Polyneuropathies due to alcohol

Besides diabetes mellitus type 2 (“diabetes”), the abuse of alcohol is one of the most common causes of polyneuropathy. Experts estimate that 15-40 % of all alcoholics suffer from polyneuropathy. Alcohol therefore damages the nerve cells and is therefore “neurotoxic”.

In chronic or long-term abuse, those affected usually develop symmetrical sensations in both legs (especially in the lower legs). Patients complain of tingling, burning and pain in the calves or feet. Often, motor deficits are added to this, so that patients report walking disorders or frequent stumbling.

These failures are usually preceded by muscle atrophy. Occasionally, the small hand muscles may also be affected first. In the case of alcohol-induced polyneuropathy, patients also sweat more on the palms of their hands and feet.

The skin becomes increasingly thin and can even develop painful ulcers. Since the sensation is reduced, patients often develop chronic wounds. Fortunately, with strict abstinence from alcohol, one can observe a slow but almost complete reduction in symptoms.

Dialysis patients with severe kidney disease in particular complain of nightly calf cramps and burning feet. The distribution pattern of paralysis is symmetrical. Polyneuropathy can also occur in patients with chronic liver failure.

Polyneuropathy can occur in connection with hereditary diseases such as porphyria. Porphyria is an inherited disorder of the synthesis of heme, a complex with iron in the red blood cells. It leads to tachycardia, high blood pressure (hypertension) and severe, contraction-like abdominal pain (colic).

Neurologically, this is either motor mononeuropathy multiplex or symmetrical paralysis of all four extremities. According to international classification, a distinction is made between hereditary motor sensitive and hereditary sensitive neuropathies. HMSN type I is the hypertrophic (“enlarged”) form of muscle atrophy, also known as Charcot-Marie-Tooth disease, which is usually inherited dominantly.

It is the most common of the hereditary neuropathies and manifests itself between the ages of 10 and 30 years. It is characterized by a symmetrical, sensitive and motor polyneuropathy with calf atrophy (“stork legs”), hollow foot and hammer toe formation and an early reduction in motor and sensitive nerve conduction velocity due to thickening of the nerve cords. HMSN Type II is the neuronal form of muscle atrophy.

In this form, the nerve conduction velocity is normal compared to type I and the distribution pattern can also be asymmetrical. The HMSN type III is inherited recessively. Typical are the even more thickened nerve cords and the even more reduced nerve conduction velocity compared to type I. HMSN type IV, Refsum-Kahlke syndrome, is a symmetrical polyneuropathy that spreads from the extremities to the trunk of the body.

It is based on a recessively inherited disorder of the metabolism of a certain fatty acid (phytanic acid). Symptoms include disturbances in movement coordination (ataxia), night blindness (hemeralopia), damage to the retina (retinal degeneration) and deafness. Also in this type the nerve conduction velocity is considerably delayed.

HMSN types V, VI and VII are rare forms combined with symptoms in the eye. The lack of perception of pain (analgesia) leads to bone fractures, injuries or mutilation. In diseases of the blood vessels, which are accompanied by inflammation of the blood vessel wall of a so-called vasculitis, damage to the nerves can result from insufficient blood circulation or nutrition.This leads to sensitive and motor paralysis, which is either symmetrical or distributed according to the multiplex type. In addition, disturbances of the nutritional or metabolic state of the body can occur.