Psychology PSYA3

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Schizophrenia
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Clinical classifications and explanations of schizophrenia.Classifications (psychopathology- dominated by biology approach)- it assumes that mental disorders is similar to physical disorders, so it suggests that mental disorders should be treated, diagnosed and classified as physical disorder.When a disorders is being classified, clinicians used the symptoms and signs to identify the group the disorder is classified into. Positive symptoms these are the Symptom, Explanation and Example * Delusions- False beliefs that the sufferer thought to be true. * Persecution – having special knowledge or a belief that powers, thought or actions are being controlled by an external force. * Hallucinations- Imagined sensory perceptions. * Auditory – hearing imagined voices (And holding prolonged conversations with these voices) * Thought Disorder- Confused thinking that is evident in what they say and how they say it. * Incoherent speech – jumping from one subject to another with little or no logical connection. The grammar may be strange and only makes sense to the speaker. They may claim that thoughts are being broadcast or stolen from them or are being controlled or influenced by an alien, demon, or foreign power. * Bizarre Behaviour- Strange and inappropriate behaviour (Contravening social norms). Undressing in public or making odd faces, body gestures and postures for no apparent purpose.Negative Symptoms these are the Symptom, Explanation and Example * Blunted Emotional Responses- No emotional involvement in or response to things in their immediate environment * Unchanging facial expression, gestures, or tone of voice regardless of whether the environment would require a happy or sad response, or an inappropriate response e.g. laughing at a funeral. * Loss of drive- Has little interest or motivation to work or enjoy leisure activities * Inability to wash and feed to take decisions and being entirely passive, which leads to social withdrawal from the individual causing a lack of friends or the difficulty making and keeping friends acquaintances or more intimate relationships. Also relates in a reluctant and negative way towards social interaction. * Poverty of Thought- Considerable reduction in cognitive activity: Thinking limited to immediate concerns. As well as, a limited amount of speech and may answer questions with ‘yes’ ‘no’ or ‘I don’t know’.

Genetic Explanations for Schizophrenia: Sample sizes and modestly positive results do not add up to certainty, however, a summary of evidence to this end includes: Twin studies showing higher than expected probability that if one twin presents symptoms the other is likely to do so; The closer the genetic relative to the sufferer, the higher the probability that they might develop schizophrenia. Adopted children whose natural family contained a member who had developed schizophrenia were more at risk; a child adopted by a family where a member later develops schizophrenia is no more likely to develop the illness itself. Where biological changes do occur they could be the result of the schizophrenia rather than the cause, or linked in ways in which has yet to be discover. The longitudinal Copenhagen High Risk Study (1962 - early 90’s) examined children who’s mothers were diagnosed as having schizophrenic symptoms and found them much more likely to develop the illness compared to those who did not. There was less than 1 in 10,000 chance (p that these findings could have occurred by chance. However, this study cannot differentiate between the effects of genes and the effects of the environment.Adoption studies provide some of the strongest evidence in support of the argument that genetics play a key role in the development of schizophrenia. Below shows the evidence indicating strong genetic links between genetics and schizophrenia. However, it must be remembered that sample sizes are small and that circumstances of each study were not directly comparable (lacks of population validity- difficult to generalise). Also, there are issues to do with the fact that NOT ALL SOCIAL GROUPS ARE EQUALLY LIKELY TO BE DIAGNOISED WITH SCHIZOPHERIA. Evaluation: · Research evidence is pretty persuasive for genetic linked risk factors; · Degree of risk for relatives is never 100% - even with Mz Twins its less than 50%, therefore genetics cant be a complete explanation. · Search for the relevant gene: Without knowing the exact gene it’s impossible to isolate the underlying mechanisms that lead from genetic risk to symptoms of the disorder. The search for the gene continues.

Biochemical explanations of schizophreniaDopamine is a brain chemical that increases the sensitivity of the brain cells that promote the individual’s awareness of danger or aroused and when under stress. If, however, the individual’s level of brain activity is already highly aroused, then the effects of additional dopamine activity may trigger the onset of a psychotic state, such as schizophrenia. Neurons that have dopamine as their transmitter substance (Dopaminergic neurons) are overactive in individuals who exhibit schizophrenic symptoms. The dopamine hypothesis suggests that ‘excessive activity’ in the dopamine neurons leading to increased dopamine production and limited absorption of existing dopamine is associated with schizophrenia. An interesting parallel exists with Parkinson’s Disease, where a dopamine increasing drug (L Dopa) seems to have the opposite effect. Further support for the dopamine hypothesis comes from the post-mortems (dead patients- corpse) of patients with schizophrenia. These have revealed specific increase of dopamine in the left amygdale (Falkai et al. 1988) and increased dopamine receptor density in the caudate nucleus putamen (Owen et al. 1978) Wong et al. (1986) shows in live patients using pet scans that the dopamine receptor density in the caudate nuclei is indeed greater in those with schizophrenia than in controls. This however is not supported in subsequent studies.Evaluation of Dopamine Hypothesis:Positive evaluation + Current available evidence supports some form of the dopamine hypothesis.+ Effects of different drugs on different sub types (Type I and II)Negative evaluation- Drugs alleviate positive symptoms but are not so effective with negative symptoms.- Cause or effect can’t be establishedNeutral evaluation-/+ Amphetamines worsen positive symptoms (associated with acute schizophrenia) and lessen negative symptoms (Associated with chronic) while phenothiazine's (Anti-psychotics) alleviate positive symptoms but aren’t as effective in lessening negative symptoms.Role of dopamine in other disorders:Dopamine also implicated in mania and other disorders which have quite different symptoms. Main evidence in dopamine schizophrenia is the effectiveness of phenothiazine in alleviating symptoms.

Neuroanatomical explanationsTwo such scanning technologies are Positron Emission Tomography (PET) and Magnetic Resonance Imaging (MRI).PET scans are used in the diagnosis of problems in bodily organs, particularly the brain.MRI is a complex diagnostic technique whereby a patient is surrounded by a cylinder that contains a strong magnet. These technologies have shown abnormal brain structures in many patients exhibiting schizophrenic symptoms,the differences in the density of receptor cells for dopamine in schizophrenia patients who were being treated with anti-psychotic drugs and those who were not. Evidence for neuro-anatomical explanations: Brown et al (1986) found decreased brain weight and enlarged ventricles, which are the cavities in the brain that hold cerebrospinal fluid. Flaum et al. (1995) also found enlarged ventricles along with smaller thalamic hippocampal and superior temporal volumes.Buchsbaum (1990) found abnormalities in the frontal hippocampus and the amygdale. As more MRI studies are being undertaken, more abnormalities are being identified.

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