Alcoholic neuropathy: MedlinePlus Medical Encyclopedia

Nursing care begins with establishing a rapport with the patient during the health history interview and head-to-toe assessment. The goals of nursing care for patients with alcohol-induced PN are to control pain, promote optimal nutritional status and mobility, and evaluate the patient's responses to treatment. Ensuring patient safety and interprofessional collaboration are major frameworks for achieving these goals. A skin biopsy of the sural nerve may be conducted and will initially show small fiber neuropathy, which results from injury to nerve fibers that may be myelinated or unmyelinated.

In general, the nerves in lower limbs were more affected than the upper limbs [3, 37,38,39]. Four studies reported abnormalities only in sensory nerves [33, 47, 63, 64], while ten reported abnormalities in both sensory and motor nerves [2,3,4, 16, 38, 54, 56, 58, 59, 65]. This may be a reflection of the severity of the neuropathy in which motor nerve function is affected at a later stage. The abnormalities were usually of reduced amplitude, in https://ecosoberhouse.com/article/alcohol-neuropathy-symptoms-and-treatment/ 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]. H and F wave latencies were not routinely reported but were found to be prolonged in those with alcohol-related peripheral neuropathy in studies that did [4, 67]. Particular attention was paid to radial SNAPs, tibial CMAPs, and sural SNAPs due to them being spared in entrapment neuropathies unlike the median, ulnar, and peroneal nerves.

What causes alcohol-related neurologic disease?

This activity describes the evaluation and management of alcoholic neuropathy and reviews the role of the interprofessional team in improving care for patients with this condition. The investigators found that neuritic symptoms persisted in all cases and some worsened, despite alcohol cessation. All patients improved, but only 2 patients showed demonstrable improvement in motor and sensory deficits. They also failed to account for malnourishment and the improvement that could be seen from enhanced nutritional status. The median and ulnar nerves are evaluated for motor function and the median, ulnar, and sural nerves are evaluated for sensory function.

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. PKC is involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth and in learning and memory. These functions are achieved by PKC mediated phosphorylation of other proteins [16]. Apart from above function, over-activation of epsilon form of protein kinase C (PKCε) is known to be involved in mediating neuropathic pain, such as pain induced by cancer chemotherapy (vincristine) [56] and diabetes [57]. PKC and protein kinase A (PKA) are both known to be important in nociceptor function [57–59].

Alcohol-induced cerebellar degeneration

Other vitamin deficiencies seen with alcohol abuse include, but are not limited to, B-vitamins, folic acid, and vitamin-E. Poor absorption and low intake of these vitamins have clinical features of dermatitis, neuropathy, and anorexia. Alcohol causes neuropathy via multifactorial processes, many of which are still under investigation. Alcohol enters the bloodstream from the digestive system within 5 minutes of consumption, and peak absorption is seen within 30 to 90 minutes.

As a result, it is usually necessary to get medical help to manage alcohol use disorder. Alcohol also alters the function of the stomach, liver, and kidneys in ways that prevent the body from properly detoxifying waste material, which then builds up and harms many regions of the body, including the nerves. Another prominent effect of alcoholic neuropathy involves painful and uncomfortable sensations. Alcoholic neuropathy can result in hypersensitivity to touch and even resting pain.

Nutritional factors responsible for alcoholic neuropathy (indirect toxicity)

Patients with small fiber neuropathy commonly report burning pain and may tell you, “My feet burn.” Patients may be hypersensitive to a stimulus (hyperesthesia). Patients may also experience numbness, restless legs syndrome, dry eyes and mouth, increased sweating, stomach problems, bladder control issues, skin discoloration, and cardiovascular symptoms. In a study by Mellion et al. (2013) with three different strains of rats, they investigated the effects of alcohol exposure on nerves and muscles. This phenomenon varied according to different susceptibility of genetic patterns, suggesting that nerve injury is influenced by individual genetic characteristics, in addition to chronicity and ingested volume of alcohol (Goldman et al., 2005, Mellion et al., 2013). Thus, treatment with anticonvulsant drugs may provide another therapeutic alternative for the symptomatic relief of pain in patients with alcoholic neuropathy.

Deficiencies in B6 and B12, thiamine, folate, niacin, and vitamin E can make it worse. Regarding the parasympathetic division of ANS, most of the studies are focused on the assessment of nerve conduction mainly in oculomotor and vagus nerves; these include pupil cycle time (PCT) and cardiovascular reflex tests correspondingly [160]. Further, ECG changes and functions of the digestive tract (dyspeptic symptoms, stomach and gallbladder motility, orocecal transit time) can also be assessed [162, 165].

Therefore, alcoholic neuropathy may occur by a combination of the direct toxic effects of ethanol or its metabolites and nutritional deficiencies, including thiamine deficiency. The precise mechanisms responsible for toxicity on the peripheral nervous system, however, have not yet been clarified. The amount of ethanol which causes clinically evident peripheral neuropathy is also still unknown. The onset of ALN is intensified by several risk factors such as malnutrition, thiamine deficiency, direct and indirect toxic effects of alcohol and its metabolites on nerve fibers, and genetic predispositions of patients [55, 139,140,141,142,143]. It is still unclear what is the major determinant in the pathogenesis of ALN. Primarily, thiamine deficiency is the crucial risk factor of ALN since it induces the progression of Korsakoff’s syndrome and beriberi [144, 145].

Deficiency of vitamins other than thiamine may also contribute to clinical features of alcoholic neuropathy. Chronic alcoholism can alter the intake, absorption and utilization of various nutrients (nicotinic acid, vitamin B2, vitamin B6, vitamin B12, folate or vitamin E). Deficiencies of B vitamins other than thiamine also may contribute to variation in clinical features, but characteristic symptoms of multiple vitamin deficiency were not seen in patients with thiamine deficiency neuropathies due to gastrectomy and dietary imbalance [26]. Thus, these vitamin deficiencies were not considered to be major causal factors of neuropathy [26].

Avoiding alcohol and improving your diet can sometimes lead to a moderate to full recovery. If you have tingling, numbness, loss of coordination, muscle weakness, or other things that don’t seem normal, see your doctor right away. In many cases, treating the condition or problem that causes your neuropathy can curb nerve damage and ease your symptoms. Alcoholic neuropathy is progressive damage to peripheral nerves and, in extreme cases, the autonomic nervous system, through chronic, heavy alcohol use.