The evidence in support of this explanation has come from the fact that antipsychotic drugs reduce the symptoms of schizophrenia by blocking dopamine receptors. This suggests that it’s the overactive dopamine receptors causing the symptoms. // Also, drugs like amphetamines, which increase dopamine function, can sometimes cause schizophrenia-like symptoms in people without schizophrenia. // Autopsies have also found that people with schizophrenia have a more than usual amount of dopamine receptors – a Falkai et al 1988. Curran et al concluded that effects of taking illegal stimulant drugs were similar to that of schizophrenia. Since the illegal drugs work on the dopamine system, schizophrenia would also appear to have a link to dopamine. // Chan et al conducted research into the rate of blinking in those with schizophrenia. They concluded that blink rate, which is said to be linked to the dopamine system in the brain, was significantly higher in patients with schizophrenia than controls. // Also the dopamine distribution in Parkinson’s disease can help support the dopamine hypothesis for schizophrenia. In a patient with Parkinson’s, dopamine activity is considerably lower and is increased with the patient taking a drug called L-dopa. If they overdosed on this drug, an abnormal amount of dopamine will be produced and schizophrenic symptoms will begin to show. //
The evidence in support of the dopamine hypothesis isn’t conclusive, and there is additional evidence that raises some questions about the role dopamine plays in schizophrenia. One important thing to note is that amphetamines and some effective schizophrenia drugs alter levels of other neurotransmitters in addition to affecting dopamine, meaning that their effect on schizophrenia symptoms may not be strictly linked to dopamine levels. // Another question is raised by the fact that dopamine-blocking drugs work to reduce dopamine levels immediately, but it can take days for symptoms of schizophrenia to improve. If dopamine levels are directly responsible for schizophrenia symptoms, one would assume that symptom improvement would begin immediately. //
Traditionally, the biological treatment of schizophrenia involved ECT and psychosurgery, however nowadays biological therapies involve more scientifically robust methods. For example, the treatment for schizophrenia involves drug therapy. This type of treatment is based on the dopamine hypothesis. Antipsychotic drugs (neuroleptics) work by blocking dopamine receptors.
Drug therapy is effective at reducing positive symptoms, e.g hallucinations. It’s successful for a large number of schizophrenia patients, meaning that more people can live in the community rather than being institutionalized. It’s the most widely-used and effective form of treatment of schizophrenia. Almost all other treatments are used alongside drug therapy.
Drug therapy isn’t very affective for treating negative symptoms like social withdrawal. It treats the symptoms of schizophrenia and not the cause. Symptoms often come back if people stop taking antipsychotic drugs and this can lead to the ‘revolving door phenomenon’, where patients are constantly being discharged and re-admitted to hospital. There are ethical issues surrounding the use of drug therapy. Some people argue that drug treatment is a ‘chemical straightjacket’ – it doesn’t really help the patient, it just controls their behaviour to make it more socially acceptable and easier to manage. Most people will experience some short-term side effects when taking antipsychotic drugs, e.g. drowsiness, blurred vision, dry mouth, constipation and weight gain. Long-term side effects include increased risk of diabetes and tardive dyskinesia (involuntary repetitive movements that continue even after they’ve stopped taking the medication). However newer antipsychotic drugs seem to have fewer long-term side effects than the older ones.
This is good but not relevant to the question….
Genetic: The genetic explanation proposes that schizophrenia is an inherited disorder, caused by genes passed on from parents. Psychologists use family, twin and adoption studies to see how likely it is that genetics plays a part in determining schizophrenia. They chiefly use concordance rates to work out the chance that someone will develop a disorder if a close family member also has it. For example, if there is a 100% concordance rate for the disorder in identical twin studies, we can conclude that there is a high chance the disorder is caused by genetic factors, since identical twins have exactly the same DNA. However, the results have not shown a 100% concordance rate, so there is evidence both for and against the role of genetics. /
Gottesman (1991) reviewed concordance rates from many twin studies and found that there was just under a 50% chance of both identical twins having schizophrenia and just under a 20% chance of both non-identical twins having it. Additionally, Shields (1962) had previously found very similar concordance rates of just under for identical twins despite studying identical twins who had been raised apart. This suggests that there is certainly a genetic factor involved, but that it is not exclusively responsible for the onset of schizophrenia. //
Because twins tend to be raised in very similar environments and children have been known to imitate behaviours of those they are close with, it is hard to differentiate how much of their behaviour is a result of their environment and how much is caused by genetics. Therefore, other factors need to be considered in order to determine the causes of schizophrenia. //
Neuroanotomical: Abnormal brain structure, caused by abnormal brain development, could be the cause of schizophrenia.
Johnstone et al (1976) compared the size of he ventricles in schizophrenics brains with non schizophrenics brains. They found that the people with schizophrenia had enlarged ventricles, which suggests that schizophrenia is linked to a loss of brain tissue. Buchsbaum (1990) carried out MRI scans on schizophrenics brains and found abnormalities in the prefrontal cortex. /
Evidence against neurological factors include the fact that non-schizophrenics can also have enlarged ventricles, which contradicts Johnstone’s evidence. However, there’s conflicting findings amongst schizophrenic patients too. These findings are correlational, so they don’t show cause and effect. It may be that abnormal brain structure is a symptom of schizophrenia, rather than a cause of it. //
14/24 There are excellent points in this essay I am impressed by the science in the dopamine hypothesis explanation. However you lost your way speaking about the therapy, this made lose marks as it took a lot of your word allowance!
Well done this is a great improvement on the last essay! Read the comments