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 alcohol neuropathy stages (B1, B2, B3, B5, B6, B7, B9, and B12) [84, 88]. The peripheral nervous system is comprised of axons—clusters of nerve fibers within a neuron that transmit electrical impulses to and from the central nervous system.

Other areas of the body

alcohol neuropathy stages

Electrophysiologic and pathologic findings mainly indicate axonal neuropathy with reduced nerve fibre densities. Densities of small myelinated fibres and unmyelinated fibres were more severely reduced than the density of large myelinated fibres, except in patients with a long history of neuropathic symptoms and marked axonal sprouting [2]. Subperineurial oedema is more prominent in thiamine deficient neuropathy, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier is more frequent in alcoholic neuropathy [3]. In general, the nerves in lower limbs were more affected than the upper limbs [3, 37,38,39].

Effects due to nutritional deficiency

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These studies correlated the autonomic alterations with the total alcohol dose and the number of doses multiplied by the consumption period (El-Mas and Abdel-Rahman, 2013; de Zambotti et al., 2015). In our study, it was not possible to detect all autonomic alterations because the consumption period was not long enough to induce these types of alterations, which should occur after a consumption of alcohol greater than those observed in our animals. The prevalence of impairments in ANS in alcohol-dependent patients varies from 20 to 99% [160]. Symptoms of AAN are due to impairments in both sympathetic and parasympathetic autonomic fibers of the cardiovascular, digestive, and urogenital systems. Appenzeller and Ogin (1974) showed that alcohol-dependent and diabetic patients had a reduced number of large fibers (greater than 5 μm) and greater density of autonomic fibers (possibly because of the degeneration followed by a partial regeneration) [161].

Alcoholic Myopathy

Parameters measured included vibration perception in the great toe, ankle and tibia, neural pain intensity, motor function and paralysis, sensory function and overall neuropathy score and clinical assessment. Although benfotiamine therapy was superior to Milgamma-N or placebo for all parameters, results reached statistical significance only for motor function, paralysis and overall neuropathy score. The reason for better results in the benfotiamine alone group than in the Milgamma-N group, despite the fact that the benfotiamine dosage was equivalent, is not completely understood.

  • Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis also seem to be implicated in the pathophysiology of this alcoholic neuropathy.
  • Its diagnosis requires prior exclusion of other causes, including optic nerve compression, inflammation, infection and drug toxicity (ethambutol, disulfiram, etc.).
  • Lettsom has observed that paralysis and hypoesthesia related to ALN presented a higher prevalence rate in lower limbs compared to upper limbs [60].
  • The US National Library of Medicine (NLM) warns that around 50 percent of long-term heavy drinkers will suffer from alcoholic neuropathy.
  • Besides blood chemistry test and complete blood count (CBC), esophagogastroduodenoscopy is needed when a patient vomits and has nausea for an unknown reason; X-rays of the gastrointestinal tract can also be performed.

Alcoholic polyneuropathy

Signs and symptoms

  • Recently findings from our laboratory also suggest the benefecial effects of both α-tocopherol and tocotrienol, isoforms of vitamin E, in the prevention of hyperalgesia and allodynia in rats administered ethanol for 10 weeks [55].
  • The abnormalities were usually of reduced amplitude, in keeping with axonal loss [2, 3, 5, 11, 12, 16, 21, 27, 37–39, 47, 51, 53, 54, 56, 63–68].
  • Of all the deleterious effects of excessive alcohol consumption, neuropathy is the most common.
  • It is estimated that in the United States 25% to 66% of chronic alcohol users experience some form of neuropathy; however, the true incidence in the general population is unknown.

Progressed disease

  • With the right approach and support, we can achieve significant improvements in our symptoms and quality of life.
  • The abnormalities were usually of reduced amplitude, in keeping with axonal loss [2, 3, 5, 11, 12, 16, 21, 27, 37,38,39, 47, 51, 53, 54, 56, 63,64,65,66,67,68].
  • Fortunately, abstaining from alcohol can help restore your nutritional health.
  • It is estimated that consumption of more than 100 ml of ethyl alcohol per day significantly increases the risk of ALN [56].
  • The majority of patients were middle-class, working men and continuous drinkers were more affected than episodic drinkers.