Major Depressive Disorder (MDD)
- Symptoms for most of day & almost every day.
- Symptoms for at least 2 weeks.
- Sad mood / loss of pleasure / sleep disturbance / low appetite and weight loss.
- Feelings of death & suicide / worthlessness.
- Episodic - symptoms present for short while then pass.
- Depressed mood more than half the time for 2 years.
- Other symptoms similar to MDD but not as extreme.
- Chronic condition - symptoms present for longer periods of time without passing.
- Manic Symptoms are defining feature--> mania = state of intense elation / irritability.
- Depressive episodes still occur, highly changeable mood.
- Chronic form of bipolar --> symptoms milder but ups and downs still noticeable.
- Symptoms for at least 2 years.
Depression Epidemiology (Prevalence)
- One of most common disorders.
- Approx 16.2% meet criteria at some point in their lives (Kessler et al, 2005).
- Approx 2x more common in women.
- High variability accross cultures.
- Much rarer than MDD
- Approx 2.5 meet criteria at some point (Kessler et al, 2005).
- Bipolar I very rare = approx 1% meet criteria (Weissman et al, 1996).
- Bipolar II = approx 2% meet criteria (Merikangas et al, 2007).
- Average onset = early 20s.
- Women have more depressive episodes.
- Cyclothemia = approx 4% meet criteria --> more common than full bipolar disorder.
Medical Aetiology of Mood Disorders (Causes)
- 1) Genetics - average 37% heritability in MZ twins, higher than DZ (Sullivan et al, 2000).
- chromosome 3 possibly implicated
- BUT! --> families/twins also share environment as well as genes.
- 2) Neurochemicals - Noradrenaline (NA) - Lower levels = depression.
- Serotonin - Lower levels =depression.
- Dopamine- Lower levels = depression.
- Cortisol - high levels = depression & lower levels of serotonin.
- 3) Brain functioning - Neurogenesis --> reduced neurogenesis linked to depression. Anti- depressants led to development of new neurons in mice.
- Stress can suppress neurogenesis & cause depression.
- Neurogenesis slows down as we age but all elderly not depressed.
- Amygdala - emotional thermostat - elevated activity in MDD (Sheline et al, 2001).
- Dorsolateral PFC - underactive/diminished volume in MDD (Davidson et al, 2002)
- Stressful life events may trigger episodes of depression (Kessler et al, 1999)
- Loss and humiliation likely triggers (Kessler et al, 2003)
- But not everyone becomes depressed after these social experiences
- Some people must be more vulnerable
- Genetics / neurochemicals as predisposing factors?
- Freud - "Mourning and Melancholia" - 1917.
- Depression from fixation at oral psychosexual stage
- Causes person to become dependent on others to maintain self-esteem.
- Depression can be caused by loss of a loved one.
- Person tries to identify with lost one but feels resentment and anger for desertion.
- Anger is not expressed --> turned inward causing self hatred.
- Negative thinking is what causes depression.
- Beck (1967)
- Negative triad (negative views of self, world and future)
- Negative schemata (acquired in childhood due to negative events)
- Cognitive biases (tendency to process info in negative ways / ignore positive info)
- But cause and effect is a major issue:
- Negative Thinking <======?=====> Depression
Examples of Cognitive Biases:
- Arbitrary Influence = friend didn't answer phone, must be avoiding me.
- Overgeneralisation = argument with friend, everyone hates me.
- Magnification= overplay -ve events/ underplay +ve events.
- Excessive Responsibility - if goes wrong it is my fault.
- Self - reference = my failures must be uppermost in other people's thoughts.
- Skinner (1953) - lack of positive reinforcement = loss of positive behaviours.
- Lewinsohn et al (1990) - fewer rewards for positive behaviour = fewer behaviours.
- Depression is often maintained by bringing attention and sympathy.
- The depressive mood is reinforced and is maintained in this way.
- Depression similar to learned helplessness--> Aspects of life uncontrollable = give up (Seligman, 1974).
INTEGRATION OF AETIOLOGY BECOMING MORE WIDELY ACCEPTED!
- E.g. predisposed with genes/faulty neurotransmitters but may be triggered / maintained by social factors, cognitive factors etc.
Biomedical Treatments of Depression
1) Anti-depressant drugs
- Monoamine Oxidase Inhibitors (MAOI)
- stops action of an enzyme which causes breakdown of neuron activity.
- Raises levels of NA and Serotonin raised activity.
- BUT! can cause stroke, hypertension, toxicity, death.
- Tricyclics (TCAs)
- prevent reuptake of NA = increased levels and may also increase serotonin levels.
- Better than MAOI (Stern et al, 1980) but not all respond.
- Selective Serotonin Reuptake Inhibitors (SSRIs)
- Inhibit reuptake and reabsorption of serotonin = serotonin in synapses longer = increased chance of binding to receptors.
- Noradrenaline Reuptake Inhibitors (NRIs)
- selectively block reuptake of NA = more NA improved mood.
- Seperate SSRI and NRI useful for distinction between serotonin and NA deficiency.
- Serotonin and Noradrenergic Reuptake Inhibitors (SNRIs)
- More effective than SSRI (Willard et al, 2002)
- Aim to balance NA and Serotonin
- Side effects = cardiovascular disease ---> hypertension.
Efficacy of Drug Treatments
- Effective in around 2/3 patients (Fawcett & Barkin, 1997)
- Data only provided for those who remain in the studies (Bollini et al, 1999).
- Bollini et al (1997) meta analysis --> best improvement on medium dose, 53% improved.
- Moncrieff (2007) - drugs don't relieve symptoms, just sedatives, don't improve prognosis.
- Kirsch et al (2008) - for most patients anti-deps no more effective than placebo.
- Fournier (2010) - anti-deps work better for more severely depressed.
- If drugs so effective why still so many sufferers?
- Seem to reduce symptoms but do they cure?
- Over-prescribed? --> may be seen as the easy option to treat depression.
- If they are just sedatives but are beneficial then does this matter?
Medical Treatments Continued
Electro Convulsive Therapy (ECT)
- Cerletti (1938) - electric current to skull = cortical seizure and convulsions.
- For MDD if no response to drugs.
- 6-10 treatments over 3-4 weeks.
- Rey & Walter (1997) - 60% show improvement.
- BUT!! - memory loss, painful and often terrifying.
Transcranial Magnetic Stimulation (TMS)
- Gentle ECT? --> brain stimulated without seizure.
- Lyons & McLoughlin (2001) --> may be more popular and effective than ECT.
- Mark et al (2010) - 15% showed improvement.
- Moniz (1930s) - frontal lobotomy --> controls thoughts and emotions.
- Cut pathways = fewer emotional thoughts & behaviours.
- High success rates - 50% improvement.
- BUT! - memory problems, withdrawal, seizures.
Behavioural Activation Therapy
- Aims to use principles of learning to change maladaptove behaviours (Weitan, 1998).
- Behaviour has been learnt so can be unlearned in the same way.
- 1) pleasant events schedule --> reintroduce pleasurable activities.
- 2) rewarded for non-depressive behaviours.
- 3) trained in effective social skills.
- All steps must be done for improvement.
- Works best with mild depression (Jacobson et al, 1996).
- Based on Behavioural Activation component of Beck's therapy.
- Problems caused by inconscious childhood conflicts and loss.
- Defence mechanisms employed but anxiety and guilt may still surface.
- Must bring unconscious conflicts to surface so can be dealt with --> remove repression.
1) Free Association
- client free to talk about whatever comes to mind.
- relaxation leads to free flow of ideas
- gradually will uncover unconscious material.
2) Dream Analysis
- Ego defences lowered during sleep --> unconscious material comes forward.
- Often disguised in symbolic form --> analyst must interpret symbols.
- Transference - client transfers emotions to therapist --> therapist interprets.
- Resistance - painful memories may be blocked --> stop talking / change topic --> therapist must interpret these blocks.
- Shedler (2010) - very effective (0.97 and 1.51 effect sizes) but very lengthy process.
- All seek to be self-actualised - if prevented from doing so can cause anxiety.
- Clients assisted to find own course of action (not very directive)
1) Client-Centred Therapy (CCT) (Rogers, 1951)
- Provides supportive emotional climate, client dictates pace and direction of therapy.
- Focus on present and conscious material.
- Distress due to incongruence between actual self and ideal self.
- Aim to help foster self-acceptance and restore congruence.
- 40% recovered (Pearce & Goss, 2011).
2) Encounter Groups - Talk in groups through structured activities - climate of trust helps to accept self.
3) Gestalt Therapy
- Help client become whole by acknowledging all aspects of them (Rathus, 1994)
- Talk about conflicting aspects of personality.
- Smith, Glass & Miller (1980) - 474 studies - improvement seen than 75-80% untreated.
1) Rational-Emotive Therapy (Ellis, 1977)
- irrational thoughts and expectancies cause distress.
- encourage clients to challenge and correct expectations.
- replace with more rational / realistic ones.
2) Cognitive-Behaviour Therapy (Beck, 1976)
- Negative schemata = negative thoughts --> from early negative events.
- Focus on negative events and ignore positive --> draw negative conclusions.
- Must make client aware of errors and change thinking --> show how irrational.
- Effect size of 0.83 --> Thase et al (2000) - effective in 77% at 16 weeks.
- Now computerised CBT.
3) Mindfulness Based Therapy
- Aim to reduce relapse in those who have had multiple episodes.
- Help to show link between negative thinking and negative mood.
- 8 week therapy - Breathing, Meditation and Yoga.
Teasdale (2000) relapse reduced from 66% to 37%
Kuyken (2008) 60% relapse for drugs only, 47% in joint group.
Overall Evaluation of Therapies.
- Eysenck (1952) - 2/3 recovered with treatment but 2/3 without treatment also recovered.
- Bergin (1995) - 83% improved - psychoanalysis showed best improvement
- Seligman (1995) - 54% treated said "made things better"
- Stiles et al (2008) - CBT, Psychoanalytic and Person-Centred equally effective.
- Cuijpers et al (2008) no major diffs between therapies, all effective.
- Gloaguen (1998) - CBT = more relapse prevention than drugs.
- Other therapies effective without side effects of drugs.
- Mulhauser et al (2010) - therapies effective but pinning down reason for effectiveness is tricky.
- Not all therapies work for everyone - usually a case of long trial and error to find correct treatment.