Four definitions of abnormality

• Statistical infrequency — a behaviour is abnormal if it is numerically rare, i.e. it falls far from the mean on a normal distribution. Example: an IQ below 70 is in the bottom 2% and is a criterion for intellectual disability disorder. Weakness: many rare traits are desirable (an IQ of 150), and many disorders are common (depression), so rarity is neither necessary nor sufficient.
• Deviation from social norms — a behaviour is abnormal if it breaches the unwritten rules of a society. Example: antisocial personality disorder involves failing to conform to 'lawful and culturally normative ethical behaviour'. Weakness: norms vary between cultures and eras, so the definition risks social control — homosexuality was classified as a disorder in the UK until 1973 in the DSM.
• Failure to function adequately — a person cannot cope with the demands of everyday life. Rosenhan and Seligman proposed signs including severe personal distress, irrational or dangerous behaviour, and a failure to observe interpersonal rules or conform to standard social norms. Strength: it takes the person's own subjective distress into account. Weakness: it is easy to label as dysfunctional any lifestyle that a majority disapproves of.
• Deviation from ideal mental health — Jahoda (1958) defined mental health positively; we are abnormal if we lack these criteria: self-attitudes (high self-esteem, strong sense of identity), self-actualisation, autonomy, accurate perception of reality, resisting stress, and environmental mastery (including successful relationships and work). Strength: it is comprehensive. Weakness: the criteria are so demanding that almost everyone fails some of them, and they are culture-bound (autonomy and self-actualisation are individualist values).

Exam craft: no single definition works alone — a strong essay concludes that clinicians use them in combination, alongside diagnostic manuals such as the DSM-5 and ICD-11.

Which definition?

Behavioural, emotional and cognitive characteristics

For each disorder you must be able to describe characteristics under three headings.

Phobias — an irrational fear out of all proportion to the danger.

• Behavioural: panic (crying, screaming, running); avoidance of the phobic stimulus; endurance (remaining but in high anxiety).
• Emotional: anxiety and fear, which are unreasonable — disproportionate to the actual threat.
• Cognitive: selective attention to the phobic stimulus; irrational beliefs; cognitive distortions.

Depression — a mood (affective) disorder.

• Behavioural: reduced (or, rarely, increased) activity levels; disruption to sleep and eating (insomnia or hypersomnia; increased or decreased appetite); increased aggression and, in some cases, self-harm.
• Emotional: persistent lowered mood; anger, often directed at the self; lowered self-esteem (self-loathing).
• Cognitive: poor concentration; dwelling on the negative; absolutist ('black-and-white') thinking.

OCD — an anxiety disorder with obsessions (intrusive thoughts) and compulsions (repetitive behaviours).

• Behavioural: compulsions that are repetitive and performed to reduce anxiety; avoidance of situations that trigger the obsession.
• Emotional: anxiety and distress; depression (accompanying low mood); guilt and disgust.
• Cognitive: obsessive thoughts; cognitive coping strategies (e.g. praying, counting); insight into excessive anxiety — sufferers know their obsessions are irrational, which is part of the diagnostic criteria.

Classify the symptom

The two-process model

Mowrer (1960) explained phobias in two stages:

• Acquisition by classical conditioning. A neutral stimulus (e.g. a dog) is paired with an unconditioned stimulus that produces fear (being bitten). The dog becomes a conditioned stimulus producing a conditioned response of fear. This can also happen through generalisation — the fear spreads to similar stimuli.
• Maintenance by operant conditioning. Avoiding the phobic stimulus removes the unpleasant anxiety, which is negative reinforcement. Because the person never re-encounters the stimulus, the fear is never extinguished.

Watson and Rayner (1920) — Little Albert. A 9-month-old showed no fear of a white rat. The researchers then struck a steel bar behind his head (UCS → fear, UCR) each time the rat was presented. After several pairings, Albert showed fear (CR) at the sight of the rat alone (CS). The fear generalised to other white, furry things — a rabbit, a fur coat, a Santa Claus beard.

Evaluation: the model has clear real-world application: it directly generates exposure therapies, which work. But it is incomplete. It ignores the cognitive component — irrational beliefs are central to phobias and are untouched by conditioning. It also cannot easily explain why phobias of snakes and the dark are far commoner than phobias of cars, despite cars being more dangerous. Seligman's (1971) biological preparedness answers this: we are innately prepared to fear stimuli that were dangerous in our evolutionary past. Finally, many people acquire a phobia without any traumatic experience, and many people are bitten by dogs without becoming phobic.

Systematic desensitisation and flooding

Systematic desensitisation (SD) — Wolpe's gradual method, based on counter-conditioning:

• The anxiety hierarchy — client and therapist together build a ladder of feared situations, from least to most frightening.
• Relaxation — the client is taught deep relaxation (breathing exercises, sometimes drugs or mental imagery).
• Exposure — the client works up the hierarchy, relaxed at each stage, moving up only when anxiety has subsided. Because it is impossible to be relaxed and afraid at the same time (reciprocal inhibition), the fear response is replaced by relaxation.

Flooding — immediate, prolonged, full-intensity exposure with no gradual build-up (e.g. a spider-phobic in a room with a tarantula on their arm). Sessions are long — typically two to three hours. Fear is a physiological response that cannot be sustained, so it eventually exhausts itself; the client learns the stimulus is harmless (extinction), and because escape is prevented, avoidance cannot be negatively reinforced.

Evaluation: Gilroy et al. (2003) followed 42 people treated with SD for spider phobia and found they were less fearful than a control group at both 3 months and 33 months — the effect lasts. SD is acceptable to clients (low refusal and drop-out rates) and can be delivered as self-help or in virtual reality. Flooding is cost-effective — it works in fewer sessions — but it is highly traumatic, so drop-out is high and clients must give fully informed consent. Both work best on simple phobias and are far less effective for complex phobias such as social phobia and agoraphobia, which have a strong cognitive element that behavioural therapy does not address.

Which therapy?

Beck's negative triad and Ellis's ABC model

Beck (1967) — the cognitive vulnerability to depression. Three elements:

• Faulty information processing — depressed people attend to the negative and think in absolutes (black-and-white thinking).
• Negative self-schema — a package of beliefs about the self, often developed in childhood, through which all information is interpreted.
• The negative triad — automatic, irrational negative views of (1) the self, (2) the world, and (3) the future.

Ellis (1962) — the ABC model. Depression results not from events but from our beliefs about them:

Ellis called the demanding, absolutist beliefs behind depression 'musturbatory thinking' — for example utopianism ('life must always be fair') and the 'I must be perfect' belief. It is the irrational belief, not the event, that produces the depressive consequence.

Evaluation: there is good supporting evidence — Grazioli and Terry (2000) assessed 65 pregnant women and found that those judged to have high cognitive vulnerability before birth were more likely to suffer post-natal depression, supporting Beck. But the approach only explains the cognitive aspects: it does not explain anger, hallucinations or delusions in severe cases, and it says nothing about the strong genetic and neurochemical evidence for depression. There is also a blame issue — Ellis's model can imply the depressed person is responsible for their own irrational thinking, which is unhelpful and ignores real adversity. Crucially, we cannot tell whether irrational thinking causes depression or is a symptom of it.

Cognitive behaviour therapy (CBT)

CBT begins by assessing the problem and agreeing goals, then works to identify and challenge the irrational thoughts, and finally sets behavioural homework to test them.

• Beck's cognitive therapy — identify the automatic thoughts of the negative triad and challenge them. The client is treated as a scientist: they gather evidence from their own life (a diary of things they enjoyed, or of when others were kind) which is then used to disprove the negative belief. This is 'patient as scientist'.
• Ellis's REBT (rational emotive behaviour therapy) — extends ABC to ABCDE: Disputing the irrational belief and Effect. Disputing may be empirical ('where is the evidence?'), logical ('does that really follow?') or pragmatic ('how does that belief help you?'). The aim is to break the link from irrational belief to depressive consequence.
• Behavioural activation — a depressed person withdraws, which removes the sources of pleasure that would lift their mood. The therapist works with them to reintroduce enjoyable, active behaviours.

Evaluation: March et al. (2007) compared CBT, antidepressants and a combination in 327 depressed adolescents. After 36 weeks, 81% of the CBT group and 81% of the antidepressant group had significantly improved, and 86% of the combined group — so CBT is as effective as drugs, and the combination is best. But CBT may not suit severe cases, where clients cannot engage with the demanding cognitive work, or clients with learning disabilities (though Taylor et al. (2008) found CBT can be effective when suitably adapted). It also has a high relapse rate, and its focus on the client's own cognition risks ignoring the client's circumstances — abuse, poverty or bereavement are real, and telling someone their beliefs about them are irrational may be neither true nor helpful.

Which technique?

Genetic and neural explanations of OCD

Genetic explanation. OCD is polygenic — many genes each contributing a small increase in vulnerability.

• Candidate genes include the COMT gene (which regulates dopamine; a variant that produces lower COMT activity, and so higher dopamine, is more common in OCD patients) and the SERT gene (which affects serotonin transport, lowering serotonin levels).
• Taylor (2013) analysed previous studies and found evidence that up to 230 different genes may be involved in OCD.
• OCD is also aetiologically heterogeneous — different combinations of genes may cause OCD in different people.

Neural explanation.

• Neurotransmitters: low serotonin is associated with OCD — serotonin is involved in mood regulation, and antidepressants that raise serotonin reduce OCD symptoms. Some cases (especially those involving planning) involve impaired decision-making and abnormal functioning of the lateral (side) frontal lobes.
• Brain structures: the 'worry circuit' — the orbitofrontal cortex (OFC) sends 'worry' signals to the thalamus; normally the caudate nucleus (part of the basal ganglia) suppresses these. If the caudate nucleus is damaged, the thalamus is flooded with worry signals and a loop is set up between the OFC and the thalamus.

Evaluation: twin studies support the genetic account — Nestadt et al. (2010) reviewed twin studies and found 68% of identical twins shared OCD compared with 31% of non-identical twins. But concordance well below 100% shows environment matters: Cromer et al. (2007) found over half of OCD patients in their sample had experienced a traumatic event, and OCD was more severe in those with more than one trauma. The diathesis-stress model is the sensible conclusion: genes create vulnerability, environmental stressors trigger the disorder. Neural evidence is also correlational — abnormal brain activity may be a consequence of having OCD, not its cause.

Drug therapy for OCD

• SSRIs (selective serotonin reuptake inhibitors) — the standard treatment, e.g. fluoxetine. Serotonin released by the presynaptic neuron is normally reabsorbed (reuptake) and broken down. SSRIs block the reuptake mechanism, so serotonin remains in the synapse for longer and continues to stimulate the postsynaptic neuron. This compensates for whatever is wrong with the serotonin system. It takes 3–4 months of daily use for a noticeable improvement.
• Combining drugs with CBT — drugs reduce emotional symptoms so that clients can engage more effectively with the psychological work. Drugs are often used alongside CBT rather than instead of it.
• Alternatives — tricyclics such as clomipramine act on the same system but have more severe side effects, so they are kept for patients who do not respond to SSRIs; SNRIs (serotonin-noradrenaline reuptake inhibitors) are a newer second-line option.

Evaluation: drugs are effective — Soomro et al. (2009) reviewed 17 randomised controlled trials comparing SSRIs with placebo and found SSRIs significantly more effective in reducing OCD symptoms in all of them. Drugs are also cost-effective and non-disruptive: you simply take a tablet, with none of the time and effort demanded by therapy. But drugs have side effects — indigestion, blurred vision and loss of sex drive with SSRIs; erection problems, weight gain and heart-related problems with clomipramine — which reduces adherence. Most importantly, drugs treat symptoms, not causes: when the drug stops, symptoms typically return. There is also serious concern about biased evidence, since much drug research is sponsored by the pharmaceutical companies that profit from it.

How do SSRIs work?

Jahoda's criteria

Two-process model

Match the approach to the disorder

AQA pairs each disorder with one approach and its therapy. Tap a card, then the approach it belongs to.

Definition and description

Tap an item on the left, then its partner on the right.

The big ideas to know

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