Alcoholic neuropathy associated with chronic alcohol intake PMC

This possibility opens the door to consideration of other possible causes, including problems with thiamine utilization unique to alcohol abuse or alcohol as a direct neurotoxin in which thiamine deficiency may be a superadded problem (Fig. 1). Alcoholic neuropathy is a type of peripheral neuropathy, which means it affects the nerves outside the brain and spinal cord. The toxic effects of alcohol on nerve tissue, combined with nutritional deficiencies caused by alcohol abuse, can lead to nerve damage and dysfunction. The clinical presentation of alcohol-induced PN is similar to other etiologies of PN. However, the pathophysiology of alcohol-induced PN is different than other forms of PN. Multiple variables contribute to this painful neuropathic syndrome, including the toxic effects of alcohol on neurons and nutritional deficiencies.

  • In chronic myopathy, myoglobinuria is absent, and creatine kinase (CK) is normal, reduced, or mildly elevated, unless an acute myopathy is superimposed.
  • Other non-specific biomarkers useful in the diagnosis of alcohol use disorder are gamma-glutamyl transferase (GGT), mean corpuscular volume (MCV) of the red blood cells, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels.
  • Other associations with alcoholism, such as malnutrition, liver dysfunction, vitamin deficiencies, hormonal alterations, and phosphate deficiency, are independent factors for alcohol myopathy development.
  • Treatment options include steps to quit alcohol use and managing symptoms of the disease.
  • The sural nerve was the most commonly reported nerve [2, 3, 5, 11, 27, 37,38,39, 51, 53, 59, 63, 68].

However, alternative therapies do not have side effect and tackle nutritional deficiencies and oxidative stress. Intensive research has been done on medications like alpha-lipoic acid, benfotiamine, acetyl-l-carnitine, and methylcobalamin. Other botanical or nutrient therapies include myo-inositol, vitamin E, topical capsaicin, and N-acetylcysteine.

Neurologic Complications of Alcoholism

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].

  • When identified, alcoholic neuropathy is indistinguishable from other distal sensorimotor axonal processes.
  • His calves were mildly swollen and thighs tender; his right deltoid was noticeably sore, as well.
  • 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.
  • Medicines may be needed to treat pain or uncomfortable sensations due to nerve damage.

Furthermore, females tend to be more vulnerable to the brain damage and neurotoxic effects of alcohol [134]. Computed tomography (CT) scans showed that among alcohol-dependent patients, the brain volumes were reduced to increase the volume of cerebrospinal fluid; these changes were induced in females in less time [135, 136]. Ammendola et al. (2000) showed an inverse correlation of the sensory-evoked potential (SEP) amplitude of the sural nerve which informs about sensory dysfunctions and is altered even in asymptomatic patients throughout the course alcohol dependence [137]. The mouse model of the injection of β-estradiol in males resulted in higher activity of cytosolic alcohol dehydrogenase (ADH), microsomal aniline hydroxylase (ANH), and aldehyde dehydrogenase (ALDH) which are crucial in ethanol metabolism [138]. Female mouse with injected testosterone showed the decreased activity of cytosolic isoform of ALDH which implies that those enzymes are sensitive to estrogen and testosterone and alcohol metabolism is greater in females.

History and Physical

Thiamine deficiency resulted in the progression of sensory dysfunctions; further, histological examination of the sural nerves revealed the loss of small nerve fibers and segmental demyelination. Patients with non-alcoholic thiamine deficiency neuropathy showed more abrupt onset of symptoms, mainly in a form of motor dysfunctions; biopsy showed damage to greater fibers alcohol neuropathy stages with subperineurial edema. ALN with thiamine deficiency was manifested as a variable mixture of these symptoms. It was proposed that ALN pathogenesis, besides thiamine deficiency itself, could be due to its inappropriate use in the organism or transketolase deficiency [150]. Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153].

  • An accumulation of acetaldehyde in the serum causes direct damage to the axon in alcohol-induced PN.
  • No patients with grade III (severe sensory impairment, absent reflexes, foot drop, muscle wasting) neuropathy showed clinical improvement over the 4-week period, but 4/8 did show an improvement over 3–6 months.
  • A careful, open-ended alcohol history is very important, particularly among patients who may be unable to provide complete histories upon initial presentation.
  • As described later in this article, gait ataxia of Wernicke syndrome may be masked by thiamine neuropathy.

Alcohol Use Disorder (AUD) is a chronic and progressive condition involving young people and adults worldwide (Diagnostic and Statistical Manual of Mental Disorders-5; World Health Organization, 2018). A recent global alcohol abuse report indicated that approximately 3 billion people consume alcohol worldwide (Global Status Report on Alcohol and Health, 2016). Early alcoholic neuropathy, usually presenting as sensory symptoms in the extremities, is reversible if the patient stops drinking and establishes proper nutrition.

Alcohol Abuse Diagnostic Criteria and Biomarkers

Later, the results have been supported by Victor and Adams (1961)—among 12 patients with ALN, neuropathic symptoms were alleviated just after thiamine supplementation, even though the alcohol consumption was previously completely reduced [149]. Koike et al. (2003) compared clinical and histological differences between ALN with and without thiamine deficiency [65]. Also, the results of the group of 32 patients with non-alcoholic thiamine deficiency neuropathy were considered.

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