Abstract
This article describes the prototypical clinical presentation, electrodiagnostic and neuropathological findings and treatment of a patient with painful peripheral neuropathy due to disulfiram toxicity. Although a review of the literature fails to reveal cases of painful peripheral neuropathy due to disulfiram toxicity, there has been heightened publicity of its risk in the treatment of persistent symptoms of Lyme disease following a standard of care course of antibiotics known as post-treatment Lyme disease syndrome. This article reviews the etiopathogenesis and diagnosis of predominant small fiber neuropathy resulting from disulfiram neurotoxicity, and offers recommendations for its use in Lyme disease and alcoholism.
Highlights
Disulfiram is an oral prescription drug for the treatment of alcohol abuse disorders [1]
A review of the literature fails to reveal cases of painful peripheral neuropathy due to disulfiram toxicity, there has been heightened publicity of its risk in the treatment of persistent symptoms of Lyme disease following a standard of care course of antibiotics known as post-treatment Lyme disease syndrome
This article reviews the etiopathogenesis and diagnosis of predominant small fiber neuropathy resulting from disulfiram neurotoxicity, and offers recommendations for its use in Lyme disease and alcoholism
Summary
Disulfiram is an oral prescription drug for the treatment of alcohol abuse disorders [1]. Post-treatment Lyme disease syndrome (PTLDS) is an example of I-Cubed (I3) that posits post-infectious immunity according to the simple relationship of Infection > Immunity > Inflammation [7] due to direct cytotoxicity by the spirochete with neuroinflammation [8]. While pre-existing nervous system injury due to alcohol exposure, and B. burgdorferi infection, and post-infectious autoimmunity all contribute to disulfiram-mediated damage, the observed clinical improvement after drug discontinuation suggests a mechanism of reversible iatrogenic neurotoxicity involving the peripheral nervous system (PNS) [13] [14]. The literature lacks references to painful small fiber sensory polyneuropathy (SFPN) as an associated neurotoxicity among large reviews of histologically-proven cases of SFPN due to toxic and metabolic causes [15], even though both alcohol exposure [16] and PTLDS [8] are both recognized proximate causes. Nor are there published cases of disulfiram neuropathy treated with immune globulin (Ig) [17] as an alternative or adjunct to discontinuing disulfiram or reducing the drug to the lowest dose to avert emergent SFPN as in the patient below
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