Alcoholic polyneuropathy Wikipedia

The development of an appropriate therapy will include cessation of alcohol ingestion but will also need to be aimed at the toxic target(s) of alcohol, which is the goal of ongoing research. Although the clinical and animal studies have focused on nutritional deficiency, biochemical studies provide evidence that alcohol may affect thiamine utilization rather than cause thiamine deficiency. Thiamine levels in the ALN group were comparable to those of normal subjects, whereas there was a significantly lower concentration among those in the Wernicke–Korsakoff group. The transketolase activity was lower in both groups as compared with controls.10 The investigators suggested that thiamine utilization rather than lack of thiamine itself was implicated in the development of ALN. The clinical correlates of white matter atrophy vary widely from having no detectible signs or symptoms, to exhibiting overt cognitive impairment [114].

alcohol neuropathy stages

The spectrum of dementias includes, Wernicke-Korsakoff syndrome (WKS), Marchiafava–Bignami, and acquired hepatocerebral degeneration [26, 163]. In addition, alcoholics often sustain traumatic brain injuries, and can secondarily develop debilitating or fatal CNS diseases due to hepatic encephalopathy, central pontine myelinolysis, or nutritional deficiencies pellagrous encephalopathy (due to niacin deficiency), [26]. Symptoms of AAN are non-specific; in the sympathetic division, these include impairments in perspiration, orthostatic hypotension, whereas in parasympathetic hoarseness, swallowing difficulties, or cardiac arrhythmias [111, 166]. Gastrointestinal symptoms include delayed stomach emptying and intestinal transit, dyspepsia, and faster emptying of the gallbladder [165].

Alcohol-related metabolic brain injury and disease

For example, alcohol poisoning causes acute injury and swelling of catecholaminergic and dopaminergic neurons in the mesocorticolimbic dopaminergic and ventral mesencephalic tegmentum [38]. Chronic injury and degeneration reduce the areas occupied by neuronal cell processes in the dorsal raphe nucleus of serotonergic neurons, reflecting impairment of serotonergic transmission to the cortex [158]. Alcohol abuse contributes to peripheral neuropathy development involving both somatic and autonomic nerves [154, 155].

  • Professional and peer help through programs such as Alcoholics Anonymous or other substance abuse programs can help you reduce your alcohol consumption.
  • White matter (myelin) is another major target of alcohol toxicity in the CNS [19, 26, 33, 78, 106].
  • Alcohol’s toxic/metabolic effects on the brain are mediated by hepatic encephalopathy, as well as other complex factors that are not entirely understood, despite decades of research in this field.
  • Further, alcohol impairs vitamin B1 absorption and its storage in the liver [151,152,153].

Patients may also have a deficiency in vitamin B12 (cobalamin), affecting the axon and causing muscle weakness, sensory disturbances, and anemia. Vitamin B9 (folic acid) levels tend to be decreased, reducing the density of small and large nerve fibers. Important in carbohydrate metabolism and neuron function, vitamin B3 (niacin) may also be decreased. Epidermal nerve fibre density was assessed in two studies, both of which 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.

Cortical and subcortical nuclear degeneration

The H-reflex and F-wave are measures of peripheral nerve conduction, often delayed or absent in alcohol-induced PN. Abnormalities in the F-wave response are a sensitive and early indicator of alcohol-induced PN. An analysis of lab data may correlate with the patient’s neuropathic syndrome and systemic symptoms. Elevated levels of the liver enzymes gamma-glutamyl transpeptidase, aspartate aminotransferase, alcohol neuropathy stages alanine aminotransferase, and alkaline phosphatase may indicate long-standing heavy alcohol consumption and its effects on hepatic function. Decreasing albumin, increasing bilirubin, and prolonged clotting factors may indicate hepatic decompensation. Red blood cells (RBCs) tend to be larger than normal (macrocytosis) and reduced in number from a deficiency in vitamin B9 or B12 or GI bleeding.

Rich sources of vitamin B1 include organ meats, beef, pork, poultry, pasta, bread, rice, nuts, whole-grain cereals, and beans. The morbidity and mortality of chronic heavy alcohol consumption encompass a wide range of systemic diseases with negative health outcomes that may be interrelated with a patient’s neuropathic syndrome (see Selected systemic effects of heavy alcohol consumption). Clinical correlation of signs and symptoms and close patient surveillance are essential.

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