Schizophrenia
Schizophrenia is a psychiatric disorder denoting an often chronic, major mental illness primarily affecting thinking, with attendant difficulties in perception of reality, which in turn can affect behavior and emotion. The term schizophrenia comes from the Greek words σχίζω (schizo, split or divide) and φρενός (phrenos, mind) and can be translated as "shattered mind."
Cause
Genetic and environmental influences
While the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that a combination of genetic vulnerability and environmental stressors can act in combination to cause schizophrenia.
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The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for schizophrenia. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.
Related Topics:
High blood pressure - Genes
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Some researchers estimate schizophrenia to be highly heritable (some estimates are as high as 70%). However, genetic evidence for the role of the environment comes from the observation that identical twins do not universally develop schizophrenia. A recent review of the genetic evidence has suggested a 28% chance of one identical twin developing schizophrenia if the other already has it{{Fn|7}} (see twin study).
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There is also considerable evidence indicating that stress may trigger episodes of schizophrenia. For example, emotionally turbulent families{{Fn|8}} and stressful life events{{Fn|9}} have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. Unstable emotional environments have also been shown to be a risk factor for developing schizophrenia {{Fn|46}} {{Fn|49}} {{Fn|50}}.
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However, the estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies{{Fn|37}} {{Fn|40}} showing rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins.
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A recent review of linkage studies, listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing schizophrenia{{Fn|26}}. Evidence comes from research suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Some genetic association studies have demonstrated a relationship to a gene known as COMT that is involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase{{Fn|27}}. This is particularly interesting because of the known link between dopamine function, psychosis, and schizophrenia.
Related Topics:
Linkage - Chromosomal - COMT - Dopamine
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There is also considerable evidence indicating that stress may trigger episodes of schizophrenia psychosis. For example, emotionally turbulent families{{Fn|8}} and stressful life events{{Fn|9}} have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. In common with other forms of mental illness, abuse as a child and early traumatic experience have also been suggested to be a risk factor for developing schizophrenia later in life{{Fn|46}} {{Fn|49}} {{Fn|50}}, although the "bad parenting" theory of causation is now largely held in disrepute on the grounds that it overlooks the likelihood that the parental incompetences may have been a result of schizophrenia in the parents, and the disorder itself in the offspring was actually transmitted genetically from the parents.
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Other factors such as poverty and discrimination may also be involved. This may explain why minority communities have much higher rates of schizophrenia than when members of the same ethnic groups are resident in their home country. On the other hand, the "social drift hypothesis" suggests that people affected by schizophrenia may be less able to to hold steady or demanding, higher-paying jobs, consigning them to lower incomes.
Related Topics:
Poverty - Discrimination
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One particularly stable and replicable finding has been the association between living in an urban environment and risk of developing schizophrenia, even after factors such as drug use, ethnic group and size of social group have been controlled for{{Fn|29}}. A recent study of 4.4 million men and women in Sweden found a 68%–77% increased risk of psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be accounted for by schizophrenia{{Fn|30}}.
Related Topics:
Urban - Drug use - Ethnic group - Social group - Sweden - Psychosis
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One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring{{Fn|32}} (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.
Related Topics:
Winter - Spring - Northern hemisphere
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Neurobiological influences
It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia{{Fn|10}}. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939–1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy{{Fn|11}}, suggesting that even psychological trauma in the mother may have an effect.
Related Topics:
Neurodevelopment - Dutch famine of 1944 - Finnish - Winter War - 1939 - 1940 - Psychological trauma
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Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered to be sensitive to features of dysfunctional social settings, such as trauma, violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. It is thought that the effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. This is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years{{Fn|51}}.
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In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.
Related Topics:
Mesolimbic pathway - Dopamine hypothesis of schizophrenia - Phenothiazines
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However, this theory is now thought to be overly simplistic as a complete explanation. Partly as newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments{{Fn|12}}.
Related Topics:
Atypical antipsychotic - Typical antipsychotic - Serotonin - Dopamine - David Healy - Pharmaceutical companies
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Much recent research has focused on differences in structure or function in certain brain areas in people diagnosed with schizophrenia.
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Early evidence for differences in the neural structure came from the discovery of ventricular enlargement in people diagnosed with schizophrenia, for whom negative symptoms were most prominent{{Fn|35}}. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients.
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More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia{{Fn|36}}. However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.
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Studies using neuropsychological tests and brain scanning technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes{{Fn|13}}. These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.
Related Topics:
Neuropsychological tests - Brain scanning - FMRI - PET - Frontal lobes - Hippocampus - Temporal lobes - Neurocognitive deficits - Memory - Attention - Problem solving - Executive function - Social cognition
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Electroencephalograph (EEG) recordings of persons with schizophrenia performing perception oriented tasks showed an absence of gamma band activity in the brain, indicating weak integration of critical neural networks in the brain.{{Fn|53}} Those who experienced intense hallucinations, delusions and disorganized thinking showed the lowest frequency synchronization. None of the drugs taken by the persons scanned had moved neural synchrony back into the gamma frequency range. Gamma band and working memory alterations may be related to alterations in interneurons which produced the neurotransmitter GABA. Alterations in a subclass of GABAergic interneurons which produce the calcium binding protein parvalbumin have been shown to exist in the DLPFC in schizophrenia. {{Fn|54}}
Related Topics:
Electroencephalograph - Gamma band - GABA - Parvalbumin - DLPFC
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