Medical Aspects of Chemical Warfare (2008) - The Black Vault

Medical Aspects of Chemical Warfareexposure. But no measurements were taken between 8and 24 hours, and the maximal inhibition might havebeen in this period. Often it is overlooked that theremay be a long delay between exposure on the skinand onset of signs or symptoms. The study authorsstressed that psychological impairment might occurbefore the onset of other signs or symptoms or mightoccur in their absence. 84Although the frequency, onset, and duration of eachreaction were not noted, some of the behavioral effectsreported in the VX subjects were fatigue, jitterinessor tension, inability to read with comprehension, difficultieswith thinking and expression, forgetfulness,inability to maintain a thought trend, a feeling of beingmentally slowed, depression, irritability, listlessness,poor performance on serial 7s (subtracting from 100 by7s) and other simple arithmetic tests, minor difficultiesin orientation, and frightening dreams. Illogical or inappropriatetrends in language and thinking were notnoted, nor was there evidence of conceptual looseness.The investigators found no evidence of perceptualdistortion resulting in delusions or hallucinations.A severe, accidental exposure to soman caused oneperson to become depressed, withdrawn, and subdued,have antisocial thoughts, and sleep restlesslywith bad dreams for several days immediately afterthe exposure (see Exhibit 5-1). 20 He received oral dosesof scopolamine hydrobromide on 3 of the following6 days and was given scopolamine methylbromide,which does not enter the CNS, on the other days tomimic the peripheral effects of hydrobromide salt, suchas dry mouth. On the hydrobromide days, the subjectwas more spontaneous and alert, less depressed, andslept better; his performance on a simple arithmetic testalso improved. Because scopolamine hydrobromideis more effective in the CNS than the methylbromidesalt of scopolamine or atropine, it seemed likely thatthe drug reversed the CNS effects, at least temporarily.The subject ’ s performance on standard psychologicaltests 16 days after exposure was below that expectedfor one of his intellectual capabilities, but it improvedto his expected level of functioning when he was tested4 months later and again 6 months later when he wasdischarged from further care. The author suggestedthat the use of scopolamine hydrobromide deservesfurther evaluation in patients who have these lingeringeffects while recovering from nerve agent poisoning.Changes in the ability to perform certain laboratoryor field tests after exposure to sarin have been reported.Generally, at the exposures used (Cts of 4–14.7mg/min/m 3 ), there was some impairment on tasksrequiring vision, hand-eye coordination, dexterity,response time, comprehension, and judgment. 85,86 Nodecrements were found on physical tasks 87 (at a Ct of14.7 mg/min/m 3 ). On a military field exercise, 88 mosttasks were performed satisfactorily, if suboptimally, inthe daylight. Nighttime performance, however, wasdifficult, if not hazardous due to a miosis-induceddecrement in dark adaptation and subsequent visualacuity.The behavioral effects of exposure to nerve agentsor other potent organophosphorus compounds in humanscan be conceptually grouped into three classes:effects on cognitive processes, effects on mood oraffect, and disturbances of sleep-wakefulness. Thiscluster of CNS and behavioral effects of nerve agentsis consistent with what is known about the role ofACh and cholinergic neurons within the brain. Centralcholinergic circuits are involved in both cognition andshort-term memory, as demonstrated by the effectsof drugs, 89 experimentally produced lesions, 90 andnaturally occurring pathological states of cholinergicinsufficiency (such as Alzheimer ’ s disease). 91 It has alsobeen hypothesized for a number of years that depressionis due to an imbalance between the cholinergicand adrenergic systems within the brain, and thatdepressive symptoms are associated with cholinergichyperactivity. 92–94 Finally, sleep cycle control, specificallythe initiation and maintenance of the rapid eyemovement (REM) stage of sleep, the sleep stage that isassociated with dreaming, is controlled by increasedactivity of cholinergic neurons within specific nucleiin the pontine brain stem. 95–98 Administration ofcarbamates, organophosphorus anticholinesterasecompounds, or cholinergic agonists that act like nerveagents can induce REM sleep in both animals andhumans. 98–102Electroencephalographic EffectsInformation is scanty on the electroencephalographic(EEG) effects in humans who have been severelypoisoned by ChE-inhibiting substances. In an earlystudy, 103 DFP, administered intramuscularly daily,caused EEG changes in 19 of 23 subjects (19 normal, 4with myasthenia gravis). The changes were• greater-than-normal variations in potential;• increased frequency, with increased betarhythm; and• more irregularities in rhythm and the intermittentappearance of abnormal waves (highvoltage,slow waves; these were most prominentin the frontal leads).These changes usually followed the onset of CNSsymptoms, they could be correlated with decreasesof RBC-ChE activity (but not with BuChE decreases),176