Peripheral neuropathy Symptoms and causes

According to many studies, alcohol-induced autonomic neuropathy (AAN) not only leads to potential damage to internal organs but also increases the mortality rate of patients [157, 158]. It was observed that abstinence may lead to the regression of several symptoms of AAN [159]. A priority treatment approach is to increase the patient’s caloric intake of nutritious foods. Chronic heavy alcohol consumption depletes hepatic proteins for energy and leads to a lack of B vitamins for carbohydrate metabolism and optimal functioning of the central and peripheral nervous systems.

Persons with alcoholism may consume smaller amounts of essential nutrients and vitamins and/or exhibit impaired gastrointestinal absorption of these nutrients secondary to the direct effects of alcohol. Spinal cord glial cells are implicated in the exaggerated pain state created by diverse manipulations such as subcutaneous inflammation, neuropathy and spinal immune activation [65, 66]. It has been recognized that spinal cord glial cells, astrocytes and microglia are activated by neuropathic pain or peripheral inflammation [42]. Furthermore, astrocytes and microglia are activated by such pain relevant substances as substance P, calcitonin-gene related peptide (CGRP), ATP and excitatory amino acids from primary afferent terminals, in addition to viruses and bacteria [67, 68]. Many different stimuli, including growth factors, cytokines, viral infection, ligands for heterotrimeric G protein-coupled receptors, transforming agents, and carcinogens, activate the ERK pathway.

Patient Education

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. They may have peroneal nerve damage, causing foot drop with difficulty raising the feet sufficiently to walk safely without stumbling. Patients may have difficulty buttoning a shirt or blouse and with handwriting and holding objects.

alcohol neuropathy

The thermal sensitivity was evaluated after the tactile sensitivity test (Miller et al., 2013). Both function and integrity of the afferent fibers can be inferred by the tactile response that is impaired in neuropathic conditions. To evaluate the tactile sensitivity of animals, the sensibility test with the Von Frey monofilaments (Touch Test™ Sensory Evaluator Kit of 20 – Leica Biosystems, Germany) was conducted, which is inexpensive and used in the clinical settings as well. These monofilaments were used in an increasing order of thickness (starting at 6 g), on the plantar surface of the pelvic limb of the animal only when it was immobile and standing on the four limbs on a mesh floor. The monofilaments were applied until they bent slightly and were held for two seconds.

Diagnosing Alcoholic Neuropathy

Primarily, it was assumed that the progression of ALN symptoms is due to malnutrition and micronutrient deficiency (mainly B1 hypovitaminosis) [82, 83]. Indeed, these factors contribute to the progression of ALN symptoms; however, they do not constitute direct factors that manifest in ALN development [84]. 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].

A deficiency of vitamin B1 in chronic alcoholics can be due to inadequate dietary intake, reduced capacity for hepatic storage, inhibition of intestinal transport and absorption or decreased formation of the active coenzyme form. In an animal study, it has been found that chronic alcohol consumption in rats resulted in a significant depletion in thiamine diphosphate (TDP), the active coenzyme form of thiamine. Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl [96]. An 8 week, randomized, multicentre, placebo-controlled, double-blind study compared the effect of benfotiamine alone with a benfotiamine complex (Milgamma-N) or placebo in 84 alcoholic patients. 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.