Causes

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Schizophrenia is not due to a single cause. As with other common chronic diseases, such as diabetes and heart diseases, it is believed that schizophrenia develops as a result of a number of concomitant factors.

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Stock photo. Posed by model.

Genetic and environmental factors, or a perinatal brain damage can significantly contribute to the development of the disease.1, 13

Each of these factors can increase the risk of psychotic symptoms in certain people; these symptoms can be triggered by various life situations or events such as social isolation or stress, in particular in young adulthood.

The use of street drugs (such as cannabis) can also be associated with the development of schizophrenia and transitory psychotic symptoms.1

Mental illness specialists agree that the symptoms of schizophrenia stem from problems in information transmission and processing in the brain [APA Clinical Guidelines, 2004].1

These problems develop when the communication resulting from normal release of chemicals between the neurons in the brain is disturbed.9

Though the development of schizophrenia cannot be prevented, the occurrence frequency of schizophrenia symptoms (known as a “psychotic episode”) can be controlled and even reduced with proper treatment.1

  • References

    1. APA Clinical Guidelines. American Psychiatric Association. Practice guidelines for the treatment of patients with schizophrenia. 2004
    2. Falkai P et al. World J Biol Psychiatry 2005; 6: 132-191.
    3. Kendler KS et al. Arch Gen Psychiatry 1996; 53: 1022-1031.
    4. World Health Organization. The World Health Report: 2001: Mental health: new understanding, new hope.
    5. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th Edition Text Revision (DSM-IV-TR). Arlington: American Psychiatric Publishing Inc. 2000.
    6. Lieberman JA et al. J Clin Psychiatry 1996; 57(suppl 9): 5-9.
    7. Breier A et al. Am J Psychiatry 1994; 151: 20-26.
    8. Robinson DG et al. Am J Psychiatry 1999; 156: 544-549.
    9. National Institute for Clinical Excellence. National Clinical Practice Guidelines Number 82.
    10. Howard R et al. Am J Psychiatry 2000; 157: 172-178.
    11. Angermeyer MC et al. Schizophr Bull 1990; 16: 293-307.
    12. Murray RM and Fearon P. J Psychiatr Res 1999; 33: 497-499.
    13. Lang UE et al. Cell Physiol Biochem 2007; 20: 687-702.
    14. Harrigan SM et al. Psychol Med 2003; 33: 97-110.
    15. Bottlender R et al. Schizophr Res 2003; 62: 37-44.
    16. Lynn Starr h. et al: Comparison of long-acting and oral antipsychotic treatment effects in patients with schizophrenia, comorbid substance abuse, and a history of recent incarceration: An exploratory analysis of the PRIDE study; Schizophr Res. 2018 Apr;194:39-46. doi: 10.1016/j.schres.2017.05.005. Epub 2017 Jun 7
    17. Awad AG et al. Pharmacoeconomics 2008; 26: 149-162.
    18. Keith SJ et al. Psychiatr Serv 2004; 55: 997-1005.
    19. Lieberman JA et al. Pharmacol Rev 2008; 60: 358-403.
    20. Tandon R et al. Psychoneuroendocrinology 2003; 28(suppl 1): 9-26.
    21. Wyatt RJ. Schizophr Bull 1991; 17: 325–351
    22. Robinson DG et al. Arch Gen Psychiatry 1999; 56: 241-247.
    23. Weiden PJ et al. Psychiatr Serv 2004; 55: 886-891.
    24. Koen L et al. Psychosomatics 2007; 48: 128-134.
    25. Novick D et al. Psychiatry Res 2010; 176: 109-113.
    26. Kozma CM et al. Changes in schizophrenia-related hospitalization and ER use among patients receiving paliperidone palmitate. Current Medical Research and Opinion. 2011.27;1603-1611

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