Alcoholic neuropathy Information New York

ALN further manifests as weakness and atrophy of muscles due to the damage of greater motor fibers and impaired neuromuscular transmission. It is likely to get worse if the person continues to use alcohol or if nutritional alcohol neuropathy stages problems are not corrected. Alcoholic neuropathy is usually not life threatening, but it can severely affect quality of life. Thus, treatment with TCAs may provide symptomatic relief in patients with alcoholic neuropathy.

These relationships make chronic alcoholism a risk factor for thiamine deficiency. In addition to thiamine deficiency, recent studies indicate a direct neurotoxic effect of ethanol or its metabolites. Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5].

Food and water consumption; body mass variation; alcohol intake and its concentration in the blood

Human studies have also suggested a direct toxic effect, since a dose-dependent relationship has been observed between severity of neuropathy and total life time dose of ethanol [6, 13]. The exact mechanism behind alcoholic neuropathy is not well understood, but several explanations have been proposed. Some other studies have indicated that chronic alcohol intake can decrease the nociceptive threshold with increased oxidative-nitrosative stress and release of pro-inflammatory cytokines coupled with activation of protein kinase C (Figure 1) [10, 16]. Therefore, alcoholic neuropathy may occur by a combination of the direct toxic effects of ethanol or its metabolites and nutritional deficiencies, including thiamine deficiency. The precise mechanisms responsible for toxicity on the peripheral nervous system, however, have not yet been clarified. The amount of ethanol which causes clinically evident peripheral neuropathy is also still unknown.

• The median and ulnar nerves are evaluated for motor function and the median, ulnar, and sural nerves are evaluated for sensory function.
• Painful sensations with or without burning quality represent the initial and major symptom of alcoholic neuropathy [2, 4].
• Of absolute alcohol per day also confirmed the neurotoxicity of alcohol to peripheral nerves.46 Seventeen exposed children were compared with 13 non-exposed children at birth and again at 12–14 months of age.
• Benfotiamine was found to be beneficial in patients with alcoholic polyneuropathy [98].
• The damage may be the direct result of long periods where you drank too much alcohol.

The sural nerve plays an important role in the diagnosis of alcohol-induced PN because it’s located in the calf and innervates sensory function in the lower legs where symptoms begin. Nerve conduction velocity may be normal or mildly diminished in the early stages of axonal degeneration, whereas demyelination causes significant slowing of conduction. The sensory nerve action potential shows decreased conduction amplitude in axonal injury.

Preventing Alcoholic Neuropathy

Current postulation holds that dysfunctions within the central and peripheral nervous system are due to both direct and indirect toxic effects of alcohol [31, 85,86,87]. Indirect effects are mainly induced by vitamin deficiencies (B1, B2, B3, B5, B6, B7, B9, and B12) [84, 88]. Ethanol has been linked to insulin/insulin-like growth factor-1 (IGF-1) resistance in the brain in patients with alcoholic dementia and alcoholic liver disease. This mechanism has been investigated in both an adult rat model of chronic ethanol exposure and in human alcoholics.

Damage to nerves caused by alcoholic neuropathy, however, is usually permanent. Seek medical care right away if you notice unusual tingling, weakness, or pain in your hands or feet. Early diagnosis and treatment give you the best chance for controlling your symptoms and preventing further damage to your peripheral nerves. The peripheral nervous system sends information from the brain and spinal cord, also called the central nervous system, to the rest of the body through motor nerves.

Systemic effects of heavy alcohol consumption

ALN can manifest differently, and patients might experience one, two, or even more clinical manifestations of ALN. Patients who have ALN might present such symptoms as cramps, impaired movement of the limbs, muscle atrophy, muscle weakness, spasms, or contractions, loss of sensation, or feeling of tingling. Besides, the gastrointestinal and urinary systems are also affected and include the presence of diarrhea, constipation, nausea, swallowing difficulties, abdominal bloating, and urinary retention. Impotence, diarrhea, constipation, or other symptoms are treated when necessary. These symptoms often respond poorly to treatment in people with alcoholic neuropathy.

Ethanol and its toxic metabolites affect neural metabolism including metabolic activities in the nucleus, lysosomes, peroxisomes, endoplasmic reticulum, and cytoplasm [104]. The morphological basis of post-alcoholic damage of neural tissue includes primary axonopathy and secondary demyelination of motor and sensory (especially small) fibers [105]. Demyelination is probably the effect of axoplasmic transmission slowdown; such degeneration so-called dying back bears semblance to Wallerian degeneration [64, 84]. An animal study on axonal transport in vitro using dorsal roots of the sciatic nerve showed decreased axonal transmission after long-term ethanol consumption [106]. Thus, ALN might be induced by the combination of the effects of the direct activity of alcohol metabolites on the nerve fibers along with nutritional deficiencies primarily in a form of thiamine deficiency.

Conclusions about Thiamine in ALN

Alcohol-induced neuropathy, also known as alcohol-related peripheral neuropathy (ALN), is a toxic polyneuropathy that leads to the damage of sensory, motor, and autonomic nerve fibers leading to the thinning of the myelin sheaths and further impairments of neural functions [14, 49]. ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia. Besides, the key mechanism of chronic pain includes the long-term potentiation of glutamatergic transmission. The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54].