Fax +41 61 306 12 34 E-Mail karger@karger.ch www.karger.com Letter to the Editor Eur Neurol 2006;56:253–255 DOI: 10.1159/000096675 Sequelae of Thallium Poisoning: Clinical and Neurophysiological Follow-Up J. Kalita U.K. Misra Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India poisoning. Gradually the patient became drowsy and developed ptosis, glossitis, sto- matitis, 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, potas- sium, laxatives and high-dose multivita- mins. Gradually his sensorium improved, and ptosis and head tremor disappeared, but he developed grade 3 quadriplegia with glove and stocking sensory loss. Bi- ceps, triceps and knee reflexes were nor- mal, and ankle reflexes were absent bilat- erally. His Mini-Mental State Examina- tion (MMSE) score was 22, and the patient had postural hypotension. At the 3-month follow-up, the patient was completely bald (fig. 1a) and dependent for activities of daily living. He had masking of face, abu- lia, 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 pin- prick sensations were diminished bilater- ally below the ankle. His biochemical tests for liver and kidney functions were nor- malized. By 6 months he was able to walk independently with mild unsteadiness but was unable to resume duty due to poor vi- sion. His symptoms related to autonomic dysfunction such as postural giddiness, dryness of mouth and eyes, and reduced sweating improved by 1 year but the de- creased 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 cata- lyst 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 col- orless, odorless and tasteless. Acute thalli- um poisoning is characterized by multisys- tem involvement, and neurological mani- festations include severe paresthesia, peripheral neuropathy, ptosis, tremor, en- cephalopathy and cerebellar symptoms [3– 6]. Subacute poisoning manifests itself slowly with alopecia and peripheral neu- ropathy. Chronic poisoning manifests it- self with extrapyramidal features, espe- cially parkinsonian tremor and choreoath- etosis [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 pa- tients [7, 8]. There is no study evaluating delayed sequelae of acute thallium poison- ing employing multimodality evoked po- tentials. We have reported acute complica- tions of a patient with homicidal thallium poisoning [4]. In this communication we report clinical and neurophysiological se- quelae of the same patient 3 years later. Case Report A 42-year-old male presented with symptoms of peripheral neuropathy, diar- rhea, vomiting, and renal and hepatic dys- function following homicidal thallium Received: May 12, 2006 Accepted: July 23, 2006 Published online: October 31, 2006 Dr. J. Kalita Department of Neurology, Sanjay Gandhi PGIMS Rae Bareily Road Lucknow 226014 (India) Fax +91 522 266 8017, E-Mail jkalita@sgpgi.ac.in © 2006 S. Karger AG, Basel 0014–3022/06/0564–0253$23.50/0 Accessible online at: www.karger.com/ene Mearson’s sign, broken saccades and pur- suit eye movements, and loss of associated movement during walking) and cerebellar signs (gaze evoked nystagmus, defective tandem walking). The visual impairment remained the same (6/60). Cranial nerves, power and sensations were normal. De- tailed autonomic function tests revealed mild abnormality. There was a 10-mm drop of systolic blood pressure on stand- ing, an expiration-inspiration heart rate variation of 10 (n 1 15), an expiration-in- spiration R-R ratio of 1.1 (n 1 1.5) and a blood pressure rise on cold immersion of 8/6 mm Hg. His sural nerve biopsy per- formed on the 40th day revealed loss of axons, active axonal degradation, and in- creased endoneurial collagen and inflam- matory cell infiltration. Kulchitsky Pal stain showed demyelination. Neurophysiological Evaluation Nerve conduction study revealed pro- gressive deterioration till month 3, which became normalized at 3 years (fig. 1b). Ini- tial unrecordable peroneal F response be- came normal at the 3-year follow-up, al- though peroneal F persistence was only 10%. The details of the nerve conduction studies are summarized in table 1. P100 la- tency of visual evoked potential (VEP) and tibial somatosensory conduction time were prolonged at 1 month and remained so even at 3 years (fig. 1 c, d), but the central motor conduction time to the tibialis ante- rior was normal. Cognitive evoked poten- tial using the auditory paradigm at the 3- year follow-up revealed normal P300 laten- cy (272 ms) and amplitude (23.5  V).