Essay: Does dysfunction of the prefrontal cortex lead to antisocial behaviour?

The prefrontal cortex (PFC) is the cerebral cortex covering the frontal lobe, crucial for executive functions and widely believed to be responsible for personality and other cognitive behaviour, including impulsivity and caution (Deyoung, Hirsh, Shane, Papademetris, Rajeevan & Gray, 2010). As these functions allow us to respond and react appropriately in social situations, it is unsurprising dysfunction of the prefrontal cortex has been linked to antisocial behaviour (ASB). Evidence largely supports this link, though there are alternative explanations to consider, and some studies to disprove the claim.
A key study to consider is Harlow\’s infamous 1848 case study of Phineas Gage, who lost a large amount of his left frontal lobe after an iron rod was driven through his eye socket. This provides an indisputable link between dysfunction of the prefrontal cortex causing antisocial behaviour, as those who knew him stated \”he was no longer Gage\”, as he became \”fitful, irreverent, indulging… in the grossest profanity\” (Harlow, 1848). This clear change in his personality supports the responsibility of the PFC, as he was previously \”regarded.. the most efficient and capable foreman\”, and only after the accident did he engage in ASB. This is interesting to consider in comparison to another case study, in which the patient GK had early frontal lobe damage from birth (Price, Daffner, Stowe & Mesulam, 1990). From a young age, GK demonstrated antisocial behaviour, unable to make friends as a child. As GK aged, he was imprisoned 8 times, and was a suspect in rape cases. Price et al. (1990) also found further support in another case study, female MH. Damage to her PFC occurred age 4, before which she “was developing appropriately”. After the accident, she became violent, suicidal and neglected her child. As case studies are so unique, support offered by multiple strengthens this link, as both partook in ASB, despite GK’s being from birth and Gage and MH having a clear before and after. This highlights that at the very least there is a clear link, and may lead psychologists to conclude damage to the PFC is a cause for antisocial behaviour.
Alcoholism and substance abuse have also highlighted a link between the dysfunction of the prefrontal cortex and antisocial behaviour, as alcohol has a significant impact on both the functions and the structure of the PFC (Abernathy, Chandler & Woodward, 2010). One study found that alcoholics often misinterpret facial expressions, which may lead to antisocial behaviour, such as misunderstanding of intentions, or inappropriate reactions (Frigerio, Burt, Montagne, Murray & Perret, 2002). When shown facial expressions varying in intensity (neutral to angry/happy/sad with increasing intensity of 0%, 33%, 66% and 100%), alcoholics made more errors in correctly identifying the expressions shown, particularly in sad faces, which they interpreted as hostile. These results are echoed in another study, where alcoholics showed significant difficulties in identifying facial expressions correctly, as well as consistently overestimating their intensity (Philippot, Kornreich, Blairy, Baert, Den Dulk, Le Bon, Streel, Hess, Pelc & Verbanck, 1999). This supports the link between the dysfunction of the prefrontal cortex leading to antisocial behaviour, as alcohol abuse often elicits ASB, which may be attributable to the functional and structural changes of the prefrontal cortex (a direct result of the substance abuse).
Another study found that in patients with damaged PFC, the ability to amend previously learned associations is severely impaired (Hornrak, Rolls, Wade & McGrath, 1994). In a reversal/extinction test (where previously ‘correct’ stimuli became ‘incorrect’ in the second condition), even if participants knew there would be negative consequences (the reduction of their score), they still pressed the previously correct, now incorrect, stimuli. The patients involved in this study had acquired damage to the PFC in a variety of ways, generally through head trauma or a stroke, suggesting it is dysfunction of the PFC that leads to antisocial behaviour, as this remained consistent between all patients. The inability to unlearn associations may account for those with damage to the PFC reacting inappropriately to stimuli, as well as difficulty in recognising how to modify behaviour, as though participants could see the stimuli had changed, they were unable to mimic their behaviour accordingly. These results were echoed in another study, which found patients with damage of the PFC acted in similar ways to substance dependents, choosing an immediate reward when offered, even if they recognised it may elicit negative consequences in the future (Bechara, 2003). This highlights the link between dysfunction of the PFC and antisocial behaviour, indicating a direct influence and clear example of ASB.
However, there has been contrasting evidence raised in a study examining brain morphometry (Chanraud, Martelli, Delain, Kostogianni, Douaud, Aubin, Reynaud & Martinot, 2006). Investigating the relationship between structural brain damage and alcoholism, they found that there were significant clusters of decreased grey matter in the PFC, with the volume of the dorsolateral frontal cortex decreased by an average of 20% in alcoholics compared to healthy patients. However, despite this dysfunction, patients did not display any “neurological, somatic or psychiatric complications”, and all were socially apt and employed. This suggests that perhaps biological explanations are limited, and other theories should be considered, such as Bandura’s social learning theory (Bandura, 1977). Bandura proposed learning occurs through social observation, and can be strengthened through vicarious reinforcement. This theory has been frequently applied to explain aggression and ASB, suggesting an alternative cognitive model to the biological approach. Other explanations of ASB include institutional aggression, as deprivation and situational factors can all influence the severity and frequency of antisocial behaviour (Welsh, Bader & Evans, 2013).
In conclusion, it is clear there is an indisputable link between the prefrontal cortex and antisocial behaviour, with the majority of studies concluding dysfunction of the prefrontal cortex does lead to antisocial behaviour. However, there are other studies that suggest this is not true, implying this is an incomplete explanation, and that in order to fully understand the cause of antisocial behaviour, we should consider other theories, including cognitive and situational models.