Biological Explanation and Treatment for Schizophrenia

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  • Created by: RihanaG
  • Created on: 16-01-16 20:15
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  • Biological Explanation and Treatment for Schizophrenia
    • Explanation: The Dopamine Hypothesis
      • Evidence for the dopamine hypothesis
        • Chlorpormazine, a drug given to Schizophrenics, alleviates the symptoms of schizophrenia and works by blocking dopamine receptors. If the receptors are blocked, then less dopamine will be taken up so that the effects of excess dopamine are avoided.
        • Scans show that if schizophrenics are given amphetamines (illegal, addictive, mood-stabilising drugs) there is a greater release of dopamine than if non-schizophrenics are given the same drugs. So this shows that schizophrenics are more sensitive to excess dopamine.
        • Drugs that are given to sufferers of Parkinson's disease which adds to dopamine production result symptoms similar to that in schizophrenia.
        • Genes that are likely to increase sensitivity to dopamine are found with greater frequency in those with schizophrenia.
        • The brains of those with Schizophrenia seem to be different (such as grey matter differences in the front and temporal lobes). These brain changes link sensitivity to dopamine.
      • Evidence against the dopamine hypothtesis
        • PET scans have suggested that drugs that block dopamine did not reduce symptoms of schizophrenia in patients who have had schizophrenia for more than 10 years, even if 90% of the receptors were blocked.
        • Anti-Schizophrenic drugs block dopamine receptors almost immediately but the effect is not noticed for several days. This suggests something other than excess dopamine is causing the symptoms.
        • Amphetamines only produce symptoms similar to positive symptoms in schizophrenia.
        • Research suggests that there are three areas of the brain where there are excess dopamine receptors in everyone. When different types of dopamine receptors are considered, there are different results from excess or reduced receptors.
        • Another neurotransmitter, glutamate, is also thought to cause psychotic symptoms if there is excess present, so perhaps dopamine is not the only neurotransmitter involved.
    • Treatment: Drug Therapy
      • Drug tratment follows the idea that if neurotransmitter functioning causes symptoms, drugs can help to treat the symptoms. these drugs are called anti-psychotic drugs and they work to supress hallucinations and delusions.
        • Antipsychotics are known as 'typical' and 'atypical'. Typical ones are well-established and atypical ones are newer and less widely used, so may have more side effects.
      • Strengths of Drug treatment
        • Drugs are more effective and more ethical than treatments used pre-1950s, such as lobotomy.
        • There is strong biological evidence about the causes of schizophrenia so is supported by theory, which strengthns its effectiveness.
      • Weaknesses of Drug treatment
        • Schizophrenics do nor always continue to take the drugs they are prescribed. This can be because the effects of schizophrenia means they do not remember when to take their medication, or they may find the side effects uncomfortable.
        • From an ethical point of view, drugs have been called 'a chemical strat-jacket' and such control. by society is unacceptable.
        • Drugs have unpleasant side-effects, and anti psychotic drugs only seem to help with most positive symptoms rather than negative ones.
        • Drugs do not take into account a patients social or environmental problems, which might contribute to relapses or re-hospitalisation.
  • Biological explanation suggests that schizophrenia is related to neurotransmitter functioning- an excess of dopamine must be the cause of schizophrenia, as the drugs used to treat schizophrenia works by blocking dopamine receptors at the synapse in the brain, and it has been successful.
    • A sensitivity to dopamine can arise from genetic inheritance to brain lesioning- so there are many ways to develop the illness.
    • Explanation: The Dopamine Hypothesis
      • Evidence for the dopamine hypothesis
        • Chlorpormazine, a drug given to Schizophrenics, alleviates the symptoms of schizophrenia and works by blocking dopamine receptors. If the receptors are blocked, then less dopamine will be taken up so that the effects of excess dopamine are avoided.
        • Scans show that if schizophrenics are given amphetamines (illegal, addictive, mood-stabilising drugs) there is a greater release of dopamine than if non-schizophrenics are given the same drugs. So this shows that schizophrenics are more sensitive to excess dopamine.
        • Drugs that are given to sufferers of Parkinson's disease which adds to dopamine production result symptoms similar to that in schizophrenia.
        • Genes that are likely to increase sensitivity to dopamine are found with greater frequency in those with schizophrenia.
        • The brains of those with Schizophrenia seem to be different (such as grey matter differences in the front and temporal lobes). These brain changes link sensitivity to dopamine.
      • Evidence against the dopamine hypothtesis
        • PET scans have suggested that drugs that block dopamine did not reduce symptoms of schizophrenia in patients who have had schizophrenia for more than 10 years, even if 90% of the receptors were blocked.
        • Anti-Schizophrenic drugs block dopamine receptors almost immediately but the effect is not noticed for several days. This suggests something other than excess dopamine is causing the symptoms.
        • Amphetamines only produce symptoms similar to positive symptoms in schizophrenia.
        • Research suggests that there are three areas of the brain where there are excess dopamine receptors in everyone. When different types of dopamine receptors are considered, there are different results from excess or reduced receptors.
        • Another neurotransmitter, glutamate, is also thought to cause psychotic symptoms if there is excess present, so perhaps dopamine is not the only neurotransmitter involved.

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