Thallium neuropathy …

Michael T Pulley MD PhD

Peripheral Neuropathies

Updated 07.17.2024
Released 10.06.1999
Expires For CME 07.17.2027

Thallium neuropathy

Author: Michael T Pulley MD PhD

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Editor: Louis H Weimer MD

Thallium neuropathy

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Introduction

Overview

Thallium poisoning is still a source of toxic exposure. Dermatologic changes along with alopecia are key clues to the diagnosis of this painful neuropathy. In this article, the author reviews the clinical and laboratory features.

Key points

	• Alopecia is one of the clues to thallium poisoning, as it is almost always present.
	• Thallium neuropathy is usually predominately sensory, affecting both small fibers (pain) and large fibers (ataxia).

Historical note and terminology

Pesticides and rodenticides based on thallous salts were commonly used in the past. Although they are rarely used now, poisoning from accidental (mostly children), suicidal, or homicidal ingestion continues to occur (22; 26). Although industrial occupations may result in exposure to thallium, this is usually low level and chronic, rather than acute and high level (08). Consumption of contaminated food and water (17; 12) may also be a source of intoxication. Thallium intoxication has also been reported with contaminated drugs, including heroin and cocaine (01).

Clinical manifestations

Presentation and course

The peripheral neuropathy associated with thallium intoxication is a distal, symmetric axonopathy that affects small and large diameter fibers. The symptoms are sensory much more than motor with pain as a prominent feature. Degeneration affects the distal portion of the longest axons initially with sparing of the proximal segments. The most vulnerable are the large diameter sensory fibers. A delayed autonomic neuropathy due to involvement of small unmyelinated fibers may also appear after acute intoxication (19).

Three distinct syndromes of thallium neuropathy occur based on the temporal course and intensity of exposure (03). Acute, high dose poisoning is the most common scenario (28). This results in symptom onset within 1 to 2 days after a massive ingestion. Severe gastrointestinal distress with associated vomiting, abdominal pain, and diarrhea occurs within hours but may be delayed up to a day. Intense joint pain and severe burning distal paresthesias in the legs develop within 2 to 5 days. Small and large fiber sensory modalities are affected (12). The hands and trunk may occasionally be involved in the sensory disturbance. Weakness is evident on examination although it may not be a prominent complaint (16). A report of nine cases confirmed the sensory greater than motor predominance of acute thallium poisoning (24). In spite of the sensory dysfunction, tendon reflexes tend to be preserved early in the disease process, which may help to distinguish thallium neuropathy from Guillain-Barré syndrome (28). Severe cardiac and respiratory failure may occur with massive ingestion, leading to death (15). The mental status may decline to lethargy or coma and death may result (23). The classic sign of thallium intoxication is alopecia. This appears 15 to 39 days after ingestion and is not helpful in the acute setting (20). Alopecia is not always present and is not specific for thallium poisoning. Renal insufficiency and paralytic ileus may complicate acute thallium poisoning. A case report regarding a patient who was poisoned on two separate occasions highlighted a possible rapid evolution of the neurologic manifestations on second exposure in the absence of gastrointestinal symptoms and the possibility that this was related to delayed clearance of thallium from the nervous system (13).

With a somewhat smaller initial ingestion, the subacute variety of neuropathy is seen. In a family with three adults and six children affected by eating rice contaminated by thallium, symptom onset was delayed 1 to 2 weeks, and only two of nine had sensory neuropathy (27). Subacute thallium neuropathy evolves more slowly, beginning more than a week after exposure. The neuropathy is characterized by sensory greater than motor deficit. All modalities are affected (proprioception, light touch, and pin). Walking may be affected early on, primarily due to the painful paresthesias in the feet. Although some degree of distal weakness is usually detected, it is rarely severe. The deep tendon reflexes are slightly reduced or normal. Tachycardia or hypertension due to autonomic dysfunction may occur. Skin, hair, and nail changes may be associated. These include alopecia, hyperkeratosis, blackening of the hair roots (22), and Mees lines (white striae of the nails). Other neurologic features include cranial neuropathies, chorea, and ataxia (04). Cranial nerve involvement may include retinal damage or retrobulbar neuritis (21).

The chronic form of thallium neuropathy is rarely seen. This neuropathy results from prolonged low-level exposure to moderate levels of thallium. The neuropathy is the predominate finding here and is identical to that described above.

Prognosis and complications

In survivors of acute thallium intoxication, the recovery tends to be incomplete. Frequently, there is residual central nervous system dysfunction due to anoxic injury. The recovery of the peripheral nerves is slow and there is often permanent injury with persistent sensory loss (20; 02). One report indicated persistent psychiatric problems in five of nine victims of thallium poisoning (22). Subacute neuropathy tends to be milder and have a much better prognosis. With termination of exposure, the prognosis for recovery is excellent, and most patients recover within 6 months. Hair regrowth begins earlier at about 10 weeks after withdrawal.

References

01: Afshari R, Mégarbane B, Zavar A. Thallium poisoning: one additional and unexpected risk of heroin abuse. Clin Toxicol (Phila) 2012;50(8):791-2. PMID 22889036
02: Ammendola A, Ammendola E, Argenzio F, Tedeschi G. Clinical and electrodiagnostic follow-up of an adolescent poisoned with thallium. Neurol Sci 2007;28:205-8. PMID 17690853
03: Berger AR, Schaumburg HH. Effects of occupational and environmental agents on the nervous system. Neurology in clinical practice. In: Bradley WG, Daroff RB, Fenichel GM, Marsden CD, editors. Butterworth Heinemann, 1996:1389-401.
04: Davis LE, Stadefer JC, Kornfeld M, Abercrombie DM, Butler C. Acute thallium poisoning: toxicological and morphological studies of the nervous system. Ann Neurol 1981;13:38-44. PMID 7271231
05: Davis RK, Hoffmann J, Dart D, Datz FL. Unilateral parathyroidectomy: the role of thallium-technetium subtraction scans. Otolaryngol Head Neck Surg 1990;102(6):635-8. PMID 2165235
06: Douglas KT, Bunni MA, Baindur SR. Thallium in biochemistry. Int J Biochem 1990;22:429-38. PMID 2189755
07: Dumitru D, Kalantri A. Electrophysiological investigation of thallium poisoning. Muscle Nerve 1990;13:433-7. PMID 2161080
08: Feldman RG. Thallium. Occupational and environmental toxicology. Philadelphia: Lippincott-Raven Publishers, 1999:115-28.
09: Ghannoum M, Nolin TD, Goldfarb DS, et al. Extracorporeal treatment for thallium poisoning: recommendations from the EXTRIP Workgroup. Clin J Am Soc Nephrol 2012;7(10):1682-90. PMID 22837270
10: Hoffman RS. Thallium poisoning during pregnancy: a case report and comprehensive literature review. J Toxicol Clin Toxicol 2000;38:767-75. PMID 11192464
11: Hoffman RS. Thallium toxicity and the role of Prussian blue in therapy. Toxicol Rev 2003;22:29-40. PMID 14579545
12: Kuo HC, Huang CC, Tsai YT, Chu CC, Hsieh ST, Chu NS. Acute painful neuropathy in thallium poisoning. Neurology 2005;65:302-4. PMID 16043805
13: Kuroda H, Mukai Y, Nishiyama S, et al. Tardily accelerated neurologic deterioration in two-step thallium intoxication. J Clin Neurosci 2016;34:234-6. PMID 27692615
14: Lehmann PA, Favari L. Parameters for the absorption of thallium ions by activated charcoal and Prussian blue. J Toxiol Clin Toxicol 1984;22(4):331-9. PMID 6527397
15: Li S, Huang W, Duan Y, Xing J, Zhou Y. Human fatality due to thallium poisoning: autopsy, microscopy, and mass spectrometry assays. J Forensic Sci 2015;60(1):247-51. PMID 25407479
16: Liu H, Liao G. Long-term misdiagnosis and neurologic outcomes of thallium poisoning: A case report and literature review. Brain Behav 2021;11(3):e02032. PMID 33438838
17: Moeschlin S. Thallium poisoning. Clin Toxicol 1980;17:133-46. PMID 7408429
18: Moore D, House I, Dixon A. Thallium poisoning. Diagnosis may be elusive but alopecia is the clue. BMJ 1993;306(6891):1527-9. PMID 8518684
19: Nordentoft T, Andersen EB, Morgensen PH. Initial sensorimotor and delayed autonomic neuropathy in acute thallium poisoning. Neurotoxicology 1998;19:421-6. PMID 9621348
20: Pau PW. Management of thallium poisoning. Hong Kong Med J 2000;6:316-8. PMID 11025853
21: Pelclova D, Urban P, Ridzon P, et al. Two-year follow-up of two patients after severe thallium intoxication. Hum Exp Toxicol 2009;28(5):263-72. PMID 19755458
22: Rusyniak DE, Furbee RB, Kirk MA. Thallium and arsenic poisoning in a small midwestern town. Ann Emerg Med 2002;39:307-11. PMID 11867986
23: Sharma AN, Nelson LS, Hoffman RS. Cerebrospinal fluid analysis in fatal thallium poisoning: evidence for delayed distribution into the central nervous system. Am J Forensic Med Pathol 2004;25(2):156-8. PMID 15166769
24: Wang Q, Huang X, Liu L. Analysis of nine cases of acute thallium poisoning. J Huazhong Univ Sci Technolog Med Sci 2007;27:213-6. PMID 17497301
25: Wang TT, Wen B, Yu XN, et al. Early diagnosis, treatment, and outcomes of five patients with acute thallium poisoning. World J Clin Cases 2021;9(19):5082-91. PMID 34307559
26: Yumoto T, Tsukahara K, Naito H, et al. A successfully treated case of criminal thallium poisoning. J Clin Diagn Res 2017;11(4):OD01-OD02. PMID 28571191
27: Zhang HT, Qiao BP, Liu BP, Zhao XG. Study on the treatment of acute thallium poisoning. Am J Med Sci 2014;347(5):377-81. PMID 23811578
28: Zhao G, Ding M, Zhang B, et al. Clinical manifestations and management of acute thallium poisoning. Eur Neurol 2008;60:292-7. PMID 18824857

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Michael T Pulley MD PhD

Dr. Pulley of the University of Florida, Jacksonville received consulting fees from Argenx, Alexion, and UCB/Ra.
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Editor

Louis H Weimer MD

Dr. Weimer of Columbia University has no relevant financial relationships to disclose.
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Former Authors

Alan R Berger MD

Patient Profile

Age range of presentation: 0 months to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: Cement factory workers

Miners

Plant smelters

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Thallium neuropathy

Differential Diagnosis

arsenic neuropathy
Guillain-Barré syndrome

Also Relevant

Clinical evaluation of peripheral neuropathies
Metal neurotoxicity
Toxic peripheral neuropathies

Thallium neuropathy …

Thallium neuropathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

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	• Urine, blood, or tissue levels are mandatory.
	• Electrodiagnostic testing (nerve conduction/EMG) provide nonspecific findings of axonal neuropathy.

Thallium neuropathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

NF2-related schwannomatosis

Familial dysautonomia

Peripheral nerve complications of HIV-1 infection

Neuropathies associated with cytomegalovirus infection

Metal neurotoxicity

Medications and substances causing headache

Disulfiram neuropathy

Mercury neuropathy

This is an article preview.
Start a Free Account
to access the full version.