This article reviews the neurobiology of vitamin E, neurologic disorders considered to be due to vitamin E deficiency, and the role of vitamin E in the management of neurologic disorders. Vitamin E is a scavenger of free radicals; it plays a role in the control of brain prostaglandin synthesis, regulation of nucleic acid synthesis, and gene expression. Neurologic and muscle dysfunction due to vitamin E deficiency may result from lack of antioxidant protection in susceptible tissues. Vitamin E has been used therapeutically in a large number of neurologic disorders wherein oxidative stress is implicated in pathophysiology, such as in neurodegenerative disorders. Vitamin E exerts antioxidant effects in combination with other antioxidants, including carotene, vitamin C, and selenium.
• Deficiency of vitamin E can produce neurologic disorders.
• Vitamin E has antioxidant and neuroprotective effects.
• Vitamin E has been found to be beneficial in the management of some neurologic disorders not characterized by deficiency of vitamin E.
Historical note and terminology
Vitamin E, or tocopherol, is one of the fat-soluble vitamins. The term tocopherol (which in Greek, tokos meaning childbirth, and phero meaning to bring forth) was first used to describe something found in lettuce that prevented fetal resorptions and enabled an animal to have offspring (Evans and Bishop 1922). To indicate the alcohol nature of the molecule, “ol” was added to the ending. This unknown substance was designated vitamin E. The neurologic role of vitamin E was first reported in 1928 when suckling offspring of vitamin E–deficient mother rats developed paralysis (Evans and Burr 1928). Degeneration of the brain in a vitamin E–deficient rat was reported a few years later (Pappenheimer and Goettsch 1931). The antioxidant properties of vitamin E were demonstrated in the 1940s, and applications in several human disorders believed to be due to free radical damage were suggested. The first documentation of the effect of vitamin E deficiency on the human nervous system was in patients with abetalipoproteinemia, in which beta-lipoprotein cannot be secreted, resulting in severe malabsorption and vitamin E deficiency. Vitamin E deficiency was shown to be the cause of ataxic neuropathy in these patients (Kayden et al 1965). In 1981, Burck and colleagues first reported neurologic abnormalities resulting from vitamin E deficiency in a patient without abnormalities of gastrointestinal function or lipid malabsorption and with normal plasma proteins. This was subsequently labeled familial isolated vitamin E deficiency.
The similarity of nutritional muscular dystrophy in animals and Duchenne muscular dystrophy led to several trials of high-dose vitamin E in patients. However, a number of studies showed that this therapy was not beneficial (Backman et al 1988).
This article will briefly review the neurobiology of vitamin E, neurologic disorders considered to be due to vitamin E deficiency, and the role of vitamin E in the management of neurologic disorders.
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