Alcoholic Neuropathy Clinical Presentation

Updated: Feb 01, 2021
  • Author: Scott R Laker, MD; Chief Editor: Robert H Meier, III, MD  more...
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Ascertaining the symptomatic history of a patient with alcoholic neuropathy is not specific for diagnosis. Pure alcoholic neuropathy is characterized by a progressive, sensory-dominant symptomatology. Interestingly, concomitant thiamine deficiency creates a much more variable presentation. A detailed history of alcohol use should be obtained from any patient presenting with symptoms of general neuropathy. Additionally, nutritional history and questioning regarding other neuropathy risk factors should be documented. [25]

Patients with alcoholic neuropathy typically present with a history of chronic consumption of alcohol and an insidious onset of distal lower extremity paresthesias, dysesthesias, or weakness. The most common presenting complaint seems to be paresthesias in the feet and toes. Over time, these symptoms usually progress proximally and symmetrically. Less commonly, patients present with a more rapid, acute onset of symptoms.

Patients also may have a history of gait ataxia and difficulty walking or a history of frequent falls.

In cases of more severe and advanced presentation, patients may report distal upper extremity symptoms.

In rare cases, vagus or recurrent laryngeal nerve involvement has been described. These patients may present with hoarseness and a weak voice.



Classic physical examination findings associated with alcoholic neuropathy may include the following:

  • Diminished sensation to vibration or pinprick stimulation in a "stocking-to-glove" distribution

  • Thermal and proprioceptive sensation abnormalities

  • Muscle stretch reflexes, especially of the gastrocnemius-soleus muscle complex

  • Weakness of ankle/toe dorsiflexion and/or ankle plantar flexion strength

  • Intrinsic atrophy of foot muscles in advanced cases

  • Gait ataxia with a widened base of support or bilateral foot drop

  • Patellar and Achilles deep tendon reflexes are often reduced or absent

Evidence of other alcohol-related end-organ damage also may be observed on physical examination. The patient should be examined for additional manifestations of chronic alcohol abuse such as caput medusae, ascites, digital clubbing, Dupuytren contractures, palmar erythema, gynecomastia, and jaundice.



Excess alcohol consumption causes alcoholic neuropathy. The factors most directly associated with the development of alcoholic neuropathy include the duration and amount of total lifetime alcohol consumption. Indeed, the aforementioned literature review by Julian et al indicated that total lifetime ethanol dose is the greatest risk factor for alcohol-related peripheral neuropathy. Genetics also play a role, according to the study, as do male gender and the type of alcohol ingested. [21]

As previously stated, further studies must be performed to determine genetic influences on this disorder.