A Level Psychology- Schizophrenia key studies & explanations

Genetic explanationsCardno et al. (2002) found that 26.5% of MZ twins both suffered from Sz, but a 0% concordance of DZ twins. MZ twins are often treated identically, causing more imitation of eachother's actions, causing a greater predisposition to the disorder (diathesis-stress model). Heston (1966) found 16% of children born to schizophregnic mothers & adopted at a young age developed Sz.

Dopamine hypothesis Neuroleptic drugs block dopamine at its synapse, which reduces the firing & overactivity of the neurotransmitter, therefore reducing the symptoms. Post-mortem examinations & neuroimaging shows more dopamine receptors in Sz patients. Iverson (1979) proposed the relationship between dopamine & Sz; Sz is a result of dopamine over-production/ over-sensitivity of neurons.

Neural correlates: study of brain activity & how it causes & affects an experience/ condition by comparing a schizophrenic brain with an anatomical (normal) brain. Swayze & Anderson (1990) looked at 50 schizophrenic brains & all had enlarged ventricles (fluid-filled cavities due to brain cell loss)

Brown et al. (1958) proposed that family interactions that had high expressed emotion (EE)/ emotional over-involvement can maintain schizophrenic behaviours.

Family dysfunction explanation, Bateson et al. (1956) Sz develops as a result of poor communication and/or faulty family relationships.

Double-blind communication: contradictory communication between parent & child. 

(1) say something where body language/ tone of voice doesn't match. (2) mixed/ ambiguous messages causing confusion & mistrust- child questions feelings & trust of parent. (3) grows up mistrusting communication & withdrawing from society (symptoms of Sz).

Lidz et al. (1957) two types of dysfunctional environments that may lead to Sz; both create confusion/ psychological harm, which can develop into Sz:

(1) Schismatic: both parents are in conflict & compete for the attention of other family members.

(2) Skewed: one parent dominates & encourages the child to follow them.

Sz can be explained in terms of faulty/ dysfunctional though processing. The breakdown of self-monitoring processes makes it difficult to interpret thoughts/ feelings accurately.

Frith's (1979) attention defict theory- (1) Processing- Concious: high level processing that requires selective attention. Preconcious: thoughts without awareness/ occur automatically. (2) Filtering- cannot determine the distinction between concious & preconcious thoughts. (3) Overload- thoughts that are usually filtered out as unimportant are made concious, causing delusions & hallucinations.

Hemsley's (1993) model- disconnection between stored expectations (schemas) & what's actually happening; the confusion between internal & external stimuli causes hallucinations.

• PET scans show a reduced activity in the frontal lobe (linked to self-monitoring operations) of schizophrenics; supports Frith's theory.
• patients have a range of cognitive deficts & varying symptoms, where theories & models are inadequate & reductionist in its complexities of the disorder.

Interactionist approach: examines how the combination of biological, psychological & social factors explains the development of schizophrenia; these factors are linked to the cause of schizophrenia to understand how the symptoms develop and help treat the disorder.

Diathesis-stress model: where an environmental stressor triggers a genetic predisposition/ vulnerability to the disorder.

• increased awareness of environmental factors increases the likelihood of genetic vulnerability- preventative strategies can be enforced due to wider knowledge of disorder
• unclear of how the factors interact to cause the disorder- reduces the reliability of the explanation.

Tarrier (1998) randomly placed patients either on anti-psychotics or CBT & found a combined treatment improved positive symptoms & reduced hospital visits.

• holisitic; intergrates different explanations for a more complete understanding of disorder.
• more hypothetical approach; doesn't have predictive power/ scientific validity.