Schizophrenia

EDUQAS GCE A-Level Psychology - Component 3 - Schizophrenia

What is schizophrenia?

A profound disruption of cognition and emotion, which affects a person's language thought, perceptions and sense of self. It is a syndrome that is split into positive and negative symptoms.

What are positive symptoms?

Positive symptoms do not have a 'typical' behavioural counter-part. They are in addition to typical behaviours.

What are hallucinations?

Unusual sensory experiences that can be related to environmental stimuli or completely random.

What are the main types of hallucination?

Auditory, Tactile, Visual, Olfactory and Gustatory.

What is meant by hypnopompic and hypnagogic hallucinations?

The hallucinations must occur outside those regarded as 'normal' experience; those that occur whilst falling asleep (hypnagogic) or waking up (hypnopompic) are considered to be within the range of normal experiences.

What is a delusion?

Strongly held false beliefs, which persist even when there is evidence against their beliefs.

What is a delusion of grandiosity?

For example, believing they are an important historical or political figure, such as Jesus or Napoleon.

What is a delusion of reference?

For example, believing that people are trying to send messages or make contact through the TV or radio.

What is a delusion of persecution?

For example, paranoid delusions where they believe that others are plotting to harm them.

What is a delusion of erotomania?

For example, when an individual believes that another person is in love with them.

What is a delusion of control?

For example, they believe that an outside source is controlling their actions.

What is the difference between a bizarre delusion and a non-bizarre delusion?

Delusions are deemed to be bizarre if they are clearly implausible and not understandable to peers of the same culture.

An example of a bizarre delusion would be that an outside force has removed his or her internal organs and replaced them with somebody else's.

An example of a non-bizarre delusion is the belief that one is under surveillance by the police, despite a lack of convincing evidence.

What is disorganised thinking?

The result of abnormal thought processes. The person has trouble organising thought processes which then manifests in their speech, and can be quickly switching between topics (derailment), sometimes mid-sentence, or speaking incoherently.

What are negative symptoms?

Negative symptoms are the removal of typical processes. They are atypical symptoms that are disruptions to normal emotions or behaviours; can sometimes be mistaken for depression.

What is avolition?

Difficulty beginning or keeping up with goal-directed activity and loss of motivation to carry out day to day tasks.

What is alogia?

Reduction in amount and quality of speech, sometimes experiencing delayed responses in conversation.

What is the flat affect?

Reduction in range and expression of emotion, e.g. facial expression, eye contact, body language and a lack of prosody (intonation and tempo) in speech.

What is anhedonia?

Loss of pleasure from all activity, this can include eating, social contact or previously pleasurable activities.

What is catatonic behaviour?

Can range from fast, repetitive movements, to no movement at all. Unexpected gestures and loud utterances and echopraxia (mimicking the movement of those around them) are common.

What are the two biological explanations for schizophrenia?

• Genetics

• Dopamine Hypothesis

What is the genetic explanation for schizophrenia?

The idea that schizophrenia can be inherited. It is investigated by concordance rates.

Gottesman (1991)

If you have schizophrenia:

• 5% concordance that grandchildren will have it.

• 6% concordance that parents will also have it.

• 9% concordance that siblings will have it.

• 13% concordance that your children will have it.

• 17% concordance that fraternal twins will have it.

• 48% concordance that identical twins will have it.

What did Gottesman’s study suggest about genetics as an explanation for schizophrenia?

Genes have a significant effect on the development of schizophrenia but the percentages of concordance suggest that there may be other causes too. 

Gottesman and Shields (1972)

Showed a concordance rate of 42% for MZ/monozygotic (identical twins) and 9% concordance rates for DZ/dizygotic (fraternal twins).

Cardno et al (1999)

Showed a 40% concordance rate in MZ twins compared with 5.3% in DZ twins.

What do Gottesman & Shields and Cardno et al.’s family studies suggest about genes as an explanation for schizophrenia?

Higher concordance rate in monozygotic twins than dizygotic twins suggests that genes play a significant role in the development of schizophrenia.

What are adoption studies?

Studies which attempt to highlight the genetic influence by separating nature and nurture.

Heston (1966)

They compared 47 children of schizophrenic mothers who were adopted before the age of one month with a control group of 47 children raised by their non-schizophrenic adopted mothers​. 10% of the children with schizophrenic mothers developed it themselves whereas none of the children from the control group did​.

Tienari et al (1987)

They compared 112 cases of adopted children who had biological mothers who had been diagnosed with schizophrenia with 135 adopted children who had non-schizophrenic biological mothers​ (control). 7% of the experimental group developed schizophrenia compared to 1.5% of the control group.

What do Heston and Tienari et al.’s adoption studies show about the influence of genes on schizophrenia?

Genetics play a significant role in the development of schizophrenia as those with a biological link were more likely to develop schizophrenia than those who did not have a biological link. 

What are the strengths of the genetic explanation of schizophrenia?

• Supporting Evidence

  • Gottesman (1991) found that the closer the genetic relationship to someone with SZ the higher the likelihood of SZ developing. For example, the occurrence of SZ in the general population is approximately 1%, but if a parent has SZ then it jumps to 6%.

• Difficult to separate nature vs nurture in family studies

  • This is because it is difficult to separate the link between genetics and environment, as families tend to share similar or the same environments so concordance rates may be caused by genetics or other causes. For example in Gottesman's study, the concordance rate for siblings is 9% and the concordance rate for dizygotic twins is 17%, despite them sharing the same percentage of DNA.

What is the initial dopamine hypothesis?

The brains of schizophrenic patients produce more dopamine than normal brains (hyperdopaminergia). It is this increased dopamine that is believed to be responsible for positive symptoms of the disorder.

Why was the initial dopamine hypothesis discredited?

The explanation was found to be oversimplified as treatments that reduced dopamine levels in the brain were effective at reducing positive symptoms but not negative symptoms.

How did post-mortems lead to the development of the initial dopamine hypothesis?

Autopsies have found that people with schizophrenia have a larger than usual number of dopamine receptors in brain structures and an increase in receptor density (excess of dopamine found in left amygdala). Concluded that dopamine production is abnormal for schizophrenia compared to “normal controls”.

How did Parkinson’s disease lead to the development of the initial dopamine hypothesis?

Those who suffer from Parkinson’s disease were given the drug L-Dopa. L-Dopa raises dopamine activity in the brain, reducing Parkinsonian symptoms, but patients began to develop schizophrenic symptoms. This allowed the link between dopamine and schizophrenia to be seen.

How did PET Scans lead to the development of the initial dopamine hypothesis?

Lindstroem et al. (1999) administered L-Dopa to 10 patients with schizophrenia and 10 with no diagnosis of schizophrenia (control group). 

• L-Dopa stayed in the brain of the schizophrenic patients for longer (synapses did not absorb it because the D2 receptors inhibited the transmission). 

This suggests why schizophrenics have excess levels of dopamine (and have more dopamine receptors).

How did drug use lead to the development of the initial dopamine hypothesis?

LSD/Amphetamines increase the effects of dopamine in the brain. In large quantities, they can lead to delusions and hallucinations.

• If drugs are taken by schizophrenic patients their symptoms get worse. 

What is the revised dopamine hypothesis?

Overactivity of the mesolimbic pathway is where hyperdopaminergia occurs and mesocortical pathway dysfunction is where hypodopaminergia occurs.

• Both pathways start at the VTA (ventral tegmental area), which is the main place of dopamine production.

What is the mesolimbic pathway?

This pathway runs from the ventral tegmental area to the nucleus accumbens. Too much dopamine in this pathway causes overstimulation of the D2 receptors leading to positive symptoms as the receptors on the postsynaptic neurone are unable to absorb the excess dopamine.

What is the mesocortical pathway?

This pathway runs from the ventral tegmental area to the frontal lobe and is important for emotional response and motivation.

• Hypodopaminergia in this pathway (meaning that there is a lack of dopamine being produced) leads to less absorption by the D1 receptors on the post-synaptic neurones, leading to negative symptoms.

How can the dopamine hypothesis be evaluated in terms of its scientific status?

• It is scientific.

  • There is a lot of supporting research for schizophrenia, e.g. Lindstroem et al (1999)'s study; L-dopa stayed in the brain of the schizophrenic patients for longer- (synapses did not absorb it because the D2 receptors inhibited the transmission), suggesting this is why schizophrenics have excess levels of dopamine.

  • PET scans are scientific methods of research, they provide objective data - they actively see what is going on in living brains which means the data is less likely to be required to be interpreted by the researcher. This increases the validity of the research.

How can the dopamine hypothesis be evaluated in terms of its successful applications?

• It has successful applications to drug therapy.

  • Antipsychotics are drugs developed to treat disorders like schizophrenia, by targeting the release of neurotransmitter at the synapse. First generation antipsychotics were developed as dopamine antagonists which targeted hyperdopaminergia, which tackled positive symptoms. Second generation antipsychotics were later developed which tackled negative symptoms.

  • Typical antipsychotics were developed based on the dopamine hypothesis based on the idea of hyperdopaminergia in the mesolimbic system and hypodopaminergia in the mesocortical system and work by blocking the transmission of dopamine on the D2 receptors on the postsynaptic neurone - which leads to a reduction in neural activity. This then leads to a reduction in positive symptoms like hallucinations and delusions.

How can the dopamine hypothesis be evaluated in terms of its supporting evidence?

• It has supporting evidence in terms of post mortems.

  • Post mortems have found that people with schizophrenia have a larger than usual number of dopamine receptors (issue because there is not enough dopamine production to match the number of receptors which leads to an overstimulation in the production of dopamine, leading to an over transmission of dopamine in the post-synaptic neurone which leads to positive symptoms).

  • However, the study can be critiqued in terms of issues with post-mortems. Post-mortems do not look at live brains, meaning that important information may be missed, and we cannot draw causal conclusions.