OCR psychology - Explanations of Dysfunctional Behaviours

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  • Created by: Ella
  • Created on: 29-01-14 18:04

Explanations of Dysfunctional Behaviour


Social --> Dysfunctional behaviours are a product of the Social Learning theory (observation of role models).

Psychodynamic --> Early childhood trauma (fear is displaced onto a secondary stimulus - repression).

* Biological --> passed on in genes/instinct. Can be used to explain Schizophrenia.

* Behavioural --> Classical Conditioning: association of innate fear response with a secondary stimulus, which is then maintained by operant conditioning (positive or negative reinforcement). Can be used to explain Phobias.

* Cognitive --> Faulty cognitions/thinking patterns - irrational and exaggerated. Can be used to explain Depression.

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The Behavioural Explanation

Used to Explain Phobias...

  • Classical Conditioning - Association of innate fear response/reflex with stimulus.
  • Operant Conditioning -  Maintains phobic response, through either positive reinforcement (e.g. comfort) or negative reinforcement (avoidence behaviour).
  • Social Learning - Learning through observing others around us.

Evaluation of the Behavioural Explanation:

Problems with experimental testing - is often unethical as it has possible lifetime impact/damage in the individual.

Classical Conditioning cannot explain all dysfunctional behaviours - e.g. you can't be conditioned to have schizophrenia/auditory or visual hallucinations. --> lowers validity.

However, has high validity as an explanation because you can observe the conditioning process/changes in behaviour.

Lead to treatments based on classical conditioing principles - systematic desensitisation and flooding --> high validity.

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Watson & Raynor

Behavioural Explanations of Dysfunctional Behaviour...

Aim: To see if...

  • ...It's possible to induce fear of a previously unfeared object through classical conditioning.
  • ...The fear response will be transferred to similar objects.
  • ...What effect time will have on the fear response.
  • ...It's possible to remove the fear response in the Lab.

Methodology: A Case Study under controlled Lab. conditions.


  • 8 month old Little Albert who was the son of a wet nurse and had lived in the hospital environment all his life.
  • According to Watson & Raynor, he was a solid and unemotional child who showed no fearful reactions to a rat, rabbit, dog, monkey a mask with hair or cotton wool.

However, Little Albert did react violently to a suspended steel bar being hit by a hammer - unconditioned (innate) fear response.

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Watson & Raynor - continued...

Procedure in Brief:

  • Albert's baseline reactions to the stimuli were noted as having no signs of fear response to any situation.
  • Experiments started when Albert was 11 months old.

Session 1: LA presented with the rat in the lab with loud noise - 2 presentations.

Session 2: (a week later) 3 presentations - one with rat only, followed by 2 presentation of the rat with the loud noise.

Session 3: (5 days later) To see if fear was transferred. Albert played with blocks whilst stimuli presented - presented with rat, rabbit, dog, fur coat & cotton wool. Some stimuli presented a negative response.

Session 4: (5 days later) LA was presented with rat which poduced a weaker fear response. It was decided to 'freshen up' the response to the rat and alos the rabbit and dog.

Session 5: (1 month later) LA was testes with various stimuli and continued to show fear to all of them with varying degree - time had not removed the fear response.

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Watson & Raynor - continued 2...


  • From Session 2: After 5 paired presentations, the conditioning of a fear response was evident so it's possible to condition fear through classical conditioning.
  • Sessions 3 & 4: Transference of the fear response had been made to other similar objects --> objects less like the original stimulus (e.g. cotton wool) resulted in a less negative fear response.
  • Session 5: Time had not removed the fear response.

Evaluation of study:

Case study in controlled laberatory conditions --> Can collect large amounts of data. Means that study can follow a standardised procedure so can easily repeat & look for consistancies in results (high reliability). However, mean study is low in ecological validity so cannot generalise findings to other settings/may not reflect learning in everyday life.

However, Little Albert was also unusual as he had lived in a hospital/lab environment all his life and had never been seen to show fear by staff so he may have responded differently in this study to how other children may have...making the findings unique to him. Also too small 'sample size' to be able to generalise findings to wider population. 

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"A psychotic disoder involving the individual having a 'break' with reality."

Diagnosis at least needs two of the following:

  • Hallucinations (visual & auditory).
  • Delusions & paranoia.
  • Disorganised speech.
  • Disorganised or catatonic behaviour.
  • Negative symptoms (e.g. loss of perceptions, speech, movement or control).

4 characteristics:

  • Paranoid schizophrenia
  • Catatonic schizophrenia
  • Disorganised schizophrenia
  • Undifferentiated schizophrenia

Type 1 - Episodeic, mainly positive symptoms

Type 2 - Chronic, mainly negative symptoms

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The Biological Explanation

In brief:

  • Too much or too little neurotransmitters in the brain - e.g. people with too much dopamine have schizophrenia.
  • Twin (and possibly adoption) studies - looking at concordance rates between monzygotic (Identical) and dizygotic (non-identical) twins.
  • Brain scans - that show brain damage to the brain which (could) cause the dysfunctional behaviour --> e.g. damage to the part of the brain that controls the production of neurotransmitters or emotions etc...

3 types of genetic studies that can be conducted:

  • Twin studies - Concordance rates. The incidence of schizophrenia in the general population is 1%. If the incidence within families is higher than this, then it suggests a genetic link.
  • Family/ adoption studies - if disease is inherited then family members should be at a higher risk & risk should increase with closer ties --> high % of genetics showed high pre-disposition to develop the disorder.
  • Genotyping - Analysing DNA for (positions of) varience.
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The Biological Explanation continued...

Specific biological explanations that can be given for schizophrenia, depression and phobias:

Schizophrenia --> genetic/is inherited: Gottesman & Shields looked at concordance rates between MZ & DZ twins (58% MZ, 12% DZ). Biochemical explanations say people with schizophrenia have more dopamine receptors so are more sensitive to the neurotransmitter. Neurodevelopment - Johnson (1989) reported that some schizophrenics have a reduced blink reflex, evidence of neurological damage. Others have reported that some schizophrenics have difficult births which could have starved their brains of O2. This would explain why the incidence of schizophrenia is declining as monitoring techniques at birth improve. Diathesis Stress - Diathesis is a person's genetic pre-disposition to a particular disorder. Because of the genes they've inherited, some people are more likely to develop schizophrenia than others.

Depression --> genetic - Bipolar has been shown to have a 72% concordance rate in MZ twins (vs. 14% for DZ). Biochemical - Noradrenaline too high = mania, and too low = depression. Too low seratonin = depression.

Phobias --> Personality types (inherited?). Someone who is more introverted, worried or shy may be more likely to develop a phobia. Also Seligman (1971) suggests it could be an evolutionary advantage to have certain phobias.

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Gottesman & Shields

Aim: To research the genetic transmission of schizophrenia --> A review of adoption & twin studies into schizophrenia between 1967 & 1976.

Studies reviewed:

  • 3 Adoption studies - 711 participants.
  • 5 Twin studies - 210 Monozygotic twins & 319 Dizygotic twins.


Incidence of chizophrenia in adopted children and monozygotic twins was extrapolated from the research

  • --> by comparing biological parents and siblings and adoptive parents and siblings in the adoptive studies.
  • --> In twin studies, concordance rates for MZ & DZ twins was compared (the probability that if one of the twins had schizophrenia, the other one also had it).

An increased incidence of schizophrenia in biological relatives and higher concordance rates between MZ twins would indicate a genetic basis for schizophrenia.

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Gottesman & Shields continued...


In Gottesman & Shield's own study (1972) concordance rates were 58% for MZ twins --> meaning that if one twin had schizophrenia, there was a 58% chance that the other twin had it. Whereas DZ twins had a concordance rate of 12%.

One of the studies by Kety (1975) found that biological siblings of children with schizophrenia showed a much higher % of schizophrenia --> 19.2% compared with adoptive siblings: 6.3%.

All 3 adoption studies found an increased incidence of schizophrenia in adopted children with schizophrenic biological parent --> Whereas normal children fostered to schizophrenic parent & adoptive parents of schizophrenic children showed little evidence of schizophrenia.


There is obviously a significant genetic input into the oneset of schizophrenia.

However, with concordance rates less than 100% means that there must be some interaction with the environment  --> there is also still some confusion to whether one or more genes are responsible for predisposing a person to schizophrenia.

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The Biological Explanation Evaluation

Reductionist --> Only accounts for biology/nature. However, could argue that it's less reductionist than the behaviour and cognitive explanations as it does acknowledge that there must be some interaction with the environment as concordance rates aren't 100%, and also that our biology must influence our cognitions. Also interaction between nature and nurture as predisposition to certain dysfunctional behaviours need to be triggered by an external event (Diathesis Stress Model).

Validity of theory -->Treaments (e.g. drug therapy) have been developed that target specific neurotransmitter systems that have been shown to be effective/work. However, are they treating the symptoms or cause?

Valid --> methods used to investigate the biological explanation of dysfunctional behaviour are falsifiable (to some extent) & objective. However, genetic research is reliant on correlations.

Determanistic --> Implies that genes (or other biological explanations/factors) causes that dysfunctional behaviour - no free will in the development of the disorder. If inheriting genes from schizophrenic family member, you are pre-disposed to develop the disorder.

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The Cognitive Explanation

States that dysfuncional behaviours are caused by faulty/negative cognitions or thinking patterns...

--> These negative thinking processes are influenced by past experiences, upbringing (nurture) etc... - This has a biological basis

Beck's cognitive triad:

...................Perception of Self..................

...Experiences............................. Future...

*Can use CBT to help break this cycle

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People with depression are prone to making faulty judgements. For example:

  • Catastophising - over exaggerating minor events
  • Overgeneralisation - Incorrectly assuming that negative outcomes will occur for all situations.
  • Selective Thinking - Focusing on the negatives
  • Black & White - Either all positive or all negative.

Symptoms of depression include:

  • Loss of interest into things tha used to make you happy.
  • Lack of sleep or too much sleep.
  • Persistant low mood
  • Poor concentration
  • Weight loss or weight gain
  • Hair loss (alopecia)
  • Inflated self esteem (bipolar: mania)
  • Flight or racing thoughts (bipolar: mania)
  • Decreased need for sleep (bipolar: mania)
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Aim: To understand cognitive distortions in patients with depression --> using clinical interviews with an independent design.


  • 50 patients diagnosed with depression.
  • 16 men, 34 women.
  • Aged 18 to 48 with a median age of 34.
  • Most were judged to be middle or upper class and at least average intelligance.

Patients were compared with a group of 31 non-depressed patients, all undergoing psychotherapy, matched for age, sex and social position.


  • Face to face interviews with retrospective reports of patients thoughts before the session as well as spontaneous reports of thoughts during the session.
  • Some patients kept diaries of their thoughts & bought these to the therapy sessions.
  • Records were kept of the non-depressed patients verbalisations to compare with those of the depressed patients.
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Beck continued...

Findings: Certain 'themes' appeared in the depressed patients that didn't appear in the non-depressed patients. These were :

  • Low self esteem
  • Self Blame
  • Overwelming responsibilities
  • Desire to escape
  • Anxiety caused by thoughts of personal danger, paranoia & accusations against other people.
  • Depressed patients had stereotypical responses to situations, even where inappropriate e.g. If a passer by did not smile at them, the patient felt inferior.
  • Some patients felt themselves unloveable & alone even when others showed them friendship.
  • Self blame was also shown, even when illogical.

*These distortions tended to be automatic, involuntary, plausible and persistant.

Conclusion: Even in mild depression, patients have cognitive distortions that deviate from realistic and logical thinking.

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The Cognitive Explanation Evaluation

Relies on self report methods --> Can't falsify explanation & also allows social desireability bias for testing for dysfunctional behaviours, therefore lowering the validity.

Effective treatments --> Development of cognitive behavioural therapy (CBT), used to treat disorders such as depression/anxiety - high validity to explanation as deals with faulty cognitions.

Can't establish cause & effect relationship --> Can't be 100% sure that faulty cognitions are the root cause or just symptoms.

Holistic --> more than behavioural or biological explanation to some extent - cognitions are influenced by upbringing/past experience and also biology/genes (has a neurological basis).

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