[Epidemiology of restless legs syndrome]. / Epidémiologie du syndrome des jambes sans repos.

INTRODUCTION: Restless legs syndrome (RLS) is a chronic sensorimotor disorder where patients complain of an almost irresistible urge to move their legs. This urge can often be accompanied by pain or other unpleasant sensations, it either occurs or worsens with rest particularly at night, and improves with activity. The International Restless Legs Syndrome Study Group has established four essential criteria for clinical diagnosis of RLS. STATE OF ART: Affecting an estimated 7.2 to 11.5% of the adult population, the symptoms of RLS may be associated with significant sleep disturbance and may have a negative impact on quality of life. The prevalence of RLS increases with age, and women are more frequently affected than men. In France, the estimated prevalence is 8.5%. Among sufferers, 4.4% complain of very severe symptoms. Although RLS is mainly idiopathic, several clinical conditions have been associated with it, especially iron deficiency with or without anemia, end-stage renal disease and pregnancy. These conditions may share a common pathophysiological mechanism involving a disorder of iron metabolism. By contrast, controversy persists as to whether polyneuropathy, particularly when associated with diabetes, is to be considered as an important cause of secondary RLS. This association is difficult to demonstrate as conventional electromyography is not adequate to detect small fiber neuropathy often associated with diabetes. CONCLUSION AND PERSPECTIVES: RLS is often underdiagnosed and few subjects receive recommended RLS drug treatment. There is a clear need for complementary education to improve the accurate diagnosis of RLS. Indeed, better knowledge of this syndrome is a prerequisite to prompt an appropriate therapeutic management.

Evolution of postural stability after subthalamic nucleus stimulation in Parkinson's disease: a combined clinical and posturometric study.

OBJECTIVES: The occurrence of postural and balance disorders is a frequent feature in advanced forms of Parkinson's disease (PD). However, the pathological substrate of these disturbances is poorly understood. METHODS: In the present work, we investigated the evolution of posturometric parameters [center of pressure (CoP) displacement and CoP area] and axial scores between the pre-operative period and 3 months post-operative in seven PD patients who underwent bilateral deep brain stimulation (DBS) of the subthalamic nucleus (STN). RESULTS: After surgery, the patients leaned backwards much more regardless of the STN stimulation, suggesting that surgery could have a deleterious effect on postural adaptation. During the post-operative period, the improvement in axial and postural scores was similar under levodopatherapy and DBS. On the other hand, DBS of the STN significantly reduced the CoP displacement and the CoP area, whereas levodopatherapy tended only to reduce the CoP displacement and to increase the CoP area significantly. CONCLUSIONS: These data suggest that DBS of the STN and levodopa do not act on the same neurological systems involved in posture regulation. DBS of the STN could improve posture via a direct effect on the pedunculopontine nucleus, which is known to be involved in posture regulation.

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy).

This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals pre-lesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.

The metabolism of exogenous L-dopa in the brain: an immunohistochemical study of its conversion to dopamine in non-catecholaminergic cells of the rat brain.

The characterization and localization of non-catecholaminergic cells producing dopamine after L-Dopa load have been investigated in the normal rat brain by a direct immunohistochemical labelling of amines using specific antibodies. The detection of dopamine-containing non-catecholaminergic cells has been achieved in rats given a commonly used mixture of L-Dopa plus peripheral decarboxylase inhibitor, and compared to controls. Results indicate that serotoninergic neurons tend toward a switch of their metabolism into dopamine production after L-Dopa load in a dose-dependent manner. In addition small non-aminergic cells, identified as aromatic amino-acid decarboxylase-containing cells, were observed to produce dopamine after exogenous L-Dopa load. Possible implications of such results concerning the mode of action of L-Dopa in the brain are discussed.

Immunohistochemistry of endogenous L-DOPA in the rat posterior hypothalamus.

The aim of this work was to study L-DOPA-containing neuronal structures of the rat posterior and dorsal hypothalamus by means of immunohistochemistry using antiserum against glutaraldehyde conjugated L-DOPA. Aspects and distribution of L-DOPA immunoreaction among cells of the supramammillary nucleus and the A11, A13c and A13 cell groups are described and compared to dopamine immunoreactivity, mainly through a double colored labelling procedure employing a color modification of the DAB reaction by metallic ions. Differences between L-DOPA and dopamine stainings within cell groups as the presence of cells with predominant or exclusive L-DOPA coloration are tentatively explained under the light of previous findings using immunohistochemistry of catecholamines synthesizing enzymes and catecholamines histofluorescence.