Peripheral neuropathy: pathogenic mechanisms and alternative therapies
Peripheral neuropathy (PN), associated with diabetes, neurotoxic chemotherapy, human immunodeficiency virus (HIV)/antiretroviral drugs, alcoholism, nutrient deficiencies, heavy metal toxicity, and other etiologies, results in significant morbidity. Conventional pain medications primarily mask symptoms and have significant side effects and addiction profiles. However, a widening body of research indicates alternative medicine may offer significant benefit to this patient population. Alpha-lipoic acid, acetyl-L-carnitine, benfotiamine, methylcobalamin, and topical capsaicin are among the most well-researched alternative options for the treatment of PN. Other potential nutrient or botanical therapies include vitamin E, glutathione, folate, pyridoxine, biotin, myo-inositol, omega-3 and -6 fatty acids, L-arginine, L-glutamine, taurine, N-acetylcysteine, zinc, magnesium, chromium, and St. John's wort. In the realm of physical medicine, acupuncture, magnetic therapy, and yoga have been found to provide benefit. New cutting-edge conventional therapies, including dual-action peptides, may also hold promise. (Altern Med Rev 2006;11(4):294-329)
Peripheral neuropathy (PN)--characterized by pain, numbness, and tingling in the extremities and slow nerve conduction--affects a significant percentage of the U. S. population and can be extremely debilitating. A 1999-2000 report, National Health and Nutrition Examination Survey (NHANES), of 2,873 men and women ages 40 or older (419 with diabetes), found a PN prevalence of 14.8 percent. (1) PN was defined as at least one insensitive area on the foot with monofilament testing; it was also assessed by self-reported symptoms. The incidence of PN was significantly higher (62%) in the subset with diabetes. The incidence of PN also increased significantly with age. NHANES found 8.1 percent of the 40-49 year age group had PN, compared to 34.7 percent of individuals over age 80.
Peripheral neuropathy manifests as axonal degeneration. Diagnosis of PN involves a complete evaluation to determine the extent of the neurological deficit as well as a complete history and physical examination to determine the possible etiology. Despite thorough history and physical exam, etiology remains a mystery in approximately 50 percent of cases. (2)
Peripheral neuropathy can be the result of genetics, chronic disease, environmental toxins, alcoholism, nutritional deficiencies, or side effects of certain medications.
Among chronic diseases, diabetes mellitus is the most common cause of PN. Mechanisms involved in diabetes-associated PN are discussed in depth in a later section. Other endocrinological abnormalities that can result in neuropathy include hypothyroidism and acromegaly. (3) The neuropathy associated with hypothyroidism commonly manifests as carpal tunnel syndrome. Other manifestations resemble diabetic neuropathy, with tingling paresthesias in a stocking-glove distribution. PN of acromegaly (excess growth hormone) includes carpal tunnel syndrome and sensorimotor polyneuropathy. Human immunodeficiency virus (HIV) also results in PN, usually involving distal, nonpainful paresthesias, decreased ankle reflexes, and abnormal pain and temperature perception. (4) Amyloidosis is another chronic disease resulting in PN.
Environmental neurotoxins that can cause peripheral neuropathy include exposure to mold in water-damaged buildings, (5) solvents such as n-hexane and methyl n-butyl ketone, (6) and heavy metals, including thallium, (7) arsenic, (7) lead, (8) mercury, (9) and germanium. (10)
Peripheral neuropathy is common among chronic alcohol abusers, with prevalence as low as nine percent and...