This nerve damage causes an individual to experience pain and motor weakness, first in the feet and hands and then progressing centrally.

[1] Alcoholic polyneuropathy usually has a gradual onset over months or even years, although axonal degeneration often begins before an individual experiences any symptoms.

[3] Motor symptoms may include muscle cramps and weakness, erectile dysfunction in men, problems urinating, constipation, and diarrhea.

[1] The general cause of this disease appears to be prolonged and heavy consumption of alcohol accompanied by a nutritional deficiency.

However, there is ongoing debate over the active mechanisms,[6][7] including whether the main cause is the direct toxic effect of alcohol itself or whether the disease is a result of alcoholism-related malnutrition.

This may cause an alcoholic to change their eating habits including more missed meals and a poor dietary balance.

A lack of thiamine in the cells may therefore prevent neurons from maintaining necessary adenosine triphosphate (ATP) levels as a result of impaired glycolysis.

Thiamine deficiency alone could explain the impaired nerve conduction in those with alcoholic polyneuropathy, but other factors likely play a part.

Schwann cells produce myelin that wraps around the sensory and motor nerve axons to enhance action potential conduction in the periphery.

In peripheral nerves, oxidative enzyme activity is most concentrated around the nodes of Ranvier, making these locations most vulnerable to cofactor deprivation.

Lacking essential cofactors reduces myelin impedance, increases current leakage, and slows signal transmission.

The slowed conduction of action potentials in axons causes segmental demyelination extending proximally; this is also known as retrograde degeneration.

[1] Many researchers favor the nutritional origin of this disease, but the possibility of alcohol having a toxic effect on the peripheral nerves has not been completely ruled out.

One of the first presenting symptoms of diabetes mellitus may be peripheral neuropathy, and hemoglobin A1C can be used to estimate average blood glucose levels.

[13] Once an individual stops consuming alcohol it is important to make sure they understand that substantial recovery usually isn't seen for a few months.

Tricyclic antidepressants such as amitriptyline, or carbamazepine may help stabbing pains and have central and peripheral anticholinergic and sedative effects.

[3][5] Anticonvulsant drugs like gabapentin or pregabalin block the active reuptake of norepinephrine and serotonin and have properties that relieve neuropathic pain.

[12] During the early stages of the disease the damage appears reversible when people take adequate amounts of vitamins, such as thiamine.

[2] If the polyneuropathy is mild, the individual normally experiences a significant improvement and symptoms may be eliminated within weeks to months after proper nutrition is established.

[1] When those people diagnosed with alcohol polyneuropathy experience a recovery, it is presumed to result from regeneration and collateral sprouting of the damaged axons.

[12] Even after the restoration of a balanced nutritional intake, those patients with severe or chronic polyneuropathy may experience lifelong residual symptoms.

[1] In 2020 the NIH quoted an estimate that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy.

ALDH2 is an isozyme of ALDH and ALDH2 has a polymorphism (ALDH2*2, Glu487Lys) that makes ADLH2 inactive; this allele is more prevalent among Southeast and East Asians and results in a failure to quickly metabolize acetaldehyde.

[4][12] The first description of symptoms associated with alcoholic polyneuropathy were recorded by John C. Lettsome in 1787 when he noted hyperesthesia and paralysis in legs more than arms of patients.

This debate continues today over what exactly causes this disease, some argue it is just the alcohol toxicity, others claim the vitamin deficiencies are to blame and still others say it is some combination of the two.

Some argue it is a direct result of alcohol's toxic effect on the nerves, but others say factors such as a nutritional deficiency or chronic liver disease may play a role in the development as well.