Sequelae of Thallium Poisoning: Clinical and Neurophysiological Follow-Up

poisoning. Gradually the patient became drowsy and developed ptosis, glossitis, stomatitis, alopecia, Mees lines, head tremor and nystagmus. His blood thallium level was 40,980
g/ml and urine 608 g/ml. He was treated with hemodialysis, potassium, laxatives and high-dose multivitamins. Gradually his sensorium improved, and ptosis and head tremor disappeared, but he developed grade 3 quadriplegia with glove and stocking sensory loss. Biceps, triceps and knee reflexes were normal, and ankle reflexes were absent bilaterally. His Mini-Mental State Examination (MMSE) score was 22, and the patient had postural hypotension. At the 3-month follow-up, the patient was completely bald ( fig. 1 a) and dependent for activities of daily living. He had masking of face, abulia, gaze evoked nystagmus and unsteady gait. Vision was 6/60 bilaterally and the fundus normal. Muscle power was grade 4 at the knee and grade 3 at the ankle, with loss of ankle reflex. The touch and pinprick sensations were diminished bilaterally below the ankle. His biochemical tests for liver and kidney functions were normalized. By 6 months he was able to walk independently with mild unsteadiness but was unable to resume duty due to poor vision. His symptoms related to autonomic dysfunction such as postural giddiness, dryness of mouth and eyes, and reduced sweating improved by 1 year but the decreased libido persisted even at the 3-year follow-up. At the 3-year follow-up he was independent for activity of daily living, and his MMSE score was 30. He had mild extrapyramidal signs (masking, positive Dear Sir, Thallium is a heavy metal and is used as rodenticide, in the manufacture of optical lenses, semiconductors, low temperature thermometer, switching devices, green firework, imitation jewelry, chemical catalyst and as an isotope in nuclear scan [1, 2] . Industrial and suicidal thallium poisoning in recent years is rare due to unavailability and strict regulation; but still it is used as a homicidal agent, as thallium salts are colorless, odorless and tasteless. Acute thallium poisoning is characterized by multisystem involvement, and neurological manifestations include severe paresthesia, peripheral neuropathy, ptosis, tremor, encephalopathy and cerebellar symptoms [3– 6] . Subacute poisoning manifests itself slowly with alopecia and peripheral neuropathy. Chronic poisoning manifests itself with extrapyramidal features, especially parkinsonian tremor and choreoathetosis [3] . Studies on long-term follow-up of acute thallium poisoning are few, and persistent cognitive, visual and peripheral neuropathy have been reported in some patients [7, 8] . There is no study evaluating delayed sequelae of acute thallium poisoning employing multimodality evoked potentials. We have reported acute complications of a patient with homicidal thallium poisoning [4] . In this communication we report clinical and neurophysiological sequelae of the same patient 3 years later.