Impulsive-reactive violent offenders show increased autonomic activity in response to negative emotional and threatening stimuli. A volume reduction and/or activity decrease of frontal brain structures associated with impulse control and the regulation of fear and anger are likewise found in combination with a fear-related hyperactivity of the amygdala. In addition, impulsive aggression is facilitated by variants of gene polymorphisms influencing the serotonergic system. Conversely, proactive-instrumental violent offender with psychopathy, who are characterized by a lack of empathy and remorse, demonstrate an autonomic hypo-responsivity as well as dysfunctions of the amygdala and of cortical regions related to empathic and social behavior. Developmentally, aggressive children exhibit temperamental differences from early childhood on that are characteristic of a developmental pathway towards either reactive or proactive violence later in life. Exposure to negative environmental factors like ineffective parenting or childhood maltreatment has been related to a heightened risk for developing reactive violence. A developmental trajectory of proactive violence, however, has been related to a mostly genetically determined callous unemotional temperament of the child that disrupts the parental socialization efforts during childhood.

Neural and psychologic factors have been implicated as risk factors for ventricular arrhythmias and sudden death in man. However, the relation between these factors and arrhythmia has hitherto not been systematically explored. We examined the effect of psychologic stress testing in 19 patients with advanced grades of ventricular arrhythmias. Psychologic stress consisted of mental arithmetic, reading from colored cards and recounting emotionally charged experiences. Such testing induced a significant increase in ventricular premature beat frequency in 11 of 19 patients (P less than 0.05). One patient experienced paroxysms of ventricular tachycardia. In 14 of these 19 patients elicitation of vagal or sympathetic autonomic reflexes failed to induce significant arrhythmia in all but one patient. It is concluded that (1) objective psychologic tests may precipitate ventricular arrhythmia in susceptible patients, and (2) evocation of peripheral autonomic reflexes is an insufficient trigger for enhanced ventricular ectopic activity.

Uterine adrenergic and cholinergic nerves were examined histochemically and chemically in combination with surgical denervation. There was a clear regional variation with a greater number of axon terminals in the tubal end of the uterine horn and in the cervix compared to the remainder (major part) of the uterine horn. No cholinergic nerves were found in the uterus but were abundant around the uterine artery and its primary ramifications. Clusters of ganglion cells were located near the cervix: the majority were acetylcholinesterase positive, whereas the remainder stored catecholamines. Unexpectedly, the suspensory ligament (connecting the tubal end of the uterine horn with the two lower ribs) was found to contain an extensive number of adrenergic nerves. The major part of the uterine horns, as well as the cervix, was innervated mainly from two sources contributing almost equally: the paracervical ganglia (short adrenergic neurons) and postganglionic fibers running in the hypogastric nerves. A restricted area at the tubal end of the uterus received most of its via the suspensory ligament.

Cerebral blood flow (CBF) measurements have been made at systolic pressures between 40 and 170 mm Hg in 8 patients with chronic autonomic failure and widespread sympathetic efferent defects. Hypotension was produced by head up tilt. Cerebral autoregulation was preserved over a wide range and only failed at a systolic pressure close to 60 mm Hg, which is below the level at which it fails in normal subjects. Therefore, although autoregulation is probably mediated largely by local myogenic factors, its lower limit appears to be reduced by defective sympathetic function. These findings help to explain the remarkable tolerance of severe postural hypotension in autonomic failure.