Lecture 8- Depression

Question 1

Name items on the DSM 5 for depression (MDD)

Answer 1

5+ symptoms present during a 2 week period (most of the day nearly every day)

• depressed mood
• diminished interest in activities
  Weight loss - decrease / increase in appetite
  Insomnia or hypersomnia
  Agitation/ retardation
  Feelings of worthlessness or guilt
  Fatigue - loss of energy
  Recurrent thought of death- suicidal attempts / plan

Symptoms cause clinically significant distress and impairment in social occupational or other areas of functioning
Episode not atrrivuted to psychological eggects of substance or medical condition
Not schizophrenia
There has never been a manic or hypermanic episode

Question 2

What is the prevelance of MDD

Answer 2

U.K. = 5-10% (nice 2014)
Variations in severity
Single lifetime prevelance - 6.4% 
Moderate recurrent MDD (12.2%)
Servers recurrent MDD =7.2%
Lifetime prevelance =16.4%

X2 as common in women than men

Question 3

What is the prevelance difference in men and women

Answer 3

Women x2 as likely to get it

Question 4

What is persistent depressive disorder also known as

Answer 4

Dysthymia

Question 5

What is the dsm for persistent depressive disorder?

Answer 5

• depressed mood for most of the day more days than not
• 2+ years
• presence while depressed of 2+ of following-
  Poor appetite/ overeating
  Insomnia/ hypersomnia
  Low energy or fatigue
  Low self esteem
  Poor concentration or difficulty making decisions
  Feelings of hopelessness

During 2 year period never been with out above symptoms for more than 2 months
Criteria for MDD may be present for 2 years

Question 6

What are the genetic causes of MDD

Answer 6

Sullivan 2000

Twin studies =37% heritability
Confirmed with adoption studies
Heridtability stronger in women

Question 7

What are the biological arguments for MDD (neurotransmitter)

Answer 7

• norepinephrine , dopamine and seretonin strongly implicated (low levels in MDD)
• may not be as simple as that , as drugs immediately change neurotransmitter levels and these aren’t effective for at least 2-3 weeks

Poss relate to dopamine receptors
(Lack of sensitivity in MDD)

Question 8

What are the 2 psychodynamic theories causing MDD

Answer 8

Early theories = due to self hatred

Later = neurotic parents
Inconsistent lack warmth inconsiderate
Child feels isolated
Child realises parents only means of survival
Internalises anger
Conflicting feelings- lead to neuroticism
More prone to depression

LITTLE SPOORTING EVIDENCE

Question 9

Explain some behaviourist theories of MDD causes

Answer 9

Depression due to environment stressors and lack of personal skills
Stressors-> low positive reinforcement -> less likely to repeat actions

Depressed people have poor coping skills
Less equipped to deal with temporary lack of reinforcement

Overly self aware of coping skills
Self criticise and socially withdrawn
Get even less pod reinforcement

Family members and friends reinforce depressive behaviours
Person more likely to shave in a depressed manner
Get special attention

Theories understate told of cognition and what people feel when depressed

Question 10

What are the cognitive theories of depresssion / MDD

Answer 10

Aaron beck
Depression caused by negative thoughts
Generated by dysfunctional beleifs

Triad of negative thoughts
Schemas
Negative cognitions about the world

Person who believes they are inadequate for everything
All of their experiences result in defeat and failures

Depressed person sees job losses as a personal failure- whereas non depressed would say due to economic climate

Depressed people may pay selective attention to a negative environment
Cognitive attention and bias dominates depression

Selectively focus on info that matches negative expectations
Magnify meg events
Minimises pos events
Over generalise cause and effect

Arbitrary inference
Quickly draws neg conclusion without evidence

Question 11

Describe the phonomenq of cognition and reinforcement as a reason for depression

Answer 11

Seligman- learned helplessness
Depressed person has learnt to behave helplessly
Even when presented with disconfirming info
Perpetual negative and pessemistic outlook

Attribution
Failure is internal global and stable
Reinforces helplessness

Hopelessness
Feeds on negative cognition

Question 12

What environmental factors influence and cause depression

Answer 12

Social factors such as stressful life events
- relationship problems, health problems, loss of jobs, childhood abuse/ trauma , health problems

Lack of social support may act as a trigger

Question 13

Impact of mood disorders on your life

Answer 13

Poorer quality of life

• MDD showed significant poorer outcome at 5 year follow up
• compared to baseline/ controls

Employment

• depress study (Levine 1997)
• MDD pots lost 4x more working days over 6 months than controls
• greater burden on society

Question 14

What are the risks of being suicidal on depressive people

Answer 14

Significant risk of being suicidal

• suicide in general pop is 1/100000 (0.01%)
• 3.1% for people with mild depression and 13.8% for people with servers

Links with antidepressants and suicide
But little evidence to support that

Study of the link =
24000 adults with MDD
No sig increase of suicide when using ssris

Question 15

How do drug treatments treat mood disorders

Answer 15

Low levels of norepinephrine, dopamine and seretonin in MDD

Reduced melatonin may also play a cause

Question 16

name the biological treatments of Mood disorders (antidepressants)

Answer 16

• maois
  original antidepressants
  Increase availability of norepinephrine, serotonin, dopamine, and melatonin
• e.g. tranylcypromine, phenelzine, selegiline
  o Very effective BUT increase presence of tyramine
• Can lead to increase in blood pressure
• Tyramine present in many foods and drinks
• If taken with MAOIs outcome could be lethal
  o Despite problems, MAOIs can be useful as 2nd line treatment
• When other antidepressants fail (Amsterdam & Shults, 2005)
  o Results from selegiline promising (first antidepressant ‘patch’)
• Works via blood stream, not stomach
• Tricyclics (TCAs)
  o Also first used in late 1950s
  o TCAs increase availability of serotonin and norepinephrine
• But no effect on dopamine
  o Common examples of TCAs:
• Amitriptyline, clomipramine, imipramine, trimipramine…
  o Generally, very effective BUT less well tolerated
• Side effects include: Dry mouth, blurry vision, constipation, cognitive and/or memory impairment, drowsiness…
• TCA overdose is a significant cause of fatal drug poisoning
  o Mostly replaced by newer antidepressants (SSRIs/SNRIs)
  o But still very commonly used
• Especially useful where sleep a problem (Mayers & Baldwin 2005)
• Selective serotonin reuptake inhibitors (SSRIs)
  o Formally introduced in 1986
  o For many years, most commonly used of the antidepressants
• Although SNRIs are becoming more so (see later)
  o SSRIs increase availability of serotonin
  o Common SSRIs:
• Fluoxetine (Prozac), citalopram, paroxetine, sertraline…
  o Generally, very effective treatment
• Often first-line treatment (Cipriani et al 2008)
  o Equally effective as TCAs
• But better tolerated (Vaswani et al 2002)
• Serotonin effect almost immediate with SSRIs
  o But SSRI efficacy can take 4-6 weeks
• And side effects can appear in 1-4 weeks
• Major challenge to medical model
• Challenge is maintaining pt compliance
• As many as 40% of patients stop taking medication
  o Typical side effects
• Insomnia, nausea, headache, dizziness, constipation, sexual dysfunction, photosensitivity … to name just a few!
  o Some of the most challenging side effects:
• Insomnia (Mayers & Baldwin 2005)
• Sexual problems (Baldwin & Mayers 2003)
• Selective serotonin-norepinephrine reuptake inhibitors (SNRIs)
  o First introduced 1994
  o SNRIs increase availability of serotonin and norepinephrine
  o Common SNRIs
• Venlafaxine, duloxetine, nefazodone, milnacipran
  o Becoming increasingly popular as first-line treatment
  o Most studies compare SNRIs to SSRIs
• Some suggest efficacy for SNRIs is better (Papakostas et al 2007)
• And side effects are fewer
• Although some studies have found no difference

Question 17

name the biological treatments of Mood disorders (antipsychotics)

Answer 17

Sometimes used in severe treatment-resistant MDD
o Several meta-analyses confirm cautious use (e.g. Kennedy & Lam 2003)
* Resistance to treatment =
o > 6 weeks without meeting an adequate treatment response
* But studies lack data on long-term effect (Goodwin et al 2009)

Question 18

name the biological treatments of Mood disorders (phsycical procedures- ECTS)

Answer 18

Electroconvulsive therapy (ECT)
* ECT - Patient put to sleep with a hypnotic drug
o A temporary muscle relaxant is also added
* Miniscule current passed through electrodes on scalp (< 1 second)
o Causes a small seizure (fit)
o Electroencephalogram (EEG) monitors seizure activity
* ECT appears to regulate neuroendocrine system
o Increases neurotransmitters release
* Very useful treatment for severe depression
o Psychotic depression
o Pts who cannot take antidepressants
o Suicidal patients
* See Merkl, et al. 2009 for overview
* Side effects
o Confusion on arousal is common but brief
o Rapid changes in blood pressure and heart rate also common
* But not serious for most pts
* Pts with prior problems with BP/HR would not undergo ECT
* 1985 NIMH Consensus Conference concluded
o Some memory loss after ECT
* But only 0.5% ECT pts suffer severe loss
* Memory deficit usually resolved within 7 months
* But for period immediately surrounding treatment

Question 19

explain behaviourist theories of treating mood disorders

Answer 19

Behavioural
* Depression may be conditioned by environmental stressors
o Reinforced by lack of personal skills
* Stressors ð low positive reinforcement ð less likely to repeat actions
* Lewinsohn’s (1979) therapy uses role playing in groups
o Patient learns how to be assertive
* Often in class-based settings
* But little empirical evidence for behavioural therapies
o Cognitive methods are more popular

Question 20

explain cognitive theories of treating mood disorders

Answer 20

Aim is to monitor and identify automatic (dysfunctional) thoughts
o Replace negative thought with neutral or positive thought
* Relationship built between therapist and client
o Challenge assumptions about distorted thought
o Break the self-fulfilling prophecy
o Should help patient to change feelings towards those thoughts
* Focus on Beck’s theory (triad of negative thought)
o World, future, and self

Question 21

eplain how cbt ca be used to treat mood disorders

Answer 21

CBT adds cognitive and behavioural therapies
o Treat conditioned behaviour and irrational thought
* MDD may be explained by a cycle of factors
o Situation drives thoughts actions and feelings
* CBT Key points
o 5-20 sessions, each 30-60 minutes
o Therapist gains patient history
* Useful to identify prior events and relationships
* Identified ‘problems’ are broken down to component parts
o Client keeps a diary
* Record current thoughts, emotions, bodily feelings and actions
* More key points of CBT
o Therapist works with patient
* Change thoughts and behaviours
o Therapist sets homework
* Practise these changes in real-life situations
* Success discussed at next meeting
o Explore strategies for improving this still further
* Help paient self-criticise irrational thought
* Replace it with more realistic thought
o THE key part
* Identify faulty behaviour and irrational thought
* Develop and practice skills to address these

Question 22

evaluate CBT as a form of treating mood disorders

Answer 22

Success of cbt
o One of most successful treatments for depression
* The most effective psychological treatment
* As effective as antidepressants for most depression (Royal College of Psychiatrists)
o Some evidence CBT better than antidepressant (Melvin et al 2006)
* But not all research agrees (March et al 2004)
o CBT plus antidepressant better than drug alone (Vitiello 2009)
* Particularly in cases of treatment-resistance

Question 23

explain mindfulness as a form of treating mood disorders

Answer 23

Mindfulness-based Cognitive Therapy (MBCT; Teasdale et al 1995)
* Comprehensive cognitive therapy for dep and other mental illness
* Involves about 8 weekly classes
o Aims of MBCT
* Help pt understand ‘patterns of their mind’
* Recognise when mood is about to deteriorate
* Reinvigorate motivation
* Halt escalation of negative thought
* Focus on ‘now’ – rather than relive past
* Shift thinking paradigms to escalate positive thought
* Help pt experience and evaluate own emotion
* Confront and challenge negative mood
o Evidence suggests promising outcomes for MBCT
* Helps prevent dep recurrence (Teasdale et al 2000)
o Outcomes measured in Australian longitudinal study (Ree & Craigie 2007)
* Pre-treatment, post-MBCT, 3 month follow-up
* Sig improvement in mood and self-esteem across time
o MBCT vs. CBT (Manicavasgar, et al 2010)
* RCT baseline vs. 8-week, 6-month and 12-month follow-up
* MBCT similar to CBT for improved mood
* But CBT better for multiple episodes (4 or more)
* No such differences for MBCT
* So CBT appears better for chronic depression