Lecture 3 - Unipolar Depressive Disorders

Question 1

Emotion

Answer 1

• a complex reaction pattern to deal with a personally significant matter
• type depends on the events significance
• involves feelings but differs from feelings in having an overt or implicit engagement with the world

Question 2

Feeling

Answer 2

• A self contained phenomenal experience.
• subjective, evaluative and independent of sensations, thoughts or images
• purely mental and do not engage with world

Question 3

affect

Answer 3

• Any experience of feeling or emotion from the simplest to most complex sensations of feeling
• described as positive/negative

Question 4

Mood

Answer 4

• a disposition to respond emotionally in a particular way (hours, days, weeks) perhaps with unknown prompting
• differs from emotion in lacking an object
• refers to a change in a person that is difficult to normal and is relatively long lasting

Question 5

Mood disorders

Answer 5

• Mental health condition in which the feature is prolonged, intense, pervasive affective disturbance
  1. unipolar = only depressive episodes
  2. Bipolar = manic/hypomanic & depressive episodes. may have ‘normal’ mood states between.

Question 6

criteria for depressive episode

Answer 6

A. In 2-week period 5+ present every day most of the day. MUST include 1 or 2 or both
1. Depressed mood
2. Diminished interest/pleasure
3. weight loss/gain
4. insomnia/hypersomnia
5. psychomotor agitation/retardation
6. Fatigue/loss of energy
7. worthlessness/guilt
8. thoughts of death
9. can’t concentrate/indecisive
B. significant clinical distress from symptoms
C. not caused by substances or medical condition
MDD also needs:
D. disturbance not better explained by schizophrenic-spectrum disorder
E. absence of manic/hypomanic episodes

Question 7

depressive disorder diagnostic specifiers (additional symptoms)

Answer 7

• anxious distress
• mixed features (mania/hypomania)
• melancholic features (more heritable)
• atypical features (mood reactivity, appetite inc)
• psychotic features
• catatonia
• peripartum onset (started in pregnancy/<4wk after birth)
• seasonal pattern

Question 8

other depressive disorders

Answer 8

• pervasive depressive disorder: MDD symptoms >2yrs, any break <2m
• premenstrual dysphoric disorder: symptoms 7d before menstruation, remit in week after
• dysruptive mood dysregulation disorder: onset before 10 years, under 18 above 6 at diagnosis, 3+ weekly temper outburst, persistant irritable, symptoms 12+m

Question 9

Beck (2008) cognitive triad

Answer 9

• negative thoughts of the self, environ and future maintain depression
• basis of CBT
• early in life develop negative coping and feeds into negative thinking

Question 10

cognition in MDD

Answer 10

• moderate dec in processing speed, attention, EF, learning & memory
• cog affective bias
  > distorted info processing or focus moving away from positive stimuli and toward negative stimuli
  > abnormal responses to negative feedback and decision making
• cog impairments can partially remain during symptom remission
• recurrent episodes inc risk of progressive function loss

Question 11

MDD typical course

Answer 11

• depressive ep 6-9m if untreated. recurrence in 40-50%
• median onset 31. more prevalent in women
• prevalence inc with age

Question 12

relapse and recurrence in MDD

Answer 12

• 10-20% exp symptoms for >2yrs = persistent depressive disorder
• most remit
• 40-50% see recurrence
• recurrence more likely as no. previous episodes inc and if other mh issues present

Question 13

epidemiology of MDD

Answer 13

• affects 6% pop
• inc likelihood in: ethnic groups, young adult, women, transgender

Question 14

odds ratio

Answer 14

• likelihood of diagnosis in women vs men
• women 3X likely than men at age 15, 2X likely at age 25 & over
• age is strongest predictor of effect size for symptom severity

Question 15

gender differences in depression

Answer 15

• men likely to exp for achievement reasons while women have risk factors e.g. inequality
• gender discrim
• diferential exposure to childhood or adult adversities
  biologically different stress response (HPA)

Question 16

HPA axis

Answer 16

• our stress hormones vary by gender & brain activation
• human stress response is associated with inc activity of HPA axis controlled by norepinephrine & serotonin
• norepinephrine in hypothalamus releases CTRH triggering ACTH to release from pituitary which travels to adrenal cortex to release cortisol.
• other endocrine axis important in depression as hypothalmic-pituitary-thyroid axis where people with low thyroid levels (hypo) often become depressed. drugs to treat thyroid hormone levels help to treat depression
• both branches of stress response activate when we detect a threat and sends energy to places needed for survival and respond to flight/fight
• in depression feedback loops abolished due to stress = dysregulate and hyperactive = elevated cortisol & can damage emotion reg areas

Question 17

Functional differences in MDD

Answer 17

• affective salience circuit - amugdala hyperactive and hyper connected. dorsal anterior cingulate and anterior insula also hyperactive
• default mode network - particularly active in MDD. hyperconnectivity = higher self directed thoughts
• fronto-parietal cognitive control circuit - hypoconnectivity = difficulties in goal directed tasks. impairs top down control of neg thoughts

Question 18

the brain as a bigger system in MDD

Answer 18

• brain communicates with CNS, stress response, ANS and immune system
  1. psych stressors = HPA response = elevated cortisol
  2. diminished feedback capacity = chronic elevation of cortisol
  3. chronically elevated levels of inflammatory mediators
  4. combo of stress response and immune activation affects CNS: alters neural plasticity, connectivity & neurotransmission
  5. may feedback w/o intervention

Question 19

chronic stress

Answer 19

• stress affects hormones as well as behaviours e.g. alcoholism, poor diet & can be exaccerbated by MDD
• immune response protects body and acute info tells brain to rest. see inc in inflammatory activity that offsets after pathogen terminates. chronic stress = chronic low grade inflammation = behaviours e.g. less exercise

Question 20

early life experiences programme immune and stress response

Answer 20

• early life experiences can alter immune response e.g. childhood adversity = cog, bio, emotional stress
• childhood obesity and diety etc (early systemic inflammation) predispose inflammatory responses
• disadvantaged children face more stressors
• early experiences can calibrate inflammatory response and affect us as adults too

Question 21

social drift hypothesis

Answer 21

• MDD people may impaired functioning = harder to work & function socially = work/family problems (social drift)
• compounded by systemic stigma, discrim, marginalisation etc.
• once in cycle is difficult to get out and harder to recover

Question 22

genetic risk factors for depression

Answer 22

• heritability of MDD is 35%
• MZ twin 2x likely to develop the disorder as DZ co-twins
• higher heritability for more severe, early onset or recurrent depression
• greater proportion of individual difs in risk for MDD can be explained by nonshared environment
• Diathesis stress model = stress can precipitate development in those already vulnerable

Question 23

epigenetic risk: 5-HTTLPR

Answer 23

• 5HTTLPR is serotonin transporter gene for reuptake. 2 versions: either have SS, LL or SL. people with SS 2x likely to develop mDD
• meta analysis shows no strong interaction.
• there may be interactions with other genes?
• some environmental effects act via epigenetic mechanissm to produce MDD

Question 24

antidepressant medication

Answer 24

• SSRIs - block reuptake of serontonin so it remains longer in cleft
• tricyclic - block reuptake of serotonin and norepinephrine
• MAOI - monoamine oxidase removes serotonin and norepinephrine and dopamine. MAOIs stop this. side effects.

Question 25

5-HT

Answer 25

- monoamine hypothesis focussed on deficiencies of 5-HT (serotonin) noradrenaline and dopamine - change to 5-HT conc in brain not consistent with delayed onset of symptom release in SSRIs - lowering 5-HT conc does not induce depression - LT use downregulates 5-HT - no evidence of problems with monoamine receptor dysfunction in brains of people with MDD

Question 26

moncrieff et al.

Answer 26

- key findings: no consistent evidence between serotonin & depression, some evidence that LT antidepressents = reduce serotonin - key criticisms: argues against SSRIs which are clinically effective, combined studies measuring proxies for serotonin, missed out key evidence for links, scientists do not asbribe to chemical imbalance theory, depression ivnolves many mechanisms

Question 27

serotonin-targeting drugs: other mechanisms

Answer 27

- delay in symptom release from drugs = new neurons need to grow - antidepressents may help resyore some functions chronic stress caused (plasticity) - stress alters neuronal circuits - antidepressants may inc neural plasticity via BDNF

Question 28

CBT

Answer 28

- helps recognise relaitonship between thoughts, behaviours and emotions, making changes to enhance emotional experiences & symptoms - thoughts behaviours and emotions can be reciprocally deterministic - 16-20 sessions over 3-4m often with homework - provides skills to test and challenge negative thoughts - behavioural activation helps patient inc positive activities that provide pleasure

Question 29

CBT for MDD: collaborative empiricism

Answer 29

- collaborative empiricism = patient and therapist become co-investigators both in ascertaining goals for treatment and identifying thoughts - use techniques e.g. cog restructuring, problem solving - challenges you to see alt perspectives of reframing interactions and the thoughts that follow in leading to a different emotion - CBT overall more effective than nothing and effect size moderate to large