CLINICAL
AND
by
Edited
LABORATORY
NOTES
ROBERT S. SCHWAB
CASE R E P O R T O F A L D R I N P O I S O N I N G W I T H SPECIAL R E F E R E N C E T O EEG A N D C E N T R A L N E R V O U S SYSTEM F I N D I N G S 1 EUGENE
J.
SPIOTTA,
M.D. a n d D o ~ L. WL~Vn~LD, P h . D .
Kennedy VA Hospital, Memphis, Tennessee Aldrin (hexahydro-hexachloro-dimenthano-napthalone) is a recently developed insecticide for the control of boll weevils. T h e following is believed to be the first recorded case of human poisoning with this agent and its effects on the electroencephalogram. Fig. 1
the stomach, the local physician reported that he could find no evidence of the poison in the fluid return as determined by appearance or odor. W i t h i n a few minutes the patient had another generalized convulsion and while being restrained the left shoulder was dislocated. Barbiturates, morphine sulphate, and atropine sulfate were given intramuscularly in rather large doses. Before sufficient sedative effect could be obtained he had his fourth generalized convulsion. During the next four days a rather deep sedation was maintained by frequent doses of sodium pentobarbital. No further seizures occurred, but he continued to be very restless and completely irrational.
Fig. 2
Case report. On August 7, 1950 a 23 year old white male farmer was seen to drink a coca cola bottle full of Aldrin mixture in an attempt at suicide following an argument with his wife. W i t h i n 20 rain. he had a generalized convulsion and was then rushed to a local hospital. He was given magnesium sulfate solution as an emetic, without results. A stomach tube was passed and during its passage the patient had another generalized convulsion which lasted approximately one minute. After lavage of 1 Reviewed
in
the
Veterans
Administration
and
published
with the approval of the Chief Medical Director. The statements and conclusions published by the authors are a result of their own study and do not necessarily reflect the opinion or policy of the
Veterans Administration.
O n August 12, 1950. he was transferred to Kennedy V A Hospital. Thd patient was restless but quite stuporous and responded only to v e r y painful stimulation. T h e pupils were equal and reacted to light. E x t r a ocular-and facial movements were nor-
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ELIGENE |, S P I O T T A
real. Funduscopy was normal. There was 9ood strength in all extremities, but reflexes could not be obtained. There were no meningeal signs. The spinal fluid was under normal pressure. X-ray of the skull was normal. Prophylactic antibiotics were given and barbiturates were administered for restlessness. On August 14, 1950, paraldehyde 10 cc. every 2-4 hours as needed was substituted for the barbiturates and there~ after sedation was decreased slowly. Sedation was discontinued August 19. 1950, when he became lucid, oriented, and quieter. Patient remained amnesic concerning the suicidal attempt. Fig. 3 LF TO I~OTH
LT 5 0 MV.
and D O N L. W I N F I E L D plitude frequencies seen in the ~ronrals a~d i,.~rietais The E E G taken January 15. ~!~51 was ,~;ideri:'d to be within normal limits. Although E E G changes were marked, ~i~c~ were no symptomatic or physical evidence of ar~.;. ,~,rtrai nervous system abnormality odler than ti~: initiai episode of convulsions. There was no ~:*.:~y ~i epileptic seizures prior to the suicida! attempt Fami]'/ history recealed a maternal uncle who was : kno,~a epileptic. Psychological testing was done Auoast 23, through September 11, 1950, for evidence of organic brain damage. Other than the continued amnesia for the act of ingestin 9 the Aldrin, memory f~mction appeared to be intact for recent as well :~a remote events. The Rorschach, Wechster~Be!levuc '.'igotsky, Bender-Gestalt and Shipley Institute of Living tests revealed the patient to be an essentially normal individual with high average intelligence. None c~f the tests revealed behavior generally considered to be correlated with brain damage. The psychological testing was repeated November 27, 1950, w~d~ no significant changes. Fig. 4
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mid
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RP4IO sEPT. 12, 1950
The initial electroencephalogram ( fig. 1 ) on August 25, 1950, 18 days after the ingestion of the poison, showed a basic 6 p e r sec. generalized slowing and 3 per sec. spike and wave discharges with a multiple spike component. A follow up E E G (fig. 2) on September I, 1950, showed a 6-7 per sec. generalized slowing of a lower amplitude but containing many more 3 per sec. spike and wave discharges. E E G tracings on September 12, 1950 (fig. 3), September 21, 1950, November 28, 1950. and January 15, 1951 (fig. 4) showed continuous improvement from l'ecord to record. T h e waves became faster, the amplitude was lower, and the build~up with hyperventilation became less marked, with a quicker return to normal activity on successive recordings. The spike and wave di~.harges h a d disappeared by September 12, 1950, ahhou~h in the September 21, 1950 recording, there were some 5 per sec. moderate am-
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DISCUSSION Little is known regarding the effect of A l d r i n poisoning upon the central nervous system in man or animal. Few experimental studies have been reported to date. Findings in this particular case other than
ALDRIN POISONING the central nervous system findin0s appears elsewhere. The patient drank approximately 6 oz. of a diluted mixture of Aldrin equivalent to 1.8 gr. of concentrated Aldrin or 25.6 mg/kg. Comparable single doses in experimental animals (Boromann) have not produced death in 100 per cent of the cases. The L.D. 50 of laboratory animals weighing up to 15 kg. (approximately 35 lbs.) ranges from 44-99 rno/ko. Deaths have occurred at lower levels. Although the exact action of Aldrin on the central nervous system is not known, signs and symptoms generally appear here first. These may be convulsions, coma, hyperirritability a n d / o r hyperactivity. The onset of these signs in experimental animals may be immediate, as occurred in this patient, or delayed for several days. Large intravenous doses of barbiturates should be 9iven at the first signs of toxicity for these drugs apparently oppose the "'irritative" action of Aldrin on the central nervous system. Borgmann decreased by 20 per cent the mortality rate in rats through the prompt use of sodium Nembutal. T h e effects of Dieldrin (hexachloroepoxyoctalydro~dimethalene), a chemically related insecticide producing similar central nervous system symptoms, were also inhibited by large doses of sodium phenobarbital (Nagel). Histological findings in animals that died as a result of Aldrin poisoning revealed oeneralized vascular congestion with blood vessel cuffing and severe 0anglion-cell degeneration. Eccentric hyperchromic nuclear straining of neuronophaoia were also seen (Dutra).
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Electroencephalographic changes have been seen in Dieldrin poisoning in monkeys. There were spike discharges as seen in this patient's initial tracing. T h e serial E E G s of this patient over a 5 ~ month period show complete clearing of the abnormalities seen in the first tracing. Other than the initial convulsions no central nervous system organic signs could be found as determined by careful analysis of the patient's symptoms, physical examination or psychological study, Relapses have occurred within two months after Dieldrin poisoning (NageI), but none are known to occur from Aldrin poisoning. The only anti-convulsive therapy given to the patient was the administration of the barbiturates for 12 days after the inaestion of the poison. The initial slowing in the E E G appeared to be similar to that which is sometimes seen after the brain has been subjected to trauma. In light of the patient having had no known epileptic seizure from September 1950 to August 1951, with an accompanying normal E E G in January 1951, the prognosis would seem to be favorable. REFERENCES BORGMANN, A. R. Toxicological studies of Aldrin in laboratory animals. Unpublished data. DUTaA, FRANK R. Unpublished data. NAGEL, L. R. Personal communication. SPIOTTA, EUGENE J. Aldrin poisonin 9 in man with report of a case. Arch. Ind. Hyg. Occup. Med., 1951, 4: 560.
Re[erence: SPIOTTA, E. J. and WINFIELD, D. L I. Case report of Aldrin poisoning with special reference to E E G and central nervous system findings. EEG Clin. Neurophysiol., 1952, 4: 215-217.