Depression Summary Cards (Diagnosis, Epidemiology, Aetiology and Treatments)

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. 

Dysthemia

• 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. 

Bipolar Disorders

• Manic Symptoms are defining feature--> mania = state of intense elation / irritability. 
• Depressive episodes still occur, highly changeable mood. 

Cyclothemia

• Chronic form of bipolar --> symptoms milder but ups and downs still noticeable. 
• Symptoms for at least 2 years. 

MDD

• 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. 

Dysthemia

• Much rarer than MDD
• Approx 2.5 meet criteria at some point (Kessler et al, 2005). 

Bipolar Disorders

• 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 View

• 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. 

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. 

• 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?

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. 

Psychosurgery (Lobotomy)

• 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. 

• 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. 

BUT!!

• 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.