Brain Factors That Influence Psychopathy
Psychopathy is among the conditions that burden the performance of most global states in the current contemporary society. A variety of factors causes psychopathy. The factors include biological, environmental, and brain factors. Psychopathy presents with different symptoms including, violence, deceitfulness, aggression, irresponsibility, lack of guilt, and impulsiveness among other symptoms associated with it. Significant researches conducted in the past have failed to create an understanding of the brain factors that cause the psychopathy. Therefore, the following essay presents an analysis of the brain factors that cause the psychopathy. The analysis presents results obtained from studies conducted to create an understanding of the relationship.
According to Verona, Sprague, and Sadeh (2012) psychopathy refers to a condition characterized by diminished abilities for remorse and low abilities to control behaviors. Cale and Lilienfeld (2002) show in their definition that defining psychopathy should not only focus on the antisocial behaviors an individual presents with but also the emotional impairment such as lack of guilt. Individuals with psychopathy present with a variety of symptoms such as impulsiveness, irritability, lack of guilt, bullying, and irresponsibility among other symptoms. The risk factors associated with psychopathy include parental inconsistency, family dysfunction, history of individual abuse, and family history of the disorder among other risks factors. Therefore, this essay presents an analysis of the brain factors that have a high relationship with psychopathy.
Brain factors that cause psychopathy
While significant evidence has shown psychopathy to be associated with criminal behaviors such as murder and rape, Anderson et al., (2014) recognize that the biological mechanism of psychopathy is poorly understood. For instance, few researches have been conducted to bring an indulgence of the association between the impaired function of particular regions of brain and psychopathy. According to Cale & Lilienfeld (2002), psychopathy occurs due to the impairment of the amygdala. Amygdala regulates instrumental learning and aversive conditioning alongside sad facial expressions and fearful behaviors. However, impairment in the functioning of the amygdala results in psychopathy due to the functional impairments associated with it. A study conducted by Anderson et al., (2014) confirmed the involvement of the amygdala in causing psychopathy. In the study, two modern imaging studies showed that reduced amygdaloid volume is associated with high rates of psychopathy. Similarly, individuals with reduced amygdaloidal volume caused low-PCL-R scores during the processing of verbal words of negative valence (Anderson et al., 2014).
Significant evidence has that individuals presenting with psychopathy have dysfunctional neural systems. As such, basing on the above, imaging studies reveal that psychopathy and its related behaviors such as violent offending are associated with dysfunction of the frontal cortex. Volumetric MRI study performed by Coid and Ullrich (2010) showed that individuals who presented with psychopathy had reduced prefrontal gray matter volume. The authors postulated that a high correlation exists between the reduced size of the prefrontal cortex and psychopathy between the participants. Moreover, the failure of the orbitofrontal cortex (OFC) has been highly linked to symptoms among psychopaths. The orbitofrontal cortex (OFC) performs the responsibility of receiving extensive projections from the cortex and sends them to the amygdala. It also regulates instrumental learning and reversal responses that are often impaired in individuals with psychopathy (Verona, Sprague, & Sadeh, 2012). As such, impairment of the orbitofrontal cortex (OFC) causes psychopathy.
Similarly, lesions of the orbitofrontal cortex (OFC) have shown a great association with psychopathy among the patients presenting with psychopathy. Lesions of the orbitofrontal cortex cause a neurological condition referred to as acquired psychopathy that is evidenced by aggression and socially undesired behaviors. Moreover, lesions of the orbitofrontal cortex (OFC) cause impairment of the basic brainstem modulating mechanisms that control flight-flight responses to threat, thereby, psychopathy. Verona, Sprague, and Sadeh (2012) found that the pathology affecting the noradrenergic system could cause severe dysfunction of the amygdala. Therefore, there is a high relationship between the pathology of the amygdala functioning, orbitofrontal cortex, and noradrenergic and psychopathy.
Moreover, the individual’s lifestyle has a high relationship with psychopathy. Significant evidence shows that one’s lifestyle might exacerbate neurological impairments that cause the psychopathy. For example, substance abuse causes apparent impairment due to the disturbance of the functions that are mediated by the orbitofrontal cortex. Similarly, chronic amphetamine abuse results in OFC dysfunction, thereby, predisposing to psychopathy. According to Cale & Lilienfeld (2002), substance abuse affects the functioning of the amygdala, a fact considered contributing significantly to psychopathy. Therefore, Anderson et al., (2014) recommends lifestyle modification as among the strategies that should be adopted to prevent occurrences of psychopathy.
Apart from the above, Harmer et al., (2009) postulate that an excellent relationship exists between the brain developments of an individual with psychopathy. Research shows that individuals with a history of abnormalities in their central nervous system development are two at risk of developing psychopathy as compared to those with a history of normal development of the central nervous system. Among the abnormalities that have a high correlation with psychopathy include hyperactivity, learning disorders, and personality disorders.
Moreover, Ogloff (2006) recognizes that protein deficiency in the brain increases the likelihood of psychopathy as evidenced by imaging studies of the brains of the affected individuals. Evidence has that deficiency of proteins in the brain increases the likelihood of a reduction in the concentration of DNA in the forebrain, thereby, psychopathy. Maternal behaviors during infancy also influence the predisposition of a child to psychopathy at their later stages of life. For example, children born to mothers who abuse alcohol shows a high risk of psychopathy. Abuse of alcohol causes fetal alcohol syndrome that contributes to structural and functional brain deficits, hence, psychopathy. Similarly, behaviors such as smoking during pregnancy increase the risks of violence and antisocial behaviors of the born child due to the involvement of the brain, hence, the disorder. Violence occurs due to a reduction in the oxygen levels in the fetal brain, a fact that causes structural and functional deficits of the brain, thereby, psychopathy (LaBrode, 2007).
Earlier studies conducted by Verona, Sprague, & Sadeh (2012) and Warren & South (2006) showed that the dysfunction of other brain parts other than the ones identified above causes psychopathy. Such areas include the uncinate fasciculus (UF) and the white matter that links the amygdala and the OFC cause psychopathy. The pathology of the above regions affects the fundamental functioning of the regions involved, thereby, the psychopathy. Early health factors such as birth complications also play a part in contributing to structural deficits of the brain that contribute to psychopathy. Birth complications cause cell death in the hippocampus that is highly linked to psychopathy and violence. Similarly, environmental factors have been shown to contribute to psychopathy. Such environmental factors include head injury that affects the normal functioning of the brain, a fact considered contributing to psychopathy. Head injury also causes imbalances in the neurotransmitter and component functioning, thereby, psychopathy (Anderson et al., 2014).
In summary, brain factors play a significant role in contributing to psychopathy. Aside from environmental and biological factors, brain factors such as brain injury, dysfunction of the amygdala and the OFC cause psychopathy. It is appreciable that preventive strategies should be adopted. Such strategies include minimizing the contributing factors such as lifestyle modification, injury prevention, early diagnosis, and management. Above all, health education plays a critical role in reducing incidences of psychopathy by creating public awareness and ensuring the adoption of socially friendly strategies that recognize the needs of the affected in the society.
Anderson, J.L., et al., (2014). Examining the Associations between Section III Antisocial Personality Disorder Traits and Psychopathy in Community and University Samples. Journal of Personality Disorders, 12(3), 1-23.
Cale, E.M., & Lilienfeld, S.O. (2002). Histrionic Personality Disorder and Antisocial Personality Disorder: Sex-Differentiated Manifestations of Psychopathy?. Journal of Personality Disorders, 16(1), 52-72.
Coid, J., & Ullrich, S. (2010). Antisocial Personality Disorder Is On A Continuum With Psychopathy. Comprehensive Psychiatry, 51(4), 426-433.
Harmer, C., Perrett, D., Cowen, P., & Goodwin, G. (2001). Administration of the beta-adrenoceptor blocker propranolol impairs the processing of facial expressions of sadness. Psychopharmacology, 154(4), 383-389.
LaBrode, R.T. (2007). Etiology of the Psychopathic Serial Killer: An Analysis of Antisocial Personality Disorder, Psychopathy, and Serial Killer Personality and Crime Scene Characteristics. Brief Treatment and Crisis Intervention, 7(2), 151-160.
Ogloff, J.R. (2006). Psychopathy/antisocial Personality Disorder Conundrum. Australian and New Zealand Journal of Psychiatry, 40(6-7), 519-528.
Verona, E., Sprague, J., & Sadeh, N. (2012). Inhibitory control and negative emotional processing in psychopathy and antisocial personality disorder.. Journal of Abnormal Psychology, 12, 121-138.
Warren, J.I., & South, S.C. (2006). Comparing the constructs of antisocial personality disorder and psychopathy in a sample of incarcerated women. Behavioral Sciences & the Law, 24(1), 1-20.
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