ABSTRACT: Over 100 years ago Lombroso [(1876/2006). Criminal man. Durham: Duke University Press] proposed a biological basis for criminality. Based on inspection of criminals’ skulls he theorized that an imbalance of the cerebral hemispheres was amongst 18 distinguishing features of the criminal brain. Specifically, criminals were less lateralized than noncriminals. As the advent of neuroscientific techniques makes more fine-grained inspection of differences in brain structure and function possible, we review criminals’ and noncriminals’ structural, functional, and behavioural lateralization to evaluate the merits of Lombroso’s thesis and investigate the evidence for the biological underpinning of criminal behaviour. Although the body of research is presently small, it appears consistent with Lombroso’s proposal: criminal psychopaths’ brains show atypical structural asymmetries, with reduced right hemisphere grey and white matter volumes, and abnormal interhemispheric connectivity. Functional asymmetries are also atypical, with criminal psychopaths showing a less lateralized cortical response than noncriminals across verbal, visuo-spatial, and emotional tasks. Finally, the incidence of non-right-handedness is higher in criminal than non-criminal populations, consistent with reduced cortical lateralization. Thus despite Lombroso’s comparatively primitive and inferential research methods, his conclusion that criminals’ lateralization differs from that of noncriminals is borne out by the neuroscientific research. How atypical cortical asymmetries predispose criminal behaviour remains to be determined.
KEYWORDS: Lateralization, criminal, brain, handedness, psychopathy
Check also: A population-specific HTR2B stop codon predisposes to severe impulsivity. L Bevilacqua et al. Nature. 2010 Dec 23;468(7327):1061-6. doi: 10.1038/nature09629. Erratum in Nature, 2011 Feb 17;470(7334):424.
Abstract: Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency > 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.
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