Schizophrenia

Schizophrenia

The Role of Social Environment and Stress in the Aetiology and Course of Schizophrenia

DSM-V Diagnostic Criteria for Schizophrenia

Schizophrenia is a mental condition characterized by physical agitation, incoherence, hallucinations, and delusions. The condition is classified as a thought disorder. The condition is diagnosed based on the DSM-V diagnostic criteria (Tandon et al. 2003). According to the DSM-V diagnostic criteria, to be diagnosed with schizophrenia, three basic diagnostic criteria should be met as outlined below.

1. Identifying symptoms: Two or more of the symptoms outlined below should manifest for much of the period during a month’s time (or for lesser time if the symptoms subside with treatment) (Tandon et al. 2003).

• Hallucinations
• Delusions
• Disorganization is speech that manifests as a result of thought disorder (criterion is met if the severity of the disorganization can impair communication)
• Negative symptoms such as avolition, alogia or affective flattening
• Catatonic or grossly disorganized behaviour

Note: Only one symptom is necessary for diagnosis from the above list if the presenting delusions are bizarre or the manifest hallucinations include voices that keep a running commentary on the patient’s thoughts or behaviours, or if there two or more conversing voices (Tandon et al. 2003).

2. Occupational/Social dysfunction: One or more major functional areas such as self-care, interpersonal relations, and work should be significantly below the level achieved before the onset of the condition for a significant part of the time since the start of the disturbance presented (Tandon et al. 2003).
3. Duration: The disturbance signs should persist for at least six months, and this period must be marked with at least a month of active manifestations of symptoms, which meet criterion one (or for lesser time if the symptoms subside with treatment) (Tandon et al. 2003).

Schizophrenia may not be diagnosed if schizoaffective disorder and mood disorder are notably present, or if the manifest signs are caused by physiological results of medication or substance abuse. Additionally, the condition cannot be diagnosed if there is a history of pervasive developmental disorders or its symptoms. The exemption to this may only occur if prominent hallucinations and delusions are also present for at least one month or less if treated (Tandon et al. 2003).

The Role of Different Factors in the Incidence and Course of Schizophrenia

            The aetiology of schizophrenia has been a subject of a contentious debate. Studies informing this debate have shown that early environment, prenatal development, childhood trauma, migration, neurobiology and social, and psychological processes are significant determinants of the condition’s occurrence (Meyer-Lindenberg, 2010). Even though no outright cause of the condition has been identified, scholars in related fields believe the condition is a result of brain acquired or inherited vulnerabilities coupled with life’s events. The probability of developing the condition has been found to increase as social adverse factors such as social exclusion and socioeconomic disadvantage increase in childhood (Wicks et al. 2005; Mueser & McGurk, 2004). According to Selten and Cantor-Graae (2005), these adverse factors cause social stress, which underlies the condition especially when persistent.  According to Meyer-Lindenberg (2010), social stress may play an out through activation of dopaminergic sensitization and the hypothalamic–pituitary–adrenal axis, which negatively impacts the brain (Lieberman, Sheitman & Kinon, 1997). Immigration and urbanicity have also been cited as possible environmental stressors that are a potential risk factor for schizophrenia (Selten and Cantor-Graae, 2005). In fact, MacCabe and Nicholas (2012) have shown that urban upbringing is linked to twice the rate of schizophrenia when compared to rural upbringing. This suggests that the socio-cultural environment has a significant role in determining the occurrence of the condition. The difference in environment is perhaps a reflection of the difference in stress levels within the different environments. According to MacCabe and Nicholas (2012), the occurrence of the condition is also influenced by marginalization and social inferiority often experienced among minority groups. This influence is linked to social defeat due to ‘outsider status,’ psychosocial adversity, poor housing, unemployment, and racial discrimination (Selten and Cantor-Graae, 2005). In a nutshell, stressful events precede the condition’s occurrence (Day et al. 1987). Social environment influences such as substance use-especially cannabis- has also been shown to increase the risk of developing the condition (MacCabe & Nicholas, 2012). The use of other drugs such as Ketamine, amphetamine and ecstasy has also been shown to precipitate the experienced psychotic states that characterize the condition. Childhood antecedents are also a major influence in determining the possible occurrence of the condition, and these rely both on developmental progress and family involvement as measured in terms of understanding and skills (Jones et al. 1994). As an example, solitary play preferences, social anxiety at an early age and mother’s skills have been found to have a direct relation with the occurrence of schizophrenia (Jones et al. 1994).  Apart from socio-cultural and environmental factors, Cromwell (1993), states that schizophrenia runs in families, and is thus genetically influenced. The fact that the condition may run in families is attested to by the fact that an estimated 89% schizophrenics have a known schizophrenic relative in their lineage. Sullivan et al. (2003), also shows that results from family and twin studies show that the condition has a degree of heritability of approximately 80%. However, concordance is about 50% for identical twins, and thus suggesting that environmental, epigenetic and most likely stochastic factors also have a significant influence (Sullivan et al. 2003; Gogos, Kvajo, & McKellar, 2012). In relation to this, Cromwell (1993) concludes that the pathogenesis of the condition is a result of interplay of genetic and environmental factors.

The alternative explanation for the role of these social factors finds its basis in Cromwell’s (1993) conclusion, which assigns the social factors a predisposition role rather than a primary role in the pathogenesis of the condition. Although the condition is strongly linked to genetic heredity, there is also evidence to show that not all cases of the condition are a result of heredity. In fact, not all people that have schizophrenia-linked genes develop schizophrenia (Carlson, 2013). Recent research efforts suggest that genetic vulnerability to the condition is multifactorial, and it depends on the interaction of various genes and the environment (Owen, Craddock & O’Donovan, 2005). This approach that is widely adopted is termed as the ‘stress-vulnerability’ model (Zubin, 1977). The social factors highlighted are thus assumed to be predisposing factors, which determine if an individual will develop the condition when exposed to a certain environment. Meyer-Lindenberg (2010) shows how the social factors intervene at physiological level to create conditions that favor the development of schizophrenia. One such proposed mechanism is the activation of dopaminergic sensitization and the hypothalamic–pituitary–adrenal axis by various stress agents (Meyer-Lindenberg, 2010). Even though, direct evidence for the hypothesis is not available, experimental studies offer a link to key neural system features that are implicated in the risk of the condition. In animals, stress increases the dopaminergic neurons’ rate of firing in the mid-brain and activities in the ventral striatum, which depend on brain-derived neurotrophic factor (BDNF) (Meyer-Lindenberg, 2010).  This shows an association to neural plasticity for which the BDNF gene associated with schizophrenia is essential, and also to the pathogenesis of psychosis outlined. Though specific findings have not yet been determined in humans, psychosocial stress evokes dopamine release in the striatum (Meyer-Lindenberg, 2010). These results link the environmental risk in social factors to the physiological precedents that lead to the development of the condition in people already predisposed to the condition due to their genetic makeup. The social factors are therefore an essential ingredient in the development of the condition, but they cannot solely lead to the development of the condition. Similarly, genes cannot be a sole cause because there is no clear Mendelian pattern of transmission yet established between generations and also because there is no specificity of genetic transmission identified (Cromwell, 1993; Blasi & Bertolino, 2009).

The dynamics of these social and biological factors in causing the development of the condition support the model of schizophrenia as a brain disease. Diseases often require genetic predisposition and favorable environments in order to thrive or invade. The above highlighted information shows that schizophrenia is indeed a disease like any other, and it can be modeled on this same framework showing dependency on the two factors in order to establish and thrive. The biological and social factors therefore play a double role-that of development and establishment of the disease as well as the progression of the condition. As such, the role of these factors can be integrated into the disease model of the condition as part of the factors that determine its establishment and progression.

 

 References

 

Blasi, G. & Bertolino, A. (2009). The Genetics of Schizophrenia. Neuroscience, vol. 164, pp. 288-299.

Carlson, N. R. (2013). Physiology of Behavior, 11th edition, Pearson Education, Limited p.568.

Cromwell, L. R. (2003). Searching for the origins of schizophrenia. Psychological Science, vol. 4 (5), pp. 276-0279

Day R, Nielsen JA, Korten A et al. (1987). Stressful life events preceding the acute onset of schizophrenia: a cross-national study from the World Health Organization. Cult Med Psychiatry, vol. 11 (2), pp. 123–205.

Gogos, J. A. Kvajo, M. & McKellar, H. (2012). Avoiding Mouse Traps in Schizophrenia Genetics: Lessons and promises from current and emerging Mouse Models. Neuroscience, vol. 211, pp. 136–164.

Jones, P. Rodgers, B. Murray, R. & Marmot, M. (1994). Child development risk factors for adult schizophrenia in the British 1946 birth cohort. Lancet, vol. 344 (8934), pp. 1398–402.

Lieberman, J. A., Sheitman, B. B. & Kinon, B. J. (1997). Neuro-chemical sensitization in the pathophysiology of schizophrenia: Deficits and dysfunction in neuronal regulation and plasticity. Neuropsychopharmacology, vol. 17, pp. 205–229.

MacCabe, H. J. & Nicholas, M. (2012). Schizophrenia, Journal of Psychiatric Disorders, vol. 40 (11), pp. 586-590.

Meyer-Lindenberg, A. (2010). From maps to mechanisms through neuro-imaging of schizophrenia. Nature, vol. 468 (11), pp.194-202.

Mueser, K. T. & McGurk, S. R. (2004). Schizophrenia. The Lancet, vol. 363 (9426), pp. 2063–72.

Owen, M. J. Craddock, N. & O’Donovan, M. C. (2005). Schizophrenia: genes at last? Trends Genet, vol. 21 (9), pp. 518–25.

Selten, J. P. & Cantor-Graae, E. (2005). Social defeat: risk factor for schizophrenia? British. Journal of Psychiatry, vol. 187, pp.101–102.

Sullivan, P.F. Kendler, K. S. & Neale, M. C. (2003). Schizophrenia as a complex trait: Evidence from a meta-analysis of twin studies. Arch Gen Psychiatry, vol. 60, pp. 1187–1192.

Tandon, R., et al., (2003). Definition and description of schizophrenia in the DSM-5, Schizophrenia. Res, vol. 50 (1), pp. 1-8.

Wicks. S. Hjern, A. Gunnell. D. Lewis, G. & Dalman, C. (2005). Social adversity in childhood and the risk of developing psychosis: A national cohort study. The American Journal of Psychiatry, vol. 162 (9), pp.103–26.

Zubin, J. & Spring, B. (1977). Vulnerability–a new view of schizophrenia. J Abnorm Psychol, vol. 86 (2), pp. 103–26.

 

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