Social Recovery of Cognitive Disorder
Cognitive disorders (including mental illness and brain injury) affect a multitude of species, communities, and cultures; with high incidence in the global burden of disease in humans (Elstad and Eide, 2017). Recent research indicates that social cognition is unique in its functional effects, exceeds that of basic cognition, and has the ability to mediate between neuro-cognition and functionality in some mental health disorders (Horan et al., 2008; Schmidt et al., 2011). As a result, mental health treatments and policies are sometimes driven by the integration and inclusion of patients within the social environment (Elstad and Eide, 2017).
Social support, defined as positive interactions provisioned by individuals, groups, and the wider community, has been associated with levels of cortisol in the brain. In a review of literature, Uchino (2006) referenced several papers, consistently finding decreased cortisol levels where social support was high, indicating the neurochemical implications of social interaction. Cortisol has been observed to play a complex part in the development of major depressive disorder, via the disturbance of circadian rhythms (wake/sleep cycles) and a resistance to glucocorticoid negative feedback mechanisms (regulation of the stress response) where cortisol levels are elevated (Herbert, 2012; Herman et al., 2012). Therefore, evidence suggests positive social support can provide resilience to stressors, resulting in reduced neuroendocrine responses, and subsequently, reduced depressive symptoms. It is interesting to note comments frequently made regarding the interaction of genes, and the environment in the development of mental health disorders. Uchinio (2006) makes reference to the genetic vulnerabilities for cognitive deficits, suggesting that the social environment can merely support, or counter, a heritable predisposition for mental illness. Should this be true, health care policy should arguably place greater emphasis on the identification and treatment of at-risk patients early on in life as a preventative measure against future maladaptive thought processes.
An additional factor causing cognitive deficits, traumatic brain injury (TBI), can be remediated by environmental enrichment, including social interaction. TBI is a critical issue in humanity, in terms of health, socio-economy, and social integration, with individuals suffering long-term cognitive defects (Cristofori and Levin, 2015) and, in some cases, further decline (Frasca et al., 2013). Patients have been seen to evolve differently from TBI cases, depending on a variety of factors, including: severity, mechanisms involved, and the brain regions affected (Cristofori and Levin, 2015), hence rehabilitation programs should focus on targeted recovery, perhaps employing the theory of the Social Brain. As stated in a previous post, the cognitive demands of social integration required evolution to cope with these interactions. Therefore, social recovery may help improve cognition post-injury, by causing the brain to evolve and cope with the social environment, in spite of lesions.
Johansson (2004) investigated the reaction of laboratory rats to induced acute cerebral trauma in varying housing conditions. Those kept in enriched environments with increased social interaction, larger cages, and greater opportunity for physical activity, were seen to have improved functional outcome compared to those kept in more rudimentary environments. Not only this, but further observation saw the altered activation of genes, increased branching of dendrites, and an increase in the number of contra-lateral cortex dendritic spines (key in synaptic transmission in memory, attention, perception and awareness). Johansson (2004) concluded that clinical attention should focus on how the environment can inform specific interventions to help target cognitive rehabilitation and recovery, as evidence shows the socially-induced changes in brain morphology which adapt the patient to their new cognitive capabilities.
In conclusion, high quality social support can increase stress-resistance, mediate the effects of depressive-neurotransmitters, and decrease the functional effects of trauma-related brain deficits (Ozbay et al., 2007). Research such as this can help to inform potential therapies and rehabilitative treatments for patients of TBI. Survivors, despite returning to positive and fulfilled home environments, can still be subject to emotional, physical, and cognitive maladaptations, resulting in an inability to engage effectively in the social environment (Frasca et al., 2013). Treatments which help patients to adapt to the social setting (even with altered cognitive functioning) can promote recovery long-term, and prevent further decline. However, more in-depth research still needs to be done so that effective therapies can be introduced. For instance, investigating the specific characteristics of social interaction that aid recovery can help to provide clarity on how to treat people effectively.
References
Cristofori, I. and Levin, H.S., 2015. Traumatic brain injury and cognition. In Handbook of clinical neurology. 128(issue unknown), pp.579–611.
Elstad, T.A. and Eide, A.H., 2017. Social participation and recovery orientation in a “low threshold” community mental health service: An ethnographic study. Cogent Medicine. 4(1), pp.1362840.
Frasca, D., Tomaszczyk, J., McFadyen, B.J. and Green, R.E., 2013. Traumatic brain injury and post-acute decline: what role does environmental enrichment play? A scoping review. Frontiers in human neuroscience. 7(issue unknown), p.31.
Herbert, J. 2013. Cortisol and depression: three questions for psychiatry. Psychological Medicine. 43(3), pp.449–469.
Herman, J.P., McKlveen, J.M., Solomon, M.B., Carvalho-Netto, E. and Myers, B. 2012. Neural regulation of the stress response: glucocorticoid feedback mechanisms. Brazilian Journal of Medical and Biological Research. 45(4), pp.292–298.
Horan, W.P., Kern, R.S., Green, M.F. and Penn, D.L., 2008. Social cognition training for individuals with schizophrenia: emerging evidence. American Journal of Psychiatric Rehabilitation. 11(3), pp.205–252.
Johansson, B.B. 2004. Functional and cellular effects of environmental enrichment after experimental brain infarcts. International Journal of Psychology. 39(5–6), pp.158–158.
Ozbay, F., Johnson, D.C., Dimoulas, E., Morgan III, C.A., Charney, D. and Southwick, S., 2007. Social support and resilience to stress: from neurobiology to clinical practice. Psychiatry (Edgmont). 4(5), pp.35.
Schmidt, S.J., Mueller, D.R. and Roder, V. 2011. Social Cognition as a Mediator Variable Between Neurocognition and Functional Outcome in Schizophrenia: Empirical Review and New Results by Structural Equation Modeling. Schizophrenia Bulletin. 37(issue unknown), pp.S41-S54.
Uchino, B.N. 2006. Social support and health: A review of physiological processes potentially underlying links to disease outcomes. Journal of Behavioral Medicine. 29(4), pp.377–387.