Schizophrenia causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
Schizophrenia is a psychiatric diagnosis that describes a mental disorder characterized by impairments in the perception or expression of reality and by significant social or occupational dysfunction.
The causes of schizophrenia have been the subject of much debate over many decades with various factors proposed and discounted. To date none has been fully elucidated, but evidence suggests that genetic vulnerability and environmental stressors act in combination to result in schizophrenia.
Studies suggest that genetics, early environment, neurobiology and psychological and social processes are important contributory factors. Current psychiatric research into the development of the disorder often focuses on the role of neurobiology, although a reliable and identifiable organic cause has not been found. In the absence of a confirmed specific pathology underlying the diagnosis, some question the legitimacy of schizophrenia's status as a disease. Furthermore, some propose that the perceptions and feelings involved are meaningful and do not necessarily involve impairment. Although no common cause of schizophrenia has been identified in all individuals diagnosed with the condition, currently most researchers and clinicians believe it results from a combination of both brain vulnerabilities (either inherited or acquired) and stressful life-events. This widely-adopted approach is known as the 'stress-vulnerability' model, and much scientific debate now focuses on how much each of these factors contributes to the development and maintenance of schizophrenia.
It is also thought that processes in early neurodevelopment are important, particularly prenatal processes. In adult life, 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. However, this theory is now thought to be overly simplistic as a complete explanation. These drugs have now been developed further and antipsychotic medication is commonly used as a first-line treatment. Although effective in many cases, these medications are not well tolerated by some patients due to significant side-effects. The positive symptoms are more responsive to medications; negative symptoms being less so.
Differences in brain structure have been found between people with schizophrenia and those without. However, these tend only to be reliable on the group level and, due to the significant variability between individuals, may not be reliably present in any particular individual. Significant brain atrophy and enlarged ventricles are the most conspicuous of such differences.
Causes
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), evidence suggests that genetic vulnerability and environmental stressors can act in combination to result in diagnosis of schizophrenia.[1]
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 diagnosis of complex inheritance. Thus, it is likely that several genes interact to generate risk for schizophrenia or for the separate components that can co-occur to lead to a diagnosis.[2] 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.
It is thought that causal factors can initially come together in early neurodevelopment, including during pregnancy, to increase the risk of later developing schizophrenia. One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring[3] (at least in the northern hemisphere). However, the effect is not large. Some researchers postulate that the correlation is due to viral infections during the third trimester (4–6 months) of pregnancy. There is now significant evidence that prenatal exposure to infections increases the risk for developing schizophrenia later in life, providing additional evidence for a link between in utero developmental pathology and risk of developing the condition.[4]
Schizophrenia is most commonly first diagnosed during late adolescence or early adulthood suggesting it is often the end process of childhood and adolescent development. Studies have indicated that genetic dispositions can interact with early environment to increase the risk of developing schizophrenia, including through global neurobehavioral deficits,[5] a poorer family environment and disruptive school behaviour,[6] poor peer engagement, immaturity or unpopularity[7] or poorer social competence and increasing schizophrenic symptomology emerging during adolescence[8] These developmental problems have also been linked to socioeconomic disadvantage or early experiences of traumatic events.[9]
There is on average a somewhat earlier onset for men than women, with the possible protective influence of the female hormone oestrogen being one hypothesis made and sociocultural influences another.
Other
Calcium channel abnormalities are currently being explored as a factor in schizophrenia. Related to this, three small studies have found some improvements on some measures, in schizophrenia with tardive dyskinesia, with the calcium channel blocking agent nilvadipine added to an existing antipsychotic regimen[10]
Currently, there is growing evidence of the crucial role of autoimmunity in the etiology and pathogenesis of schizophrenia. This can be seen as a study of the statistical correlation schizophrenia with other autoimmune diseases[11] and the recent work on the direct detailed study immune status of patients with schizophrenia.[12][13]
References
- ↑ Harrison PJ, Owen MJ. (2003). Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet, 361(9355), 417–9. PMID 12573388
- ↑ Owen MJ, Craddock N, O'Donovan MC. (2005). Schizophrenia: genes at last? Trends in Genetics, 21(9), 518–25. PMID 16009449
- ↑ Davies G, Welham J, Chant D, Torrey EF, McGrath J. (2003). A systematic review and meta-analysis of Northern Hemisphere season of birth studies in schizophrenia. Schizophrenia Bulletin, 29 (3), 587–93. PMID 14609251
- ↑ Brown, A.S. (2006). Prenatal infection as a risk factor for schizophrenia. Schizophrenia Bulletin, 32 (2), 200–2. PMID 16469941
- ↑ Hans SL, Marcus J, Nuechterlein KH, et al (1999). Neurobehavioral deficits at adolescence in children at risk for schizophrenia: The Jerusalem Infant Development Study. Arch Gen Psychiatry. 56(8):741–8. PMID 10435609
- ↑ Carter JW, Schulsinger F, Parnas J, Cannon T, Mednick SA. (2002). A multivariate prediction model of schizophrenia. Schizophrenia Bulletin 28(4):649–82. PMID 12795497
- ↑ Hans SL, Auerbach JG, Asarnow JR, Styr B, Marcus J. (2000). Social adjustment of adolescents at risk for schizophrenia: the Jerusalem Infant Development Study. J Am Acad Child Adolesc Psychiatry. 39(11):1406–14. PMID 11068896
- ↑ Dworkin RH, Bernstein G, Kaplansky LM, et al (1991). Social competence and positive and negative symptoms: a longitudinal study of children and adolescents at risk for schizophrenia and affective disorder. Am J Psychiatry. Sep;148(9):1182–8. PMID 1882996
- ↑ Read J, Perry BD, Moskowitz A, Connolly J (2001). The contribution of early traumatic events to schizophrenia in some patients: a traumagenic neurodevelopmental model. Psychiatry, 64, 319-45. PMID 11822210Full text) (PDF), Retrieved on 2007-05-16
- ↑ Yamada K, Ashikari I, Onishi K, Kanba S, Yagi G, Asai M. (1995). Effectiveness of nilvadipine in two cases of chronic schizophrenia. Psychiatry Clin Neurosci. Aug;49(4):237–8. PMID 9179944
- ↑ Eaton WW, Byrne M, Ewald H, Mors O, Chen CY, Agerbo E, Mortensen PB (2006). Association of Schizophrenia and Autoimmune Diseases: Linkage of Danish National Registers. American Journal of Psychiatry 163, 521–528. PMID 16513876
- ↑ Jones AL, Mowry BJ, Pender MP, Greer JM. (2005). Immune dysregulation and self-reactivity in schizophrenia: do some cases of schizophrenia have an autoimmune basis? Immunol Cell Biol, 83 (1), 9–17. PMID 15661036
- ↑ Strous RD, Shoenfeld Y (2006). Schizophrenia, autoimmunity and immune system dysregulation: a comprehensive model updated and revisited. Journal of Autoimmunity 2006 Sep;27(2):71–80. PMID 16997531