Abstract

Chronic lead poisoning, commoner in low and middle income countries can cause neurological disorders. We present such a case with long standing cerebellar syndrome and sensory neuropathy, presenting as status epilepticus where chronic lead toxicity was confirmed to be the cause. A 35 year male presented with status epilepticus. Over a period of 7 years he suffered from cerebellar ataxia and sensory neuropathy. He was also hypertensive. MRI brain showed bilateral cerebellar and thalamic hyperintensities (Fig 1). Latest MRI also shows significant cerebellar atrophy. CSF showed albumin-cytological dissociation (fig 2). The serum lead level was 33 micromol/litre (Normal less than 5). No history of direct ‘occupational’ exposure noted. He lived adjacent to a main road within the central city limits. Given the clinical presentation and biochemistry chelation with peniclillamine was initiated. Chronic lead toxicity causes encephalopathy and sensory predominant peripheral neuropathy as seen here.Hypertension is known to be associated. Albumin-cytological dissociation in CSF is a rare but consistent finding. MRI typically shows hyperintensities in basal ganglia, thalami and cerebellum. Serum lead levels remain the best marker of toxicity. However in chronic disease the levels may not correlate with the outcome. Chelating agents used are either EDTA, DMSA, or penicillamine. Seizures were controlled with anti-epileptics. Lead toxicity should be considered a possibility in ataxia due to combined sensory neuropathy & cerebellar dysfunction. Presentation with status epilepticus was unusual. It is a reversible condition with chelation.

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