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Episodically aggressive offenders, both impulsive and predatory, constitute one of the most pressing problems for law enforcement, courts, and corrections, not to mention the general public. This subgroup of offenders is largely responsible for the following: (a) a disproportionate amount of aggressive crimes against persons, (b) high recidivism rates, (c) a significant number of institutional rule violations, (d) high rates of substance abuse, and (e) intractability and poor treatment outcomes. Repetitively aggressive offenders are often diagnosed with antisocial personality disorder (ASPD), and a subset of these as psychopathic. Their personal histories are typified by childhood aggression, insensitivity to punishment, emotional dysregulation, risk taking, and sensation seeking. These inmates are recommitted more often than other inmates, a majority of them recidivate with aggressive offenses, and they are likely to develop an early and more severe course of drug abuse. Yet few community, private, or correctional programs are available to treat these offenders or, more importantly, to prevent the development of these behaviors before they stabilize. There are clear public safety benefits to being able to accurately identify and characterize these offenders in terms of conditions that may underlie or contribute to their dysregulated behavior in order to direct more effectively treatment and prevention resources.
Recent research on underlying mechanisms in aggression may be applicable to this problem and has implications for more effective interventions. Various neuropathological conditions (attenuated frontal P300 amplitude, reduced prefrontal glucose metabolism, subdued physiological responses to alcohol, neuropsychological deficits, differences in neurotransmitter metabolism and activity levels, and heightened stress dampening) have been associated with these dysregulated behaviors, suggesting that neurobiological processes may underlie risky behaviors. In particular, studies have consistently found that deficits in certain neuropsychological functions correlate with and predict aggression, impulsivity, violence, and other forms of persistent misconduct in both children and adults. What is emerging from these studies is that although many offenders may function adequately in terms of basic cognitive skills such as memory, intelligence, and learning ability, those who repeatedly engage in very risky behaviors may have deficits in what is called executive cognitive functions (ECFs), higher-order neuropsychological skills. ECFs include a subset of higher-order neuropsychological abilities and their measurement has become more refined, non-invasive, and reliable, making it more amenable to conducting these studies with offenders.
ECF abilities include social skills, impulse control, assessment of and sensitivity to consequences, motivation, attention, and emotional perception and regulation. Deficits in these abilities have been implicated in aggression and are thought to be responsible for a number of traits often seen in aggressive offenders, such as poor social skills and decision-making ability, insensitivity to punishment, impulsivity, inattention, impaired problem solving, cognitive inflexibility, and lack of goal-directed behaviors. And because ECFs regulate and, in most cases, inhibit emotional responses, ECF deficits are also associated with poor emotional regulation and inaccurate perceptions of emotion in others. In essence, impaired ECF may compromise the ability to interpret social cues during interpersonal interactions, which may lead to misperceptions of threat or hostility. As a result, difficulties arise in generating socially adaptive behaviors and in executing responses to avoid aggressive or stressful interactions. Also, compromised cognitive control over behavior may permit hostility, negative affective states, and other maladaptive responses to dominate.
Neural regulatory mechanisms in cognitive impairments that may specifically subserve dysregulated behaviors involve the prefrontal cortex (PFC) and its circuitry to areas of the limbic system. Certain regions of the PFC play a role in neuropsychological functions that support forethought, behavioral inhibition, and capacity to learn from experience. The PFC also plays a role in the regulatory system, controlling emotional perceptions, regulation of emotional responses, and moods. Populations with damage to this circuitry show increased extroversion, impulsivity, irritability, aggressiveness, and various antisocial behaviors, as well as impairments in ability to make rational decisions and difficulties in processing emotion.
There is evidence that a disconnect between the PFC and structures in the limbic system (an emotional center) may be responsible for these dysregulated behaviors via neuropsychological impairments. Sources of damage to this circuitry that may disrupt ability to assess consequences and regulate impulses include head injury, adversity, prenatal drug exposure, neurotoxins, childhood deprivation, child abuse, and chronic drug use. Many of these factors are environmental, suggesting that the PFC is sensitive to external physical and social influences. Psychosocial stress can alter PFC function and contribute to ECF impairment. The volume and function of particular brain structures, including the PFC and limbic system, are associated with social stress and adversity. Perhaps not coincidentally, the incidence of adverse social (e.g., child abuse) and physical (e.g., head injury) experiences is high in offender populations. Those with brain dysfunction are significantly more likely to have been indicted for violent crimes.
Of particular interest is the connection between neuropsychological impairment and psychopathy. Psychopaths with aggressive behavior have been distinguished from nonpsychopaths on the basis of neuropsychological functioning of the PFC. Prefrontal lobe damage has been reported in a significantly greater percentage of subjects with a history of violent crimes than those with no such damage. Neuroimaging studies report diminished brain activity in the PFC in individuals with persistent violent behavior.
In summary, the prevalence of neuropsychological dysfunction is significantly greater in violent offenders than in nonaggressive offenders and in the general population. This evidence suggests that treatments designed to enhance functionality and connectivity between neural systems may be effective behavioral modifiers.
References:
- Barratt, E. S., Stanford, M. S., Kent, T. A., & Felthous, A. R. (1997). Neuropsychological and cognitive psychophysiological substrates of impulsive aggression. Biological Psychiatry, 41, 1045-1061.
- Davidson, R. J., Putnam, K. M., & Larson, C. L. (2000). Dysfunction in the neural circuitry of emotion regulation—A possible prelude to violence. Science, 289, 591-594.
- Elliott, F. A. (1992). Violence: The neurologic contribution: An overview. Archives of Neurology, 49, 595-603.
- Fishbein, D. H. (Ed.). (2000). The science, treatment and prevention of antisocial behaviors: Applications to the criminal justice system. Kingston, NJ: Civic Research Institute.
- Fishbein, D. H. (Ed.). (2004). The science, treatment and prevention of antisocial behaviors (Vol. 2). Kingston, NJ: Civic Research Institute.
- Kandel, E., & Freed, D. (1989). Frontal-lobe dysfunction and antisocial behavior: A review. Journal of Clinical Psychology, 45, 404-113.
- Mirsky, A. F., & Siegel, A. (1994). The neurobiology of violence and aggression. In A. J. Reiss, Jr., K. A. Miczek, & J. A. Roth (Eds.), Violence: Biobehavioral influences (Vol. 2, pp. 59-172). Washington, DC: National Academy Press.
- Raine, A. (1993). The psychopathology of crime: Criminal behavior as a clinical disorder. New York: Academic Press.
- Raine, A., Buchsbaum, M., & LaCasse, L. (1997). Brain abnormalities in murderers indicated by positron emission tomography. Biological Psychiatry, 42, 495-508.
- Volavka, J. (1995). The neurobiology of violence. Washington, DC: American Psychiatric Press.
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