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Published on: January 21, 2020
Pathophysiological concepts of restless legs syndrome
Walter Paulus1, Pascal Dowling1, Roselyne Rijsman2
1Department of Clinical Neurophysiology, University of Göttingen, Göttingen, Germany.
Summary
Restless Legs Syndrome (RLS) involves a dopaminergic system dysfunction, potentially affecting spinal and striatal dopamine receptors. Neurophysiological methods reveal altered spinal excitability impacting sensory processing in RLS patients.
Area of Science:
- Neuroscience
- Neurology
Background:
- Current understanding of Restless Legs Syndrome (RLS) pathophysiology relies on neuroimaging, neurophysiological data, and treatment effects.
- Genetic research is anticipated to further elucidate RLS mechanisms.
Purpose of the Study:
- To outline the established pathophysiological concepts of Restless Legs Syndrome.
- To highlight the role of the dopaminergic system and the A11 neuron group in RLS.
Main Methods:
- Review of neuroimaging and neurophysiological data.
- Analysis of treatment effects on RLS.
- Discussion of neurophysiological methods including pain thresholds, H-reflex testing, and quantitative sensory testing.
Main Results:
- A dysfunction in the dopaminergic system is the prevailing concept in RLS pathophysiology.
- The A11 neuron group in the hypothalamus plays a role in modulating spinal excitability, which is altered in RLS.
- Altered spinal excitability affects sensory processing of leg afferents in brain stem structures.
Conclusions:
- The dopaminergic system, particularly striatal/spinal dopamine receptors and the A11 neurons, is central to RLS pathophysiology.
- Neurophysiological alterations in spinal excitability are measurable and contribute to RLS symptoms.
- Further genetic insights are expected to refine the understanding of RLS.
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