Year : 2012  |  Volume : 16  |  Issue : 1  |  Page : 38--39

Neuropsychiatric manifestations of methyl iodide


Shubhangi R Parkar, Tushita S Mayanil 
 Department of Psychiatry, Seth G.S.M.C. & K.E.M. Hospital, Mumbai, India

Correspondence Address:
Shubhangi R Parkar
Department of Psychiatry, G.S.M.C. & K.E.M. Hospital, Parel, Mumbai - 12
India

Abstract

Methyl iodide is a monohalomethane and with a chemical formula CH 3 I. Acute exposures to methyl iodide have frequently occurred in the workplace. Predominantly, neuropsychiatric symptoms of acute exposure to monohalomethanes consist of headache, nausea, vomiting, drowsiness, dizziness, giddiness, diarrhea, confusion, ataxia, slurred speech, paralysis, convulsions, delirium, coma, and death. We report two cases who presented to our emergency services after accidental exposure to methyl iodide for a short duration. These case reports highlighted concurrence of frankly psychotic features and acute confusional state in workers vulnerable to industrial exposure to toxic chemicals. Understanding the mechanism of neuro-toxicity will perhaps throw some light on co-existence of both psychiatric and neurological symptoms. Awareness of these toxic effects at vulnerable work places will lead to timely and appropriate interventions. Importance of safety precautions and education of both workers and supervisors cannot be overemphasized here



How to cite this article:
Parkar SR, Mayanil TS. Neuropsychiatric manifestations of methyl iodide.Indian J Occup Environ Med 2012;16:38-39


How to cite this URL:
Parkar SR, Mayanil TS. Neuropsychiatric manifestations of methyl iodide. Indian J Occup Environ Med [serial online] 2012 [cited 2019 May 25 ];16:38-39
Available from: http://www.ijoem.com/text.asp?2012/16/1/38/99694


Full Text

 Introduction



Methyl iodide is a monohalomethane and with a chemical formula CH 3 I. It has been used as methylating agents, laboratory reagents, pesticides, and in microscopy. Many recent studies indicated neurotoxic as well as fetal toxic effects in laboratory animals. There are 11 cases of acute methyl iodide exposure in the medical literature. [1] The human exposure to methyl iodide occurs through routes like dermal, inhalation, and oral ingestion. Acute exposures to methyl iodide have frequently occurred in the workplace. Predominantly neuropsychiatric symptoms of acute exposure to monohalomethanes consist of headache, nausea, vomiting, drowsiness, dizziness, giddiness, diarrhea, confusion, ataxia, slurred speech, paralysis, convulsions, delirium, coma, and death. [2],[3],[4],[5],[6] One case of suicidal parenteral exposure has been reported. [7] Prominent delayed neuropsychiatric manifestations as behavioral disturbances, cognitive deficits, psychoses, and emotional liability have also been noted lasting for months to years. [8] The primary target organs in cases of severe poisoning are lungs, liver, kidney, and brain. Animal studies have shown methyl iodide to be a potential carcinogen and teratogen. [9],[10] A case presenting with repeated overexposure producing recurrent attacks of multifocal neurological dysfunction mimicking multiple sclerosis has also been reported. [1]

We report two cases who presented to emergency services of tertiary care public hospital, after accidental exposure to methyl iodide for a short duration.

 Case Reports



Case 1

A 23-year-old industrial worker, was accidentally exposed to an unknown quantity methyl iodide vapors for 5 to 10 seconds at his place of work. This resulted in loss of consciousness for few minutes. After regaining consciousness, he had altered behavior in the form of muttering to self, running around aimlessly, picking at his clothes and saying fearfully that somebody is coming to kill him. Mental status examination further revealed that he was disoriented in time, place, and person; physical examination showed pulse was 102 per minute and weak and blood pressure was 100/70 mmHg at the time of emergency evaluation. His pupils were dilated and he had a left seventh nerve palsy of lower motor neuron type and depressed gag reflex. Routine investigations were within normal limits except for a transient elevation in liver transaminases.

Gradually, his sensorium and neurological signs improved. The patient reported fearfulness, persecutory delusions, and occasional auditory hallucinations after resolution of neurological symptoms. The psychotic features gradually settled over a week with 4 mg of lorazepam.

Case 2

A 34 year industrial worker, was brought with accidental workplace exposure to methyl iodide for 15 to 30 s. He had been working there for the past 9 years. On his entry to emergency unit, his pulse was 90/min and blood pressure was 110/80 mm of Hg and respiratory rate was 30/min. He had a lower motor neuron type left seventh nerve palsy and horizontal nystagmus. All routine investigations revealed no abnormality except for small pleural effusion on the chest x-ray.

Gradually, the patient's sensorium improved over next 2 days, he complained of extreme anxiety, fear, restlessness, and poor sleep. This continued for next 10 days and gradually subsided on 2 mg of clonazepam. Over the same time span, the patient showed complete resolution of the neurological signs.

In both these cases no history of any other organic, metabolic, infective, or intoxication causes was found on detailed enquiry. They were given benzodiazepine drugs for symptomatic relief, i.e. to control anxiety and agitation. They were supervised closely. These patients did not have neuropsychiatric manifestations on follow up.

 Discussion



These case reports highlight concurrence of frankly psychotic features and acute confusional state in workers vulnerable to industrial exposure to toxic chemicals. Understanding the mechanism of neurotoxicity will perhaps throw some light on co-existence of both psychiatric and neurological symptoms. All methyl halides follow the same metabolic pathway. In the major pathway, glutathione S tranferase conjugates methyl iodide with glutathione (GSH). This results in formation of final products methanethiol, H 2 S and free radicals. All three of the above have been linked to neurotoxicity of methyl iodide. These have been shown to bind to cytochrome oxidase in the mitochondria and thus disrupt the oxidative pathway of ATP generation leading to cell death and neurotoxicity. Depletion of GSH has also shown to decrease cell's ability to combat oxidative stresses and thus the cytotoxicity. [11],[12],[13]

Further, the presence of psychotic features in such patients does not warrant treatment with antipsychotic drugs and caution should be maintained while doing the same in an already compromised nervous system. No specific antidote or treatment modality has been studied except for efficacy of N-acetylcysteine in a few cases. Supportive treatment for maintenance of general medical condition should be provided to patients. Monitoring of these patients for long-term neuropsychiatric sequelae is important.

Awareness of these toxic effects at vulnerable work places will lead to timely and appropriate interventions. Importance of safety precautions and education of both workers and supervisors cannot be overemphasized here. Relatively, the Indian literature is found to be inadequate regarding safety exposure limits (SELs) of individual industrial chemicals. Occupational Safety and Health Administration (OSHA), 1989, and American Conference of Governmental Industrial Hygienists (ACGIH), 1984-85, recommend Permissible Exposure Limit (PEL) of methyl iodide as (for 8 h) 2 ppm. [14] However, timely identification of toxic effects and early intervention will go a long way in these unfortunate accidental events.

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