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Table of Contents    
Year : 2011  |  Volume : 59  |  Issue : 5  |  Page : 768-769

Methyl bromide poisoning presenting as acute ataxia

1 Department of Neurology, Christian Medical College, Vellore, India
2 Department of Radiodiagnosis, Christian Medical College, Vellore, India

Date of Submission02-Sep-2010
Date of Decision02-Sep-2010
Date of Acceptance12-Jan-2011
Date of Web Publication22-Oct-2011

Correspondence Address:
Mathew Alexander
Department of Neurology, Christian Medical College, Vellore
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.86561

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How to cite this article:
Balagopal K, Muthusamy K, Alexander M, Mani S. Methyl bromide poisoning presenting as acute ataxia. Neurol India 2011;59:768-9

How to cite this URL:
Balagopal K, Muthusamy K, Alexander M, Mani S. Methyl bromide poisoning presenting as acute ataxia. Neurol India [serial online] 2011 [cited 2021 Oct 16];59:768-9. Available from:


Methyl bromide is a widely used industrial compound. Exposure to it causes acute toxicity, with severe giddiness, confusion, and slurred speech. We present a patient with an acute onset of ataxia who was later found to have had exposure to methyl bromide.

A 32-year-old man with no significant past medical history presented with imbalance while walking, slurred speech, and tremulousness of the upper limbs, which was more when reaching an object. All symptoms had been present for 1 week. His history revealed that he was working as a contract laborer in a factory that processed raw materials for a pharmaceutical company. His symptoms had started after accidental inhalation of fumes at the workplace; this was later found to be methyl bromide. On examination, he had cerebellar dysarthria, scanning speech, bilateral limb incoordination, and gait ataxia.

His complete blood picture and blood biochemistry were normal. Magnetic resonance imaging (MRI) of brain [Figure 1] and [Figure 2] revealed mild swelling and significant hyperintense lesions in the posterior pons, bilateral olivary nuclei, and dentate nuclei, with focal central restricted diffusion in the splenium of the corpus callosum on T2-weighted sequence. Since the occupational exposure to bromide was significant, bromide toxicity with encephalopathy was considered likely. High serum levels of chloride supported this diagnosis. Workup, including cerebrospinal fluid (CSF) examination, for other diagnostic possibilities was negative.
Figure 1: ADC, DWI axial section at the level of the lateral ventricles showing focal restricted diffusion in the splenium of the corpus callosum

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Figure 2: ADC, DWI axial section at a similar level a week later showing resolution of restricted diffusion

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He was started on forced diuresis therapy with intravenous saline and loop diuretics. With 2 days treatment he improved significantly and could walking without support, and his speech also became normal over the next 2 days. Repeat imaging of the brain [Figure 3] showed significant resolution of the hyperintense lesions. He was educated about the toxicity of the chemicals at his workplace and was advised to either take adequate precautions or to avoid exposure altogether. He was also advised follow-up in the outpatient department.
Figure 3: T2W axial sections at the level of the medulla and pons showing symmetric hyperintensity in the olivary nuclei, dentate nuclei, and the dorsal pons. These findings have been described in methyl bromide toxicity and metronidazole toxicity

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Neurological manifestations of acute methyl bromide poisoning have been categorized into three stages: [1]

(1) a premonitory stage, with vomiting, headache, vertigo, ataxia, and visual disturbances; (2) a cerebral irritation stage, with convulsions, delirium, and mania; and (3) a recovery stage, with hallucinations, amnesia, apathy, and incoordination that may last for many years. The features of acute intoxication are varied and may include headache, nausea, vomiting, sense of drunkenness, ataxia, slurred speech, and confusion. The mechanism of action of methyl bromide on the nervous system is not completely understood.

There have been earlier reports of MRI abnormalities in methyl bromide poisoning. Ichikawa et al.[2] reported a case of chronic methyl bromide intoxication showing bilateral symmetric lesions in the putamen, subthalamic nuclei, dorsal medulla, inferior colliculi, and periaqueductal gray matter of the midbrain. Lesions in the splenium of the corpus callosum have been reported by Kang et al.[3] The treatment of methyl bromide poisoning is mainly symptomatic, besides hydration and loop diuretics. In severe cases, anticonvulsant therapy and intensive unit care may be required. Hemodialysis is the treatment of choice in severe cases. [4]

  References Top

1.Shield LK, Coleman TL, Markesbery WR. Methyl bromide intoxication: Neurologic features, including simulation of Reye syndrome. Neurology 1977;27:959-62.  Back to cited text no. 1
2.Ichikawa H, Sakai T, Horibe Y, Kaga E, Kawaura M. A case of chronic methyl bromide intoxication showing symmetrical lesions in the basal ganglia and brain stem on magnetic resonance imaging. Rinsho Shinkeigaku 2001;41:423-7.  Back to cited text no. 2
3.Kang K, Song YM, Jo KD, Roh JK. Diffuse lesion in the splenium of the corpus callosum in patients with methyl bromide poisoning. J Neurol Neurosurg Psychiatry 2006;77:703-4.  Back to cited text no. 3
4.Hustinx WN, van de Laar RT, van Huffelen AC, Verwey JC, Meulenbelt J, Savelkoul TJ. Systemic effects of inhalational methyl bromide poisoning: A study of nine cases occupationally exposed due to inadvertent spread during fumigation. Br J Ind Med 1993;50:155-9.  Back to cited text no. 4


  [Figure 1], [Figure 2], [Figure 3]

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