Alcoholic neuropathy: Causes, symptoms, and treatment

alcohol neuropathy stages

Tricyclic antidepressants (TCAs) are often the first line drugs to alleviate neuropathic pain symptoms. They have central effects on pain transmission and block the active re-uptake of norepinephrine and serotonin. TCAs have been shown to relieve various neuropathic pain conditions in many trials 115. In agreement with this, one recent study has confirmed the efficacy of TCAs in central pain 116. The serotonin/norepinephrine re-uptake inhibitors (SNRIs), duloxetine and venlafaxine, have a well-documented efficacy in painful polyneuropathy 117, 118. SSRIs have been studied in a few trials which have demonstrated a weak analgesic effect but the clinical relevance of these compounds is questionable 119.

  • Benfotiamine was found to be beneficial in patients with alcoholic polyneuropathy 98.
  • 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.
  • Alcoholic neuropathy is damage to the nerves that results from excessive drinking of alcohol.
  • It was shown that patients with liver cirrhosis (regardless of its etiology) present dysfunctions in ANS, primarily within the vagus nerve 170.
  • Supplementation with benfotiamine significantly increased concentrations of TDP and total thiamine compared with supplementation with thiamine HCl 96.

Causes of Alcoholic Neuropathy

alcohol neuropathy stages

Distal latency, conduction velocity, and minimum F-wave latency (when present) are normal or consistent with the degree of axonal loss and show no signs of demyelination. H reflexes are absent at an early stage and correlate with absent ankle reflexes. Autonomic testing of parasympathetic and sympathetic reflexes is often abnormal, including analysis of heart rate variability, Valsalva maneuver, handgrip, tilt table, and standing maneuvers. 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 of nerve health and function. Alcohol also contributes to liver damage, impairing the body’s ability to absorb and utilize vital nutrients.

alcohol neuropathy stages

Alcohol Abuse and Nerve Damage

The primary axonal damage and secondary demyelination of motor and sensory fibres (especially small diameter fibres) are considered to constitute the morphologic basis of alcoholic damage to nerve tissue at present 20. The demyelination is explained as the result of a slowing down (decceleration) of axoplasmic flow and a degradation of the quality of biological properties of axonal enzymes and proteins. This type of degeneration, so called ‘dying-back’, resembles Wallerian degeneration.

alcohol neuropathy stages

How are Alcohol-Related Neurological Diseases Treated?

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. When this message is interrupted due to damaged nerves, the muscles cannot function as they normally would.

Neurobehavioral symptoms may initially be erroneously ascribed to a mood disorder such as alcoholic depression; patients often experience some degree of social decline but typically have frank depression as a relatively minor clinical https://ecosoberhouse.com/ component. 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.

Long-Term Effects Of Alcoholic Neuropathy

Treatment for alcoholic neuropathy first focuses on stopping or significantly reducing alcohol intake. A person who drinks alcohol excessively may start to feel a tingling sensation in their limbs. Another prominent effect of alcoholic neuropathy involves painful and uncomfortable sensations. Alcoholic neuropathy can result in hypersensitivity to touch and even resting pain. Light touch can feel exaggerated and painful, particularly in the fingers and toes. People with a lengthy history of alcohol misuse might experience loss of balance, pain, tingling, weakness, or numbness after drinking alcohol.

alcohol neuropathy stages

Symptoms of alcohol-related neuropathy are similar to those of peripheral neuropathy. These can affect both your controlled and involuntary movements, as well as sensations. Thus, there is a need to screen acetyl-L-carnitine in both preclinical and clinical models of alcoholic neuropathy.

Wernicke-Korsakoff Syndrome

  • Alcohol-related peripheral neuropathy appears to be characterised by severe loss of myelinated fibres; and although profound small fibre loss can also be present, this appears to occur more variably 3, 51, 53, 59, 85.
  • A healthcare professional can offer support for people with alcohol use disorder.
  • Other studies have shown a direct, negative effect of alcohol and its many metabolites on the nervous system.
  • A mechanism of cisplatin chemotherapy-induced peripheral neuropathy was elucidated in an in vitro mouse model.

Paresthesia is usually mild to moderate in severity alcohol neuropathy stages but can become quite unpleasant or even frankly painful. Although patients may initially present with hand dysesthesia, more commonly hand symptoms follow anesthesia in the legs, which may be otherwise unrecognized or overlooked until more bothersome symptoms evolve. Neuropathic “Charcot” joints, a traumatic arthropathy typically of the ankle, may develop in advanced cases with severe loss of nociception as the patient forcefully strikes the ground to perceive placement of footing leading to joint destruction. Autonomic signs are difficult to demonstrate at the bedside unless frank orthostatic hypotension is present. Cerebellar degeneration may occur in alcoholics with or without micronutrient deficiency states, such as thiamine deficiency.

Deficiencies in these nutrients can harm overall health and prevent nerves from functioning correctly. Keep reading to learn more about the symptoms, causes, and treatments for alcohol-related neuropathy. Research suggests that up to 66% of people with AUD have some type of alcohol-related neuropathy. Addiction helplines, like the one operated by American Addiction Centers, can also be powerful resources for those seeking help of alcohol addiction. Our compassionate staff is available 24/7 and may be able to help answer your questions about alcohol addiction and related health issues, help you locate suitable rehab centers, and help you to verify your insurance coverage. B, Fluid-attenuated inversion recovery (FLAIR)–weighted MRI depicting hyperintense white matter lesions predominantly involving the splenium of the corpus callosum.

How Does Alcohol Impact the Brain and Central Nervous System?

C, Diffusion-weighted images revealing marked restriction with corresponding low apparent diffusion coefficient values. Reprinted with permission from Tozakidou M, et al, Neurology.16 © 2011, American Academy of Neurology. It is important to seek medical attention as soon as symptoms appear, as early detection and intervention can help manage the condition and potentially slow its progression. If liver damage is evident, appropriate consultation with a transplantation service is recommended. However, neuropathy is generally an exclusion criterion for transplantation. Your health care provider will perform a physical exam and ask about symptoms.

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