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Subacute polyneuropathy of a patient under treatment with disulfiram, suffering from alcohol use disorder
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Abstract
Disulfiram is a drug commonly used in the treatment of chronic alcohol use disorder. It works by inhibiting the enzyme acetaldehyde dehydrogenase, causing highly unpleasant symptoms upon alcohol intake, which supports abstinence by deterring alcohol consumption. We present the case of a 31-year-old male with a long history of alcohol dependence, since the age of 14. The patient had no other comorbidities. His addiction problem determined him to pursue alcohol withdrawal and psychiatric treatment. He had been on disulfiram therapy for one year. The onset of his symptoms started three months prior to admission to our clinic; he developed progressive, symmetric lower limb weakness, which notably worsened during the two weeks prior to hospitalization. According to collateral history, this exacerbation coincided with significant alcohol consumption while on disulfiram treatment. Neurological Examination Findings revealed: no meningeal signs, right-sided hearing loss, stepping gait achievable only with partial assistance, flaccid paraparesis (MRC grade 4 in the lower limbs muscle groups), tongue tremor, upper limb postural tremor, and palpebral myoclonus, symmetrical deep tendon reflexes, decreased in the lower limbs, no pyramidal signs, pallhypesthesia of the legs with reduced vibratory sense in the distal lower limbs, lower limb muscle hypotrophy, no sphincter or erectile dysfunction, preserved coordination and orientation in time and space. Electromyography and electroneurography revealed bilateral active denervation in the lower limb muscles, consistent with progressive poly(radiculo)neuropathy. Laboratory tests, cranial CT, spinal MRI, and cerebrospinal fluid analysis showed no other pathological findings to explain the neuropathy. Disulfiram therapy was discontinued, and the patient was treated with neurotrophic medications and physical therapy, leading to a gradual resolution of his symptoms. Although peripheral neuropathy due to disulfiram is rarely reported in the literature, in this case, the combination of disulfiram treatment with concurrent alcohol use likely contributed to the acute exacerbation of peripheral nerve damage.
Walter de Gruyter GmbH
Title: Subacute polyneuropathy of a patient under treatment with disulfiram, suffering from alcohol use disorder
Description:
Abstract
Disulfiram is a drug commonly used in the treatment of chronic alcohol use disorder.
It works by inhibiting the enzyme acetaldehyde dehydrogenase, causing highly unpleasant symptoms upon alcohol intake, which supports abstinence by deterring alcohol consumption.
We present the case of a 31-year-old male with a long history of alcohol dependence, since the age of 14.
The patient had no other comorbidities.
His addiction problem determined him to pursue alcohol withdrawal and psychiatric treatment.
He had been on disulfiram therapy for one year.
The onset of his symptoms started three months prior to admission to our clinic; he developed progressive, symmetric lower limb weakness, which notably worsened during the two weeks prior to hospitalization.
According to collateral history, this exacerbation coincided with significant alcohol consumption while on disulfiram treatment.
Neurological Examination Findings revealed: no meningeal signs, right-sided hearing loss, stepping gait achievable only with partial assistance, flaccid paraparesis (MRC grade 4 in the lower limbs muscle groups), tongue tremor, upper limb postural tremor, and palpebral myoclonus, symmetrical deep tendon reflexes, decreased in the lower limbs, no pyramidal signs, pallhypesthesia of the legs with reduced vibratory sense in the distal lower limbs, lower limb muscle hypotrophy, no sphincter or erectile dysfunction, preserved coordination and orientation in time and space.
Electromyography and electroneurography revealed bilateral active denervation in the lower limb muscles, consistent with progressive poly(radiculo)neuropathy.
Laboratory tests, cranial CT, spinal MRI, and cerebrospinal fluid analysis showed no other pathological findings to explain the neuropathy.
Disulfiram therapy was discontinued, and the patient was treated with neurotrophic medications and physical therapy, leading to a gradual resolution of his symptoms.
Although peripheral neuropathy due to disulfiram is rarely reported in the literature, in this case, the combination of disulfiram treatment with concurrent alcohol use likely contributed to the acute exacerbation of peripheral nerve damage.
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