EEG, PSYCHOLOGICAL, AND NEUROLOGICAL ALTERATIONS IN HUMANS WITH ORGANOPHOSPHORUS EXPOSURE *

In the early 195O’s, the University of Colorado Medical Center conducted a multidisciplinary investigation of industrial and agricultural workers acutely exposed to a variety of pesticides. The focus of this program was a special project involving the intensive study of workers engaged in the manufacture of several organophosphorus (OP) anticholinesterase compoh,. ’.,. Because of the acute confusional states induced by O P exposure and because of the need for more information regarding the central effects of OP exposure in humans, an effort was made to examine certain psychological, neurological, and clinical-neurophysiological variables; additionally, a number of biochemical parameters were investigated. Since January, 1965, a group of men from this same industrial population has been studied; many of the current subjects have been continuously employed in the same capacity since 1950. This report is concerned primarily with some of the psychological, neurological, and clinical-neurophysiological results of these studies. In the 1952 program, psychological testing involved a large battery of measures designed to search for classic evidences of brain damage. Data analysis revealed no formal evidences of organic brain damage in psychological test terms. Testing done within 72 hours of exposure almost always showed erratic and slowed functioning, interpreted as indicating the presence of clinical delirium for many individuals within three days of a symptomatic exposure. The one differentiating test in the original study was the Rotary-Pursuit task, a test of hand-eye coordination. Recently exposed men had worse performance than controls, but we have since found that this type of test is unreliable because of technical limitations. Neurological examinations revealed multiple minor signs such as generalized weakness and confusion shortly after exposure; hard neurological signs were absent after treatment and clinical recovery. In the 1952 study, electroencephalograms were done as close to time of exposure as possible and, in many cases, repeated after treatment and recovery. Typical slow-wave bursts after activation by overbreathing were observed if EEGs were done soon after untreated exposure (FIGURE 1 ). These findings were similar to those reported by Grob (1953). A t this time, it was believed that adequate treatment normalized the EEG. These old EEGs have been reevaluated in light of findings from our current investigations and modern knowledge of the neurophysiology of drowsiness and sleep. Upon reevaluation, we find an increase in medium-voltage, irregular theta activity, OCcurring in bursts of one to five seconds’ duration, most often seen during light drowsiness. Special characteristics of the drowsy EEG-there is a normal increase in slow activity-made it easy to overlook this change. In the 1952 study, psychiatric interviews were done o n 78 men: 56 with histories