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The syndrome was first mentioned by an English doctor, Thomas Willis, in 1672. In 1861, a German doctor, Theodor Wittmaack, described it as Anxietas tibiarum (literally anxiety of the lower leg muscles: the tibialis). The Swedish doctor Karl Ekbom in 1945 reported his observations in 34 persons with the condition and used the term "restless legs;" later, he observed 70 additional typical cases. Ekborn founded the department of clinical neurology of Uppsala University in 1956, continuing his studies of restless legs, which was known for some time as Ekbom's Syndrome or Wittmaack-Ekbom Syndrome. Much progress in understanding the disorder has been made recently as new study techniques have been developed.
Restless Legs Syndrome may have a genetic component (especially when onset is before age 50), and it is partly related to dopamine activity in the brain affecting function of the cerebral cortex; this is the same neurotransmitter involved in Parkinson's disease. Dopamine agonists (drugs that stimulate the dopamine receptors in the same way dopamine does) and dopamine itself (e.g., l-dopa) are often effective in treating the condition. However, studies suggest that the specific dopamine systems in the brain differ in Restless Legs Syndrome versus Parkinson's disease; the two disorders can coexist when dopamine levels are quite low.
Restless Legs Syndrome mainly occurs past age 50, and affects about 10% of those in that age group; it is particularly common in women. Poor circulation in the legs-which may result from history of smoking, diabetes, lack of exercise, and other factors-contributes to the development of the condition. Nutritional deficiency, particularly lack of bound iron, is known to exacerbate the disorder. The syndrome may also occur temporarily during late pregnancy, possibly as the result of reduced circulation in the legs and lower levels of folate (a B vitamin, B9).
Tests have suggested that serum levels of both ferretin and folate are involved in nutritional aspects of Restless Legs Syndrome (3-5). The levels of these nutrients within cells may not be relevant, nor, apparently, are levels of hemoglobin or free iron. Administration of iron and folate in deficiency cases can provide some relief and sometimes resolve the problem entirely. Folate deficiencies can result from genetic defects, low absorption, or dietary insufficiency (recommended intake for adults is 400 ?g/day). The following table displays good sources of folate (see the article Iron Deficiency Anemia for good dietary sources of iron; suggested daily iron intake is 7 mg for men; 12-16 mg for women). Some foods are rich sources of both folate and iron, especially liver (and, to a lesser extent, other meats), spinach (and, to a lesser extent, most green leafy vegetables), and several legumes (beans and peas). Fortified foods, such as breads and cereals, are also good sources of these nutrients. Folate was named for leaves (foliage) that were noted to be a significant source; the supplement form is called folic acid. Current recommendations suggest limiting intake of supplements with folic acid to 1,000 ?g (= 1 mg) per day, but the concern for high doses is eliminated when vitamin B12 is also administered.
