Abnormalities in the frontal lobe have been widely implicated as contributing to the pathophysiology of violent behavior. The prefrontal cortex is imperative for executive functions; it is responsible for regulating inhibition, emotions, movement, self-monitoring, self-correcting, and overall social and cognitive behavior. Damage or dysfunction of the frontal lobes results in unregulated behavior. Lesion studies that date back to the late 1800s have repeatedly found that damage to the frontal lobes results in an altered personality marked by an increase in impulsivity and a lack of judgment and decision-making skills (1
). These reports suggest that frontal lobe areas are significantly compromised and may serve as structural markers for predisposed violent behavior.
The diagnostic characteristics of antisocial personality disorder include impulsivity, failure to conform to social norms, aggressiveness, disregard for safety, glibness, and deceitfulness. Not all violent criminals have antisocial personality disorder, but there is a higher rate of severe violence among subjects with antisocial personality disorder compared to the general population. This suggests that there may be a specific pattern of cortical deficits that underlie this violent behavior. There is a lack of brain imaging data regarding the neural correlates that underlie antisocial personality disorder. However, two studies have shed some light on this topic. One study revealed that when corrected for total brain volume, individuals with antisocial personality disorder have an 11% reduction in prefrontal gray matter volume in relation to healthy comparison subjects (5
). Another study showed that violent individuals with antisocial personality disorder, in relation to healthy comparison subjects, have a decrease in total brain and temporal lobe volumes and an increase in putamen volume (6
Evidence from behavioral and functional magnetic resonance imaging (fMRI) studies further implicate frontal brain regions as contributing to the neuropathology of antisocial personality disorder. For example, a neuropsychological study by Dinn and Harris (7
) reported that individuals with antisocial personality disorder performed significantly worse than healthy comparison subjects on cognitive tasks sensitive to orbitofrontal function. Furthermore, fMRI data showed that violent individuals with antisocial personality disorder had deficits in working memory and reduced brain activations in the left frontal gyrus, anterior cingulate, and precuneus in relation to comparison subjects (8
). Impaired emotion and behavioral inhibition, personality traits representative of antisocial personality disorder, have also been attributed to orbitofrontal dysfunction (9
). Notably, functional imaging evidence supports that the mesial prefrontal cortex is highly involved in emotional processing and more regularly activated by emotional tasks than cognitive tasks (10
). Thus, dysfunction of the mesial prefrontal cortex may result in abnormal emotional processing. Deceitfulness and psychopathic symptoms have also been attributed to antisocial personality disorder and frontal lobe abnormalities. Yang and colleagues (11
) have shown that gray matter volume in pre-frontal regions decreases in association with higher psychopathy scores. These investigators, however, also reported that within the population with antisocial personality disorder, frontal white matter volume increases and changes in gray/white matter tissue ratios are linked with lying and deceitfulness specifically (12
) and that deficits in prefrontal gray matter are evident in unsuccessful—but not in successful—psychopaths (11
). The high rates of violent and impulsive behavior among individuals with antisocial personality disorder and these earlier studies suggest that the prefrontal cortex or frontal lobes are compromised in violent individuals with antisocial personality disorder. This pattern of structural deficits may also be involved in the pathophysiology that underlies the violent behavior observed in schizophrenia patients.
Although to a lesser extent than antisocial personality disorder, the incidence of violent behavior in schizophrenia is greater than in the general population, at least in a subgroup of patients (13
). Neuropathology in schizophrenia has been widely studied in which cumulative evidence suggests that multiple brain regions are affected in the disease. Specifically, schizophrenia patients have significant reductions in brain volume and weight (6
). In addition, CSF enlargements and gray matter deficits in the lateral and medial temporal cortices, principally the superior temporal gyrus and hippocampus subcortically, are reported in the large majority of studies (14
). Gray matter abnormalities in other neocortical regions, including the frontal cortices, notably the prefrontal and orbitofrontal regions and the parietal cortices, are also reported in schizophrenia (16
). Finally, several studies have shown that cortical thinning within frontal, temporal, and parietal cortical association regions is associated with disease processes in schizophrenia (16
The existing literature concerning the structural neuropathology of schizophrenia is vast, and the literature regarding the neural underpinnings of violent behavior
in this population is growing. In a recent review by Naudts and Hodgins (19
), the authors concluded that male schizophrenia patients who consistently showed a pattern of aggressive and antisocial behavior had poorer orbitofrontal functions, an increase in the size of the putamen (6
), and reductions in the volume of the amygdala, the hippocampus, and the orbitofrontal system compared to schizophrenia patients with no violent history. These findings suggest that there may be specific deficits in the pre-frontal-limbic circuitry in violent schizophrenia patients. Notably, some studies have also shown that relationships exist between frontal white matter integrity and aggressive symptoms of schizophrenia. In a diffusion tensor imaging study, Hoptman et al. (20
) reported inverse relationships between fractional anisotropy and motor impulsiveness scores and positive relationships between diffusion tensor imaging trace measurements and aggression scores in male schizophrenia patients (N=14) in right hemisphere inferior frontal regions. In a later study, this group also reported that larger left orbitofrontal cortical gray matter volumes and larger bilateral orbitofrontal white matter volumes were associated with aggression in schizophrenia patients (21
). Remarkably, the only fMRI study to have investigated the neural correlates of seriously violent behavior in schizophrenia so far has linked bilateral frontal and right parietal activation deficits to serious violence in schizophrenia (8
). In the same study, activation deficits in the sensorimotor cortex, thalamus, and hippocampus were associated with violence across both antisocial personality disorder and schizophrenia.
Analyses of the anatomy of violent groups with antisocial personality disorder and schizophrenia may provide insight into the neural underpinnings of violent behavior. Barkataki et al. (6
) recently reported findings on structural/volumetric abnormalities in violent patients with antisocial personality disorder and schizophrenia. Their findings show that although violent subjects with antisocial personality disorder and schizophrenia have some common structural abnormalities, differences exist, suggesting that some brain systems are selectively involved in violent antisocial personality disorder compared to violent schizophrenia groups (6
). Thus, in this investigation, we set out to examine regional differences in cortical thickness in an overlapping group of the subjects included in the study by Barkataki et al. (6
), namely, violent individuals diagnosed with antisocial personality disorder, violent and nonviolent schizophrenia patients, and well-matched healthy comparison subjects. There are few to no data concerning the regionally specific cortical correlates of violent behavior in antisocial personality disorder and schizophrenia, nor are there any data that indicate whether structural changes associated with violent behavior differ in these two populations. Although previous studies have explored regional changes in cortical thickness in schizophrenia patients, none of these studies has examined the effects of violence specifically. Moreover, disturbances in laminar thickness and the structural difference associated with violence have not yet been addressed in individuals with antisocial personality disorder, to our knowledge. Cortical thickness serves as an indicator of cortical integrity and provides an overall profile of anatomical and possible functional deficit. Based on existing data characterizing structural abnormalities in schizophrenia and antisocial personality disorder, we hypothesized that violent schizophrenia patients and violent individuals with antisocial personality disorder would both exhibit regional alterations in cortical thickness within frontal neocortices. In order to elucidate changes in cortical thickness specific to violent behavior and to investigate whether violence effects differed in our two violent subject groups, we used cortical pattern-matching methods to align homologous cortical regions between subjects.