Electrophysiologic investigation of thallium poisoning (original) (raw)
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Management of Thallium Poisoning
Clinical Toxicology, 1981
A case of acute thallium poisoning in a 67-year-old Chinese woman is described. She presented with acute pain in the chest, abdomen, and lower limbs. The diagnosis was not made, however, until alopecia developed. Detoxification treatment, which included Prussian blue (potassium ferric hexacyanoferrate) was given, but further neurological damage occurred. The patient's motor function recovered after 1 year, but residual sensory neuropathy remained. This case illustrates that tissue-bound thallium may cause prolonged neurological damage if detoxification therapy is not commenced within 72 hours of the onset of acute poisoning. Acute abdominal pain and painful neuropathy in the lower extremities are important early diagnostic clues for timely therapy. However, by the time alopecia develops-typically around 2 weeks after the onset of symptoms-detoxification therapy may not be able to prevent the development of prolonged neurological damage.
Thallium poisoning: a case report
Journal of Yeungnam Medical Science
Thallium poisoning is usually accidental. We present a case of a 51-year-old woman who was evaluated in June 2018 for myalgia, vertigo, asthenia, and abdominal pain. Physical examination revealed temporal-spatial disorientation, jaundice, and asterixis. The laboratory reported the following: bilirubin, 10.3 mg/dL; aspartate transaminase, 78 U/L; alanine transaminase, 194 U/L; albumin, 2.3 g/dL; prothrombin time, 40%; and platelet count, 60,000/mm 3. Serology performed for hepatitis A, B, and C; Epstein-Barr virus; cytomegalovirus; and human immunodeficiency virus was negative, and a collagenogram was negative. Physical reevaluation revealed alopecia on the scalp, armpits, and eyebrows; macules on the face; plantar hyperkeratosis; and ulcers on the lower limbs. Tests for lead, arsenic, copper, and mercury were carried out, which were normal; however, elevated urinary thallium (540 µg/g; range, 0.4-10 µg/g) was observed. The patient was treated with D-penicillamine 1,000 mg/day and recovered her urinary thallium levels were within normal range at annual follow-up. Thallium poisoning is extremely rare and can be fatal in small doses. An adequate clinical approach can facilitate early diagnosis.
Thallium poisoning: emphasis on early diagnosis and response to haemodialysis
Postgraduate Medical Journal, 2003
Thallium poisoning is known for its diverse manifestations and these can delay the diagnosis if a clear history of poisoning is not forthcoming. A 42 year old man presented on the third day of illness with flaccid quadriparesis and paresthesia, which were confused with Guillain-Barré syndrome. Because of associated loose motions, skin lesions, and liver and kidney dysfunction arsenic poisoning was considered. In the second week he developed ophthalmoplegia, nystagmus, and neck tremor and later developed alopecia, and thallium poisoning was suspected. His serum thallium level on the 18th day of illness was 40 980 µg/ml. He was subjected to haemodialysis, potassium supplementation, laxatives, and B complex supplementation. He showed significant improvement after haemodialysis and at three months he was able to walk with support. At six months of follow up he was independent for activities of daily living. Severe paresthesia, ophthalmoplegia, cerebellar and extrapyramidal signs, and alopecia are highly suggestive of thallium poisoning. Haemodialysis may be effective even in the third week of poisoning.
A case of thallium intoxication by walking in a field
Forensic Science International: Reports, 2020
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Archives of Industrial Hygiene and Toxicology, 2010
Thallium Toxicity in HumansThallium is a naturally occurring trace element, widely distributed in the earth's crust, but at very low concentrations. It does not have a known biological use and does not appear to be an essential element for life. It has been considered one of the most toxic heavy metals.Occasionally, there are reports on thallium poisoning as results of suicide or murder attempt or accident. The main threat to humans is through occupational exposure, environmental contamination, and accumulation in food, mainly in vegetables grown on contaminated soil. Increasing use in emerging new technologies and demanding high-tech industry constantly raise concern about exposure risk to all living organisms. Thallium is considered a cumulative poison that can cause adverse health effects and degenerative changes in many organs. The effects are the most severe in the nervous system. The exact mechanism of thallium toxicity still remains unknown, although impaired glutathione ...
Electron microscopic study of the effects of thallium poisoning on the rat cerebellum
Forensic Science International, 1978
Rats were given thallium acetate (5 mg elemental thallium/kg body weight) intraperitoneally daily for 7 days. The brain was fixed by perfusion—fixation and small pieces of the cerebellum were processed for electron microscopy. Variegated mitochondrial profiles, increased incidence of electron — dense bodies and proliferation of Golgi zones were observed in the thallium — poisoned rat cerebellum. Multilamellar cytoplasmic bodies were discernible in the cerebellar cortex of the thallium-treated rats.
Subacute arsenic neuropathy: clinical and electrophysiological observations
Journal of Neurology, Neurosurgery & Psychiatry, 1981
We report a patient who developed subacute peripheral neuropathy following ingestion of a traditional medicine for obesity. A 9-year-old girl who had a residual equinus varus deformity and sphincter disturbance due to pelvic ganglioneuroma presented with subacute sensorimotor peripheral neuropathy of 2 weeks duration. Her symptoms started 3 weeks after she started taking a locally made traditional medicine for obesity. She had no other systemic features of arsenic toxicity. She had Mee's lines on her nails and high serum arsenic levels and 24-hour urine levels confirmed the diagnosis of arsenic neuropathy. Nerve conduction study on admission demonstrated axonal sensorimotor neuropathy with slowed conduction velocity. She was not given any specific treatment and recovery was slow. At 18 months, she showed complete recovery and electrodiagnostic parameters returned to normal values. Arsenic is a known ingredient of many Indian ethnic remedies and possibility of arsenic neuropathy should be thought of in patients presenting with acute or sub-acute peripheral neuropathy of unknown etiology.
Toxicity in Peripheral Nerves: An Overview
Toxics, 2021
Introduction to a collection. This article is intended to introduce a collection of papers on toxic neuropathies. Toxic neuropathies can be caused by a variety of substances and by different mechanisms. Toxic agents are numerous and can be distinguished between drugs, recreational agents, heavy metals, industrial agents, pesticides, warfare agents, biologic substances and venoms. Toxic agents reach the nervous system by ingestion, transcutaneously, via the mucous membranes, parenterally and by aerosols. The most frequent types are cumulative toxicities. Other types are acute or delayed toxicities. Pathogenetic mechanisms range from a specific toxic substance profile causing axonal or demyelinating lesions, towards ion channel interferences, immune-mediated mechanisms and a number of different molecular pathways. In addition, demyelination, focal lesions and small fiber damage may occur. Clinically, neurotoxicity presents most frequently as axonal symmetric neuropathies. In this work...