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Alcoholic neuropathy: possible mechanisms and future treatment possibilities PMC

The best way to prevent alcoholic neuropathy is to avoid excessive alcohol consumption and to seek treatment for alcoholism if you have difficulty doing so. The prevalence of alcohol-induced PN varies depending on demographics and the diagnostic criteria used in individual research studies. According to studies by the CDC, nearly 30% of adults in the US consume alcohol excessively. Excessive or heavy alcohol consumption is defined by the CDC when men have 15 or more drinks each week and women have 8 or more drinks each week. The National Institute on Alcohol Abuse and Alcoholism reports that 16 million people in the US have been diagnosed with alcohol use disorder (AUD).

Chronic abuse of alcohol depletes the pool of liver proteins which are consumed for energy production and insufficient intake of proteins only worsens this imbalance. Resulting disturbances in protein and lipid metabolism lead to undernourishment which adversely influences other metabolic pathways, including those influencing the function of the nervous system. Four studies addressed the management of patients with alcohol-related peripheral neuropathy.

Chronic Complications

Because ALN is a length-dependent axonopathy, it manifests mainly in a “stocking-glove” form, affecting the lower extremities at the beginning [28, 113]. The main symptoms of ALN include dysesthesia, paresthesia, numbness, and pain in the lower extremities which progressively reach higher parts of the body [114,115,116,117]. The pain is described as burning, cramp-like, or itching; also, a common symptom is a subjective feeling of cold in both feet alcohol neuropathy stages [118,119,120,121,122,123]. The symptoms deteriorate through touch and pressure which intensify pain while standing or walking [124]. Further progression of ALN leads to the weakening of tendon reflexes or total areflexia and disturbed proprioception, which additionally impair the ability to walk [28, 113]. ALN further manifests as weakness and atrophy of muscles due to the damage of greater motor fibers and impaired neuromuscular transmission.

alcohol neuropathy stages

These studies addressed abstinence from alcohol consumption and administration of vitamins. Symptoms of AAN are non-specific; in the sympathetic division, these include impairments in perspiration, orthostatic hypotension, whereas in parasympathetic hoarseness, swallowing difficulties, or cardiac arrhythmias [111, 166]. Gastrointestinal symptoms include delayed stomach emptying and intestinal transit, dyspepsia, and faster emptying of the gallbladder [165].

Relationship between alcoholic neuropathy and thiamine deficient neuropathy

On examination her strength was normal except for Medical Research Council (MRC) grade 4/5 in her extensor hallucis longus muscles bilaterally. Sensory examination was notable for profound loss of vibration and temperature sensation in the feet and to a slight degree in her hands. Gait was normal, and she could tandem for several steps, https://ecosoberhouse.com/ although an examiner needed to catch her during the Romberg test. Laboratory tests revealed normal electrolytes and mildly increased transaminase levels. Screening laboratory testing for identifiable causes of neuropathy was negative. Cessation from ethanol is paramount to improvement, as it is for disorders of CNS involvement.

Myopathy in the presence of a chronic, high ethanol intake is needed for diagnosis. Because of similar challenges and factors relevant to chronic alcoholics with regard to peripheral neuropathy, symptoms and signs of myopathy may be overlooked. Proximal weakness is seen, sometimes accompanied by severe muscle wasting and generalized loss of muscle mass (up to 30%).