Malnutrition has been implicated in the pathology of alcohol-related neuropathy by several authors. The majority of studies which investigate the relationship between malnutrition and neuropathy focus on thiamine deficiency as an aetiological factor, drawing upon existing knowledge of Beri Beri. A smaller number of publications do attribute thiamine deficiency, but generally speaking these studies were older or of lower quality evidence [4, 6, 30, 58, 76, 77]. While the data herein presented can contribute to this collective effort, there are limitations worth mentioning. The absence of evaluation of biochemical indicators regarding toxicity in nervous system that could better explain the alcohol-induced neurodegeneration process, what we intend to perform in future studies.
Fennelly and colleagues evaluated the response to vitamin therapy in 29 individuals with alcohol-related neuropathy [30]. Patients were admitted and treated with a diet containing thiamine, nicotinic acid, pantothenic acid, pyridoxine, folic acid, and vitamin B12. This study found that the response to treatment depended upon the severity of neuropathy and whether there was severe cirrhosis. Thiamine replacement improved signs of neuropathy in 7/13 patients with grade I neuropathy (objective signs of reduced pain and vibration sensation but normal reflexes) and 3/8 with grade II (marked sensory changes and decreased reflexes) neuropathy within 4 weeks. No patients with grade III (severe sensory impairment, absent reflexes, foot drop, muscle wasting) neuropathy showed clinical improvement over the 4-week period, but 4/8 did show an improvement over 3–6 months.
Sensory, motor, and autonomic symptoms
Your health care provider will perform a physical exam and ask about symptoms. In total, 585 papers did not meet the inclusion/exclusion criteria and were excluded. By scanning the reference lists of included studies, an additional 4 papers were identified. This study is reported in accordance with the preferred reporting items for systematic reviews and meta-analysis (PRISMA) guidelines [7].
Chronic heavy drinkers may be at risk for several different alcohol-related neurological issues. It is likely to get worse if the person continues to use alcohol or if nutritional problems are not corrected. Alcoholic neuropathy is usually not life threatening, but it can severely affect quality of life. Epidermal nerve fibre density was assessed in two studies, both of which https://ecosoberhouse.com/ supported decremental nerve fibre density distally in the lower limb, anecdotally supportive of a length-dependent pattern [53, 63]. The sometimes-conflicting findings between biopsy findings may be representative of the complex interplay of pathological factors in alcohol-related peripheral neuropathy and is indicative of the need for further research in this area.
Signs and symptoms
Excessive or heavy alcohol consumption is defined by the CDC when men have 15 or more drinks each week and women have 8 or more drinks each week. The National Institute on Alcohol Abuse and Alcoholism reports that 16 million people in the US have been diagnosed with alcohol use disorder (AUD). A person is diagnosed with AUD when he or she meets at least 2 of the 11 criteria in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Multiple research studies indicate that 11% to 66% of people with AUD have alcohol-induced PN. N-acetylcysteine, an amino acid, is a potent antioxidant and helps to enhance glutathione concentrations. N-acetylcysteine may have application in the prevention or treatment of neuropathy.
Endoneural oxidative stress leads to nerve dysfunction in rats with chronic constriction injury [39]. A significant decrease in the activity of anti-oxidant enzymes (superoxide dismutase and catalase) and an increase in lipid peroxidation were observed in sciatic nerves of diabetic rats with established neuropathic pain [40]. ROS triggers second messengers involved in central sensitization of dorsal horn cells [41] or they activate spinal glial cells which in turn play an important role in chronic pain [42]. Reduced glutathione is a major low molecular weight scavenger of free radicals in cytoplasm.
Increased Pain and Hypersensitivity
Glucose fluctuation, hyponatremia, hypokalemia, and hypomagnesemia are common features. An elevated carbohydrate-deficient transferrin level is a sensitive indicator of chronic heavy alcohol consumption. Transferrin is a serum protein that facilitates iron transport under the control of glycosyltransferase, which is a carbohydrate chain. A review of the human literature implicates nutritional deficiencies, most often thiamine deficiency, that are common in alcoholic patients, as commonly accompanying complicating factors in the development of this neuropathy.
- The term polyneuropathy is used when multiple peripheral nerves are damaged.
- Keeping this disease process high on the differential with the right history is essential.
- Patients may be severely malnourished and dehydrated with electrolyte imbalances.
- This condition can be identified through blood tests, which can detect levels of essential nutrients in the body.
- However, the limitations of those studies include the lack of the possibility to measure the amount of vitamin B1 in the serum; further, patients who were involved in the study have received an unrefined form of the supplement.
Thus, treatment with anticonvulsant drugs may provide another therapeutic alternative for the symptomatic relief of pain in patients with alcoholic neuropathy. Therefore, topical application with capsaicin may provide symptomatic relief from neuropathic pain in patients suffering from alcoholic neuropathy. Thus, there is an urgent need to screen the vitamin E isoforms, especially tocotrienol for evaluating clinical efficacy in patients with alcoholic neuropathy.
What Are the Top Causes of Neuropathy?
People who drink heavily on a regular basis are at risk of developing this condition. 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. The mechanism of direct damage of nerve fibers due to alcohol intoxication remains unclear. Activation of spinal cord microglia, mGlu5 spinal cord receptors, and hypothalamic-pituitary-adrenal axis appear to be implicated in this process [92,93,94,95,96,97]. Oxidative stress also leads to the indirect damage of nerve fibers via the release of free radicals and proinflammatory cytokines with protein kinase C and ERK kinase phosphorylation [98,99,100,101].
Thiamine serves as an important coenzyme in carbohydrate metabolism and neuron development. The lack of thiamine in the nervous system affects the cellular structure and can cause https://ecosoberhouse.com/article/alcohol-neuropathy-symptoms-and-treatment/ cell membrane damage and irregular ectopic cells. Other vitamin deficiencies seen with alcohol abuse include, but are not limited to, B-vitamins, folic acid, and vitamin-E.