Peripheral nerves can get the same types of problems as other tissues, inflammation, toxicity, swelling, permeability, etc. However, there are some differences, due to their structural uniqueness. They exist as units of motor neurons with long axons that innervate muscle fibers. Individual nerve fibers contain the nerve axon along with its Schwann cells and protective myelin sheath coating (not all axons are myelinated). The fibers are grouped by the perineural sheath, a connective tissue wrapping containing both myelinated and unmyelinated axons. Regulation of the nerve microenvironment is accomplished by three barriers, the perineural barrier, the blood-nerve barrier, and the nerve-cerebrospinal fluid barrier. When these barriers are penetrated or otherwise dysfunctional, inflammatory cells can infiltrate, causing neuropathies with demyelination, inflammation, pain and atrophy.
Neuropathies include diabetic neuropathy, Guillain-Barré syndrome, post-herpetic neuralgia, and other forms of neuropathic pain/damage. Diabetic neuropathy is a common long-term complication that causes persistent painful sensation or loss of sensation, most commonly in the hands, feet and legs. It affects an estimated 1.3 million diabetic patients in the United States, and if severe, can lead to amputation of affected limbs. About 50% of diabetics develop neuropathy after 25 years, and approximately 56,000 amputations in the United States each year are due to diabetic neuropathy (Thomas, 1999, Resnick, 1999).
At a deeper level, neuropathies often are preceded by various forms of vasular damage, which can contribute to both to ischemic states as well as damaging iron deposits. This lends to the idea of using detoxification strategies prior to or along with vessel repair methods. It now seems clear that anti-oxidant therapy can help with diabetic neuropathy (Kahler et. al., 1993). In a double-blind study of 21 patients, 900 mg. of Vitamin E for six months showed significant results (Tutuncu et. al., 1998). Of all the anti-oxidant nutrients, alpha lipoic acid (ALA) seems to be the strongest. ALA is an approved medicine in Germany, where it has been used to treat diabetic neuropathy for over three decades. Studies have repeatedly shown that a 200-mg dose of ALA three times per day shows significant results within 6 months for most diabetics (Reljanovic et al., 1999). ALA has the ability to restore missing electrons and extend the life of other antioxidants, such as vitamins C and E (Shonhit 1995). This activity is crucial in neuropathy because it is difficult to remove inflammation from the affected nerve tissue with its complex barriers. It seems the concentration of antixoidants that ALA supports slowly builds up in the tissue, removes inflammation and allowing repair to occur over several months (Packer et al., 1995).
• To help speed and improve this antioxidant healing process I use the mentioned vitamins along with herbs from the blood-moving group, including salvia root, red peony root, and carthamus flower (Qian et al., 1987).
• To reduce the general inflammation, I use fish oil or evening primrose oil.
• Licorice root, which has been shown to reduce diabetic cataract formation in rat studies, may help reduce the inflammation of neuropathy be reducing a chemical called aldose reductase (Aida et al., 1990).
• Ginkgo leaf has shown specific benefit for optic neuropathy in a placebo-controlled human study (Chung et al., 1999).
• The wound healing herb Tien Qi root is a first line choice in my clinic.
• The Ayurvedic herb bala (Sida cordifollia) is used in treatment of neuropathy in TAM, because its warming action and nutrient composition seem to increase the circulation and supply of nutrition to nerve tissues.
• Acupuncture is often of great benefit in neuropathy, especially electro-acupuncture.
• Commercially available preparations of capsaicin, the strongly
pungent ingredient in red peppers can be applied externally to block
the pain of neuropathy (Fusco et al., 1997)