Orthotics using splints and braces should be explored to help with ambulation. Encourage patients to be active as tolerated to promote tissue oxygenation, mobility, and well-being. Nerve degeneration progresses from sensory symptoms to include motor function problems of the lower and upper extremities. Patients may stand and walk with a wide base of support to maintain balance.

• Taking these medications at bedtime may be indicated because of their sedative effects.
• 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.
• This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency.
• The National Institute on Alcohol Abuse and Alcoholism reports that 16 million people in the US have been diagnosed with alcohol use disorder (AUD).
• However, this seemingly innocuous sensation may be an early warning sign of a condition known as alcoholic neuropathy, a lesser-known but significant consequence of long-term alcohol use.

During the initial stages of ALN, the disease may appear asymptomatic and demonstrable only on electroneurographic investigation [71, 111, 112]. 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 [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].

Motor

Also, levels of alcohol in the blood higher than 60 mg/dL confirmed the consistency of this protocol and were compatible with other studies (Bell et al., 2006, Simms et al., 2008a, Simms et al., 2008b). According to Simms et al., 2008a, Simms et al., 2008b, using similar protocol of intermittent alcohol (20%; v/v) ingestion, the alcohol concentration in the blood ranged from 4 to 93 mg / dL in Wistar rats submitted to 20 ingestion sessions. In our study, https://ecosoberhouse.com/ we observed a blood concentration of 85 mg / dL in the AL group, associating the signs and symptoms of AN observed in this study with this pattern of human consumption (NIAAA, 2022). The morbidity and mortality of chronic heavy alcohol consumption encompass a wide range of systemic diseases with negative health outcomes that may be interrelated with a patient’s neuropathic syndrome (see Selected systemic effects of heavy alcohol consumption).

Axonal degeneration has been documented in rats receiving ethanol while maintaining normal thiamine status [5]. 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.

Alcohol Abuse Diagnostic Criteria and Biomarkers

It is possible that hepatic dysfunction and alcoholic toxicity each cause neuropathy independently, and that there is frequently overlap between the two. It may also be that comorbid hepatic dysfunction is a risk factor for alcohol-related peripheral neuropathy. Further studies are required to develop a greater understanding of the interaction these entities. Thiamine serves as an important coenzyme in carbohydrate metabolism and neuron development. The lack of thiamine in the nervous system affects the cellular structure and can cause cell membrane damage and irregular ectopic cells. Other vitamin deficiencies seen with alcohol abuse include, but are not limited to, B-vitamins, folic acid, and vitamin-E.

Thus, deficiency of these vitamins was felt to be unlikely in Danish beer drinkers at that time and, indeed, measured vitamin concentrations were mostly normal. Clinical features of neuropathies in the alcoholic and post gastrectomy patients were similar. These two groups, however, were distinct from the standpoint that nerve conduction velocities were slower and sural nerve biopsy specimens revealed alcohol neuropathy stages more segmental demyelination in the post gastrectomy group. The authors concluded that malnutrition, including low blood concentrations of B vitamins, is not a prerequisite for the development of alcoholic neuropathy, and ethanol per se plays a role in the pathogenesis of alcoholic neuropathy. Protein kinase C (PKC) is a family of protein kinases consisting of approximately 10 isozymes.