Eugene Ziskind

Psychophysiology of sociopathy: Electrocortical measures

The CNV, visual AEP and resting EEG were analyzed in sociopaths and controls matched for age and sex. Twenty-seven male sociopaths were selected by psychiatric interview and special rating scale, restricted to Shipley-Hartford IQs of 115-145 and separated into young (x = 20.5 yr) and older (x = 35.3 yr) age groups. Subjects participated in forewarned reaction-time tasks in which the imperative stimulus was either an innocuous or noxious tone that the subject escaped by pressing a response key. Sociopaths and controls did not differ in reaction time, vertex and occipital AEP amplitude or latency, and power spectral density of the EEG. Contrary to previous findings, there also were no significant differences between sociopaths and controls in overall CNV amplitude or topography. However, while most controls showed increased CNV amplitude in the noxious tone condition as compared to the innocuous tone condition, older sociopaths showed no change, or decreased amplitudes.

Aversive conditioning in the sociopath

Results of two experiments on differential conditioning of the skin conductance (SCR) in sociopaths and normal control subjects are described. In the first experiment it was found that an equal number of sociopaths and control subjects were aware of the conditioning contingency. However, only the normal subjects displayed reliable differential SCR conditioning. Sociopaths showed a dissociation between verbal learning and conditioning of a physiological change. The second experiment examined the differential conditioning of normal subjects and sociopaths in partial remission. The number of aware subjects in the two groups did not differ. Aware subjects in both groups showed differential SCR conditioning. Differential conditioning in sociopaths did not persist over trials as it did in control subjects. A deficiency in ACTH 4–10 as well as neurological dysfunctions were considered possible factors in the etiology of sociopathy. Further research on the relation of neuropeptides to the etiology and treatment of sociopathy is suggested.

Hallucinations in Sensory Deprivation—Method or Madness?

Ten-minute observations of visual fields in binocularly patched subjects, and self-observation for dreams yielded visual imagery similar to sensory deprivation hallucinations. The latter probably arise from fragments of normal imagery whose origins are unrecognized because of reduced awareness.

Relationship Of Nailbiting To Sociopathy

The incidence of nailbiting in 62 sociopath subjects was compared with that in 62 nonsociopath matched controls utilizing the Cornell Medical Index Health Questionnaire. Results indicated that the incidence of nailbiting in primary sociopaths (48 per cent) was significantly greater (p less than .01) than the incidence of nailbiting in the control group (24 per cent). Implications of these findings are discussed in terms of the significance of nailbiting in sociopaths, particularly the relationship of nailbiting and anxiety in primary sociopathy.

Relationship Between Insulin Dosage, Duration and Degree of Hypoglycemia and Production of Brain Damage.∗†

Conclusions 1. The larger the dose of insulin the greater the incidence of brain damage. However, irrespective of the insulin dose, brain damage did not occur in our animals unless they were kept in the “medullary stage” of hypoglycemia for at least 100 minutes. 2. In cats, not previously treated with insulin, the larger the dose the longer time it took for the appearance of neurologic signs of hypoglycemia.

Decorticate and Decerebrate Preparations Produced by Insulin Shock.

During insulin shock induced therapeutically there is a progressive depression of nervous functions, in a gradient manner, from the highest (cortical) levels to lower subcortical levels (striatum, mid-brain, medullary) which is temporary and reversible. 1 , 2 It was decided to demonstrate this gradient effect clinically with the production of animal preparations showing permanent, irreversible lesions at progressively lower levels in the nervous system by prolonging the period of hypoglycemia. Cats, fasted 18 hours, were given 15 to 20 units of insulin per kilo body weight. When clinical signs indicated early medullary decompensation, small amounts of glucose were given intraperitoneally to prevent death and still maintain a marked degree of hypoglycemia. Hypoglycemia was terminated after 12 to 20 hours. Persistent brain damage was observed in 17 animals. Group I consisted of 5 animals with variable degrees of cortical damage. Group 2 totaled 8 animals with cortical plus subcortical injury (“thalamic preparations”?). Group 3 included 4 cats with loss of function at the midbrain level or lower. The decorticate preparations (Group 1) showed impairment of vision, impairment of placing and hopping reactions (Bard), slight impairment of righting reactions, difficulty in feeding self, impairment of cleaning habits, restlessness and absence of rage reaction when confronted by a dog. They were able to walk and maintained normal body temperature. These preparations were kept alive from 6 to 90 days. Preparations in Group 2 showed in addition to the above, inability to walk, decerebrate rigidity, increased tonic neck reflexes and mock rage. These animals were also able to maintain body temperature. These signs point to loss of function at the “thalamic level.” The animals lived 19 to 48 hours after the hypoglycemia was terminated. Animals in Group 3 were not studied as carefully as the above, but are added because they showed inability to maintain body temperature.