All of the following diagnostic criteria must be met:
The frequency of symptoms varies considerably, and is defined as chronic-persistent or intermittent, as follows:
The symptoms of RLS cause significant distress or impairment in social, occupational, educational, or other important areas of functioning by the impact on sleep, energy/vitality, daily activities, behavior, cognition (thinking), or mood.
Restless legs syndrome is generally considered an “idiopathic” disorder, meaning that the exact cause of the condition is unknown. Neurology textbooks and articles focus on the theory that iron deficiency in the brain decreases the function of the dopamine brain nerve receptors. How this particular process occurs has not been proven. There are additional theories regarding how other conditions and factors can trigger RLS, including peripheral neuropathy. New discoveries have been made linking disturbances in the balance of gut bacteria and generalized inflammation with RLS. Unfortunately, acceptance of new ideas and the pace of research are slow. This information is not readily accepted by the conservative medical community, and thus, the general population may be the last to know – however, the power of the Internet is changing this process.
RLS is grouped into primary RLS (unknown causes), familial RLS (strong hereditary basis), and secondary RLS (over 50 different disorders and conditions that produce or worsen RLS). The role of small intestinal bacterial overgrowth (SIBO) is becoming recognized as a key factor in the pathophysiology of RLS. Unfortunately, the importance of SIBO is not well known amongst most physicians. Similarly, the discovery that there is endorphin deficiency in the brain of patients with RLS is also not well recognized.
Restless legs syndrome is treatable but generally cannot be cured at this time by FDA-approved therapy. List of FDA-approved medicines and other treatments:
Many other remedies are reported in the lay literature.
There are many causes for iron deficiency and an answer must be discovered. Seeing a gastroenterologist is very important in many patients.
Note: investigational studies on RLS food triggers are limited. There are many barriers and defensive mechanisms by which the intestinal tract mucosa can be exposed to antigens, bacteria and chemicals, yet still be selective about what is absorbed and secreted. Healthy commensal bacteria play a role in protecting the mucosal barrier both directly and indirectly by improving immune function. When this balance is disturbed, absorption of food antigens may be increased. When the bacterial load is increased in SIBO, carbohydrate consumption resulting in increased fermentation, increased bacterial colony counts and increased inflammation.
When SIBO has been diagnosed or IBS/SIBO diet is useful. Those with small intestinal bacterial overgrowth should refer to the SIBO diet in www.gidoctor.net. The “IBS diets” and “SIBO diets” are low in sugar, carbs, and in certain carbohydrates that are hard to digest such as gluten.
Gluten sensitivity with and without celiac disease are common conditions (combined incidence up to 3% of the population). With gluten sensitivity alone it is not known if it can directly affect RLS as it could in those with celiac disease (Jackson-2012). A number of patients do, however, find that gluten intake can trigger RLS.
Foods high in carbohydrates, or carbohydrates which are difficult to digest such as the “FODMAPs”, may be a problem for some patients. These foods are substrates for bacterial fermentation and hence could not only explain worsening symptoms in patients with IBS but also those with SIBO and possibly SIBO-associated RLS. The term FODMAPs stands for fermentable oligo-, di-, and mono-saccharides and polyls. These include lactose, fructose, fructans, galactans and sugar alcohols. Fructans are present in wheat, onions, garlic and other vegetables.
Many patients with RLS have found alcohol consumption, especially in the evening hours, can lead to an increase in RLS symptoms. Alcohol as a factor for poor sleep was not supported by one epidemiologic study of various sleep disorders including RLS (Vinson-2010). In contrast, the author (LW) has RLS patients who have RLS and concomitant SIBO who have exacerbations of RLS symptoms by alcohol intake which may be related to fructose consumption. The effect of alcohol on periodic limb movements was evaluated in 40 alcohol dependent patients (Gann-2002). Alcohol dependent patients displayed a significantly enhanced PLMS-arousal index compared to age- and gender-matched healthy subjects. The study did not address RLS per se. In one of the antibiotic treatment studies for bacterial overgrowth in RLS, an observation was made that consumption of alcohol and fruit exacerbated RLS symptoms (Weinstock-2010-C) and other of our clinic patients have had similar problems.
Caffeine can lead to an increase in RLS symptoms. A clinical, uncontrolled study of 62 RLS patients and associated anxious-depressed states suggested that caffeine worsened RLS symptoms (Lutz-1978).
This additive has been studied and was compared to cyclamate in randomized, double-blind, placebo-controlled trial with a crossover design (de Groot-2007). During a period of 48 days, the subjects took 4 capsules per day containing either 150 mg of cyclamate, 22.5 mg of saccharin, either sweeteners or placebo on two successive days. Between each of these 2-day periods there was a 2-day rest period during which no capsules were taken. The subjects had symptoms more often and more severe RLS while using saccharin or the combination of saccharin and cyclamate than when taking the placebo.