Restless Legs Syndrome and Pain Disorders: What’s in common?

Abstract

Between 10 % and 30 % of the population report chronic pain. More than half of these also have sleep complaints. From considering these data, it can be inferred there is a significant overlapping between these conditions. Restless Legs Syndrome/Willis-Ekbom Disease (RLS/WED) is characterized by complaints of an "urge to move" frequently associated with dysesthesias. From that perspective, these sensations can also have painful characteristics. By the same token, the presence of comorbid diseases as predicted by a higher prevalence RLS/WED, have many of them with pain as an important complaint. Pain is a multidimensional response involving several levels of expression ranging from somatosensory to emotional. The potential shared mechanisms between RLS/WED and pain may involve sleep deprivation/fragmentation effect, inducing an increase in markers of inflammation and reduction in pain thresholds. These are modulated by several different settings of neurotransmitters with a huge participation of monoaminergic dysfunctional circuits. A thorough comprehension of these mechanisms is of utmost importance for the correct approach and treatment choices.

Restless Legs Syndrome: From Pathophysiology to Clinical Diagnosis and Management

“…The medial thalamic nuclei are part of the limbic system, which is modulated by dopaminergic afferents. Another study found thalamic activity changes in the thalamocotrical circuit ( Goulart et al, 2014 ). Therefore, it was hypothesized that the dopaminergic dysfunction might lead to an impairment of the medial pain system ( Garcia-Borreguero and Williams, 2014 ; Goulart et al, 2014 ) and then caused the uncomfortable symptoms of RLS.…”

Restless Leg Syndrome in Neurologic and Medical Disorders

“…Notably, RLS correlates best with PLM-associated arousals rather than PLM severity 75,76 consistent with the relationship of this disorder to sleep fragmentation and deprivation. 28 Second, the morphology of basal nuclei revealed no gross abnormalities in structure, no degenerative features, and quite stable dopamine activities in patients with RLS. 77 Severity of both RLS and PLM relate to higher g-aminobutyric acid levels in the thalamus and lower levels in the cerebellum, as determined by localized magnetic resonance spectoscopy.…”

“…9 The association of RLS with sleep deprivation and/or fragmentation may be caused by reduction in pain thresholds, modulated by a variety of neurotransmitters, particularly dysfunction of monoaminergic circuits. 28 The association of RLS with autoimmune disorders has been long recognized 29 with significant comorbidity of inflammation, intestinal bacterial overgrowth, iron deficiency, and peripheral neuropathy, suggesting an immunologic basis of secondary RLS. 30 Some studies found elevated inflammatory cytokines, most prominent interleukin-6 and tumor necrosis factor-a, 30 although other studies failed to observe such a correlation.…”

Spinal Cord Stimulation for Restless Legs Syndrome: Case Series and Mechanistic Hypothesis

“…There is a sizeable population of chronic pain patients who suffer from comorbid RLS [11], as did the patients described here. Because spinal cord stimulators are already implanted with relative ease and adjustment to include areas involved in RLS is not difficult or dangerous, using SCS to target chronic pain in these patients thus also grants the additional opportunity to provide potential ancillary RLS treatment to many people.…”