Psychopathology

• Statistical deviation, e.g. 2% of people have an IQ below 70.
  • Strengths: Real-life application in clinical assessment as severity is compared to statistics
  • Limitations: Unusual characteristics can be positive; abnormality doesn't always need a label as this may have a detrimental effect.
• Deviation from social norms, e.g. psychopathy or ant-social personality disorder.
  • Strengths: Real-life application in the diagnosis of anti-social personality disorder; useful in determining whether someone may need treatment. 
  • Limitations: Cultural relativism; can lead to human rights abuses (e.g. slaves diagnosed for running away); some people choose to deviate; labelling may lead to a self-fulfilling prophecy.
• Failure to function adequately; e.g. when behaviour becomes irrational or dangerous
  • Strengths: Useful because subjective experience is accounted for; Global Assessment of Functioning Scale makes assessment easier.
  • Limitations: Ignores that some people choose to deviate (may not be maladaptive); hard to be objective.
• Deviation from ideal mental health, e.g. low self esteem or depression (Jahoda 1958)
  • Strengths: Comprehensive; clear who would benefit from treatment.
  • Limitations: Culture bound (e.g. self-actualisation is Western); criteria too high.

• Mowrer's two-process model (1960) states that phobias are aquired through classical conditioning and then continue due to operant conditioning.
  • The aquisition of phobias through classical conditioning: Unconditional stimulus (e.g. outdoors) → Paired with neutral stimulus (e.g. mugging) → Produces unconditioned response (e.g. fear and anxiety) → Unconditioned response becomes a conditioned stimulus that produces a conditioned response (e.g. outdoors produces fear).
  • The maintainance of phobias through operant conditioning: Avoidance creates a desirable response/consequences, so behaviour is likely to be repeated. A reduction in fear reinforces avoidance behaviour, so the phobia is maintained.
• Generalisation of a phobia: When a conditioned response starts occurring as a result of other similar stimuli, not just the conditioned stimulus, e.g. Little Albert.

Evaluation:

• Strengths: Explanatory power (aquisition and maintainace of phobias): practical application of the two-process model explains why patients need to be exposed to the phobic stimulus.
• Limitations: Suggests that avoidance is motivated by anxiety reduction which ignores safety factors in more complex phobias; reductionist (ignores biological preparedness); incomplete explanation; deterministic as not everyone who experiences trauma develops a phobia.

• Behavioural: Avoidance; endurance.

• Emotional: Anxiety; panic

• Cognitive: Percieving something to be a threat; thinking that something is dangerous or disgusting.

• Systematic densensitisation: Involves drawing up a hierarchy of anxiety inducing situations relating to the phobic stimulus, teaching the patient to relax and then exposing them to the hierarchal situations while maintaining relaxation.
• Counterconditioning: The phobic stimulus is paired with relaxation instead of anxiety, so a new response is learned.
• Reciprocal inhibition: It is impossible to be afraid and relaxed at the same time, so one feeling prevents the other.

Evaluation:

• Strengths: Effective; long-lasting (Gilroy 2003); suitable for a diverse range of patients; acceptable to patients; low refusal and attrition rates.
• Limitations: The possibility of symptom substitution decreases effectiveness.

• Flooding: Patients are immediately exposed to the phobic stimulus without any gradual build-up of an anxiety hierarchy. Phobic responses are stopped very quickly as there is no option for avoidance behaviour so the patient learns that the phobic stimulus is harmless.
• Extinction: A term within classical conditioning, wherein a learned response is extinguished when the conditioned stimulus (e.g. a dog) is encountered without the unconditioned stimulus (e.g. being bitten). This means that the conditioned stimulus no longer produces the conditioned response (e.g. fear).

Evaluation: 

• Strengths: Cost-effective because it is fast
• Limitations: Less effective for more complex phobias (e.g. social phobias) which limits usefulness and practical application; traumatic which increases attrition and refusal rates; the possibility of symptom substitution reduces effectiveness.

• CBT: A method for treating mental disorders based on cognitive and behavioural techniques. Cognitively, the therapy aims to deal with thinking, such as challening negative thoughts. The therapy also includes behvioural techniques such as behavioural activation. → Based on cognitive theories that some mental disorders may involve "faulty" or irrational thinking. The therapy focuses on cognitive restructuring.
• Negative and irrational thoughts: Thoughts that may interfere with happiness.
• Behavioural activation: A therapy for depression focusing on encouraging patients to engage in activities that they avoid. A cognitive behavioural therapist may encourage enjoyable activities to provide evidence for the irrational nature of beliefs.

Evaluation of CBT as a treatment for depression: 

• Strengths:Supporting evidence (March et al. 2007 → 81% improvement in CBT condition).
• Limitations: CBT may not work in severe cases (patients may be unable to motivate themselves to engage with therapy); reductionist due to an emphasis on the present which may reduce willingness to participate; overemphasis on cognition may discourage patients to change aspects of their lives.

Beck (1967) believed that cognitive vulnerability made people susceptible to depression.

Cognitive Vulnerability:

• Faulty information processing → Blowing problems out of proportion; pessimism; abolutist thinking.
• Negative self-schemas → Interpreting all information about ourselves negatively.
• The negative triad → A person develops a dysfunctional view of themselves due to 3 types of negative thinking: a negative view of the world; a negative view of the future and a negative view of yourself.

Evaluation: 

• Strengths: Good supporting evidence (Grazioli and Terry 2000 → 65 pregnant women more likely to be depressed if they had cognitive vulnerability); practical application in CBT.
• Limitations: Doesn't explain unusual or severe symptoms; assumes cognitive primacy despite the fact that this isn't always the case (the idea that emotions are influenced by cognition); theory doesn't account for how insecure attachments in infancy make you more susceptible to depression in later life as it assumes that depression is down to cognitve vulnerability.

• Seeks to identify and challenge the negative triad directly, as well as testing the reality of beliefs, e.g. a client may be set homework to record when someone is nice to them, so this can be used to counter irrational thoughts.

• States that depression is the result of irrational thinking.

A) Activating event triggers irrational thoughts → e.g. bad test score

B) Beliefs become irrational → e.g. low grade = low self worth

C) Consequences → Depression

Evaluation: 

• Strengths: Practical application in CBT; supporting evidence (Lipsky et al. 1980 → REBT therapy found to reduce negative emotions). 
• Limitations: Only explains reactive depression (doesn't account for anger or unusual symptoms); assumes cognitive primacy; doesn't account for how insecure attachment makes depression more likely as it assumes that depression is caused by irrational thinking.

REBT: Rational Emotive Behavioural Therapy

• The central technique of REBT is to identify and challenge irrational thoughts through empirical and logical argument. Here, the ABC model is extended to the ABCDE model. 
• REBT also seeks to challenge utopianism and break the link between negative life events and depression.

The ABCDE Model:

A) Activating event → Co-worker is late with required work.

B) Belief about activating event → Co-worker is lazy (irrational)

C) Consequence about irrational belief → Stress about deadline 

D) Dispute irrational thoughts to end negative link → Co-worker is busy with other things

E) Effect of dispute → Seeing good in co-worker

• OCD: A condition characterised by obsessions (recurring thoughts or images) and/or compulsions (urge to perform repetitive behaviours).

The genetic explanation for OCD:

• Suggests that genes are the cause and that OCD can be inherited.
• Supported by Lewis' 1936 study, where 37% of patients had parents with OCD and 21% had siblings with OCD.
• Genetic vulnerability: OCD runs in families, making it more likely to occur in some people.
• The Diathesis-Stress Model states that some genes make it more likely for someone to suffer from a mental disorder, but it takes environmental stress to trigger the condition.
• OCD is polygenic → More than one gene is involved.
• Candidate genes create vulnerability towards suffering from OCD. 
• OCD may be caused by different genes in different people, making the disorder aetiologically heterogenous. 

Evaluation: 

• Strengths: Good supporting evidence (Nestadt et al. 2010 → 68% of identical twins shared OCD, compared to 31% of non-identical twins).
• Limitations: Twin studies are flawed as genetic evidence because they ignore environmental factors; too many candidate genes reduce predictive value; environmental risk factors can trigger OCD (Cromer et al. 2007→ OCD more likely with trauma)

• Suggests that physical and psychological features of someone/something are determined by the behaviour of the nervous system and the structure of the brain. 
• Neurotransmitters: Chemicals which allow the transmission of signals from one neuron to the next across synapses.
• Low levels of serotonin is believed to be a cause of OCD because this is a mood regulating neurotransmitter.
• Abnormal function of the lateral frontal lobes may also contribute towards OCD because this impairs logical thinking and decision making.
• Abnormal function of the parahippocampal gyrus may also contribute because it is involved in processing unpleasant emotions.

Evaluation: 

• Strengths: Supporting evidence (effectiveness of serotonin based drugs; OCD symptoms form a part of other biological conditions (e.g. Parkinsons disease), suggesting that biological processes are responsible for OCD.
• Limitations: Isn't clear what neural mechanisms are involved as studies haven't shown a consistent part; assumes that neural abnormality causes OCD when it could be the other way round; serotonin link may be co-morbitity with depression.

How does the serotonin system work?:
1) Serotonin is released by certain neurons.

2) Serotonin is released by presynaptic neurons and travels across a synapse.

3) The neurotransmitters chemically convey the signal from the presynaptic neuron to the post- synaptic neuron.

4) The serotonin is then reabsorbed by the presynaptic neuron, where it is broken down and reused.

• SSRI's: Prevent the reabsorption and breakdown of serotonin, which increases levels in the synapse and thus continues to stimulate the post-synaptic neuron and compensates for whatever is wrong with the serotinin system, e.g. Citalopram or Prozac.
• SNRI's: Increase levels of serotonin and noradrenaline, e.g. Efexor.
• Tricylics: Work the same as SSRI's, but act as a second line of defence because they typically have worse symptoms, e.g. Amitriptyline.
• CBT is often combined with drugs to treat OCD.

Evaluation: 

• Strengths: Drugs are effective (Soomro et al. 2009→ SSRI's were better than placebos); cost-effective and non-disruptive.

• Limitations: Greatest effectiveness when used alongside a psychological treatment (70% success rate of SSRI's); may have side effects which will stop people from taking them; evidence supporting drug treatment may be biased because research is sponsered by drug companies (Goldacre 2013); reductionist as it focuses on the biological origin of the disorder when resources may be better spent tackling trauma through other treatment instead.