Brain abnormalities in psychopaths: a meta-analysis.

Yang and Raine (2009) provided a meta-analytic evaluation of 43 studies, dating from 1994 through 2007, involving brain imaging in antisocial, violent and psychopathic individuals. These studies reported significant impairments in the prefrontal cortex of antisocial individuals; specifically, impairments were shown in the right orbitofrontal cortex, right anterior cingulate cortex, and left dorsolateral prefrontal cortex. The purpose of this meta-analysis was to evaluate recent studies (2009-present) that assessed differences in functional imaging variables in the prefrontal cortex and their relationship to antisocial or psychopathic behavior.

Why is it important to study the relationship between brain physiology and psychopathy? First, it is necessary to find the cause of psychopathy in order to understand, diagnose, and formulate a program of treatment for these individuals. Second, the burgeoning field of brain imaging technology provides a more expansive look into the human brain in search of a biological basis for psychopathy. Third, the implications of these studies could advance the understanding of other related neuropsychiatric conditions such as sociopathic behavior, bipolar conditions, or aggressive tendency. Finally, it may be argued that, much like those with severe mental disabilities, the physiological determinants which cause psychopathy may diminish an individual's responsibility for criminal conduct (Hagerty, 2010).

The term psychopath has been described by Hare (1999) as a "self-centered, callous, and remorseless person profoundly lacking in empathy and the ability to form warm emotional relationships with others, a person who functions without the restraints of conscience" (p. 2). Psychopathy is considered a personality disorder and was specifically included in the Diagnostic and Statistical Manual of Mental Disorders (DSM) until it was conceptually merged in the DSM-III with antisocial personality disorder (APD). Researchers have criticized the DSM-IV's definition of antisocial personality disorder for its overemphasis on behavioral outcomes such as criminality and under-emphasis of the core personality features such as affective deficits (Hare, 1999). Recent changes in the DSM-V, however, seem to address this issue by listing the criteria for APD as a person having "significant impairments in the personality functioning manifest by: impairments in both self-functioning and interpersonal functioning as well as pathological personality traits in the domains of antagonism and disinhibition." (pp. 659-663). Unlike previous versions, this criterion takes into consideration the personality traits that are present in a psychopathic individual in addition to the antisocial behaviors.

Hare and Harpur (1991), provided the most widely used scale to measure psychopathy, the Hare Psychopathy Checklist--Revised (PCL-R). The PCL-R is a diagnostic tool created in the early 1990s for use in clinical, legal, and research settings to determine an individuals' level of psychopathic tendencies. The PCL-R assesses the following traits: "glib and superficial charm, exaggerated grandiosity, need for stimulation, pathological lying, cunning and manipulativeness, lack of remorse or guilt; shallow affect (superficial emotional responsiveness), callousness and lack of empathy, parasitic lifestyle, poor behavioral controls, sexual promiscuity, early behavior problems, lack of realistic long-term goals, impulsivity, failure to accept responsibility for own actions, many short-term marital relationships, juvenile delinquency, revocation of conditional release, and criminal versatility" (Hare & Harpur, 1991). Each of these characteristics is scored on a 3-point scale by an experienced rater during a semi-structured interview; additional materials are extracted from the subjects' institutional records. A score of 0 indicates that the item definitely does not describe the person; 1 that it describes somewhat or only in a limited sense; and 2 that it definitely does describe the individual. The scale provides a total score between 0-40, reflecting the degree to which an individual meets the characteristics of a prototypical psychopath. According to Hare and Harpur (1991), a minimum score of 30 identifies a psychopathic individual. The PCL-R was used to classify participants in all of the studies in this review.

Finger et al. (2011) and Craig et al. (2009) suggested that the behaviors inherent in psychopaths represent a disruption of the integrated functioning of the prefrontal cortex and areas of the limbic system. The specific behaviors that have been the focal points of recent brain imaging studies in relation to psychopaths are instrumental learning (Finger et al., 2001), emotional and attentional processing (Deeley et al., 2006; Dolan, 2008; Marsh et al., 2008), moral decision making (Harenski, Harenski, Shane & Kiehl, 2010), and semantic and affective verbal processing (Kiehl et al., 2004; Intrator et al., 1997). All of these processes are necessary for socialization; a collection of skills that are lacking in an individual with psychopathy.

The amygdala is the almond-shaped nucleus in the anterior temporal lobe that plays a key role in both aversive conditioning and instrumental learning (Blair, 2003). It is also thought to be involved in processing fearful and sad facial expressions. (Deeley et al., 2006) Finger et al. (2011) indicated that the amygdala is responsible for absorbing stimuli and for determining whether the stimuli are positive or negative. The information is then forwarded and stored in the orbitofrontal cortex as reinforcement-expectations which then facilitate decision making. The caudate and the orbitofrontal cortex are also implicated in error prediction which is necessary to forecast outcomes and to determine future behavior (Haruno & Kawato, 2006).

Researchers originally believed that the deficits shown by individuals possessing psychopathic traits on passive avoidance tasks were attributed to an inability to process punishment information (Lykken, 1957). More recent studies have shown that psychopathic individuals appropriately use punishment information to modify responses immediately following an error; however, the deficits lie in the inability to form and use the stimulus-reinforcement information needed for decision-making (Blair, 2004). This concept predicts that psychopaths may be less able to use reinforcement expectancies to guide behavior (Blair, 2007) than other individuals.

Other components of the limbic system may also moderate psychopathy. For example, the hippocampus, located directly behind the amygdala also regulates aggression and contextual fear conditioning. Raine et al. (2004) suggests that disruption in the circuitry connecting the prefrontal and hippocampal areas could result in the disinhibited and impulsive behavior often witnessed in psychopaths.

The third area of cortical difference in psychopaths relative to control participants is the left temporal lobe which mediates semantic processing of linguistic information. Hare (1999) notes that psychopaths show an understanding of the dictionary meaning of emotive words such as love, hate or cancer but do not comprehend or appreciate their emotional value. Keihl et al. (2004) confirmed that psychopathic individuals display deficits in neural activity in the anterior temporal gyrus and the surrounding cortex during semantic processing, a condition referred to earlier by Hervey Cleckley (1955) as "Semantic Aphasia" (p. 438).

Most of the studies outlined above were done before 2008; however, there have been significant advances in neuroimaging in recent years which allow a more detailed look at the brain and its role as a mediator of psychopathy. Therefore, this study investigated consistencies in recent research and compared current findings with those of past studies. Specifically, the goal of this study was to evaluate the relationship between psychopathy and changes in functional MRI in various areas of the brain in studies since 2008.

METHOD

This study extended the results originally published by Yang and Raine (2009). The original study was a meta-analysis of 43 studies dating from 1992 through 2007. The present study added to the cumulative literature regarding the relationship between the prefrontal cortex (specifically the orbitofrontal cortex/OFC, dorsolateral prefrontal cortex/DLPFC, ventrolateral prefrontal cortex/VLPFC, and the medial prefrontal cortex/MPFC) and psychopathic behaviors.

Study Selection

The following words and combinations were used to search PubMed, Elsevier, PsycINFO (Ebsco), and Google: antisocial behavior, and brain imaging. psychopath, brain imaging/Antisocial personality disorder (APD), antisocial behavior, conduct disorder (CD), oppositional defiant disorder (ODD), disruptive behavior disorder (DBD), psychopath, psychopathy, psychopathic, violent, violence, aggressive, aggression, offender, criminal, anatomical magnetic resonance imaging/ aMRI, volumetric magnetic resonance imaging/ vMRI, diffusion tensor imaging/ DTI, structural imaging, functional magnetic resonance imaging/ fMRI, magnetic resonance spectroscopy/ MRS, perfusion emission tomography/ PET, single photon emission computerized tomography/ SPECT, functional imaging, prefrontal cortex/ PFC/ psychopathic brain/ brain imaging, antisocial personality disorder (Yang & Raine, 2009). Additionally, all reference materials listed by each of the studies included and review articles on brain imaging and psychopathy were appraised.

Additional criteria for inclusion were that the study had at least one antisocial comparison group, that is, a "group that contains individuals with APD, antisocial behavior, conduct disorder, oppositional defiant disorder or disruptive behavior disorder, psychopaths, criminals, violent offenders, or aggressive individuals" (Yang & Raine, 2009). Each study also had to include one or more of the following imaging methods: aMRI, fMRI, DTI, MRS, PET or SPECT. Finally, the imaging technologies used had to assess either the function or the structure of the prefrontal cortex. The prefrontal cortex was defined by Yang and Raine (2009) as "the frontal region anterior to the precentral sulcus (primary and association motor areas were excluded" (p. 3).

In addition to the 43 studies included in the original meta-analysis, a systematic search of the databases produced 16 studies that fit the inclusion criteria. One of those studies was excluded because of insufficient statistical data necessary to compute effect size. Of the 15 new studies, 13 included psychopaths with PCL-R scores at or above 30; two included participants with a previous diagnosis of either conduct disorder or oppositional defiant disorder; and one study compared violent individuals diagnosed with antisocial personality disorder to violent schizophrenics, non-violent schizophrenics and a healthy control group. Of the 1781 total participants, there were 726 who were diagnosed with antisocial tendencies including psychopathy and 747 control subjects. The demographic information and antisocial sample characteristics of the remaining 58 studies included in this meta-analysis are presented in Table 1, which is available from the author upon request.

Potential Moderators

There were nine potential covariates of the effect sizes in these studies: the type of imaging technology, violent versus non-violent participants, comorbidity, inclusion of a psychiatric control, institutional based versus non-institutional based, psychopathy, mean age, percentage of males, and type of imaging technology used. The violent category included studies in which more than half of the antisocial individuals had a history of violent behavior; had been convicted or charged with violent crimes; or had displayed aggressive behavior towards a family member. Those studies whose antisocial population did not show a history of violent tendencies were listed as non-violent. Studies whose antisocial participants were diagnosed with co-morbid psychiatric conditions (such as substance abuse, drug dependency, schizophrenia, and ADHD) were coded for co-morbidity, whereas the other studies were coded without co-morbidity. Studies that compared a psychiatric control to the study group (i.e. individuals who are considered violent schizophrenics compared to non-violent schizophrenics) were coded for contrast with studies that had healthy control groups (i.e. individuals who are free of psychiatric or neurological conditions). Those studies whose antisocial population was recruited from a controlled environment like a hospital or a prison were coded as institutional-based, whereas studies whose participants were recruited from non-confined environmental settings like temporary employment agencies or outpatient clinics were categorized as non-institutional. Studies whose antisocial population was diagnosed as having psychopathy (based primarily on PCL-R scores of 25 or above) were coded for psychopathy. Additionally, the mean age of the participants as well as the percentage of males in each study group were taken into account as potential covariates.

RESULTS

A total of 58 studies (1781 cases) were selected for the initial meta-analysis. All but three of the studies (Hoptman, 2005, Muller, 2005; Schneider, 2000) were included in the study. Two studies (Hoptman, 2005; Schneider, 2000) were evaluated separately because the effects reported in these studies were the opposite of the predicted direction. The third study (Muller, 2005) was excluded because it was identified as a statistical outlier.

Analysis of the heterogeneity statistics produced a nonsignificant Q statistic (Q = 17.36, p > .05). This statistic is an estimate of heterogeneity among the effect sizes in the various studies. The fact that it was not significant indicates that the effect sizes reported in this collection of studies were consistent and did not vary significantly across the studies. Figure 1 is a simple forest plot that illustrates the variation in these effect sizes.

The average effect size (r square) for these studies was .2 which means that the hypothesized effect accounted for approximately 20% of the variance in the average study. A single sample t test computed on r square statistic was significant, t (54) = 7.308, p < .05.

Each square in the forest plot (Figure 1) represents the p value for the effect size for an individual study and horizontal line to the side of each square is the confidence interval for that p value. Any square that falls within the confidence interval for another study is not significantly different from that study. The plot indicates a remarkable similarity of effect size for the included studies.

Figure 2 is a selectivity funnel plot for the various studies. This plot displays the effect size on the X axis and a measure of within study variability (Precision) on the Y axis. The plot is used to assess the extent to which selective dissemination of evidence may have affected the conclusions of the meta-analysis. Each study is a single dot in the plot and p value lines form the funnel at various levels of significance (.1, .05, and .01). One evaluates dissemination bias by evaluating the lack of studies in the regions of non-significance. Lack of studies in this region otherwise known as "missingness" indicates potential dissemination bias. Figure 3 does not indicate any significant dissemination bias because the studies are equally distributed across the range of significance in the plot.

Dissemination selectivity refers to the extent to which the results could have been skewed by the variability within the sample. Because smaller studies will often produce larger variances and effect sizes, a correlation between the variance of the study and the effect size, otherwise known as Begg's Test, is used to evaluate this potential bias. The Begg's Test correlation of .63 was significant, Z = 6.82, p < .05, which suggests that the effect sizes reported in this collection of studies were at least partially the result of the variability within the sample studied. However, this correlation is not the result of the sample size. A non-parametric correlation computed on the sample size and effect size data did not indicate any significant relationships.

Additional analyses were computed on other variables in the study and the effect size data. Neither the percent male nor the age of the participants variables correlated significantly with the effect size measure.

Difference in effect size as a function of the type of measurement used was also examined. Box plots of the effect size (Pearson r) for the different types of measures used in the various studies indicated that two studies were outliers and these were removed. The remaining studies were then analyzed with a Kruskal-Wallis non-parametric analysis of variance which indicated that the different measures did yield different effect sizes, ChiSquare = 11.301, p < .05. The boxplots indicated that those studies that used fMRI and MRI produced smaller effect sizes relative to the studies that used aMRI, Pet, or some other measure.

Analysis of those studies in which the results were not in the predicted direction (Hoptman, 2005; Schneider, 2000) did not reveal any outstanding differences in their study characteristics relative to the larger body of included studies. Both studies used MRI procedures and sample sizes that were primarily males. The average age of the participants was approximately 35. The effect sizes were moderate (.4). Perhaps the only noticeable difference is that in the Hoptman study, the patients were co-morbid for dementia, which was not the case in any other study. It is, therefore, unclear why these two studies produced results that differed so markedly from the other 56 studies.

DISCUSSION

A meta-analysis allows one to pool the results of several similar studies and draw correlations based on the analytical data presented. The main advantage of a meta-analysis is that it increases the sample size and, therefore, the power to study effects of interest as well as the variables and outcomes. One disadvantage to meta-analysis is that studies that produce non-significant results are not regularly published. Therefore a literature search will typically include only those studies with significant effects which have been published. This phenomenon is called publication bias (Walker, Hernandez & Kattan, 2008).

It may also be difficult to summarize large amounts of varied information using a single number such as a measure of effect size. Inconsistencies among covariates, dependent measures, and experimental procedures in the various studies raise the question of whether the experiments may be combined at all to produce a single accurate measure of effect size. In order to counter this issue, we separated out and analyzed each of eight potential moderators (the type of imaging technology, violent versus non-violent participants, co-morbidity, inclusion of a psychiatric control, institutional based versus non-institutional based, psychopathy, mean age, & percentage of males) in order to rule out their influence on the effect size measure. Based on the analysis of these potential moderators we found that only the type of imaging contributed to a change in the effect size; fMRI and MRI techniques created a smaller effect size relative to those using aMRI, PET or other imaging technology.

This meta-analysis supports the previous findings that brain imaging can predict psychopathy. The average effect size in these studies is significant; the overall pattern of results across studies indicates that people diagnosed with psychopathy demonstrate reduced MRI, fMRI, aMRI, PET and SPECT activity in the frontal lobe areas. These findings suggest that damage to and neural deficiencies in the prefrontal cortex limits normal emotional display and may precipitate abnormalities in social behaviors that are exhibited by psychopathic individuals (Damasio, 1994). These results are consistent with other reported findings that related unilateral damage to the right OFC or the right VMPC with impairments in social conduct, decision-making and emotional processing as seen in psychopathic individuals (Tranel et al., 2002). Additionally, functional deficits in the DLPFC have been shown to impair the ability to allocate and sustain attention in psychopathic individuals. The OFC and Anterior Cingulate Cortex (ACC) which are implicated in processing secondary cues such as emotional contents may further impede attentional control, if damaged, by failing to effectively direct attention to important information when necessary (Yang & Raine, 2009). All of these effects are supported by the findings in this study.

There are two important models of psychopathy that are often cited in literature that are supported by these findings of deficiencies in the prefrontal cortex; the Somatic Marker Hypothesis (Damasio, 1996) and the Prefrontal Dysfunction Theory (Gorenstein & Newman, 1980). Damasio (1996) hypothesizes that when a normal person is faced with a decision, he or she must first weigh the incentive value of the choices available to them which requires both cognitive and emotional processes. When individuals are faced with more complex or conflicting decisions, they may be unable to make these decisions using cognitive processes only and must then rely on somatic markers to aid in the process.

Somatic markers are associations between reinforcing stimuli that induce an associated physiological affective state (Damasio, 1996). For example, if a specific person tends to elicit anxiety and increased blood flow to the extremities another, eventually even thoughts about that person will elicit the same responses only to a lesser degree. At some point, the individual will begin to avoid this source of anxiety by staying away from the person who elicits the emotional response. Psychopaths have shown an inability to form somatic markers by learning from previous experiences and therefore often make decisions that elicit unfavorable consequences for themselves or others (Hare, 1993).

These data support Antonio Damasio's (1994) Somatic Markers Hypothesis that damage or dysfunction in the prefrontal cortex (specifically the ventromedial frontal lobe) reduces the person's emotional responsivity. Damasio's (1994) hypothesis suggests that a psychopathic individual may have difficulty acquiring the associations necessary to form somatic markers; therefore, that individual has limited ability to consider emotions when making a decision. This impairment causes self-defeating behavior, and violation of social norms with detrimental consequences, all behaviors indicative of the psychopathic profile.

Gorenstein and Newman (1980) reported significant correlations between human disinhibition and lesions in the medial septum, the hippocampus, and the orbitofrontal cortex (SHF). These researchers found that animals with SHF lesions did not defer gratification in order to achieve greater reward; these animals were profoundly impaired on tasks requiring impulse control. This theory is also reinforced by later research (Buckholtz et al., 2010) which linked the impulsivity which is prevalent in psychopathy with dysfunction in the dopamine reward circuitry which includes the nucleus accumbens, hippocampus, amygdala, ventral tegmental area and the prefrontal lobe. This research supports these findings of abnormal functioning in the prefrontal cortex, specifically the orbitofrontal cortex/OFC, dorsolateral prefrontal cortex/DLPFC, ventrolateral prefrontal cortex/VLPFC, and the medial prefrontal cortex/MPFC) and psychopathic behaviors.

A limitation of this study is the lack of female antisocial participants available and, therefore, an inability to generalize the results to heterogeneous gender population. Female antisocial individuals in this study constituted only 13% of our overall participation of 1,856 in the study group. While there is very little information available regarding female psychopathy, some estimates (Nesca, Dalby & Baskerville, 1999) suggest that women constitute approximately one-third of the total population of psychopathic individuals.

Whereas the current study was designed to focus predominantly on the prefrontal cortex, more recent studies indicate additional areas which are necessary in the formation of social skills that are noticeably absent in the antisocial population. For example, Kiehl (2006) published a comprehensive review of the literature concerning the cognitive neuroscience of psychopathy and studies involving behavioral changes following damages to the paralimbic system. Kiehl concluded that the paralimbic system (consisting of the amygdala, hippocampus, anterior cingulate and the orbitofrontal cortex) is the relevant functional neural architecture implicated in psychopathy.

Mitchell et al. (2002) suggests that a dysfunction in the amygdala-orbitofrontal cortex circuit, limits the ability to assign motivational value to stimuli. This circuit may be the culprit in a psychopathic individual's inability to recognize and demonstrate socially appropriate behaviors in an emotional situation. Damage to the amygdala and the antero-lateral temporal lobe may also impact psychopaths' aggression, impulsivity, and poor behavioral control, as well as lack of empathy and emotional concern (Kiehl, 2006).

Additionally, structural variances in the hippocampus, the area of the brain that has demonstrated a role in classical conditioning and the social learning of psychopaths (Laakso et al., 2001; Raine et al., 2004) may account for a psychopath's limited fear conditioning and unresponsiveness in classical conditioning paradigms with aversive contingencies (Kiehl, 2006).

The cingulate gyrus, a third area of interest in studies involving brain abnormalities in psychopathic individuals, is commonly divided into two distinct functional regions: the affect and cognition components (Devinsky et al., 1995). The affect component or rostral area underlies conditioning and emotional learning, assessments of motivational content and assigning emotional valence to internal and external stimuli. The caudal region is engaged in response selection and error monitoring. As a whole, the anterior cingulate cortex appears to play a crucial role in initiation, motivation and goal-oriented behavior (characteristics that are not commonly seen in a psychopathic individual).

This meta-analysis provides clear evidence of differences between the function of the prefrontal region in the brains of psychopathic individuals versus normal individuals. However, the results indicate a need to cast a wider research net; i.e., to expand the focus of future studies to additional areas of the brain known to mediate antisocial behaviors (i.e. amygdala, hippocampus, anterior cingulate, and the antero-lateral temporal lobe). This study also underscores the critical need to replicate the findings with other populations such as female antisocial individuals.

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* Yang, Y., Raine, A., Narr, K., Colletti, P. & Toga, A. (2009). Localization of deformations within the amygdala in individuals with psychopathy. Archives of General Psychiatry, 66(9), 986-994.

* Yang, Y., Colletti, P., Raine, A., Toga, A. & Narr, K. (2010). Morphological alterations in the prefronal cortex and the amygdala in unsuccessful psychoparths. Journal of Abnormal Psychology, 119(3), 546-554.

* Yang, Y. & Raine, A. (2009). Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: A meta-analysis. Psychiatry Research, 174(2), 81-88.

Notes: A table outlining the demographic information and sample characteristics of the 58 studies used in this analysis is available from the author upon request. I would like to express my sincere gratitude to Rick Parente, PhD., for his continued guidance and analytical expertise in the completion of this publication.

Sherry D. Nickerson

Towson University

Author info: Correspondence should be sent to: Sherry D. Nickerson, 17905 Bunker Hill Road, Parkton, MD 21120 [email protected]

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Author:	Nickerson, Sherry D.
Publication:	North American Journal of Psychology
Article Type:	Report
Date:	Mar 1, 2014
Words:	5429
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Topics:	Antisocial personality disorder Research Brain Physiological aspects Psychiatric research Psychopaths Physiological aspects Psychological aspects Sociopathic personality Research