Anatomical Basis of Antisocial Personality Disorder
Updated: Jan 31, 2023
Mr. Ovioke David, Research Assistant, University of Ilorin Nigeria DOI: 10.5281/zenodo.7524641 Email ID: Oviokedavid@gmail.com
Abstract:
This literature review discusses the anatomical basis of antisocial personality disorder, including research concerning its etiology, prevalence, physiological and hormonal regulation, diagnosis and treatment. Antisocial personality disorder (ASPD) is a chronic mental condition that is characterized by a long-term violation of the right of others, disregard for societal norm with disrespect to lawful behaviors, persistent deceitfulness, impulsivity, irritability, aggressiveness, reckless disregard for safety of self or others, consistent irresponsibility, and lack of remorse etc (Matt et al., 2019). About 5-15% of the population are affected (Moran, 1999). The diagnosis of ASPD is made if there is evidence of pervasive pattern of disregard for and violation of the rights of others occurring since age 15. Thus, the diagnostic statistical manual DSM requires that the diagnosis of ASPD is only given to persons 18 years old or older and have evidence of Conduct Disorder (CD) with onset before age 15 years to meet criteria for a diagnosis (Stephane and Sheilagh, 2009). Structural and functional abnormality can be noticed among Antisocial personality disorder patients have reduced cortical thickness in orbitofrontal, superior and middle frontal gyri (Jiang et al., 2016), reduced amygdala structure and function, (Glenn and Raine 2014) striatal enlargement has also been observed among patient with antisocial personality disorder and childhood aggression (Ducharme et al., 2011). Individuals with Cavum septum pellucidum have been found to have higher scores on antisocial personality disorder, psychopathy, and criminal behavior (Raine et al. 2010). One of the neurotransmitters that has been discussed in individuals with ASPD is serotonin. Deficiencies in serotonin level are linked to antisocial personality disorder. Impulsivity is not only linked with irregularities in serotonin metabolism, but may be the most essential psychopathological aspect linked with such dysfunction (Olivier, 2004). The specific gene that is involved in antisocial personality disorder is Monoamine oxidase A (MAO-A) gene. Monoamine oxidase A breaks down neurotransmitters like; serotonin and norepinephrine. MAO-A knockout models in rodents with impulsive aggression and positron emission tomography (PET) studies of healthy subjects shows association between low brain MAO-A levels and greater impulsivity or aggression (Nathan et al., 2015). The precise etiology of ASPD remains unknown. ASPD is a multifactorial construct with biological (genetic and physiological) and environmental bases. Antisocial personality disorder is difficult to treat but there are some biological or healthy interventions that have the potential to either reduce the source of neurodevelopmental impairments very early in life or alternatively normalize dysfunctional brain systems later in life. In conclusion Antisocial personality disorder is a neurodevelopmental disorder with early onset and stable
developmental course throughout life resulting in impaired functioning of the brain. Abnormalities associated can be neurocognitive deficiency, lack of empathy or remorse as associated with reduced structure and function and amygdala among others. The abnormalities associated are significant heritable.
