Antisocial behaviour is behaviour viewed by the public as being abnormal or harming, either to the person or the public, usually in the form of verbal or physical abuse. Labelling someone with antisocial behaviour can have harmful consequences on both the person and the people close to them. Antisocial behaviour can be caused by many factors; individual differences, genetics, drug abuse and impairment to specific brain structures. The pre frontal cortex (PFC) is just one of the structures involved in executive functions such as social, emotional and moral behaviours. If damaged there can be severe consequences on social, emotional and moral behaviours, potentially causing huge problems in society.
Early damage to the PFC can precede the development of social cognition and therefore the deficits in the child when they grow up can demonstrate a lack of social capabilities. A case investigated by Price, Daffner, Stowe and Mesulam (1990) looked at a patient, GK, who had damage to the left frontal cortex from birth. GK, diagnosed as antisocial, has severe deficits in creating friendships, displaying correct behaviours in public and consequently has resulted in a large amount of criminal activity. In contrast a study conducted on a boy who damaged his right PFC at 7 years old, has revealed that PFC damage doesn’t always cause antisocial behaviour (Eslinger & Biddle 2000). JC’s deficits were mainly associated with education and his ability to stay attentive to tasks and finish them. With rehabilitation JC’s behaviour improved increasingly, remaining well liked by friends, family and the community. JC may not have experienced many social deficits due to the fact that he was 7 when the damage occurred, after social development (Piaget 1962), and therefore this previous social knowledge may have remained after the damage. The difference in outcomes between JC and GK could also be due to JC having damage to the right side of their PFC whereas GK was on the left.
As well as damage to different areas within the PFC increasing antisocial behaviour, the same could be said for other areas in the brain. The basal ganglia, for example, controls movement in people, when this is damaged such as in patients with Parkinson’s disease they lose their motor control (Carlson, 2010). The basal ganglia is part of the limbic system which has major connections to the dorsolateral PFC, therefore if damaged this can cause deficits to the PFC’s function without direct dysfunction of it. Participants with Parkinson’s disease and controls were presented with a vignette Theory of Mind (TOM) task; this asked them to think about how the characters in the story were feeling. Control participants performed as expected, all answers correct however those with Parkinson’s answered 1.5 incorrectly per patient. This shows, in comparison to controls, they were impaired in this social behaviour task (Eddy, 2009). Based on these participants it could suggest that people with damage to the basal ganglia struggle to understand social conventions and may come across antisocial in real life situations. As these structures are highly connected with the PFC it suggests the major deficits are caused when the PFC is damaged. Phineas Gage was a man in 1848 that had his PFC damaged through a steel rod being forced through it (Harlow, J. M. 1848 cited in Steegman, A. T. 1962). Phineas Gage’s impairments occurred through the decisions that he made for himself; this meant that he was irresponsible and couldn’t decipher between trivial and important decisions, he therefore lost jobs, friends and became a social outcast. This provides evidence that the PFC is the main structure where social cognition is developed, however if any structures that are connected to it are damaged then this has a direct effect on the PFC function even if it isn’t directly dysfunctional.
As with damage to the basal ganglia, consumption of alcohol can cause deficits in TOM tasks. A study into TOM in alcoholism was conducted whereby 24 joke stories were presented to participants, and the participants were asked to explain the punch line. The alcoholics score in comparison to the controls on the same task was much lower (Uerkermann, Channon, & Daum 2007). As humour is processed in the PFC (Wild, B., Rodden, F. A., Grodd, W., & Ruch, W, 2003) this could suggest that the deficit shown in this TOM task means the alcohol had a direct effect on the PFC and may cause deficits when replicated in social situations. Other studies have also found clear evidence of a link between PFC damage and antisocial personality disorder (ASPD). Raine. DPhil, Lencz. PhD, Bihrle. PhD, LaCasse. BA, Colletti. MD (2000) conducted a study which found patients with ASPD have a severe reduction of grey matter; the area with the most activity, in their PFC in comparison to controls and people who are heavily dependent on alcohol and drugs. Therefore this decrease in activity may be one of the causes of the behaviours that people with ASPD exhibit. However, a critique is that this study was only conducted on men and can’t be generalised to women who have ASPD. Whether the dysfunction is caused by alcohol consumption or a disorder of the PFC, both cause deficits in social cognitions.
In conclusion the studies mentioned provides evidence that dysfunction of the PFC, whether it is a reduction of grey matter, excessive intake of alcohol or even dysfunction of connected structures, can cause antisocial behaviour. There are many cases that demonstrate this including GK and alcoholic patients however some case studies display individual symptoms of dysfunction to the PFC, such as JC. Some of these differences could be age related or the location of the dysfunction in the PFC. All these studies provide a starter for further research into the relationship between the PFC and relevant social behaviours and deficits that may develop from damage. Furthermore research into the specific area of the PFC that manages social development may give us a clearer understanding of the role of the PFC.