Hospitalized offspring of holocaust survivors. Problems and dynamics.
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Biomedical subjects
Publications and source records attributed to J H Rau.
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Fifty-nine compulsive eaters were interviewed, had a complete waking and sleep EEG tracing, and were offered a trial with phenytoin. Forty-seven patients had an adequate pharmacological intervention. Analyses of the EEGs showed a disproportionately higher percentage of abnormal EEGs and of paroxysmal EEGs in particular among compulsive eaters as contrasted with unselected psychiatric patients and normal controls. Patients with abnormal EEGs responded to phenytoin treatment statistically more frequently than those with normal EEGs--even after conservatively classifying "uncertain" patients as non-responders. Patients with 14 & 6/sec. positive spikes alone showed a phenytoin improvement significantly greater than that seen with either normal EEG subjects or other EEG abnormalities. There are suggestions of a weight by EEG interaction in that the combination of weight deviance (viz: emaciated or obese) plus abnormal EEG seems especially highly predictive of good phenytoin response. The EEG results combined with phenytoin response suggest that neurophysiological etiological hypotheses may have merit for some compulsive eating disorders. Suggestions for additional research are made and the need for controlled replication of these data results is stressed.
Thirty patients with the syndrome of episodic compulsive eating (binge eaters) were given a neurophysiological evaluation which included a complete electroencephalogram (EEG) and a structured interview. The interview was designed to elicit 10 "neurological soft signs" (rage attacks, frequent headaches, dizziness, stomach aches, nausea, parethesias, history of convulsions, perceptual disturbances, other compulsions, and a family history of epilepsy). Afterwards, 23 patients received an adequate trial with phenytoin. The sum of the 10 neurological soft signs and the EEG (as an 11th sign) was significantly correlated with improvement. No single sign or other combination of signs was significantly a predictor of improvement. These results lend support to the thesis that in some episodic compulsive eaters, a neurophysiological substrate may be involved.
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