Metabolic, Toxic, and Nutritional Peripheral Neuropathies

ALCOHOL

The prevalence of neuropathy in alcohol use is uncertain, but has been estimated to exist in approximately 50% of alcoholics. Incidence of neuropathy in alcoholics correlates with age of the patient and the duration of alcohol use. The pathophysiology is uncertain, but the direct toxic effect of alcohol on peripheral nerves seems to be the most important etiology. Alcoholic neuropathy has a similar phenotype to other metabolic neuropathies. The neuropathy is often distal, symmetric, pure sensory, or sensory predominant and slowly progressive. There are often positive neuropathic sensory symptoms, such as tingling and or burning, as well as loss of nociceptive sensation on examination. Patients should be evaluated for other vitamin deficiencies or causes of malnutrition, because alcohol neuropathy often coexists with neuropathy due to thiamine deficiency and sometimes vitamin B₁₂ deficiency.

THIAMINE (VITAMIN B₁)

Thiamine (vitamin B₁) deficiency most commonly occurs in chronic alcohol abuse, chronic gastrointestinal problems (including recurrent vomiting), cancer patients, and after weight reduction surgery (i.e., bariatric surgery). Severe vitamin B₁ deficiency causes congestive heart failure (wet beriberi), peripheral neuropathy (dry beriberi), Wernicke encephalopathy, and Korsakoff syndrome. Neuropathy associated with thiamine deficiency may present with acute onset or insidiously with distal, symmetric, sensory, or sensorimotor neuropathy with positive neuropathic sensory symptoms (e.g., tingling) Thiamine-deficient patients may develop weakness, numbness, and loss of balance (ataxia). Evaluation of thiamine deficiency should include measurement of whole blood thiamine.

VITAMIN B₁₂ DEFICIENCY

Multiple nutritional deficiencies can result in peripheral neuropathy, with vitamin B₁₂ deficiency as one of the most recognized forms, which can lead to both a peripheral neuropathy as well as a myelopathy. Vitamin B₁₂ deficiency can result from a number of factors, both related to poor diet as well as syndromes of malabsorption, including the presence of pernicious anemia, inflammatory bowel disease, and bowel resection surgery (including gastric bypass surgeries). The usual manifestation of vitamin B₁₂ deficiency is distal numbness (large fiber sensory modalities) and paresthesias, with progressive gait unsteadiness. Vitamin B₁₂ deficiency can also cause cognitive dysfunction and should be considered in this clinical setting. Serologic testing for vitamin B₁₂ as well as methylmalonic acid is crucial for this diagnosis. Electrophysiologic studies show findings of an axonal sensorimotor peripheral neuropathy, and somatosensory evoked potentials may also show central conduction slowing, reflecting spinal cord involvement. Magnetic resonance imaging of the spinal cord may at times show abnormal T2 signal in the posterior columns of the spinal cord. Vitamin B₁₂ supplementation should be instituted. Depending on whether the etiology of the deficiency is poor dietary intake or malabsorption, oral or intramuscular administration should be chosen. Follow-up serologic studies should be done to ensure normalization of vitamin B₁₂ and methylmalonic acid levels after supplementation.

HYPOTHYROIDISM

Hypothyroidism is a common disorder most commonly affecting women. The diagnosis should be considered in patients with symptoms such as fatigue, weight gain, cold intolerance, coarse dry hair and skin, constipation, depression, and abnormal menstrual cycles. Neuropathic symptoms often include paresthesias, numbness, and pain. Patients often complain of subjective weakness but do not often have findings of weakness on examination.

UREMIA

Peripheral neuropathy due to uremia occurs in 10% to 80% of patients with chronic renal failure who are on dialysis but has become less frequent due to renal transplantation. The neuropathy in uremia is similar to other neuropathies due to a metabolic cause, being often distal, symmetric, sensory predominant, and slowly progressive. Patients often have symptoms of numbness and imbalance as well as paresthesias and burning. Other common symptoms include restless legs, cramps, and weakness. The diagnosis should be considered especially in patients with end-stage renal disease with a creatinine level of 5 mg/dL or higher or creatinine clearance less than 12 mL/min.

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