Restless legs syndrome and nocturnal myoclonus: initial clinical manifestation of familial amyloid polyneuropathy.

Salvi, Fabrizio; Montagna, Pasquale; Plasmati, R.; Rubboli, Guido; Cirignotta, Fabio; Veilleux, Martin; Lugaresi, E; Tassinari, C. A.

doi:10.1136/jnnp.53.6.522

Cited by 74 publications

(28 citation statements)

References 9 publications

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“…A number of studies confirmed these observations [19,21]. So far it remains unclear to what extent neuropathy contributes to the development of RLS symptoms [2,22,30]. Special attention has been paid to small fibre neuropathy, which can be found in secondary RLS [20] and may also be present in idiopathic RLS patients [12].…”

Section: Discussionmentioning

confidence: 82%

Idiopathic restless legs syndrome:

et al. 2004

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Section: Discussionmentioning

confidence: 82%

Idiopathic restless legs syndrome:

et al. 2004

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“…Moreover, PLMS may be the only abnormality in relatives of families with RLS inherited in an autosomal dominant fashion [14, 62,106]. PLMS have also been reported associated with a wide variety of neurological disorders such as stiff-person and Isaacs' syndromes, dopa-responsive dystonia, Huntington chorea, ALS, startle disease, attention-hyperactivity disorder, myelopathies and peripheral neuropathies [40,53,56,78,105,[110][111][112] but here the true relevance of these associations remains often undetermined given the small numbers and the lack of appropriate controls among the general population. Many different views exist in regard to the mechanisms which originate the PLMS.…”

Section: International Classification Of Sleep Disorders (Icsd) Of Thmentioning

confidence: 99%

Sleep-related non epileptic motor disorders

Montagna

2004

J Neurol

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Sleep-related non epileptic motor disorders represent a frequent but often neglected or trivialized source of neurological disability. In recent decades, the widespread adoption of videopolygraphic techniques has better characterized already known nosographic entities and described a bewildering variety of previously unrecognized clinical entities (such as REM sleep behaviour disorder, sleep-related eating disorder, benign neonatal sleep myoclonus, facio-mandibular myoclonus during sleep, fragmentary hypnic myoclonus, propriospinal myoclonus at the wake-sleep transition, rhythmic feet movements during sleep, etc). The scope of the neurophysiological investigations of sleep related disorders has therefore been much expanded. However, advances in the semeiology and clinical description of sleep-related movement disorders has rarely been matched by adequate understanding of the underlying pathophysiological mechanisms, or by major advances in treatment. The main sleep-related motor disorders are described here, following the only classification currently available, e. g. that offered by the International Sleep Disorders Classification of the American Sleep Disorders Association, which is more a classification of diseases of sleep than of movement disorders. The increasing use of functional neuroimaging in vivo and of updated neurophysiological and molecular techniques in man and in the experimental animal will hopefully lead to a better understanding of these disorders in terms of pathophysiology of disordered motor control.

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“…The association between RLS and peripheral neuropathy was initially described by Ekbom and, subsequently, confi rmed by many studies. [86][87][88][89][90][91][92][93] These studies revealed that the axonal-sensory and the small-fi ber polyneuropathies are the most common causes of RLS. [89][90][91][92][93] An imbalanced equilibrium in the dorsal horn of the spinal grey matter among the excitatory nociceptive inputs, due to the peripheral neuropathy, and the inhibitory ones descending from the diencephalon might explain the occurrence of RLS in the course of peripheral neuropathy.…”

Section: Vesper's Cursementioning

confidence: 99%

Restless legs syndrome: differential diagnosis and management with rotigotine

Merlino

Serafini²,

Robiony³

et al. 2009

NDT

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RLS is a common sleep disorder with distinctive clinical features. The prevalence of RLS in Caucasians and North Americans ranges from 5% to 10%. However, only some of these subjects (almost the 3% of the general population) report being affected by a frequent and severe form of the sleep disorder. RLS is diagnosed clinically by means of four internationally recognized criteria that summarize the main characteristics of the sleep disorder. Besides the essential criteria, supportive and associated features of RLS have been established by experts in order to help physicians treat patients with doubtful symptoms. Several clinical conditions may mimic this sleep disorder. In order to increase the sensibility and specifi city of RLS diagnosis, doctors should perform a meticulous patient history and then an accurate physical and neurological examination. Dopamine agonists are recognized as the preferred fi rst-line treatment for RLS. Rotigotine is a non-ergoline dopamine agonist with selectivity for D1, D2 and D3 receptors. The drug is administered via transdermal patches which release rotigotine for 24 hours. Four clinical trials demonstrated that this compound is able to improve RLS symptomatology with few and moderate adverse events. Head to head trials are required to compare the effi cacy and tolerability of rotigotine with other dopamine agonists administered via oral intake. Rotigotine has been approved by the FDA and EMEA for Parkinson's disease. For the treatment of moderate to severe idiopathic RLS, rotigotine has been recommended for approval by the EMEA and is under review by the FDA.

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Restless legs syndrome and nocturnal myoclonus: initial clinical manifestation of familial amyloid polyneuropathy.

Cited by 74 publications

References 9 publications

Idiopathic restless legs syndrome:

Idiopathic restless legs syndrome:

Sleep-related non epileptic motor disorders

Restless legs syndrome: differential diagnosis and management with rotigotine

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