Alcoholic neuropathy: possible mechanisms and future treatment possibilities PMC

Depending on the degree of cognitive impairment influencing accurate history taking, patients may report various neuro-ophthalmic concerns, including diplopia or more subtle visual symptoms. Examination often reveals horizontal nystagmus, which may accompany rotatory or vertical nystagmus, and bilateral but typically asymmetric lateral rectus palsy. Truncal and gait ataxia are found in most patients; symptoms may be profound and impair gait or even the ability to sit. As described later in this article, gait ataxia of Wernicke syndrome may be masked by thiamine neuropathy.

Alcohol-induced neuropathy, also known as alcohol-related peripheral neuropathy (ALN), is a toxic polyneuropathy that leads to the damage of sensory, motor, and autonomic nerve fibers leading to the thinning of the myelin sheaths and further impairments of neural functions [14, 49]. ALN is characterized by spontaneous burning pain, hyperalgesia, and allodynia. Besides, the key mechanism of chronic pain includes the long-term potentiation of glutamatergic transmission. The percentage of alcohol-dependent patients affected by ALN is estimated to be 66% [50, 51]. The pathophysiology of ALN involves underlying mechanisms that include direct or indirect effects of alcohol metabolites, impaired axonal transport, suppressed excitatory nerve pathway activity, or imbalance in neurotransmitters [52,53,54].

Natural history

One of the main mechanisms behind alcohol-induced nerve damage is the depletion of essential nutrients, particularly vitamin B1 (thiamine) and B12. Thiamine deficiency, coupled with the toxic effects of alcohol on nerve tissue, leads to the deterioration https://ecosoberhouse.com/ of nerve health and function. Alcohol also contributes to liver damage, impairing the body’s ability to absorb and utilize vital nutrients. A priority treatment approach is to increase the patient’s caloric intake of nutritious foods.

Thus, from the above discussion it is clear that stress hormones, catecholamines and glucocorticoids, from the sympatho-adrenal and HPA neuroendocrine stress axes, respectively, play a very important role in initation and maintenance of alcoholic neuropathy. The combined actions alcohol neuropathy stages of catecholamines and glucocorticoids, via their receptors on sensory neurones, demonstrate a novel mechanism by which painful alcoholic neuropathy is induced and maintained. The mechanism of direct damage of nerve fibers due to alcohol intoxication remains unclear.

Study characteristics

If you’re struggling to control your drinking and worried about alcoholic neuropathy, help is available. For a list of rehabs and treatment centers near you, visit our rehab directory. However, vulnerability to neuropathy and its severity and speed of progression varies. Women, continuous as opposed to episodic drinkers, and people with a family history of the disorder appear to be more vulnerable to alcoholic neuropathy and more severe presentations. Capsaicin is a topical agent that modulates the inflammatory effects of the neurotransmitter neurokinin A to reduce neuropathic pain.

• The most important risk factor for alcohol-related peripheral neuropathy is the total lifetime dose of ethanol, although other risk factors have been identified including genetic, male gender, and type of alcohol consumed.
• Valproate demonstrated varying effects in different studies of neuropathic pain, with three studies from one group reporting high efficacy [125–127] and others failing to find an effect [128, 129].
• Abnormalities in the F-wave response are a sensitive and early indicator of alcohol-induced PN.

Physical therapy should be included in the treatment plan to improve flexibility, strength, and balance. Occupational therapy can help the patient with self-care activities and safely navigating the home environment. 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.

Effects due to nutritional deficiency

It was shown that patients with liver cirrhosis (regardless of its etiology) present dysfunctions in ANS, primarily within the vagus nerve [170]. Proposed mechanisms include circulatory disturbances in liver cirrhosis, metabolic and neurohormonal (renin-angiotensin-aldosterone system) dysfunctions, excessive nitric oxide production, oxidative stress, and inflammatory mediators [11, 171]. There is a strong correlation between AAN and Child-Pugh scale which suggests that liver cirrhosis progression is related to impairments in ANS [172]. Alcohol-abusing patients with liver cirrhosis and vagus nerve neuropathy are at higher risk of a sudden death compared to patients without impairments within the nervous system [173, 174]. Our muscles need to receive a message from nearby nerves in order to function.