If you are struggling from the following symptoms you might have Restless Legs Syndrome (RLS): throbbing, pulling, creeping and other unpleasant sensations in the legs, which are often experienced in conjunction to impaired sleep. The relentless and tormenting course of RLS symptoms can often significantly diminish the quality of life for many of those affected and leads to significant emotional distress.
Frequently Asked Questions
- RLS is one of the most common neurological conditions that increases with advancing age and is diagnosed clinically based on four essential criteria as outlined by the International Restless Legs Syndrome Study Group:
- a desire to move the limbs, often associated with paraesthesia’s or dysesthesias;
- symptoms that are worse or present only during rest and are partially or temporarily relieved by activity;
- motor restlessness;
- Worsening of symptoms at rest or nocturnally.
- RLS is considered “the most common disorder you never heard of” and continues to be ignored by healthcare providers, mainly due to the lack of objective evidence regarding its prognostic value in determining clinical outcomes.
- Disrupted sleep is the most frequent reason RLS patients seek medical assistance, with 82–89% of patients exhibiting PLMS that results in repeated Restless legs syndrome, also known as Willis-Ekbom Disease, an overwhelming urge to move one's legs, sometimes accompanies sleep apnoea.
- In most cases the urge is immediately relieved by movement.
- The urge most frequently sets in during the evening, especially upon going to bed, and thus it can interfere with going to sleep.
Obstructive sleep apnea is often comorbid to RLS and PLMS and is established as a significant cause of sleep disturbance and risk factor for hypertension, CVD, and stroke. Read more on Sleep Renewal about Restless Legs Syndrome
- No cure exists for restless leg syndrome.
- Patients can reduce their symptoms by destressing and relaxing their muscles, such as with massage or warm baths.
- Some medications, like pramipexole, can help with symptoms.
- The National Institute of Neurological Disorders and Stroke notes that benzodiazepines for restless leg syndrome, like diazepam, can worsen sleep apnoea.
- The main goal of sleep apnoea treatment is to help patients breathe while sleeping.
- Options include nasal CPAP, bi-level positive airway pressure and oxygen.
- Doctors may need to treat an underlying cause, such as heart failure, for central sleep apnoea. Patients with obstructive sleep apnoea may need surgery, such as uvulopalatopharyngoplasty, in which the doctor removes excess tissue at the source of the obstruction.
Patients with RLS have been reported to have a higher risk of stroke and heart disease than those without the disorder.
- Much of what we know about the relationship between sleep disturbances, such as those incurred by patients with RLS and PLMS, and the increased risk for hypertension and vascular diseases comes from clinical investigations into such risks in patients with insomnia and OSA.
- Disturbances in sleep onset, sleep maintenance, and total sleep time are reported by as many as 85 % of patients with RLS with nearly a third of patients with RLS reporting severe sleep disturbances.
- Because PLMS often accompany RLS and their occurrence frequently results in arousals from sleep, PLMS can exacerbate sleep disturbances.
- Studies have suggested that shortened sleep and insomnia may increase the incidence and risk of hypertension and CVD.
- Shortened sleep also has been associated with increased risk for CVD and coronary heart disease (CHD).
- Finally, patients with insomnia have a blunted nocturnal BP dipping response that may increase the risk of higher BP, CV risk, and target organ damage.
- Studies suggest that short sleep duration and poor sleep quality may increase the risk for hypertension and CVD.
- Obstructive sleep apnoea is often comorbid to RLS and PLMS and is established as a significant cause of sleep disturbance and risk factor for hypertension, CVD, and stroke.
The relationship between sleep disturbances, such as those incurred by patients with RLS and PLMS, and the increased risk for hypertension and vascular diseases comes from clinical investigations into such risks in patients with insomnia and OSA. Disturbances in sleep onset, sleep maintenance, and total sleep time are reported by as many as 85 % of patients with RLS with nearly a third of patients with RLS reporting severe sleep disturbances.
Because PLMS often accompany RLS and their occurrence frequently results in arousals from sleep, PLMS can exacerbate sleep disturbances. Therefore, an examination of the associations between hypertension and CVD with insomnia and OSA may provide context to similar risks related to RLS and PLMS and may help in the understanding of where CV risks arise in the patients who suffer from RLS and PLMS.
Studies have suggested that shortened sleep and insomnia may increase the incidence and risk of hypertension and CVD.
Prospective and epidemiologic database studies have shown that subjects sleeping ≤5 h per night had up to a 32 % greater likelihood of being diagnosed with hypertension than subjects sleeping longer.
Shortened sleep also has been associated with increased risk for CVD and coronary heart disease (CHD).
Finally, patients with insomnia have a blunted nocturnal BP dipping response that may increase the risk of higher BP, CV risk, and target organ damage.
Significantly less day to night-time SBP dipping was observed in the subjects with insomnia (−8 %) versus controls (−15 %; p = 0.01), but day to night-time DBP dipping did not statistically differ between the two groups of subjects.
Taken together, these studies suggest that short sleep duration and poor sleep quality may increase the risk for hypertension and CVD.
Obstructive sleep apnoea is often comorbid to RLS and PLMS and is established as a significant cause of sleep disturbance and risk factor for hypertension, CVD, and stroke.
In addition to hypertension, OSA has been reported to increase the risk for atrial fibrillation and CV-related and all-cause mortality.
Limited evidence shows that treating patients with RLS/PLMS with DA agonists reduces the PLMS-related heart rate response, subsequently normalizing the increases in heart rate.
Additional studies are needed to further explore the long-term effects of pharmacologic intervention on CV variables in patients with RLS/PLMS and whether such treatment may reduce the risk of hypertension, CVD, and vascular diseases in these patients. RLS/PLMS may be associated with an increase in hypertension, CVD, and vascular diseases is perhaps not surprising. Insomnia and OSA also contribute to an increased risk for hypertension and CVD, albeit likely through different mechanisms.
Disorders such as RLS/PLMS, insomnia, and OSA do share commonalities such as reduced sleep and increased arousals during the night, all of which have been shown to increase BP through sympathetic activation and reduce nocturnal BP dipping.
The relationship between RLS/PLMS and hypertension may, in part, explain the presence of treatment-resistant hypertension in some patients.
Since many patients do not pursue treatment or receive a diagnosis for RLS until symptoms become severe enough to affect their quality of life, the effects of the disease may go unrecognized for an extended time.
The influence of RLS/PLMS and the sleep disruption they cause on heart rate and BP may help to explain why some patients do not achieve therapeutic goals for hypertension.
Although the increases in BP in many patients with RLS may be small, such increases may be high enough to elevate certain patients into a prehypertension diagnosis, which would result in an increased risk for vascular events.
Consequently, polysomnography may be indicated in patients with prehypertension or treatment-resistant hypertension to determine the RLS/PLMS contribution to hypertension.
Further research is needed to tease out the complexities of the relationship between RLS/PLMS and hypertension, to determine the effects of pharmacologic therapy on hypertension and related risks.
Restless Legs Syndrome not only has physical, but bothersome psychological symptoms too. Sleepless nights and mental anguish contribute to a considerable physical and psychological burden for patients suffering from this condition. Unfortunately, by using conventional drugs such as tricyclic antidepressants (TCAs) and selective serotonin uptake inhibitors (SSRIs) to treat psychological effects associated with RLS, these may trigger or even worsen RLS symptoms. There is thus a constant trade-off between taking medication, or not.
Pharmaceutical treatment strategies, such as dopaminergic medications, can offer relief for those with RLS. However, a pitfall of dopaminergic drugs used at high doses is that quite often they may exacerbate RLS symptoms via a phenomenon known as augmentation or rebound. Fortunately, the 2012 approval of sustained release, transdermal rotigotine may overcome this roadblock (Bell 2012; Elshoff 2012; Boroojerdi 2010; Godau 2011).
Interesting, there are two types of Restless Legs Syndrom: primary and secondary. Where primary RLS has no known cause, secondary RLS is normally linked back to to another medical ailment. As an example: patients suffering from high blood sugar often present with secondary RLS, other relted conditions include: related nerve damage or chronic vascular disease like deep vein thrombosis and arterial claudication (Gemignani 2007; McDonagh 2007).
As mentioned, the exact cause of primary RLS is unknown. However, a genetic component is present in approximately 40 to 50 percent of patients with primary RLS, and those individuals have a family history of the disorder. Certain genetic variations are also associated with the condition (Ferri 2012; Bradley 2008; Miletic 2011).
Primary RLS is thought to be a disease of the peripheral nervous system, but studies suggest that the central nervous system may also be involved. Because RLS is akin to some other movement disorders the neurotransmitter dopamine, which helps facilitate uniform, controlled movements, has been theorized to be a possible causative factor. Indeed, altered dopamine signaling within the brain has been observed in several RLS studies, but results have been insufficient to draw firm conclusions (Clemens 2006; Cervenka 2006; Ruottinen 2000; Turjanski 1999; Eisensehr 2001). Additionally, alterations in dopamine signaling in the spinal cord have been observed, which lends further support to the hypothesis that dopamine is involved in RLS (Paulus 2006; Clemens 2006).
As the name suggest, secondary RLS is a symptom of over twenty medical conditions that are connected to this condition (Miletic 2011).
- End Stage Kindney Disease: Estimates indicate that up to 60% of patients on dialysis have RLS (Walker 1995; Thorp 2001; Kavanagh 2004).
- Diabetes, or impaired glucose tolerance, are more likely to have RLS, and RLS is a prominent part of diabetic peripheral neuropathy (Bosco 2009; O’Hare 1994; Lopes 2005; Merlino 2007).
- Parkinsons's diease, another disorder associated with dopaminergic dysfunction in the nervous system. However, the link has not yet been clearly established (Guerreiro 2010; Gjerstad 2011).
- Chronic venous disorders are a major contributor to secondary RLS (McDonagh 2007). In a 2007 study, researchers found that 36% of patients suffering from chronic venous disease also had RLS. In comparison, the control group only had a 19% occurrence of RLS. However, when the control participants who showed positive for RLS were studied more closely, it was noted that 91% of them had mild indications of venous problems (McDonagh 2007). In another study, participants with RLS who received medical treatment for chronic venous disease reported a 36% increase in quality of sleep and a 67% decrease in severity of symptoms (Tison 2005).
People with RLS also have an increased risk of developing high blood pressure, possibly due to overactivity of certain parts of the nervous system (Walters 2009; Batool-Anwar 2011).
The initial medical consultation at Health Renewal will be approximately 45 minutes. You will have to complete an in depth questionnaire before the consultation so please arrive 20 minutes before the time. During the 45 minute consultation your Health Renewal doctor will obtain a full medical history from you to determine your personal risk. A physical examination will be done after which the Doctor will decide which blood tests need to be requested from your local pathology laboratory.
These results will then be analyzed by your Doctor and this will be discussed with you at your follow up appointment. The results will determine whether a definite deficiency exists, and you will be advised on your treatment options. These options for treatment may range from (and include more than one) prescription medications, and nutraceuticals.
Make an appointment to consult with your Health Renewal Doctor and they will assist you in determining your risk factors and how best to prevent any problems or conditions that you may be susceptible to.
At Health Renewal the Integrative Doctors will assist patients with a combination of nutraceutical supplements.
Iron: Due to the presumed link between iron deficiency or altered iron metabolism in the brain and RLS (Conner 2008), one of the more common alternative treatments for RLS is iron supplementation (Trotti 2009). Various routes for iron supplementation have been studied as a treatment for RLS. Oral iron supplementation has been found to significantly ameliorate RLS in patients with low-normal levels of iron in their blood (Wang 2009). However, it is unclear if oral iron supplements are as effective for patients with no signs of iron deficiency (Davis 2000). Oral iron supplementation is also beneficial for treating RLS in the elderly, particularly those with low iron levels (O’Keeffe 1994). Intravenous iron supplementation in the form of iron dextran has also been found to significantly reduce RLS symptoms (Sloand 2004; Earley 2004). Although intravenous iron may be more effective than oral iron supplementation, it can cause severe complications including anaphylaxis (Silverstein 2004). It is important to note that only those with a blood test-verified iron deficiency should take supplemental iron. Ingestion of excess iron has been linked to cancer, atherosclerosis and other degenerative diseases.
Folate: Folate deficiencies may also play a role in the development of RLS. Pregnancy often precipitates signs of RLS (Manconi 2004) and folate levels are of paramount importance during pregnancy for healthy fetal development. Researchers have also found that pregnant women with low folate levels are more likely to develop RLS (Lee 2004), whereas women who take vitamins during pregnancy are less likely to develop RLS (Tunc 2007). Low levels of folate may also play a role in non-pregnant RLS patients (Patrick 2007). Older studies have found that folic acid supplementation can help treat certain paresthesias and other disorders of the peripheral nervous system as well (Botez 1976 and 1977).
Magnesium: Low levels of magnesium can cause neurons to become more easily excited, thus affecting a person’s mental status. As a result, magnesium supplements are often used to stabilize neuronal membranes and prevent abnormal activity in the nervous system (Trenkwalder 2008). Magnesium supplementation has been studied as a treatment for RLS. One case study found that magnesium supplements were able to relieve symptoms of RLS and improve sleep (Hornyak 1998). A novel form of magnesium – magnesium-l-threonate – may be even more effective for RLS because it is better able to gain access to the central nervous system (Slutsky 2010). However, the impact of magnesium-L-threonate on RLS has yet to be clinically validated.
Diosmin: The link between chronic venous disease and secondary RLS is well established (see above) (McDonagh 2007). Although it can be difficult to treat chronic venous issues, one therapy that has gained support is diosmin. Diosmin is a natural venotonic that supports venous function, thereby preventing or reversing some of the changes of chronic venous disease. Used and researched extensively in Europe, micronized diosmin has recently been introduced to the United States and proven to be an effective treatment for chronic venous disease (Carpentier 1998; Maksimovic 2008). Although the effectiveness of diosmin for treating RLS has not been tested, it remains a promising possible treatment.
Green Coffee Extract: Diabetes is a well-known risk factor for secondary RLS. However, less appreciated is that pre-diabetes – subclinical elevations in blood sugar – may also cause RLS while remaining under the diagnostic radar of most physicians (Gemignani 2007; Bosco 2009). A study examining subjects with impaired glucose metabolism unearthed a significantly increased risk of RLS in this population. RLS affected 41% of those with pre-diabetes, while only 18% of those with healthy glucose tolerance experienced the condition (Bosco 2009).
Maintaining healthy glucose metabolism, even for those not diagnosed with diabetes, may be helpful in RLS. Even slightly elevated blood sugar can damage delicate nerve cells and contribute to unpleasant sensations called paresthesias (Yagihashi 2007). Life Extension suggests that all aging individuals should strive to maintain blood glucose levels between 70 and 85 mg/dL for optimal health. Green coffee extract, with minimal caffeine content, represents a powerful tool for those aiming to maintain healthy blood sugar levels. It may also help control glucose elevations, which have been associated with RLS. However, this theory has yet to be tested in clinical trials.
Valerian root: Often used as an herbal sedative, valerian root has shown promise at reducing symptom severity of RLS. In an 8-week clinical trial, supplementation with 800 mg of valerian root daily resulted in improvements in daytime sleepiness and RLS symptoms (Cuellar 2009). Additional data also support the effectiveness of valerian root in treating insomnia in postmenopausal women (Taavoni 2011).