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   Introduction
   Case Report
   Discussion
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 Table of Contents    
CASE REPORT  
Year : 2020  |  Volume : 62  |  Issue : 1  |  Page : 97-99
Neuropsychiatric manifestations of methyl iodide toxicity


1 Department of Psychiatry, Government Medical College and Hospital, Chandigarh, India
2 Department of Medicine, Government Medical College and Hospital, Chandigarh, India
3 Department of Radiology, Government Medical College and Hospital, Chandigarh, India

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Date of Submission21-Oct-2019
Date of Acceptance05-Dec-2019
Date of Web Publication3-Jan-2020
 

   Abstract 


Methyl iodide is an industrial chemical used in methylation for pharmaceutical intermediates. Its toxicity is a rare industrial hazard. Its toxicity is reported with both acute sudden exposure and gradual exposure. The authors report a case of methyl iodide toxicity occurring in a 47 year-old male with sudden exposure to this chemical. He presented with neuropsychiatric symptoms primarily slurring of speech, ataxia followed by delusion and hallucinations which resolved within 2 weeks with parenteral thiamine and an antipsychotic. Symptoms reappeared after a re-exposure, this time with more prominent psychiatric symptoms which were late to resolve (4 weeks) with similar treatment. Neuroimaging revealed hyperintensities in posterior regions of the brain which resolved after 4 weeks. The patient had prominent neurocognitive deficits which were persistent. The case highlights the rare chemical toxicity with neuropsychiatric manifestations with persistent neurocognitive symptoms.

Keywords: Methyl iodide, neuropsychiatric, toxicity

How to cite this article:
Sidana A, Singh A, Sawal N, Chavan B S, Gupta R. Neuropsychiatric manifestations of methyl iodide toxicity. Indian J Psychiatry 2020;62:97-9

How to cite this URL:
Sidana A, Singh A, Sawal N, Chavan B S, Gupta R. Neuropsychiatric manifestations of methyl iodide toxicity. Indian J Psychiatry [serial online] 2020 [cited 2021 Oct 23];62:97-9. Available from: https://www.indianjpsychiatry.org/text.asp?2020/62/1/97/274832





   Introduction Top


Methyl iodide is an industrial chemical. It is colorless and highly volatile substance with boiling point of 42°C.[1] It is used in methylation for pharmaceutical intermediates. Toxicity with this chemical is reported with both repeated and gradual exposure and sudden large amount of exposure. Toxicity of this chemical is a rare event with few case reports in literature.[2],[3],[4],[5],[6] The commonly reported symptoms are slurring of speech;[2],[4],[5],[6] unsteadiness of gait;[3],[4],[5],[6] confusion;[3],[5] giddiness, sleepiness, and diarrhea;[2] visual or auditory hallucination;[4],[5],[6] paranoia;[4],[6] oliguria, vomiting, restlessness, and incontinence;[2] depressive symptoms;[3] and tingling in lower extremities.[3] Prognosis of such cases has been variable with reappearance of symptoms and worsening of condition leading to coma and death.[2] The authors report a case of methyl iodide toxicity occurring in an owner of chemical plant due to accidental exposure and which responded well to high doses of parenteral thiamine and oral olanzapine within a period of 4 weeks.


   Case Report Top


A 47-year-old male, owner of an industrial plant, had accidental exposure to methyl iodide vapors due to leakage from duct at his plant 45 days before his current admission at our hospital. After 10–12 days of asymptomatic period after this exposure, the patient had sudden onset of episodic headache, ataxia, and vertigo. Within the next 2 days, the patient developed slurring of speech to the extent that it became completely incomprehensible for family members, he started having tremors while doing movements of limbs (during eating), his swaying movements increased, and he was not able to walk without support due to increased swaying and on few occasions he fell when trying to walk. He was admitted to a tertiary care teaching hospital of North India, where neurological investigations were done. Magnetic resonance imaging (MRI) brain revealed altered signal intensity predominantly involving posterior aspects of medulla oblongata including periaqueductal region, dorsal aspect of pons, midbrain, as well as dentate nuclei with sparing of dorsomedial thalami. However, cerebrospinal fluid examination and electroencephalogram were within normal range, and autoimmune encephalitis panel was also negative. On detailed neurological examination, dysarthria was present and tandem walking was impaired. He was managed with parenteral thiamine. However, within 4–5 days of admission, he additionally developed visual hallucinations, paranoid delusion, and sleep disturbance which were managed with tablet olanzapine 5 mg/d. Neurological and psychiatric symptoms started improving over a period of next 7–8 days and hence discharged from hospital. From the very next day, he resumed his work, where he had a reexposure to methyl iodide while supervising the packaging of the product. Two days after the reexposure, he again started developing swaying movements and slurring of speech which increased progressively. In addition, he became more irritable and aggressive for which he was brought to our hospital and got admitted. On examination, dysarthria was present and proprioception and tandem walking was impaired. MRI brain revealed predominant involvement of red nuclei, periaqueductal region, superior cerebellar peduncle, dorsal pons, central tegmental tract of pons, dorsal surface of medulla, left cerebellum adjacent to fourth ventricle in the region of dentate nucleus, and subtle signal alteration in the region of bilateral olivary nuclei [Figure 1]. However, the signal abnormalities were improved as compared to previous scan. He was started on high dose of parenteral thiamine. Within 2–3 days of his admission, he again started developing psychotic symptoms (visual, olfactory hallucinations, paranoid delusion, and disorganized thoughts) for which tablet olanzapine was further optimized up to 12.5 mg/d. On NIMHANS Neuropsychological Battery, the patient had cognitive deficits in the domain of processing speed, attention, verbal and category fluency, comprehension ability, verbal learning, and logical memory. In addition to the above treatment, capsule rivastigmine 3 mg/d was also added. Repeat MRI 3 weeks postadmission revealed complete resolution of previous altered signal intensities [Figure 2]. As there was improvement in both neurological and psychiatric symptoms, the patient was discharged in satisfactory condition.
Figure 1: Axial FLAIR shows signal alteration on periaqueductal region (a), central tegmental tracts (b), region of red nuclei and periaqueductal region (c), and dorsal pons and in the region of left dentate nucleus (d)

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Figure 2: Follow-up scan three weeks after readmission shows complete resolution of the signal abnormalities

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   Discussion Top


Although methyl iodide toxicity is a rare occupational exposure, it has been reported earlier with case report dating back to 1945.[2] The onset of symptoms is reported within few hours,[3],[4] 1 week,[5] and 3 weeks.[6] In the index case, this period was around 2 weeks, suggesting that there may not be immediate manifestations after exposure unlike toxicity with other gases. Majority of neuropsychiatric symptoms were seen in the index case in both the instances of exposure as reported in the literature.[2],[3],[4],[5],[6] On examination, cerebellar signs have been reported commonly[2],[3],[6] and neuroimaging has shown both a normal imaging[5] and altered signal intensities.[3],[4] Hermouet reported a lesion in the right caudate nucleus, right frontal white matter, and pigmented nuclei[3] and Ross reported high signal intensity in the cerebellum and brainstem.[4] In the index case, there was altered signal intensities in the posterior region of the brainstem which resolved in few weeks after cessation of exposure and treatment. The patient recovered in around 2 weeks after the first exposure and in 4 weeks after the second exposure with neurological symptoms recovering first in both the instances.

As the exact mechanism of methyl iodide action is unclear, the specific treatment for its toxicity is not available. It has been thought that it causes glutathione depletion leading to neurotoxicity and based on this N-acetyl cysteine has been tried, but it has not shown protective effects.[3] Symptomatic management is the option remaining in this toxicity. Saline infusion and thiazide diuretic have been used to increase clearance of the toxin.[6] Parenteral thiamine has also been used probably for its neuroprotective effects. In this case also, the patient was managed with high dose of injection thiamine.

Psychiatric symptoms usually require antipsychotics because of increased severity in some cases. Chlorpromazine has been used in such cases.[6] Due to better efficacy and tolerability, tablet olanzapine was used in the index case.

As the antidote is not available for this toxicity and sometimes this can cause fatal consequences, prevention becomes necessary in such cases. Therefore, adequate preventive measures such as apron, gloves, and mask are must in such cases.


   Conclusion Top


Methyl iodide toxicity is a rare phenomenon and neuropsychiatric manifestations can occur even after a gap of 2 weeks of exposure. Early diagnosis and high-dose parenteral thiamine is effective in reverting the neurological changes and generally antipsychotic is required to treat psychotic symptoms. It is also observed that there is reappearance of symptoms after resuming the same occupational work, so complete cessation of exposure (occupational switch) is required to prevent further worsening.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Buckell M. The toxicity of methyl iodide: 1. preliminary survey. Occup Environ Med 1950;7:122-4.  Back to cited text no. 1
    
2.
Garland A, Camps FE. Methyl iodide poisoning. Br J Ind Med 1945;2:209-11.  Back to cited text no. 2
    
3.
Hermouet C, Garnier R, Efthymiou M, Fournier P. Methyl iodide poisoning: Report of two cases. Am J Ind Med 1996;30:759-64.  Back to cited text no. 3
    
4.
Mackenzie Ross S. Delayed cognitive and psychiatric symptoms following methyl iodide and manganese poisoning: Potential for misdiagnosis. Cortex 2016;74:427-39.  Back to cited text no. 4
    
5.
Nair JR, Chatterjee K. Methyl iodide poisoning presenting as a mimic of acute stroke: A case report. J Med Case Rep 2010;4:177.  Back to cited text no. 5
    
6.
Appel GB, Galen R, O'Brien J, Schoenfeldt R. Methyl iodide intoxication. A case report. Ann Intern Med 1975;82:534-6.  Back to cited text no. 6
    

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Correspondence Address:
Dr. Ajeet Sidana
Department of Psychiatry, Government Medical College and Hospital, Sector - 32, Chandigarh - 160 030
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/psychiatry.IndianJPsychiatry_638_19

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