‘There is considerable evidence that biological factors cause schizophrenia. These can be genetic, neuroanatomical, biochemical, viral or a combination of such factors.’ Discuss biological explanations of schizophrenia. (8 marks + 16 marks) Biological explanations portray behaviour as a product of nature. It has three main assumptions: Human behaviour can be explained by looking at internal, biological structures such as hormones and the nervous system. Experimental research that uses animals can be generalized to human behaviour, And that abnormal behaviour can be removed using biological treatments- e.g. medication for schizophrenia.
Biochemical explanation: Post-mortems and PET scans have shown that people with schizophrenia have either an abnormally high amount of the neurotransmitter dopamine, a high amount of D2 receptors, sensitive D2 receptors, or all three. These findings led to the development of the dopamine hypothesis, which states that synapses that use dopamine as a neurotransmitter are overactive in the brains of people with schizophrenia.
A nerve impulse arrives at the synaptic knob of the presynaptic neuron. The arrival stimulates voltage-gated calcium ion channels to open. Calcium ions then diffuse into the synaptic knob. The influx of calcium ions into the synaptic knob causes the synaptic vesicles (containing the neurotransmitter dopamine) to move to the presynaptic membrane. They then fuse with the presynaptic membrane. The vesicles release the dopamine into the synaptic cleft by exocytosis. The dopamine diffuses across the cleft and binds to specific D2 receptors on the postsynaptic membrane.
Prices start at $12
Prices start at $11
Prices start at $14
Prices start at $12
This process is thought to be amplified, either by over-sensitive/amount of D2 receptors and the amount of neurotransmitter being released susceptible to the binding. / this is great but maybe a bit long for just one mark; however, obviously, it would give you marks for depth and breadth (are you sure you would be able to write this without your notes?) The evidence supporting 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 the effects of taking illegal stimulant drugs were similar to that of schizophrenia. Since illegal drugs work on the dopamine system, schizophrenia would also appear to link to dopamine. Finally, Chan et al. researched the rate of blinking in those with schizophrenia.
They concluded that blink rate, which is 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 would 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. Therefore, 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.
Ethical issues are surrounding the use of drug therapy. Some people argue that drug treatment is a ‘chemical straightjacket’ – it doesn’t help the patient; it 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. For example, 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 undoubtedly a genetic factor involved but 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 to determine the causes of schizophrenia. Neuroanatomical: Abnormal brain structure caused by abnormal brain development, could be the cause of schizophrenia. Johnstone et al (1976) compared the size of the ventricles in schizophrenics brains with non-schizophrenics brains.
They found that 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 includes the fact that non-schizophrenics can also have enlarged ventricles, which contradicts Johnstone’s evidence. However, there are 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 its cause. 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 of speaking about the therapy; this made you lose marks as it took a lot of your word allowance!