The data indicates that there is both small and large fibre loss in alcohol-related neuropathy, but that small fibre loss is generally predominant [3, 51, 53, 56, 59, 63, 86]. 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].
- Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth).
- ALN with thiamine deficiency was manifested as a variable mixture of these symptoms.
- 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].
- Motor nerves are the nerves responsible for all voluntary skeletal and somatic movement such as moving the leg or arm.
- This disease typically occurs in chronic alcoholics who have some sort of nutritional deficiency.
- She has over a decade of direct patient care experience working as a registered nurse specializing in neurotrauma, stroke, and the emergency room.
According to Simms et al., 2008a, Simms et al., 2008b, using similar protocol of intermittent alcohol (20%; v/v) ingestion, the alcohol concentration in the blood ranged from 4 to 93 mg / dL in Wistar rats submitted to 20 ingestion sessions. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), acute intoxication in alcohol consumption (binge drinking) corresponds to a blood concentration of 80 mg / dL or higher, and a pattern of heavy drinking to a concentration of 60 mg / dL or higher. In our study, we observed a blood concentration of 85 mg / dL in the AL group, associating the signs and symptoms of AN observed in this study with this pattern alcohol neuropathy of human consumption (NIAAA, 2022). As yet there is no effective therapeutic intervention available for relieving the neuropathic pain due to chronic alcohol consumption. Thus there is a need to understand the basic pathophysiological mechanisms involved in alcohol induced neuropathic pain so that new therapeutic modalities targeting disrupted molecular events can be developed for prevention as well as clinical management of alcoholic neuropathy. Izumi et al. [73] also demonstrated that a single day of ethanol exposure in rats on post natal day 7 results in significant apoptotic neuronal damage throughout the forebrain after 24 h of ethanol administration.
Treatment Process
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]. An essential risk factor regarding the etiology of ALN is the amount of alcohol consumed throughout the years since alcohol displays direct toxicity on nerve fibers [55]. It is estimated that consumption of more than 100 ml of ethyl alcohol per day significantly increases the risk of ALN [56]. Recent studies show contradictory information about the role of malnutrition and micronutrients (thiamine) deficiency in the pathogenesis of ALN; however, it is assumed that these might induce the progression of ataxia or movement disorders [55, 57]. Nevertheless, heavy alcohol drinkers are usually significantly malnourished because of the improperly balanced diet and impaired absorption of the essential nutrients and elements [58, 59]. Behse & Buchthal [31] compared 37 Danish patients with alcoholic neuropathy with six patients with nonalcoholic post gastrectomy polyneuropathy.
Thus, ALN might be induced by the combination of the effects of the direct activity of alcohol metabolites on the nerve fibers along with nutritional deficiencies primarily in a form of thiamine deficiency. 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 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].
What Is Alcoholic Neuropathy?
Biomarkers of alcohol abuse include carbohydrate-deficient transferrin (CDT) and phosphatidylethanol (PEth). CDT is an indirect metabolite of ethanol and constitutes either a marker of prolonged, heavy alcohol consumption or a marker of relapse. Peth on the other hand is a direct alcohol metabolite that can be measured to monitor alcohol consumption as well as for the identification of https://ecosoberhouse.com/article/how-long-does-a-hangover-last-how-to-ease-a-hangover-tips/ early signs of alcohol-related clinical manifestations. Other non-specific biomarkers useful in the diagnosis of alcohol use disorder are gamma-glutamyl transferase (GGT), mean corpuscular volume (MCV) of the red blood cells, and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Alcohol abuse causes a wide range of disorders that affect the nervous system.
- It was observed that abstinence may lead to the regression of several symptoms of AAN [159].
- Alcoholic polyneuropathy is a neurological disorder in which peripheral nerves throughout the body malfunction simultaneously.
- Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153].