Fibromyalgia patients are often concurrently diagnosed with restless leg syndrome (RLS). According to estimates, thirty to seventy percent of fibromyalgia patients also meet the diagnostic criteria for RLS, making it one of the primary comorbidities of fibromyalgia syndrome.⁽¹⁾⁽²⁾ Given this prevalence, it is constructive for fibromyalgia patients to develop an understanding of RLS and it’s relationship to fibromyalgia syndrome, including:

• similarities in clinical presentation/diagnosis
• possible common etiologies
• overlap of treatment modalities
• future trends

RLS Clinical Presentation/Diagnosis

Restless leg syndrome is a sensorimotor disorder causing unpleasant sensations and an almost irresistible urge to move the legs.⁽³⁾ The diagnostic criteria for RLS were established by the International Restless Legs Syndrome Study Group in 1995, and identify four essential components, along with several supportive and associated clinical features.⁽⁴⁾ The four essential components are:

1. Urge to move the legs
   -This is usually accompanied by uncomfortable or unpleasant sensations in the legs.
2. Onset or exacerbation with rest
   -The urge to move becomes more pronounced during periods of inactivity such as sitting or lying.
3. Relief with movement
   -The urge to move and unpleasant sensations are diminished by activity, for at least as long as the movement continues.
4. Circadian pattern
   -The urge to move is more pronounced in the evenings or night than during the day.

Disturbed sleep is the most common clinical manifestation of RLS and is often the primary reason patients seek medical attention. It should be noted, that while fibromyalgia patients also suffer from disturbed sleep patterns, RLS does not appear to be the root cause and sleep disturbances in fibromyalgia patients often occur in the absence of RLS.⁽⁵⁾ However, RLS sleep disturbances do appear to exacerbate the fatigue and cognitive impairment already present in many fibromyalgia patients.⁽²⁾

As with fibromyalgia syndrome, the vast majority of patients diagnosed with RLS are women, and there appears to be a strong hereditary component to both disorders.⁽²⁾ Additionally, some research indicates a genetic linkage between RLS, mood disorders and irritable bowel syndrome – three of the most common comorbidities of fibromyalgia syndrome.⁽⁶⁾⁽⁷⁾ Unfortunately, no laboratory test or physical exam can confirm the diagnosis of either fibromyalgia or restless leg syndrome, so timely and accurate diagnosis of each condition depends largely on the expertise of the health care provider.

Causes

The clinical study of RLS has mirrored that of fibromyalgia syndrome in the sense that researchers initially focused on possible peripheral causes but eventually concluded that CNS mechanisms were responsible for both syndromes. Current research suggests it is likely that both syndromes share a similar pathogenesis arising from dysfunction in the neuroendocrine system.⁽¹⁾ The exact mechanism of this CNS dysfunction is unclear, but it appears both pathologies involve increased spinal cord excitability and decreased regulation of sensory processing pathways.⁽⁸⁾⁽⁹⁾.

Much of the current fibromyalgia research is centered around the neurotransmitters, serotonin and norepinephrine, and the role they play in regulating pain.⁽⁸⁾ RLS research, meanwhile, has been primarily focused on dopamine, a neurotransmitter responsible for regulating motor control. Interestingly, recent evidence suggests that dopamine is also involved in pain modulation, indicating that, like restless leg syndrome, fibromyalgia may involve a disturbance of dopaminergic neurotransmission.⁽¹⁰⁾
.

Treatments

Fibromyalgia syndrome and RLS are treated with both pharmacologic and non-pharmacologic therapies. Non-pharmacologic therapies, like improved nutrition and better sleep hygiene, typically address functional symptoms of the disorders, while pharmacologic therapies usually act on neuroendocrine function in the central nervous system.⁽¹¹⁾

Drugs that increase levels of dopamine (i.e. ropinirole and pramipexole) are first-line treatments for restless leg syndrome.⁽³⁾ The majority of patients treated with these agents show improved symptoms, at least initially, but these medications can sometimes cause an augmentation, or rebound, effect and actually make symptoms worse between doses. This is especially likely to happen with older medications like levodopa. Attention should be paid to this possibility whenever initiating therapy or adjusting doses.⁽¹²⁾

It is also important to be aware that anti-depressant drugs used in the treatment of fibromyalgia can aggravate RLS symptoms in some patients, so a period of trial-and-error might be required to find appropriate therapies for an individual.⁽⁶⁾

Future

It appears that a combination of external environmental stressors and internal neuroendocrine dysfunction in genetically predisposed individuals leads to alterations in central nervous system function in both RLS and fibromyalgia syndrome.⁽³⁾⁽⁸⁾ Currently, the studies of both syndromes are directed primarily at neuroendocrine dysfunction and are likely to remain so for the foreseeable future. As the study of genetics continues to unravel the pathogenesis of fibromyalgia and RLS, the therapies should become more targeted toward specific, dysfunctional sensory pathways, leading to decreased symptoms and an improved quality of life.

Learn more about fibromyalgia at: www.myalganex.com

1. Yunus MB, Aldag JC. Restless legs syndrome and leg cramps in fibromyalgia syndrome: a controlled study. BMJ. 1996 May 25;312(7042):1339. [↩] [↩]
2. Stehlik R, Arvidsson L, Ulfberg J. Restless legs syndrome is common among female patients with fibromyalgia. Eur Neurol. 2009;61(2):107-11. Epub 2008 Dec 9. [↩] [↩] [↩]
3. Thomas K, Watson CB. Restless legs syndrome in women: a review. J Womens Health (Larchmt). 2008 Jun;17(5):859-68. [↩] [↩] [↩]
4. Walters AS. Toward a better definition of the restless legs syndrome. The International Restless Legs Syndrome Study Group. Mov Disord 1995;10(5):634-42. [↩]
5. Moldofsky H. The significance, assessment, and management of nonrestorative sleep in fibromyalgia syndrome. CNS Spectr. 2008 Mar;13(3 Suppl 5):22-6.
   [↩]
6. Hornyak M, Benes H, Eisensehr I, Haan J, Kassubek J, Peglau I, Stiasny-Kolster K, Trenkwalder C. Depression in restless legs syndrome : Pathogenesis, assessment, and implications for treatment. Nervenarzt. 2009 Apr 11. [Epub ahead of print] [↩] [↩]
7. Weinstock LB, Fern SE, Duntley SP. Restless legs syndrome in patients with irritable bowel syndrome: response to small intestinal bacterial overgrowth therapy. Dig Dis Sci. 2008 May;53(5):1252-6. Epub 2007 Oct 13. [↩]
8. Bradley LA, McKendree-Smith NL, Alarcón GS, Cianfrini LR. Is fibromyalgia a neurologic disease? Curr Pain Headache Rep. 2002 Apr;6(2):106-14. [↩] [↩] [↩]
9. Wood PB. Role of central dopamine in pain and analgesia. Expert Rev Neurother. 2008 May;8(5):781-97. [↩]
10. Wood PB, Schweinhardt P, Jaeger E, Dagher A, Hakyemez H, Rabiner EA, Bushnell MC, Chizh BA. Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 2007 Jun;25(12):3576-82. [↩]
11. Paulson, G W. Restless legs syndrome. How to provide symptom relief with drug and nondrug therapies. Geriatrics. 2000 Apr; 55(4):35-8, 43-4, 47-8. [↩]
12. Ferini-Strambi L. Treatment options for restless legs syndrome. Expert Opin Pharmacother. 2009 Mar;10(4):545-54. [↩]

Tags: fibromyalgia, fms, restless leg syndrome, rls

This entry was posted on Monday, April 13th, 2009 at 3:55 pm and is filed under Fibromyalgia. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.