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The beginning of the search for the neurological basis of crime can be traced back to Cesare Lombroso, an Italian criminologist and physician who provided one of the most influential arguments that criminals are born with a nature favorable to crime. Although no direct means exists to examine in vivo the brain anatomy of criminals at the time, Lombroso managed to identify several distinct physical features, which he called “stigmata.” This included a slanting forehead, long/no ear lobes, a large jaw with no chin, heavy supraorbital ridges, excessive/absent hair on the body, and an extreme sensitivity/insensitivity to pain. According to Lombroso, the possession of multiple physical abnormalities indicated that the individual was less developed, a “born criminal,” and thus could not adjust to the rules of modern society. Although Lombroso's argument was less than sound, the idea that criminal behavior is influenced by biological predispositions has endured and gained significant interest since then.

With the development of brain imaging, the emphasis has since shifted to establish the connection between disruptions in the neural system and elevated criminal behavior. Criminal behavior, especially aggression, can be observed even in toddlers at the age of 1 to 2 years, when the brain is far from mature to allow full control over behavior. As the neural systems mature, children learn to deal with their aggressive impulses in a socially appropriate manner, and aggressive behavior diminishes as a result. Therefore, it has been predicted that if development of the neural system were interrupted (e.g., prenatal or postnatal damage to the brain), the maldeveloped, immature brain would be unable to function properly in behavior control and moral reasoning and continue to use aggressive behavior as a means to obtain goals.

Several theories have been proposed to further explain the association between neurological deficits and criminal offending. Among them, three major theories have been most widely accepted and intensively tested: Terrie Moffitt's developmental theory, Antonio Damasio's somatic marker hypothesis, and Jeffrey Gray's dual biological model. Below, each hypothesis and the supporting evidence for it is reviewed. The discussion is extended by drawing additional evidence for these hypotheses from individuals with traumatic brain injuries (TBIs) to demonstrate the high prevalence of neuropathology in criminal offenders. This entry concludes by assessing the hypothesized links between neurology and crime and by discussing implications for future studies.

Theories on Neurology and Crime

Moffitt's Developmental Theory of Crime

This theory was developed based on Moffitt's 1993 groundbreaking work indicating that signs of persistent deviant behavior during adolescence can be detected as early as the preschool year and are influenced by the behavior of peer groups. This theory identified two groups of delinquents—the life-course-persistent (LCP) and the adolescent-limited (AL) offenders—based on their ages of onset and trajectories of conduct problems. The AL group may only be engaging in criminal activities as a way of expressing their adolescent rebellion and usually desist from any pathway toward crime. By contrast, the LCP group precociously escalates into serious criminal offenses as a way of expanding the versatility of their antisocial tendencies and usually maintain a lifestyle of repeated criminal offending. According to the theory, the LCP offenders may suffer prenatal and perinatal disruptions in neural development that contribute to their persistent criminal behavior. These neurological deficits, which in most cases were too subtle to require clinical remediation, often manifested as behavioral problems such as inattention, hyperactivity, irritability, and impulsivity. Thus, neurological deficits in the LCP offenders may put them at higher risk for early-onset conduct disorders, which often escalate to persistent delinquent behaviors when interacting with an unsupportive environment.

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