TY - JOUR
T1 - Syndrome E
AU - Fried, Itzhak
PY - 1997/12/20
Y1 - 1997/12/20
N2 - The transformation of groups of previously nonviolent individuals into repetitive killers of defenceless members of society has been a recurring phenomenon throughout history. This transformation is characterised by a set of symptoms and signs suggesting a common syndrome - Syndrome E. Affected individuals show obsessive ideation, compulsive repetition, rapid desensitisation to violence, diminished affective reactivity, hyperarousal, environmental dependency, group contagion, and failure to adapt to changing stimulus-reinforcement associations. Yet memory, language, planning, and problem-solving skills remain intact. The main risk factors are male sex and age between 15 and 50. A pathophysiological model - 'cognitive fracture' - is hypothesised, where hyperaroused orbitofrontal and medial prefrontal cortices tonically inhibit the amygdala and are no longer regulated by visceral and somatic homoeostatic controls ordinarily supplied by subcortical systems. It is proposed that the syndrome is a product of neocortical development rather than the manifestation of a disinhibited primitive brain. Early recognition of symptoms and signs could lead to prevention through education and isolation of affected individuals.
AB - The transformation of groups of previously nonviolent individuals into repetitive killers of defenceless members of society has been a recurring phenomenon throughout history. This transformation is characterised by a set of symptoms and signs suggesting a common syndrome - Syndrome E. Affected individuals show obsessive ideation, compulsive repetition, rapid desensitisation to violence, diminished affective reactivity, hyperarousal, environmental dependency, group contagion, and failure to adapt to changing stimulus-reinforcement associations. Yet memory, language, planning, and problem-solving skills remain intact. The main risk factors are male sex and age between 15 and 50. A pathophysiological model - 'cognitive fracture' - is hypothesised, where hyperaroused orbitofrontal and medial prefrontal cortices tonically inhibit the amygdala and are no longer regulated by visceral and somatic homoeostatic controls ordinarily supplied by subcortical systems. It is proposed that the syndrome is a product of neocortical development rather than the manifestation of a disinhibited primitive brain. Early recognition of symptoms and signs could lead to prevention through education and isolation of affected individuals.
UR - http://www.scopus.com/inward/record.url?scp=0031588518&partnerID=8YFLogxK
U2 - 10.1016/S0140-6736(97)09385-9
DO - 10.1016/S0140-6736(97)09385-9
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AN - SCOPUS:0031588518
SN - 0140-6736
VL - 350
SP - 1845
EP - 1847
JO - The Lancet
JF - The Lancet
IS - 9094
ER -