INTRODUCTION:

Advances in neuroscience are increasing our understanding of how our biology influences our behaviour for both good and bad. The emerging field of neurocriminology seeks to apply techniques and principles from neuroscience to improve our understanding of crime, to predict crime and ultimately to prevent crime. Such an approach would have the potential economic and social benefits that are associated with violence reduction, but it also raises neuroethical concerns. In this article, we discuss the current state of neurocriminology. This provides an overview of the neurobiological abnormalities that are associated with criminal behaviour and consider the genetic and environmental factors that may contribute to these abnormalities.

The current state of neurocriminology¹:

There are now relatively extensive literatures that document relationships between antisocial behaviour and biological functioning. A number of prospective longitudinal studies are examining whether the presence of specific biological factors, such as hormone levels, neurotransmitter levels, physiological indices or brain impairments, is predictive of future offending.

Genetics:

Heritable influences, with some exceptions, are broadly consistent across gender and ethnicity. Recently, research has focused on identifying which specific genes confer risk of antisocial behaviour. Several genetic variants that incrementally increase the risk of antisocial behaviour have been identified. Research finding underscores the idea that, as with other complex behaviours, the contribution of any single gene to antisocial and aggressive behaviour is likely to be quite small. It is possible that a combination of a larger number of gene variants substantially increases the risk of aggressive behaviour. Nevertheless, knowledge about individual genes may prove to be useful in improving our understanding of the mechanisms and pathways that increase the risk of antisocial behaviour. Importantly, the environment plays an equally influential part; indeed, some genetic variants confer risk of antisocial behaviour only in the presence of particular environmental risk factors, such as abuse in early childhood. Research in epigenetics has shown that the environment can influence how genes are functionally expressed in an individual (and even in specific brain areas); this finding undermines traditional arguments of biological determinism.

Prenatal and perinatal influences:

Early health risk factors, sometimes in conjunction with social risk factors, have been found to be associated with an increased probability that a young infant will develop antisocial and aggressive behaviour. During the prenatal and perinatal period, a number of factors may be important. Birth complications, in combination with maternal rejection of the child in the first year of life, have been associated with violent criminal offending in later period. Fetal maldevelopment during the second trimester of pregnancy, as indicated by minor physical anomalies in the child (such as low seated ears or a single palmar crease), has been associated with later violent delinquency and violent offending in adulthood. The association between fetal neural maldevelopment and childhood aggression and adolescent conduct disorder may be even more pronounced when combined with effects of poor parenting or social adversity. Criminal offending and psychopathy have been associated with another indicator of disruption in fetal development - namely, cavum septum pellucidum, which is the failed closure of the septum pellucidum, a process that normally takes place during gestation until approximately 6 months post-birth.

Maternal nicotine consumption and alcohol consumption during pregnancy are also factors that may predispose individuals to violent offending in adulthood. Even small amounts of alcohol during pregnancy have been associated with increased childhood aggression in the offspring. Lead levels have been associated with juvenile delinquency and aggressive behaviour. From a prospective viewpoint, high lead levels in the mother during the first and second trimester of pregnancy are associated with an increased risk of being arrested for violent crimes in adulthood. Higher manganese levels in the mother during pregnancy have also been associated with increased externalizing-behaviour problems (defined as aggressive, destructive and defiant behaviour) in children. Poor nutrition in either the first or second trimester of pregnancy has been associated with a 2.5-fold increase in antisocial personality disorder in the offspring. Malnutrition in infancy is associated with conduct problems in adolescence. This relationship is also mediated by low IQ. Together, these findings suggest that a number of early environmental factors may increase the risk of antisocial behaviour as late as adulthood, probably via effects on biological systems.

Hormones and neurotransmitters:

Disruptions in the hypothalamus–pituitary–adrenal (HPA) axis, the body’s stress response system that regulates the release of the hormone cortisol, are frequently observed in antisocial people. Associations between antisocial behaviour and cortisol levels vary depending on the type of antisocial behaviour and other factors. Psychological stress at various stages during development may produce lasting changes in HPA axis functioning and thereby predispose an individual to antisocial behaviour. Low levels of cortisol in childhood are predictive of aggressive behaviour 5 years later, in adolescence. Similarly, a study showed that boys who were identified as having behavioural problems and who had low cortisol levels showed more aggressive behaviour at a follow-up assessment 2 years later. Increased testosterone levels have been repeatedly associated with increased aggressive behaviour in adults. Increased levels of testosterone at the ages of 10–12 years are predictive of assaultive behaviour at the ages of 12–14 years, norm-violating behaviour at the age of 16 years and cannabis use at the age of 19 years. Higher levels of testosterone at the age of 16 years are associated with crime in adulthood.

Multiple neurotransmitter systems have been implicated in aggression, and the best-replicated correlate of human aggressive behaviour is a low level of serotonin. Low levels of serotonin in cerebrospinal fluid are a particular marker of people who show impulsive aggressive behaviour. However, aggression has also been associated with reduced monoamine oxidase A (MAOA) levels in the brain. MAOA is an enzyme that breaks down serotonin and other neurotransmitters, and hence lower levels of MAOA would presumably result in higher serotonin levels.

Psychophysiology:

Psychophysiological differences have also been observed between antisocial behaviour. Low resting heart rate may indicate a lack of fear and a reduced likelihood of experiencing negative effect in response to a criminal act. Research studies shows that, low resting heart rate was found to be as strong a predictor of future antisocial behaviour as it is of current antisocial behaviour. Psychophysiological indicators of under arousal- such as slow-frequency electroencephalographic activity and reduced skin conductance activity at the age of 15 years are predictive of crime at the age of 24 years. Poor autonomic fear conditioning (the ability to learn associations between neutral cues and aversive stimuli) is another well replicated correlate of adult criminal and psychopathic adult offending, conduct disorder in children and adolescents, and juvenile offending. A review of 46 human brain imaging studies suggests that deficits in fear conditioning may reflect abnormalities in a common core fear network that consists of the amygdala, insula and anterior cingulate.

In addition to aiding in the prediction of future offending, individual differences in fear conditioning may also provide information about which antisocial individuals may desist from future violence or be particularly amenable to treatment. For example, adolescents who were identified as being likely to commit crimes in adulthood by virtue of being antisocial at the age of 15 years but who did not go on to develop into adult criminal offenders at the age of 29 years showed superior fear conditioning compared with both antisocial adolescents who become offenders and non-criminal controls.

Brain imaging and neurology:

Reduced functioning in the frontal lobe of the brain is to date the best-replicated brain imaging correlate of antisocial and violent behaviour. In particular, structural and functional imaging studies found that the largest reductions in structure and function within the frontal lobe of antisocial individuals were observed in the orbitofrontal cortex, anterior cingulate cortex and dorsolateral prefrontal cortex. The dorsolateral prefrontal cortex is associated with self-regulatory processes, including attention and cognitive flexibility, and may be linked to the antisocial features of impulsivity and poor behavioural control. The anterior cingulate is involved in error processing, conflict monitoring and avoidance learning. Individuals with damage to this region are more disinhibited and aggressive, and demonstrate impairments in inhibitory control and emotion processing.

The ventral prefrontal cortex, including the orbitofrontal cortex, has received particular attention given its role in emotion processing, learning from reward and punishment, and decision making. The possibility of a causal connection between impaired orbitofrontal cortex structure and/or function on the one hand, and crime and/or violence on the other, has been raised by neurological studies showing that head injury in ostensibly normal individuals precedes the onset of disinhibited antisocial behaviour. For example, higher levels of aggression were found in war veterans who had experienced penetrating head injuries that were localized to the ventral prefrontal cortex. Furthermore, neurological patients who had suffered from an accidental head injury to the ventral prefrontal cortex show poor decision making, reduced autonomic reactivity to socially meaningful stimuli and psychopathic-like behaviour.

The amygdala is another brain region that is consistently identified as showing altered activity in brain imaging studies of antisocial individuals. The type of deficit may vary in different subgroups of antisocial individuals. Adults and youths with psychopathic traits, who have blunted emotional responding and may engage in more cold calculated aggression, have reduced amygdala volume and functioning, whereas individuals with a more impulsive, reactive form of aggression demonstrate exaggerated amygdala reactivity. Reduced amygdala volume in psychopathic individuals has been localized to the basolateral, lateral, cortical and central nuclei regions that are involved in emotion processing, fear conditioning and autonomic reactivity to affective stimuli.

These studies demonstrate that information about brain structure and function, regardless of whether the origins are neurodevelopmental or a result of a direct physical insult later in life, may be of some use in identifying which individuals are at an increased risk of criminal behaviour.

Remaining challenges for Neurocriminology:

In sum, in recent years, evidence of the importance of biological factors in antisocial behaviour has accumulated and is being recognized as valuable in our understanding of crime and violence. With advances in neuroscience and the design of longitudinal investigations, studies are becoming methodologically stronger. Taken together, it is becoming increasingly harder to argue that biological factors do not predispose some individuals to adult crime. This conclusion neither diminishes nor replaces social and environmental perspectives on crime causation.

Together, genetic and environmental factors shape the way that biological systems develop and function, and thus affect multiple complex psychological processes that are important in controlling and regulating behaviour and in behaving morally. A future challenge in neurocriminology lies in parsing out the specific genetic and environmental influences that induce neurophysiological changes that result in the more proximal cognitive, affective and behavioural risk factors for violence. In other words, what neurobiological processes mediate the relationship between the well-documented early social risk factors and violence in adulthood?

A few studies have begun to explore how genetic and environmental factors affect the brain. For example, researchers have found that the adolescent offspring of mothers who smoke during pregnancy have reduced thickness in two regions of the brain that have been implicated in antisocial behavior(the orbitofrontal cortex and middle frontal cortex)². Children exposed to high levels of lead early in life have been shown in adulthood to have reduced grey matter volume in the brain, particularly in the prefrontal cortex³. Males with a common polymorphism in the MAOA gene (which is present in about 30% of the population) have an 8% reduction in the volumes of the amygdala, anterior cingulate and orbitofrontal cortex⁴, which suggests that there is a causal pathway from genes to brain to antisocial behaviour.

To delineate these types of causal connections, future studies need to examine the pathways by which genes and the environment affect biological systems, and how these altered systems in turn predispose individuals to antisocial behaviour. A predisposition to criminal behaviour is unlikely to be reduced to one or even two simple brain circuits but probably involves multiple brain dysfunctions and multiple circuits that each give rise to different risk factors for violence. Thus, the future use of brain imaging in the assessment of risk of criminal behaviour will require a much more sophisticated understanding of these circuits. Although brain imaging techniques have advanced rapidly in the past few decades, there are still many limitations to these methods. However, with continued methodological improvements in neuroscience research, we will gain more information about how brain regions function together to predispose individuals to criminal behaviour.

Although only a few prospective studies have been conducted, findings from research on early risk factors suggest that information about biological factors in youths may aid in the prediction of which individuals are more likely to engage in crime and violence later in life. Such information may also help to identify individuals who are particularly amenable to rehabilitation.

In a review of ten studies implementing variants of cognitive– behavioural therapy in individuals with antisocial behaviour⁵, multiple neurobiological factors were predictive of treatment response and progress, including heart rate, hormone levels and neuropsychological measures of risk taking, sensitivity to negative consequences, impulsivity, cognitive flexibility and emotion processing. Although such initial findings are provisional, these neurobiological characteristics could ultimately help to determine which offenders are best suited to specific rehabilitation programmes and are more likely to re-integrate into society safely. A major challenge that remains to be addressed is the identification of socially acceptable psychosocial or biological intervention programmes that target biological risk factors for criminal behaviour.

The legal context

Neurocriminology interfaces with the judicial system at three main levels: punishment, prediction and prevention. To what extent does the growing body of knowledge on the neuroscience of crime and violence suggest that we should rethink our approach in these three domains? Although it is unlikely that neurocriminology will result in any radical or swift shift in the operation of the criminal justice system in the very near future, it is not inconceivable that some modest change may occur in these areas at some point, assuming that the field continues to develop and evolve, as the past two decades have suggested.

Punishment:

Punishment is predicated on blameworthiness, and the extent to which we blame individuals is a function of the extent to which they can be held accountable for their actions. Such accountability in a legal context is based on the concept of responsibility. In this context, let us assume that, to some extent, neurobiological abnormalities or insults relatively early in life predispose some individuals to a life of crime and violence. We also assume that offenders are not responsible for being exposed to these early risk factors for violence. So are these offenders responsible for their behaviour, and if so, to what degree

Currently, in the United States, an individual is deemed ‘responsible’ for their actions if two conditions are met: first, they have sufficient rational capacity; and second, they are not acting under coercion. Rational capacity is typically interpreted as whether the individual knew what he or she was doing and understood that his or her actions would have consequences. It is difficult to argue that someone with a less obvious neurobiological ‘predisposition’ to offending such as reduced functioning of the amygdala during a moral decision making task, carrying a specific variant of the MAOA gene or a significant but nonobvious volume reduction in prefrontal grey matter is not responsible for his or her actions.

In most criminal cases, the causal flow from biological risk to offending will never be known. All behaviour has a cause, and identifying the neural basis of a behaviour in an individual does not in itself establish that the individual had diminished rational capacity. Therefore, as the law currently stands all countries, the documentation of neurobiological risk factors, no matter how early they originated, does not render that individual lacking responsibility.

Despite this current legal stance, a challenging question concerns whether the current law pertaining to responsibility is in need of modest revision. This is ultimately a normative question over which there can be reasonable disagreement. Even without invoking the presence of biological risk factors to suggest impaired rational capacity, it has been argued that severe psychopaths should not be held responsible on the grounds that they have no sense of moral rationality — they are not sensitive to moral concerns and thus do not have the same moral sense as most people in society.

The judicial system acting in a practical world essentially conducts binary decision making: for example, in establishing innocence versus guilt. Risk factors associated with antisocial and criminal violence are also usually dimensional in nature (for example, the degree of prefrontal dysfunction and the resting heart rate), although some may be categorical (for example, the presence of TBI or genetic polymorphisms). Although neuroscience has no current definitional bearing on concepts of responsibility, it is not without international precedent to consider a revision to legal practice in all countries so that responsibility may, in the future, be assessed on a continuum using measures that include neurobiological variables.

Although a sensible dividing line needs to be drawn for practical reasons, in theory one can conceive of a set of multiple neurobiological and genetic influences that, combined with social influences, diminish responsibility to varying degrees. To the extent that neuroscience provides reliable methods to document these influences objectively, and assuming that methodologies become less expensive and quicker and easier to implement than hitherto, we anticipate that responsibility will eventually be conceptualized more broadly than it is today.

As recent studies have documented in psychopaths, some individuals may have deficits in brain regions that are important for generating these emotional responses. The facts that research in the field uniformly recognizes substantial affective impairments as a core feature of psychopathy and that there is no longer any reasonable doubt that such affective impairment influences behaviour^6,7raise the question of whether the legal system will eventually reformulate its current, long-standing concept of responsibility.

For example, environmental head injuries can change an otherwise responsible individual into a person who, although cognitively capable of differentiating right from wrong, lacks the neural regulatory affective and behavioural control over their behaviour⁸. It has been suggested that as neuroscience begins to offer a more detailed and specific account of the physical processes that can lead to irresponsible or criminal behaviour, the public perception of responsibility may begin to change in the same way that public viewpoints on addiction have shifted from addiction as a failure of personal responsibility towards addiction as a disease⁹.

Prediction:

If biological factors could predict future violence over and above predictions based on social variables, even opponents of a neuroscientific perspective on crime would have to agree that neurobiology has added value in this area. Whether or not such biological factors are causes or merely correlates of violence is irrelevant to the issue of prediction, the fact that they add predictive value is the currency of risk assessment in prisoners who are about to be released. Given that approximately 50% of the variance in aggressive and antisocial behaviour can be explained by genetic influences, a compelling case could in theory be made for using biological information to improve violence prediction. However, the fact that molecular genetic studies have so far largely failed to identify specific genes that can account for more than 1% of the variance in any complex behavioural trait gives considerable pause for thought^10,11.

Molecular genetic advances have, in theory, the potential to elucidate and identify specific genetic factors that predispose individuals to crime in the future, but currently the value of genotyping individuals to predict future violence is limited. Perhaps surprisingly, endophenotypes such as prefrontal dysfunction and low heart rate, which reflect compound genetic and environmental influences, may currently explain more of the variance in adult violence than any individual genotype and may have more traction in predicting future violence. The literature reviewed above has revealed several replicable early biological correlates of later violence. Some studies have shown that neurobiological markers can predict, over and above well-replicated psychosocial risk factors, which individuals will demonstrate antisocial or psychopathic traits ^12,13.

Despite the potential promise, and indeed likelihood, that neurobiology could provide at least modest increases in predictive power, methods used to predict the potential of future re-offending in about-to-be-released prisoners have so far never incorporated neurobiological markers into the risk assessment equation. There are three main reasons for this.

First, the evolving body of knowledge on neurocriminology has not yet been accepted in the social sciences and among practitioners.

Second, neurobiological measures are less easy to collect than behavioural, social and psychological data.

Third, there have been longstanding ethical concerns about collecting biological data on offenders.

Any major advances in predicting future violence will be based not just on progress in neurocriminology but also on statistical advances. If neurocriminology can identify replicable biological risk factors that provide incremental knowledge over and above the traditional variables that are currently used in dangerousness assessments, this would further aid violence prediction. Indeed, given that probation and parole decisions must be made every day in offender populations, and assuming that neurobiological data can reliably enhance the accuracy of such predictions, it could be viewed as ethically questionable not to use such knowledge. However, such a development would raise several powerful ethical concerns. The potential for future extension of such predictions from offender populations to non-offender community populations is one such concern given the egregious civil liberty violations that could arise from false positives — that is, nondangerous individuals being predicted to be at risk of committing crimes.

Intervention and prevention:

At the psychopharmacological level, it is known from over 45 randomized controlled trials that that a wide range of medications — including atypical antipsychotics, mood stabilizers, stimulants and antidepressants — are effective in reducing aggressive behaviour in children and adolescents¹⁴.

Although such effects may in part be due to the treatment of clinical conditions that are co-morbid with aggressive behaviour, such as attention-deficit hyperactivity disorder and depression, pharmacological intervention is also effective in children presenting solely with aggressive symptoms. In adults with impulsive aggression, treatment with selective serotonin reuptake inhibitors has been found to increase glucose metabolism in the orbitofrontal cortex¹⁵, suggesting a potential method for improving functioning in regions that have been identified as deficient in antisocial populations. Despite these findings, there appear to be few, if any, systematic studies on the long-term efficacy of medications or their application to offender populations.

Controversially, anti-androgen medications such as medroxyprogesterone or DepoProvera are thought to reduce recidivism in sex offenders¹⁶, but well-controlled randomized controlled trials are lacking. There is agreement that anti-androgens do reduce sexual drive, and in practice at least eight states in the United States have laws on chemical castration. Although some have argued that chemical castration violates the constitutional rights of the offender, others have countered that these medications are effective, that offenders are capable of making an informed decision and that preventing such informed choices that have appropriate safeguards in place is ethically questionable¹⁷. A more socially acceptable avenue of biological intervention may lie in nutritional supplementations such as omega-3 fatty acids.. Long-chain fatty acids are critical for brain structure and function; they constitute 30% of the cell membrane and are known to enhance neurite outgrowth and prolong cell life¹⁸. Given the existence of structural and functional neural correlates of antisocial and violent behaviour and the finding that poor nutrition is an early risk factor for antisocial and aggressive behaviour, omega-3 supplementation may prove to be modestly beneficial for at least some subgroups of offenders. From a public-health perspective, applications of neurobiological research on violence at the population level relatively early in life may help to prevent adult violence.

In one randomized controlled trial, low-income pregnant mothers were provided with prenatal and early postnatal home visitations from nurses who gave advice on reducing smoking and alcohol use and improving nutrition. The study documented a 63% reduction in the number of convictions among the 15-year-old children of these mothers¹⁹. In principle, targeted investment of resources to underserved populations at risk of future violence has the potential to enhance neurocognitive functioning and prevent offending, although these initial public health prevention programmes require replication and extension. Novel, innovative approaches to crime prevention through benign brain manipulation also have the potential to develop from basic neuroscience research.

CONCLUSIONS AND FUTURE DIRECTIONS:

Neurocriminological research in particular, and neuroscience in general, are not yet poised to make immediate changes in the prediction, prevention and punishment of criminal offenders. It is also unclear how strong and how well replicated scientific findings should be for their proper use in legal cases, although most evidence can be entered as mitigating factors in the penalty phase of a capital punishment case. At the same time, notwithstanding difficulties in determining causality, there is increasing convergence from different disciplinary perspectives that neurobiological influences partly predispose an individual to offending. It is our considered opinion that it would be valuable for researchers and practitioners to focus efforts on:

· first, the development of innovative and benign biological programmes for crime prevention;

· second, attempting to enhance the prediction of recidivism, with socially acceptable accuracy, by including neurobiological predictors;

· third, including emotion alongside cognition in how we legally conceptualize responsibility;

· fourth, considering the adoption of a dimensional concept of partial responsibility; and

· fifth, discussing the thorny neuroethical implications of this growing body of neurocriminology research that include the potential for conceptualizing crime as having a physical cause (for example, viewing crime as the result of psychological deficits), stigma and labelling (that is, the potentially harmful effects of identifying individuals based on early biological predispositions).

In conclusion, there is initial proof of concept that neuroscience can become an important future influence in society’s approach to the punishment, prediction and prevention of criminal behaviour. Hence neurocriminology is an area that needs more concentration in the present social systems.

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Received on 27.09.2016 Modified on 04.10.2016

Int. J. Nur. Edu. and Research. 2017; 5(1): 108-114.

DOI: 10.5958/2454-2660.2017.00023.0