 |
| About Bioline | All Journals | Testimonials | Membership | News |
|
||||||
|
||||||
Neurology India, Vol. 59, No. 5, September-October, 2011, pp. 768-769 Letter to Editor Methyl bromide poisoning presenting as acute ataxia Krishnan Balagopal1, Karthik Muthusamy1, Mathew Alexander1, Sunithi Mani2 1 Department of Neurology, Christian Medical College, Vellore, India PMID: 22019671 DOI: 10.4103/0028-3886.86561 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. 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. 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
Copyright 2011 - Neurology India The following images related to this document are available:Photo images[ni11231f2.jpg] [ni11231f3.jpg] [ni11231f1.jpg] |
| |||||||||
