanding of general biological vulnerabilities that underlie both (or one) kinds of syndromes)

alloy et al.s (1999) helplessness/hopelessness model - contribute to my understanding of the seq relationship, diff comorbidity, and relative lack of pure depression vs. pure anxiety - helps me understand the transition from anxiety to depression

Rumination (N-H, 2000) - contributes to my knowledge of the specific variables involved in the transition (is common to anx/depression) – rumination is one such specific variable

Question 15

epidemiology of depression: point prevalence (child, adolescent, adult); lifetime prevalence; ration between men and women; proportion of P’s with MDD who report comorbidity; porportion of P’s with Hx of MDD who report recurrent episodes?

Answer 15

80%

Where does this data come from (Kessler, 2002; a WHO study)

Question 16

Course of depression: proportion of Px’s w/ MDE that recover in the first year; prop. of Px’s w/ MDE that relapse w/in 1st year; recurrence (new episode) rates 2, 5, and 10 years after MDE

Answer 16

70%

22%

25-40; 60; 75%

Where does this data come from: (Boland & Kessler, 2002)

Question 17

conseqeunces of depression

Answer 17

According to Kessler, 2002:

WHO study ranked depression as the single most burdensome disease in the world

Estimated cost of depression-related lost productivity in US exceeds $33 billion

Depression can disrupt critical role transitions

People with untreated depression are often heavy users of primary care medical services

Question 18

What’s the mnemonic for depression symptoms

Answer 18

SIGECAPPS

Sadness (depressed mood)
Interest (anhedonia)
Guilt (excessive)
Energy (loss of)
Concentration (diminished/poor)
Appetite (loss of, increase -- weight gain/loss?)
Psychomotor (agitation/retardation)
Sleep (insomina/hypersomina, restless sleep)
Suicide

Question 19

DSM IV criteria for an MDE

Answer 19

5 or more symptoms, in same 2 week period (at least one needs to be depressed mood or anhedonia)

Not part of a Mixed Episode

Cause clinically significant distress/ impairment

Symptoms not due to effects of GMC or substance

Symptoms are not better accounted for by Bereavement

Question 20

DSM IV criteria for MDD, single episode

Answer 20

Presence of a single Major Depressive Episode

Major Depressive Episode is not better accounted for by a psychotic disorder

There has never been a manic, mixed, or hypomanic episode

Question 21

DSM IV criteria for MDD, recurrent

Answer 21

Presence of two or more Major Depressive Episodes. Note: To be considered separate episodes, there must be an interval of at least 2 consecutive months in which criteria are not met for a Major Depressive Episode

Major Depressive Episode is not better accounted for by a psychotic disorder

There has never been a manic, mixed, or hypomanic episode

Question 22

DSM IV criteria for DD

Answer 22

Depressed mood for most of the day, for more days than not, at least 2 years

while depression, experience 2 or more of the following Sx's:
CHASES
Concentration (diminshed/poor)
Hopelessness (feelings of)
Appetite (loss of, increase)
Sleep (insomnia/hypersomnia)
Energy (lack of)
Self-esteem (low)

During the 2-year period (1 year for children or adolescents) of the disturbance, the person has never been without the symptoms in Criteria A and B for more than 2 months at a time.

No Major Depressive Episode has been present during the first 2 years of the disturbance (1 year for children and adolescents); i.e., the disturbance is not better accounted for by chronic Major Depressive Disorder, or Major Depressive Disorder, In Partial Remission.

There has never been a Manic Episode, a Mixed Episode, or a Hypomanic Episode, and criteria have never been met for Cyclothymic Disorder.

The disturbance does not occur exclusively during the course of a chronic Psychotic Disorder, such as Schizophrenia or Delusional Disorder.

not due to substance/GMC

clinically significant distress/impairment

Question 23

When can DD and MDD co-occur?

Answer 23

Double depression (DD for two years, then onset MDE)

MDD, full remission, at least two months no MDE, then onset DD

Question 24

Coding MDD

Answer 24

296.xx – Major Depressive Disorder
4th digit - .2 – Single Episode, .3 – Recurrent
5th digit – severity/remission
1 = Mild
2 = Moderate
3 = Severe Without Psychotic Features
4 = Severe With Psychotic Features
5 = In Partial Remission
6 = In Full Remission
0 = Unspecified

Question 25

additional MDD specifiers

Answer 25

Chronic
With Catatonic Features
With Melancholic Features
With Atypical Features
With Postpartum Onset
With and Without Full Interepisode Recovery
With Seasonal Pattern

Question 26

In sum, how do we distinguish MDD and DD

Answer 26

based on severity, chronicity, and persistence.

Question 27

Genetics of depression: family studies, twin studies, heritability estimates (what do these data tell us?)

Answer 27

Family studies - higher rates of MDD in first degree relatives of depressed individuals

Twin studies – higher concordance rates of MDD for MZ twins than for DZ

Heritability estimates of MDD – 40-70%

Evidence that MDD results from genetic vulnerability + environmental stress

Where’s this data from?: Wallace, Schneider, McGuffin, 2002

Question 28

Depression and early life experiences…

Answer 28

Part of the environmental part of the genetics+environment equation

• Fetal exposure to stress can lead to depression
• Inadequate parenting can lead to depression
• Exposure to stressful life experiences can lead to depression

Fetal exposure to stress can lead to depression

• Maternal stress can affect fetal development (i.e. the cortisol itself; e.g. disrupted HPA axis and other regulatory mechnisms in the brain)
• Maternal stress also leads to poor health behaviors during pregnancy that can affect fetal development

Inadequate parenting

• exposure to poor model of social skills and affective expression
• which, can lead to more arousal modulation and affect regulation in child
• can also affect self-esteem, attachment-relationships social-cognitive biases, attribution style

exposure to stressful life events
-e.g. maternal depression, which is associated with financial difficulties, marital discord, etc)

this comes from (Goodman & Brand, 2009)

Question 29

depression and stressful life events

Answer 29

not everyone exposed to stressful life evetns goes on to develop depression, however:

SLE’s are associated with depression

the more severe the SLE the stronger the association with depression

ppl with hx of depression report more SLE even when not in episodes of depression

independent SLE were predictive of depression

depedent SLE were more predicitive of depression

chronic role related stressors are strongly associate with chirnically depressed mood

the enduring effects of SLE’s account for most of the effects of life events on MDD

this data comes from Kessler, 1997)

Question 30

depression in the social context…

Answer 30

MDD pos. associated with social skills deficits ( what kinds, below)

MDD negatively associated with marital and parenting relationship problems

Specific social risk factors for depression:

• Negative feedback seeking
• Interpersonal inhibition
• Dependency/Sociotropy

(Joiner, 2002)

Question 31

Gender diffferences in depression, and how the field makes sense of them?

Answer 31

roughly twice as many women as men experinces MDD at some point in their life (approx 22:13%; Kessler, 2002: WHO)

Biological explanations

• Hormonal changes associated with puberty
• –Testosterone & estradiol levels better accounted for increases in depressive sxs than age
• Genetic factors
• –Some studies show greater genetic effects among females than males, but findings are mixed

Psychological explanations

• Interpersonal orientation
• Rumination

Social explanations

• Trauma/childhood adversity
• Interpersonal stress

Question 32

Cultural difference in depression: symtpom expression

Answer 32

difference in symptom expression across cultures – many other cultures are more likely to endorse somatic (vs. emotional) symptoms

• -“Nerves” and headaches in Latino & Mediterranean cultures
• -Weakness, tiredness, “imbalance” in Asian cultures
• -Problems of the “heart” in Middle Eastern cultures or being “heartbroken” among Hopi

Chentsova-Dutton & Tsai, 2009

Question 33

cultural differences in depression: prevalence

Answer 33

Cross-cultural differences in prevalence of MDD

• higher in countries with rapidly changing economic/political conditions
• US and Canada consistently higher than E. Asian countries
• in contrast bipolar spectrum d/o’s stable across cultures

Chentsova-Dutton & Tsai, 2009

Question 34

risk factors consistently associated with depression across cultures & cultural factors associated with depression

Answer 34

female gender, low SES, stress, and not being married

• Positivity biases
• Attributional style
• Norms regarding negative emotions/ emotional expression

Chentsova-Dutton & Tsai, 2009

Question 35

name three models of depression

Answer 35

hopelessness model (abramson, 2002)

beck’s cognitive (behahvioral) model

Joorman (2009) the cognitive aspects of depression – very similar to the other two, but makes the role of negative emotion and emotion regulation deficits more explicit

Question 36

describe the CBASP model of chronic depression

Answer 36

mccullough, 2003

Chronically depressed patients are similar to preoperational children

• Think in a prelogical and precausal manner
• Egocentric views of self/others
• Talk in monologue fashion
• Unable to generate empathy with others
• Emotionally dysregulated

Question 37

sum up the research about med treatment for depression

Answer 37

Antidepressants are more effective than placebo

• Limited to severely depressed individuals (e.g., Fournier et al., 2010)
• May be more effective for mild to moderate depression when course is chronic (Keller et al., 2000)

Continued tx after acute response associated with a reduced rate of relapse (Geddes et al., 2003)

• Maintenance tx is less effective for those with chronic or recurrent depression
• No guidance for the optimal length of medication maintenance

Side effects are common

Question 38

sum up the research about psychotherapy for despression

Answer 38

Behavior therapy, Cognitive therapy and Interpersonal Psychotherapy are well-established as beneficial treatments for MDD (APA, Div. 12, Society of Clinical Psychology)

Some evidence that brief dynamic therapy, self-control therapy, and social problem-solving therapy are useful in the treatment of MDD (APA, Div. 12, Society of Clinical Psychology)

Question 39

Now, more specifcally, summarize the research around CBT for depression

Answer 39

CBT has been widely studied and validated as a treatment for depression

Outcome research has consistently found that CBT is at least as effective as TCA’s for the treatment of MDD

Several studies have failed to find the combination of CBT and medication to be superior to either treatment alone

Research has found that patients treated with CBT alone or with CBT + Meds have lower rates of relapse compared to those treated with Meds alone

Question 40

sum up treatment research for chronic depression

Answer 40

CBASP: Situational Analysis, Interpersonal Discrimination, Behavioral Skills Training

Keller et al., 2000 found CBASP and Serzone were equally effective in treating chronic depression and that the combination of the two was superior to the individual treatments