Objective:

This study is a case series of female patients who presented with significant disability attributed to acute alcoholic neuropathy. It describes their clinical presentation, laboratory, electrodiagnostic findings, and pathology of muscle and nerve biopsies.

Background:

Recent studies have shown that binge drinking may lead to more harm to health than chronic average alcohol consumption. Prior research on alcoholic neuropathy has predominantly focused on chronic, slowly progressive alcoholic neuropathies. Females are at increased risk for alcoholic polyneuropathy. Sexually dimorphic rats respond differently in models of alcohol induced neuropathy.

Design/Methods:

This is a retrospective analysis of  patients who presented with acute, axonal polyneuropathy in the context of binge drinking. Three patients were identified with a sensorimotor polyneuropathy that developed acutely (up to 4 weeks). Symptoms were neuropathic pain, paresthesias, muscle weakness, areflexia, disability and weight loss. Nutrient deficiency was not identified as an etiology. Extensive studies were performed ruling out other etiologies including inflammation and other toxins.  Trials of immunomodulators were variable in objective improvement. 

Results:

Extensive studies including serology, electrodiagnostic studies, nerve and muscle biopsy failed to identify an alternative etiology for acute polyneuropathy. Trials of treatment response were variable in objective improvement. Following extensive diagnostic studies, risk factors in these three patients include self-professed or family-ascertained history about binge drinking, nausea and vomiting prior to acute polyneuropathy. All patients were female and this was similar to other published case series of acute alcoholic/nutritional neuropathies. 

Conclusions:

We hypothesize that female patients have a predilection to developing acute/subacute axonal neuropathy after binge drinking. This could be related to a direct nerve toxicity or sexually dimorphic features given that nutrient deficiencies were not identified.