Alcoholic Neuropathy Symptoms and Treatment

In addition, 32 patients with nonalcoholic thiamine deficiency neuropathy were also evaluated for comparison. The subgroup without thiamine deficiency, considered to be a pure form of alcoholic neuropathy, uniformly showed slowly progressive, sensory dominant symptoms. Superficial sensation, especially nociception, was predominantly impaired and painful symptoms were the primary complaint in most patients in this group. The histologic features of sural nerve biopsy specimens demonstrated small fibre predominant axonal loss as characteristic of the pure form of alcoholic neuropathy. Clinical features of alcoholic peripheral neuropathy develop slowly, extending over a period of months and include abnormalities in sensory, motor, autonomic and gait functions. Painful sensations with or without burning quality represent the initial and major symptom of alcoholic neuropathy [2, 4].

Medication can help in reducing some of the symptoms of alcoholic neuropathy. The most important strategy against alcoholic neuropathy lies in preventing the symptoms from getting worse by decreasing alcohol consumption as soon as possible. The medical community has recognized that addiction is a disease and that some people are predisposed to it.

How to Prevent Alcoholic Neuropathy?

Dr. Raja is a board-certified internal medicine physician, certified by both the American Board of Internal Medicine and the American Society of Addiction Medicine. He is committed to providing the highest-quality medical care to his patients. He is conscientious and compassionate with regards to all those who have been entrusted in his care. Dr. Raja values the patient-physician relationship and makes every effort to build trust and confidence as he goes to great lengths to make sure the experience is as pleasant as possible for his patients.

• If your lab tests show no condition that’s causing the neuropathy, your health care professional might recommend watchful waiting to see if your neuropathy stays the same or gets better.
• Neuropathy, even if it badly impairs your quality of life, is more symptom than illness, and the time to treat it is after the larger problem is under control.
• Depending on the extent of the damage, symptoms may lessen or disappear when a person stops drinking alcohol; however, nerves have less self-healing ability than many other body components, and neuropathy harm is often permanent.
• Pain is usually present and characterized by burning, sharp, prickling, tingling, tickling, and pins-and-needles sensations, and may coexist with numbness.
• One patient with grade I neuropathy responded with the correction of low pantothenic acid.

Some people might feel constant pain in the feet or hands which feels like throbbing, burning or sharp needles and pins. Chronic alcohol abuse can exhaust the pool of liver proteins, which are crucial in energy production. Once alcohol enters the organism, it is degraded by ethanol dehydrogenase into acetaldehyde and then into acetate alcoholic neuropathy recovery time which is metabolized. But there is always some amount of acetaldehyde that will not get metabolized and which will bound to proteins. The disease was observed to start in the lower limbs and extend upward affecting the hands and arms. The main symptom was a pain, which was excruciating at times, but which could wax and wane.

Occupational Therapy

The term polyneuropathy is used when multiple peripheral nerves are damaged. The prevalence of PN ranges from 2.4% to 8% per 100,000 individuals worldwide. The Foundation for Peripheral Neuropathy and the US Food and Drug Administration estimate that 20 million people in the US experience PN. Alcohol-induced peripheral neuropathy (PN) is a chronic and painful condition in which the neurotoxic effects of alcohol and nutritional deficiencies cause a pathologic response in nerve function. This article presents the pathophysiology, signs and symptoms, diagnostic approaches, treatment options, and nursing care of patients with alcohol-induced PN. In one clinical study, aimed at studying distinct clinicopathologic features of alcoholic neuropathy, 64 patients were assessed.

Activator and effector caspases, defining components of programmed cell death signalling pathways, also contribute to pain-related behaviour in animals with small fibre peripheral neuropathies. The death receptor ligand, tumour necrosis factor α, and its downstream second messenger, ceramide, also produce pain-related behaviour via this mechanism. This suggests that these pathways are potential targets for novel pharmacological agents for the treatment of inflammatory as well as neuropathic pain [71]. Most patients with alcohol neuropathy initially present with symmetrical polyneuropathies in the lower distal extremities, however; heavier abuse can progress to distal upper extremity symptoms. The most common findings are sensory related and are varied to include pain, numbness, and paresthesias.