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Restless Legs Syndrome: Current Concepts about Disease Pathophysiology
Brian B Koo1, Kanika Bagai2, Arthur S Walters2
1Department of Neurology, Yale University School of Medicine, New Haven, CT, USA; Department of Neurology, Connecticut Veterans Affairs Health System, West Haven, CT, USA; Yale Center for Neuroepidemiology & Clinical Neurological Research, New Haven, CT, USA.
Tremor and Other Hyperkinetic Movements (New York, N.Y.)
|August 19, 2016
Summary
Restless Legs Syndrome (RLS) involves brain area activation and striatal iron deficiency. This neurologic disorder affects multiple biological systems, including dopaminergic and serotonergic pathways.
Area of Science:
- Neurology
- Neuroscience
- Medical Research
Background:
- Restless Legs Syndrome (RLS) pathophysiology has been extensively studied, encompassing neuropathology, neuroimaging, electrophysiology, and genetics.
- Research has identified specific brain regions and biological systems implicated in RLS.
- This review examines the current understanding of RLS pathophysiology, considering neuroanatomy, biological, organ, and genetic systems.
Purpose of the Study:
- To review the existing literature on the pathophysiology of Restless Legs Syndrome (RLS).
- To examine the neuroanatomical, biological, organ, and genetic underpinnings of RLS.
Main Methods:
- A comprehensive literature search was conducted using PubMed, covering publications from 1966 to April 2016.
- Search terms included "restless legs syndrome" combined with "pathophysiology," "pathogenesis," "pathology," or "imaging."
- English language studies focusing specifically on RLS pathophysiology were included, excluding those related to other diseases.
Main Results:
- No gross structural brain abnormalities are observed in RLS patients.
- Widespread brain activation occurs in areas such as the pre- and post-central gyri, cingulate cortex, thalamus, and cerebellum.
- Consistent pathological findings include striatal iron deficiency, alongside alterations in dopaminergic, oxygen-sensing, opioid, glutamatergic, and serotonergic systems.
- Genetic associations with RLS have been identified, including polymorphisms in BTBD9 and MEIS1 genes.
Conclusions:
- RLS is a neurologic sensorimotor disorder characterized by pathology, notably iron deficiency, in motor and sensory brain regions.
- Brain areas beyond motor and sensory functions, including the cingulate cortex and cerebellum, are implicated in RLS.
- Multiple biological systems, including dopaminergic, oxygen-sensing, opioid, glutamatergic, and serotonergic pathways, are involved in RLS pathophysiology.
- Further research is required to elucidate the primary versus secondary roles of affected anatomical locations and biological systems in RLS.
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