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| + | Some of the causes of [[schizophrenia]] have been considered in the other sections |
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| − | *[[ ICD: Schizophrenia: Known evidence of causes]] |
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| − | *[[ ICD: Schizophrenia: Theories of possible causes]] |
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| + | Considerable evidence indicates that stressful life events cause or trigger schizophrenia.<ref name="fn_15">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3595169&dopt=Abstract Day R, Nielsen JA, Korten A, Ernberg G, Dube KC, Gebhart J, Jablensky A, Leon C, Marsella A, Olatawura M et al (1987)]. Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. ''Culture, Medicine and Psychiatry'', 11 (2), 123–205<br></ref> Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.<ref name="fn_16">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11691695&dopt=Abstract Harriet L. MacMillan, Jan E. Fleming, David L. Streiner, Elizabeth Lin, Michael H. Boyle, Ellen Jamieson, Eric K. Duku, Christine A. Walsh, Maria Y.-Y. Wong, William R. Beardslee. (2001)] Childhood Abuse and Lifetime Psychopathology in a Community Sample. ''American Journal of Psychiatry'',158, 1878-83.<br></ref><ref name="fn_17">[http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TC2-4FWT420-3&_user=10&_coverDate=04%2F08%2F2005&_rdoc=1&_fmt=summary&_orig=browse&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a75a0204ebb590104747e8115cddd64a Schenkel, L.S., Spaulding, W.D., Dilillo, D., Silverstein, S.M. (2005)] Histories of childhood maltreatment in schizophrenia: Relationships with premorbid functioning, symptomatology, and cognitive deficits. ''Schizophrenia Research''<br></ref><ref name="fn_18">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14674957&dopt=Abstract Janssen I., Krabbendam L., Bak M., Hanssen M., Vollebergh W., De Graaf R., Van Os, J. (2004)] Childhood abuse as a risk factor for psychotic experiences. ''Acta Psychiatrica Scandinavica'', 109, 38-45.<br></ref> |
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| + | Evidence is also consistent that negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.<ref name="fn_70">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7991753&dopt=Abstract Bebbington P E, Kuipers E (1994)] The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. ''Psychological Medicine'', 24, 707-718.<br></ref> It is not clear whether such attitudes play a causal role in the onset of schizophrenia, although those diagnosed in this way may claim it to be the primary causal factor. The research has focused on family members but also appears to relate to professional staff in regular contact with clients.<ref name="fn_71">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14968481&query_hl=1&itool=pubmed_docsum Van Humbeeck G, Van Audenhove C. (2003)] Expressed emotion of professionals towards mental health patients. ''Epidemiologia e Psychiatria Sociale'', 12(4), 232-235. ([http://www.psychiatry.univr.it/page_eps/docs/2003_4_humbeeck.pdf full text])<br></ref> While initial work addressed those diagnosed as schizophrenic, these attitudes have also been found to play a significant role in other mental health problems.<ref name="fn_66">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10860170&query_hl=4&itool=pubmed_docsum Wearden AJ, Tarrier N, Barrowclough C, Zastowny TR, Rahill AA. (2000)] A review of expressed emotion research in health care. ''Clinical Psychology Review'', 20, 633-66.<br></ref> This approach does not blame 'bad parenting' or staffing, but addresses the attitudes, behaviors and interactions of all parties. Some go as far as to criticise the whole approach of seeking to localise 'mental illness' within one individual - the patient - rather than his/her group and its functionality, citing a [[scapegoat]] effect. |
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| − | ===Genetic and environmental influences=== |
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| + | Factors such as [[poverty]] and [[discrimination]] also appear to be involved in increasing the risk of schizophrenia or schizophrenia relapse, perhaps due to the high levels of stress they engender, or faults in diagnostic procedure/assumptions. Racism in society, including in diagnostic practices, and/or the stress of living in a different culture, may explain why minority communities have shown higher rates of schizophrenia than members of the same ethnic groups resident in their home country. The "social drift hypothesis" suggests that the functional problems related to schizophrenia, or the stigma and prejudice attached to them, can result in more limited employment and financial opportunities, so that the causal pathway goes from mental health problems to poverty, rather than, or in addition to, the other direction. Some argue that [[unemployment]] and the long-term unemployed and homeless are simply being stigmatised. |
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| − | 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 genetic vulnerability and environmental stressors can act in combination to cause schizophrenia. |
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| ⚫ | One particularly stable and replicable finding has been the association between living in an [[Urbanization|urban]] environment and schizophrenia diagnosis, even after factors such as [[drug use]], [[ethnic group]] and size of [[social group]] have been controlled for.<ref name="fn_19">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15056569 Van Os J. (2004)] Does the urban environment cause psychosis? ''British Journal of Psychiatry'', 184 (4), 287–288.<br></ref> A recent study of 4.4 million men and women in [[Sweden]] found an alleged 68%–77% increased risk of diagnosed [[psychosis]] for people living in the most urbanized environments, a significant proportion of which is likely to be described as schizophrenia.<ref name="fn_20">[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15056572 Sundquist K, Frank G, Sundquist J. (2004)] Urbanisation and incidence of psychosis and depression: Follow-up study of 4.4 million women and men in Sweden. ''British Journal of Psychiatry'', 184 (4), 293–298.<br></ref> |
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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 [[Arterial hypertension|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. |
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| + | ----- |
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| − | ====Genetic==== |
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| + | ==See also== |
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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 one identical twin does not universally develop schizophrenia if the other one does. 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|9}} (see [[twin study]]). |
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| + | ==References & Bibliography== |
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| − | However, the estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies{{Fn|10}} {{Fn|11}} showing rates as low as 11.0%–13.8% among monozygotic twins, and 1.8%–4.1% among dizygotic twins. |
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| + | <References/> |
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| + | ==Key texts== |
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| + | ===Books=== |
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| + | ===Papers=== |
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| − | A recent review of [[Genetic linkage|linkage]] studies listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing the disease{{Fn|12}}. Evidence comes from research suggesting multiple [[Chromosome|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 [[Catechol-O-methyl transferase|COMT]] that is involved in encoding the dopamine catabolic enzyme [[catechol-O-methyl transferase]]{{Fn|13}}. This is particularly interesting because of the known link between [[dopamine]] function, psychosis, and schizophrenia. |
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| + | ==Additional material== |
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| + | ===Books=== |
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| + | ===Papers=== |
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| − | There is also considerable evidence indicating that stress may trigger episodes of schizophrenia psychosis. For example, emotionally turbulent families{{Fn|14}} and stressful life events{{Fn|15}} 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|16}} {{Fn|17}} {{Fn|18}}, 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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| + | *[http://scholar.google.com/scholar?sourceid=mozclient&num=50&scoring=d&ie=utf-8&oe=utf-8&q=Schizophrenia+cause Google Scholar] |
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| + | ==External links== |
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| − | Factors such as [[poverty]] and [[discrimination]] may also be involved in increasing the risk of having a schizophrenic episode due to the high levels of stress that these lifestyles harbor. 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 hold steady or demanding, higher-paying jobs, consigning them to lower incomes thereby increasing stress levels and leaving them susceptible to lapsing into a schizophrenic episode. |
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| ⚫ | One particularly stable and replicable finding has been the association between living in an [[Urbanization|urban]] environment and |
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| − | One curious finding is that people diagnosed with schizophrenia are more likely to have been born in [[winter]] or [[spring (season)|spring]]{{Fn|21}} (at least in the [[northern hemisphere]]). However, the effect is not large and it is still not clear why this may occur. |
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| + | [[Category:Schizophrenia]] |
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| − | ===Neurobiological influences=== |
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| − | ====Early neurodevelopment==== |
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| + | {{Psych-stub}} |
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| − | 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|22}}. Similarly, studies of [[Finland|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|23}}, suggesting that even [[psychological trauma]] in the mother may have an effect. |
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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 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|24}} |
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| − | [[Image:Schizophrenia_PET_scan.jpg|frame|Data from a [[Positron emission tomography|PET]] study{{Fn|25}} suggests the less the [[frontal lobe|frontal lobes]] activated (red) during a [[working memory]] task, the greater the increase in abnormal [[dopamine]] activity in the [[striatum]] (green), thought to be related to the [[neurocognitive deficit|neurocognitive deficits]] in schizophrenia.]] |
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| − | ====Role of dopamine==== |
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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|phenothiazines]], reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment. |
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| − | However, this theory is now thought to be overly simplistic as a complete explanation, partly because 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|26}} |
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| − | ====Role of glutamate and the NMDA receptor==== |
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| − | Interest has also focused on the neurotransmitter [[glutamate]] and the reduced function of the [[NMDA receptor|NMDA glutamate receptor]] in the development of schizophrenia. This theory has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia{{Fn|27}} and the discovery that the glumatate blocking drugs such as [[phencyclidine]] and [[ketamine]] can mimic the symptoms and cognitive problems of associated with the condition.{{Fn|59}} The fact that reduced glutamate function is linked to poor performance on tests requiring [[frontal lobe]] and [[hippocampus|hippocampal]] function and that glutamate can effect [[dopamine]] function, all of which have been implicated in schizophrenia, have suggested the [[glutamate hypothesis of schizophrenia]] as an increasingly popular explanation.{{Fn|28}} Further support of this theory has come from trials showing the efficacy of molecules, which are coagonists at the NMDA receptor complex, in reducing schizophrenic symptoms. The precurosrs D-serine, glycine, and D-cycloserine all enhance NMDA function through the glycine modulatory site. Several placebo controlled trials have shown a reduction mainly in negative symptoms with high dose therapy.{{Fn|60}} Currently type 1 glycine transporter inhibitors are in late-state preclinical for the treatment of schizophrenia. They increase glycine concentrations in the brain thus causing increased NMDA receptor activation and a reduction in symptoms.{{Fn|61}} |
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| − | ====Anatomy and Physiology of the brain==== |
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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 system|ventricular]] enlargement in people diagnosed with schizophrenia, for whom negative symptoms were most prominent{{Fn|29}}. 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|30}} 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 test|neuropsychological tests]] and [[brain imaging]] technologies such as [[Functional magnetic resonance imaging|fMRI]] and [[Positron emission tomography|PET]] to examine functional differences in brain activity have shown that differences seem to most commonly occur in the [[frontal lobe|frontal lobes]], [[hippocampus]], and [[temporal lobe|temporal lobes]]{{Fn|31}}. These differences are heavily linked to the [[neurocognitive deficit|neurocognitive deficits]] which often occur with schizophrenia, particularly in areas of [[memory]], [[attention]], [[problem solving]], [[executive function]] and [[social cognition]]. |
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| − | [[Electroencephalography|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|32}} 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 that 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 [[dorsolateral prefrontal cortex|DLPFC]] in schizophrenia. {{Fn|33}} |
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Some of the causes of schizophrenia have been considered in the other sections
Environmental
Considerable evidence indicates that stressful life events cause or trigger schizophrenia.[1] Childhood experiences of abuse or trauma have also been implicated as risk factors for a diagnosis of schizophrenia later in life.[2][3][4]
Evidence is also consistent that negative attitudes towards individuals with (or with a risk of developing) schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed 'high expressed emotion' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.[5] It is not clear whether such attitudes play a causal role in the onset of schizophrenia, although those diagnosed in this way may claim it to be the primary causal factor. The research has focused on family members but also appears to relate to professional staff in regular contact with clients.[6] While initial work addressed those diagnosed as schizophrenic, these attitudes have also been found to play a significant role in other mental health problems.[7] This approach does not blame 'bad parenting' or staffing, but addresses the attitudes, behaviors and interactions of all parties. Some go as far as to criticise the whole approach of seeking to localise 'mental illness' within one individual - the patient - rather than his/her group and its functionality, citing a scapegoat effect.
Factors such as poverty and discrimination also appear to be involved in increasing the risk of schizophrenia or schizophrenia relapse, perhaps due to the high levels of stress they engender, or faults in diagnostic procedure/assumptions. Racism in society, including in diagnostic practices, and/or the stress of living in a different culture, may explain why minority communities have shown higher rates of schizophrenia than members of the same ethnic groups resident in their home country. The "social drift hypothesis" suggests that the functional problems related to schizophrenia, or the stigma and prejudice attached to them, can result in more limited employment and financial opportunities, so that the causal pathway goes from mental health problems to poverty, rather than, or in addition to, the other direction. Some argue that unemployment and the long-term unemployed and homeless are simply being stigmatised.
One particularly stable and replicable finding has been the association between living in an urban environment and schizophrenia diagnosis, even after factors such as drug use, ethnic group and size of social group have been controlled for.[8] A recent study of 4.4 million men and women in Sweden found an alleged 68%–77% increased risk of diagnosed psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be described as schizophrenia.[9]
See also
References & Bibliography
- ↑ Day R, Nielsen JA, Korten A, Ernberg G, Dube KC, Gebhart J, Jablensky A, Leon C, Marsella A, Olatawura M et al (1987). Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. Culture, Medicine and Psychiatry, 11 (2), 123–205
- ↑ Harriet L. MacMillan, Jan E. Fleming, David L. Streiner, Elizabeth Lin, Michael H. Boyle, Ellen Jamieson, Eric K. Duku, Christine A. Walsh, Maria Y.-Y. Wong, William R. Beardslee. (2001) Childhood Abuse and Lifetime Psychopathology in a Community Sample. American Journal of Psychiatry,158, 1878-83.
- ↑ Schenkel, L.S., Spaulding, W.D., Dilillo, D., Silverstein, S.M. (2005) Histories of childhood maltreatment in schizophrenia: Relationships with premorbid functioning, symptomatology, and cognitive deficits. Schizophrenia Research
- ↑ Janssen I., Krabbendam L., Bak M., Hanssen M., Vollebergh W., De Graaf R., Van Os, J. (2004) Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatrica Scandinavica, 109, 38-45.
- ↑ Bebbington P E, Kuipers E (1994) The predictive utility of expressed emotion in schizophrenia: an aggregate analysis. Psychological Medicine, 24, 707-718.
- ↑ Van Humbeeck G, Van Audenhove C. (2003) Expressed emotion of professionals towards mental health patients. Epidemiologia e Psychiatria Sociale, 12(4), 232-235. (full text)
- ↑ Wearden AJ, Tarrier N, Barrowclough C, Zastowny TR, Rahill AA. (2000) A review of expressed emotion research in health care. Clinical Psychology Review, 20, 633-66.
- ↑ Van Os J. (2004) Does the urban environment cause psychosis? British Journal of Psychiatry, 184 (4), 287–288.
- ↑ Sundquist K, Frank G, Sundquist J. (2004) Urbanisation and incidence of psychosis and depression: Follow-up study of 4.4 million women and men in Sweden. British Journal of Psychiatry, 184 (4), 293–298.
Key texts
Books
Papers
Additional material
Books
Papers
External links
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