Alcoholic polyneuropathies

Alcoholic polyneuropathies (or chronic ethanol-deficiency polyneuropathies) are among the most common types of polyneuropathies, along with diabetic polyneuropathies. They usually complicate severe and long-standing alcoholism. Their prevalence is > 30% among chronic alcoholics.

Pathophysiology

The pathophysiology of alcoholic polyneuropathies is not well understood. They are commonly believed to result from:

• Multiple vitamin deficiencies due to frequently inadequate dietary intake in alcoholics and intestinal absorption disorders due to the digestive toxicity of alcohol.
  • Thiamine (vitamin B1) deficiencies, which are thought to be exacerbated by an increased carbohydrate metabolism induced by alcohol.
• Direct neurotoxicity of alcohol.

Clinical Presentation

The typical presentation involves the gradual onset of a sensory, sensory-motor, and/or autonomic polyneuropathy, characterized by:

• Fatigability while walking.
• Cramps (++ nocturnal) and neuropathic pain.
• Motor deficits predominantly in the lower limbs, distal, bilateral, and symmetrical, often manifested by bilateral foot drop.
• Distal hypoesthesia, hyperpathia, dysesthesias.
• Hyporeflexia in the lower limbs.
• Balance disturbances with non-lateralized Romberg sign.
• Dysautonomic disorders: trophic changes, sweating disorders, erectile dysfunction, hypertension, orthostatic hypotension, plantar ulcers (rare), etc.

However, there are rarer forms characterized by rapidly developing, extensive pareses, both distal and proximal. In the most severe cases, they may lead to a flaccid, painful paraplegia that develops within less than 24 hours. These cases generally occur within the context of beriberi and are often accompanied by Wernicke's encephalopathy.

Differential Diagnosis

• See detailed article: Peripheral Neurological Syndromes: Polyneuropathies and Polyradiculopathies
• See detailed article: Peripheral Neurological Syndromes: Orientation in the Face of Polyneuropathy or Multiple Neuropathy

The diagnosis of alcoholic polyneuropathy is generally straightforward (typical clinical presentation in the context of chronic alcoholism and absence of elements suggesting another etiology).

However, in cases of atypical presentation or unacknowledged alcoholism, the differential diagnosis includes other causes of chronic polyneuropathies. It should also be noted that alcoholics have an increased frequency of compression neuropathies, but their distribution is rarely confusing.

In rare acute forms, differential diagnoses will include, depending on the presentation: acute polyneuropathies (++ Guillain-Barré syndrome), myasthenic crises, acute alcoholic myopathies, cauda equina syndrome, conus medullaris syndrome, etc.

Additional Tests

In cases of typical clinical presentation in a known chronic alcoholic and in the absence of evidence for another etiology, the diagnosis is based solely on clinical grounds, and no additional tests are recommended.

In selected cases, the utility of the following tests may be discussed based on the context:

• Nerve Conduction Velocities (NCV) and Electromyography (EMG):
  • Generally reveals axonal sensory or sensory-motor damage.
  • A demyelinating component is, however, common in advanced forms.
• Biology:
  • Hematogram-CRP, sedimentation rate (ESR), renal and hepatic function tests, electrolyte levels, HbA1c, TSH, serologies (HBV, HCV, HIV, Borrelia, Syphilis), protein electrophoresis, vitamin B12, and folates, etc.
  • Utility of CDT in cases of suspected unacknowledged chronic alcohol consumption.
• Lumbar Puncture:
  • Useful only in rare acute presentations or if there is a demyelinating character to NCV.
• 24-Hour Urine:
  • 24-hour proteinuria.
  • Myoglobinuria in acute presentations where acute myopathy is a differential diagnosis.
• Chest X-Ray or CT Scan:
  • To search for radiological evidence of sarcoidosis, amyloidosis, cryoglobulinemia, vasculitis, or pulmonary infection.
• Lumbar-sacral MRI or CT Scan:
  • Exceptionally useful in acute presentations (to exclude cauda equina syndrome and conus medullaris syndrome).

Therapeutic Management - Treatments

• Etiological Treatment:
  • Ethanol withdrawal, psychiatric follow-up.
  • Correction of deficiencies
    • polyvitaminotherapy (++ B1 and B6). To be maintained as long as ethanol consumption persists (also for the prevention of Wernicke's encephalopathy)... keeping in mind that high-dose B6 administration over a long period is neurotoxic (sensory and sensory-motor polyneuropathies). Three months of Befact Forte (high-dose B1 and B6 complex) 1 tablet/day followed by Benerva (vitamin B1 alone) 1 tablet/day can be proposed.
    • Increased protein intake.
• Symptomatic Treatment:
  • Sometimes necessary: physiotherapy and pharmacological management of neuropathic pain.

In rare acute forms, hospitalization with infusions (vitamins B1 500 to 1000 mg/day, B6 250 mg/day, Cernevit 1 ampoule/day) for 5 days (then oral vitamin supplementation for a minimum of 3 months) is recommended, modeled after Wernicke's encephalopathy (often present in these cases), though there is no strong evidence for this approach.

Prognosis

Without ethanol withdrawal, the progressive worsening of polyneuropathy is inevitable.

With ethanol withdrawal, the progression may lead to stabilization or very slow improvement (over several years). The older the alcoholism and/or the more severe the polyneuropathy, the more unfavorable the prognosis for recovery.

Bibliography

Bradley WG et al., Neurology in clinical practice, 5th ed., Butterworth-Heinemann, e-dition, 2007

Charness ME et al., Overview of the chronic neurologic complications of alcohol, UpToDate, 2022

EMC, Traité de neurologie, Elsevier, 2018

Rutkove SB, Overview of polyneuropathy, UpToDate, 2022