The word schizophrenia comes from the Greek language, Skhizein (To split) and Phren (Mind) and is a type of psychosis. Schizophrenia is a severe mental disorder disrupting cognitive processes and emotions, impacting on perception, thought, language and sense of self resulting in a loss of contact with reality. Sufferers are unaware of the effect their behaviour has on others. Schizophrenia may be many illnesses masquerading as one.
Schizophrenia is characterised by two types of symptoms in addition to social dysfunction. Positive symptoms (symptoms in addition to normal behaviour) manifesting themselves through thought disorder, hallucinations & delusions; these symptoms respond well to anti-psychotic medication. Negative symptoms (a decrease in normal behaviour) manifesting themselves through paranoia or disorganised speech & thinking, these mental deficiencies do not respond well to medication. Schizophrenia affects both men and women equally, appears in all ethic groups, appears in early teens for males, up to five years later in females and may be a lifelong illness leading to a breakdown of normal relationships in both work and home environments.
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Classification of schizophrenia by the American Psychiatric Association - DSM-IV is generally accepted & can be divided into three criteria. Diagnosis of schizophrenia is dependant on the type of symptoms exhibited & the duration of those symptoms. No single symptom is definitive for a diagnosis & the diagnosis encompasses a pattern of signs & symptoms, in conjunction with impairment of social functioning.
The DSM-IV recognises five sub-types of schizophrenia:
Paranoid schizophrenia the most common type, is characterised by paranoid delusions, hallucinations and may show little or no impairment in other respects.
Undifferentiated schizophrenia described as miscellaneous, not enough symptoms are present to classify it as any other type but does contain loss of reality amongst other symptoms.
Disorganised schizophrenia previously known as hebephrenic. This type highlights difficulty with completing ordinary tasks, disorganised loosely associated speech & behaviour with flat affect that seems lacking in emotion. This type has the poorest prognosis, Bootzin & Acocella (1984).
Catatonic schizophrenia highlights motor activity disorder. This activity can be wildly inappropriate with no purpose or completely still (wax like) while still remaining flexible, Bloom et al (1976).
Residual schizophrenia is a category used to describe people with previous history of the illness who still display some negative residual symptoms, like flattened affect and social withdrawal.
Understanding what causes schizophrenia is becoming more difficult. There are many theories of possible causes, all using different approaches but we just don't know. One simple explanation is that schizophrenia is caused by a combined disturbance of specific genes & interactions with biological and social stressors in the environment. The following essay will discuss these interactions in more detail.
Scientific advances in genetics, neuroscience, bio-chemical, neuro-imaging & pre-natal factors, give substantial support to the biological causes of schizophrenia. On the other hand some scientists support psychosocial factors, mainly cognitive explanations in terms of the diathesis-stress model. A psychological theory suggesting the causes of schizophrenia may result from a combination of genetics and early learning (Tienari, 1991). Further evidence for the psychosocial model supports the social causation theory emphasising social & economic reasons, Brown et al (2000).
Several regions of the human genome are currently being investigated to establish whether people suffering from schizophrenia had a genetic predisposition. Activities of neurotransmitters in the brain are controlled by genes and there is compelling evidence that these genes are in involved in the aetiology of schizophrenia. This evidence comes from family, twin and adoption studies. Family studies of children with a schizophrenic parent are 15 times more likely to develop the disease than the rest of the population. Twin studies (identical) have reported where one twin develops symptoms, other has a 50% chance of developing the symptoms as well, that implies half will not go on to develop the illness, Heston (1970). The strongest relationships are found between identical twins. Non-identical twins have a 10-15% chance one twin will develop schizophrenia, Nicol & Gottesmann (1983). Adoption studies gave support to the biological model, where children were adopted out with schizophrenic & non-schizophrenic birth mothers, suggesting family environment did not contribute to a child developing symptoms of schizophrenia where one twin already had the illness, this does however give credibility to the difficulty in separating the effects of genetics from environmental effects, Plomin et al (1997).
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For many years neuroscientists believed schizophrenia was caused by a surplus of dopamine in the brain. Dopamine increases sensitivity & promotes individual awareness of events when aroused, in danger or under stress. Addition levels of dopamine may increase the risk of psychotic symptoms. To determine how dopamine levels play a role in the aetiology of schizophrenia, other diseases were looked at for comparisons. Evidence for the dopamine hypothesis comes from three main sources, post-mortems, anti-psychotic drugs & amphetamine use. The first evidence to appear supporting the dopamine theory came from amphetamine users. Amphetamine has been found to increase levels of dopamine in the brain and symptoms of schizophrenia as reported by Snyder (1973) and later researched by Perreault et al (2010). Further support was realised by chance when an overdose of dopamine used in the treatment of Parkinson's disease produced similar symptoms to schizophrenia, overproduction of dopamine neurotransmitters occurs in schizophrenic patients, similar elevations were found in dopamine receptors in the brains of patients with Parkinson's & Huntington's, Seeman et al (1987). Scientists discovered that by blocking levels of dopamine with anti-psychotic drugs a noticeable reduction in symptoms of schizophrenia occurred, Howes & Kapur (2009).
Neuro-imagery allows scientists to study abnormalities in the brain structure of living schizophrenic patients. The two methods used to discuss schizophrenia from a neurobiological standpoint are: Positron Emission Tomography (PET) for assessing metabolism & Magnetic Resonance Imaging (MRI) for measuring changes of blood flow in the brain. MRI scans have revealed enlarged ventricles and cavities within the brain of schizophrenic sufferers. These ventricles are 15% larger than non schizophrenics, there is evidence to suggest increased blood flow restricts normal brain growth and development and damages healthy tissue. There is also evidence that sufferers of schizophrenia display cognitive abnormalities & negative symptoms, Andreasen (1990). Research using PET scans report reduced neural activity in the prefrontal cortex, indicating abnormal brain activity in schizophrenics. There is also evidence that metabolic rate increases in white matter & decreases in grey matter demonstrating an inefficiency in brain circuitry of patients, Buchsbaum et al (2007).
Brain structure & function may be damaged due to viral illnesses. This can increase when a pregnant woman contracts an illness such as chicken pox, measles or the flu virus. Exposure to viral infections before birth is an area within the biological framework which may explain schizophrenia. Further evidence to support prenatal factors lies in the number of people with schizophrenia who are born during the winter. Schizophrenia occurs mostly with people born from December to April, when viral infections are peaking within the population, Brown (2001). Further evidence that foetal exposure to the flu virus may be a predictor of the development of schizophrenia can be seen from research on grown up twins. Evidence of abnormal fingertip ridge count has been found in the schizophrenic twin, Cannon et al (1994).
Biological explanations have gained a lot of support from the research community but there is still plenty of scope for psychological explanations to have an influence on our understanding of schizophrenia.
Schizophrenia is characterised by profound thought disturbance. Significant cognitive impairment is common in schizophrenic patients and often pre-dates the illness, affecting up to 75% of sufferers. The cognitive model acknowledges the role of biological factors but psychosocial factors help our understanding when additional features of the disorder appear when the schizophrenic person tries to interpret their own behaviour. The schizophrenic brain is characterised by dysfunction of both hemispheres and the basal ganglia, Buchsbaum (1990). Large scale studies have been carried out comparing cognitive function in schizophrenic patients with healthy people, greatest impairments were observed in large-scale verbal memory functioning, concluding that several patterns of neuro-cognitive dysfunction may underlie schizophrenia Heinrichs & Zakzanis (1998). Other studies have indicated the inability to generate spontaneous intentions can lead to deficiency of action, perseveration and unsuitable action. The inability to monitor other people's beliefs & intentions may lead to incoherence, delusions & third-person hallucinations, Frith (1992).
This explanation suggests schizophrenia is a consequence of faulty learning and is developed in childhood. A child who receives no social reinforcement early in life may pay more attention to irrelevant environmental cues, paying more attention instead to the sound of the word instead of its meaning. Poor communication in the family has been reported as a contributing factor, Goldstein (1987). A turbulent parent-child relationship in the British 1946 birth cohort is suggested as a contributing factor, Jones et al (1994). Other recent studies have found behavioural abnormalities in healthy children prior to the development of schizophrenic symptoms, Murray (2005).
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Dysfunctional family relationships
Research suggesting that living in a dysfunctional family as a possible cause has been largely discredited, this explanation fails to establish the 'cause' and 'effect'. An adoption study carries out in Finland using psychological tests & interviews looking for a correlation between environmental factors i.e. poor parenting and schizophrenia. Results found a dysfunctional environment may be significant in turning vulnerability or biological sensitivity into schizophrenia, Tienari et al (1987). The Israeli High Risk Study reported similar findings where no 'cause' and 'effect' could be established, Marcus et al (1987). Research into dysfunctional families show that people that do go on to develop schizophrenia come from normal functioning, well adjusted families and not from socially deprived backgrounds.
Social-causation theory/Social drift
Schizophrenia tends to affect the poor rather than the rich in society. This may be down to one of two things: Did the effects of poverty cause the illness or did the illness condemn suffers to a life of poverty? Cause and effect is not established. The population of New York was surveyed, a relationship between social class and schizophrenia was found, providing evidence for both socio-economic drift and social causation, Turner & Wagenfield (1967).
Biological & Psychosocial factors
This approach argues that schizophrenia occurs where there is a known pre-disposition towards the disorder (diathesis) & is combined with social and biological stressors. High diathesis would require less stress to react in an abnormal way. The diathesis-stress model combines biological factors; genetics with levels of stress and assumes a biological sensitivity that will develop under the right conditions of environmental or emotional stress. A Finnish study reported that adopted children raised in healthy families did not go on to developed schizophrenia. In severely disturbed families however 11% of the children did go on to develop the illness, Tienari (1991). The bio-psycho-social approach combining different factors is a more diverse approach to studying and understanding schizophrenia.
Both biological and psychosocial models offer valid explanations for the aetiology of schizophrenia & search to control or find a cure for the condition. Twin studies & genetics fail to account for upbringing and environmental factors but do indicate a persons risk increases with the number of sufferers in a families, lifetime risk is much greater for first degree relatives. There is compelling evidence to support biochemical factors, however dopamine is one neurotransmitter & although an important one, many others hormones are likely to be involved as well. Neuro-imagery allows research on live patients paving the way for effective immediate treatment for sufferers, however this model is currently unable to determine whether the structural abnormalities in the brain are a result of schizophrenia and not other mental disorders. Other mental disorders display similar abnormal brain structures. There is some interesting evidence to support prenatal factors but the evidence is difficult to verify.
Psychosocial explanations take into account how behaviours are developed & how environmental factors can be controlled to stop the progression of the condition. Cognitive models combine biological factors, behaviour, environment and cognition with diverse symptomatology. This model emphasises the schizophrenics own distorted view of the world, views about themselves and their own behaviour and uses cognitive behaviour therapy (CBT) to trace the origins of their symptoms & a better understanding of how they developed. This model also supports the view that schizophrenic symptoms lie on a continuum with normal experiences. Behavioural factors are difficult to assess because it is unknown which came first, did the behaviour lead to the development of schizophrenia or did the innate predisposition to the illness lead to abnormal behaviour. Evidence for a dysfunctional family model has been largely discredited with most sufferers coming from well adjusted backgrounds. Social causation and the social drift hypotheses may be very significant as a cause but until cause & effect has been established, this view has little support. Diathesis stress model combines biological factors; genetics with levels of stress and assumes a biological sensitivity will develop under the right conditions of environmental or emotional stress into schizophrenia. Research in this area looks promising; more research is required to promote better understanding of schizophrenia.
Schizophrenia appears to be a combination of several illnesses and requires both biological and psychosocial models in the search for the aetiology of schizophrenia.