Article

The restless legs syndrome

Paracelsus Elena Klinik, Centre of Parkinsonism and Movement Disorders, Kassel, Germany.
The Lancet Neurology (Impact Factor: 21.82). 09/2005; 4(8):465-75. DOI: 10.1016/S1474-4422(05)70139-3
Source: PubMed

ABSTRACT The restless legs syndrome is a common disorder that encompasses an idiopathic form of genetic or unknown origin and symptomatic forms associated with many causes. Symptomatic forms occur during pregnancy and are coincident with uraemia, iron depletion, polyneuropathy, spinal disorders, and rheumatoid arthritis. For the hereditary forms, at least three gene loci, located on chromosomes 12, 14, and 9, have been traced so far. Prevalence in the general population is between 3% and 9%, increases with age, and is higher in women than in men. Treatment is needed only in the moderate to severe forms of the disorder and mostly in elderly people. Pathophysiology and treatment may be closely linked to the dopaminergic system and iron metabolism. Dopaminergic treatment with levodopa and dopamine agonists is the first choice in idiopathic restless legs syndrome, but augmentation and rebound should be monitored in long-term treatment. Various other drugs, such as opioids, gabapentin, and benzodiazepines, provide alternative treatment possibilities.

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    • "These sensations occur at rest, in particular in the evening or at night, and are relieved by movement. Symptoms are typically attenuated by dopaminergic drugs (Trenkwalder et al., 2005). The pathophysiology of restless legs syndrome is poorly understood. "
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    ABSTRACT: Pathophysiology of restless legs syndrome is poorly understood. A role of the thalamus, specifically of its medial portion which is a part of the limbic system, was suggested by functional magnetic resonance imaging and positron emission tomography studies. The aim of this study was to evaluate medial thalamus metabolism and structural integrity in patients with idiopathic restless legs syndrome using a multimodal magnetic resonance approach, including proton magnetic resonance spectroscopy, diffusion tensor imaging, voxel-based morphometry and volumetric and shape analysis. Twenty-three patients and 19 healthy controls were studied in a 1.5 T system. Single voxel proton magnetic resonance spectra were acquired in the medial region of the thalamus. In diffusion tensor examination, mean diffusivity and fractional anisotropy were determined at the level of medial thalamus using regions of interest delineated to outline the same parenchyma studied by spectroscopy. Voxel-based morphometry was performed focusing the analysis on the thalamus. Thalamic volumes were obtained using FMRIB's Integrated Registration and Segmentation Tool software, and shape analysis was performed using the FMRIB Software Library tools. Proton magnetic resonance spectroscopy study disclosed a significantly reduced N-acetylaspartate:creatine ratio and N-acetylaspartate concentrations in the medial thalamus of patients with restless legs syndrome compared with healthy controls (P < 0.01 for both variable). Lower N-acetylaspartate concentrations were significantly associated with a family history of restless legs syndrome (β = -0.49; P = 0.018). On the contrary, diffusion tensor imaging, voxel-based morphometry and volumetric and shape analysis of the thalami did not show differences between the two groups. Proton magnetic resonance spectroscopic findings in patients with restless legs syndrome indicate an involvement of medial thalamic nuclei of a functional nature; however, the other structural techniques of the same region did not show any changes. These findings support the hypothesis that dysfunction of the limbic system plays a role in the pathophysiology of idiopathic restless legs syndrome.
    Brain 11/2012; DOI:10.1093/brain/aws266 · 10.23 Impact Factor
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    • "These include neuromodulatory effects on nociceptive input (Jensen and Yaksh, 1984; Barasi and Duggal, 1985; Fleetwood-Walker et al., 1988; Gao et al, 2001; Wei et al., 2009), locomotion (Barbeau and Rossignol, 1991; Barriere et al., 2004), movement (Zhu et al., 2007), cardiovascular function (Lahlou et al., 1990; Maisky and Doroshenko, 1991), and sex-specific roles (Pappas et al., 2010) including male sexual function (Giuliano et al., 2001, 2002). Dysfunction of this system is hypothesized to be one factor leading to the development of Restless Legs Syndrome (RLS) in humans (Trenkwalder and Paulus, 2005; Barriere et al., 2005), a sensorimotor disorder characterized by uncomfortable sensations and an urge to move the legs. The most common treatment for RLS is DA agonist administration, but the use of opioids such as morphine has also been reported to alleviate symptoms of RLS. "
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    ABSTRACT: Dopamine (DA) neurons of the A11 diencephalospinal system represent the sole source of DA innervation to the spinal cord in mice, serving neuromodulatory roles in the processing of nociceptive input and movement. These neurons originate in the dorso-caudal diencephalon and project axons unilaterally throughout the rostrocaudal extent of the spinal cord, terminating predominantly in the dorsal horn. The density of A11 DA axon terminals in the lumbar region is greater in males compared to females, while in both sexes the activity of neurons terminating in the thoracic spinal cord is greater than those terminating in the lumbar region. The present study was designed to test the hypothesis that A11 DA neurons are activated by opioids. To test this hypothesis, male and female mice were systemically treated with agonists or antagonists acting at the μ-opioid receptor, and spinal cord concentrations of DA and its metabolite DOPAC were determined in the thoracic and lumbar spinal cord using high performance liquid chromatography coupled with electrochemical detection. Systemic administration of the μ-opioid agonist morphine led to a dose- and time-dependent increase in spinal cord DOPAC/DA ratio (an estimate of DA neuronal activity) in both male and female mice, with greater changes occurring in the lumbar segment. Blockade of opioid receptors with the opioid antagonist naloxone reversed the stimulatory effects of morphine on A11 DA neurons in both male and female mice, but had little to no effect on the activity of these neurons when administered alone. Present findings are consistent with the conclusion that spinal cord-projecting axon terminals of A11 DA neurons are activated by opioids in both male and female mice, most likely through a dis-inhibitory mechanism.
    Neuropharmacology 05/2011; 61(4):614-21. DOI:10.1016/j.neuropharm.2011.05.002 · 4.82 Impact Factor
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