TY - JOUR
PY - 1998//
TI - Reduced prefrontal and increased subcortical brain functioning assessed using positron emission tomography in predatory and affective murderers
JO - Behavioral sciences and the law
A1 - Raine, Adrian
A1 - Meloy, J. Reid
A1 - Bihrle, Susan
A1 - Stoddard, Jackie
A1 - LaCasse, Lori
A1 - Buchsbaum, Monte S.
SP - 319
EP - 332
VL - 16
IS - 3
N2 - There appear to be no brain imaging studies investigating which brain mechanisms subserve affective, impulsive violence versus planned, predatory violence. It was hypothesized that affectively violent offenders would have lower prefrontal activity, higher subcortical activity, and reduced prefrontal/subcortical ratios relative to controls, while predatory violent offenders would show relatively normal brain functioning. Glucose metabolism was assessed using positron emission tomography in 41 comparisons, 15 predatory murderers, and nine affective murderers in left and right hemisphere prefrontal (medial and lateral) and subcortical (amygdala, midbrain, hippocampus, and thalamus) regions. Affective murderers relative to comparisons had lower left and right prefrontal functioning, higher right hemisphere subcortical functioning, and lower right hemisphere prefrontal/subcortical ratios. In contrast, predatory murderers had prefrontal functioning that was more equivalent to comparisons, while also having excessively high right subcortical activity.
RESULTS support the hypothesis that emotional, unplanned impulsive murderers are less able to regulate and control aggressive impulses generated from subcortical structures due to deficient prefrontal regulation. It is hypothesized that excessive subcortical activity predisposes to aggressive behaviour, but that while predatory murderers have sufficiently good prefrontal functioning to regulate these aggressive impulses, the affective murderers lack such prefrontal control over emotion regulation. © 1998 John Wiley & Sons, Ltd.
Language: en
LA - en SN - 0735-3936 UR - http://dx.doi.org/10.1002/(SICI)1099-0798(199822)16:3<319::AID-BSL311>3.0.CO;2-G ID - ref1 ER -