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Antiviral therapy for cryoglobulinemic neuropathy: comment on the article by Saadoun et al. Arthr Rheum 2007;56:2810 (letter)
No full text
MICRORGANISMI DI PROVENIENZA ITTICA: ATTENDIBILITA' DEL TEST DI NIVEN E REALE POTENZIALITA' ISTAMINOGENA
No full textRestless legs syndrome in diabetic neuropathy: a frequent manifestation of small fiber neuropathy
No full textAs the occurrence of restless legs syndrome (RLS) in diabetes is controversial, the aim of this study was to assess the prevalence of RLS in a cohort of patients with diabetic neuropathy and to analyze the features of the associated neuropathy. We investigated the occurrence of RLS diagnosed in accordance with the criteria of the International Restless Legs Syndrome Study Group in a cohort of patients with polyneuropathy and mononeuropathy multiplex associated with diabetes mellitus (DM), or impaired glucose tolerance (IGT), or impaired fasting glucose (IFG) in a retrospective study. RLS was present in 33/99 patients with neuropathy associated with DM/IGT/IFG (84 with distal polyneuropathy and 15 with multiple mononeuropathy). Comparing patients with or without RLS, small fiber sensory neuropathy was more common in the RLS patients (15/33 vs. 15/66), as were symptoms of burning feet (10/33 vs. 6/66). In several patients, RLS was responsive to neuropathic pain medications. The frequent occurrence of RLS in association with thermal dysesthesias may reflect the involvement of small sensory fibers in the form of hyperexcitable C fibers or A-delta fiber deafferentation. We suggest that RLS may be triggered by abnormal sensory inputs from small fibers, especially involved in neuropathy associated with DM/IGT/IFG. Our data show that RLS is a relevant feature of diabetic neuropathy, as a frequent and potentially treatable manifestation of small fiber involvement in the course of DM and IGT/IFG
Restless legs syndrome and painful neuropathy—Retrospective study. A role for nociceptive deafferentation?
No full textOBJECTIVES:
Restless legs syndrome (RLS) occurs in polyneuropathy with small fiber
involvement, possibly as a peculiar form of neuropathic pain; however, the
relationship between pain and RLS has been poorly investigated in
polyneuropathy.
DESIGN, SETTING, AND PATIENTS:
We evaluated retrospectively the occurrence of RLS in 102 consecutive patients
with polyneuropathy manifesting with neuropathic pain or dysesthesia, referred
to the Neuromuscular Center, using the National Institutes of Health criteria
for RLS. The patients were classified in subgroups characterized respectively by
allodynia (hyperphenomena), with reported unpleasant sensations evoked by
tactile stimuli, and hypoalgesia (hypophenomena), with absent pain sensation to
pinprick, according to putative mechanisms of pain.
RESULTS:
RLS was present in 41/102 patients (40.2%). It was significantly more frequent
in the "hypoalgesia" (23/37) than in the "allodynia" subgroup (9/31; P = 0.008)
and in the not classifiable cases (9/34; P = 0.004).
CONCLUSIONS:
RLS is frequent in painful polyneuropathy and is significantly associated with
decreased small fiber input, thus nociceptive deafferentation may represent a
factor interacting with RLS "generators," possibly at spinal level. We suggest
that overactivity of the spinal structures implicated in RLS may be triggered by
nociceptive deafferentation in a subgroup of patients with painful
polyneuropathy. Our findings, prompting a mechanistic characterization of RLS
associated with painful polyneuropathy, have to be confirmed in a prospective
study
Restless legs syndrome: differential diagnosis and management with pramipexole
No full textFrancesca Brindani, Francesca Vitetta, Franco GemignaniDepartment of Neurosciences, University of Parma, ItalyAbstract: Restless legs syndrome (RLS) is a condition characterized by discomfort at rest and urge to move focused on the legs. RLS may occur as an idiopathic, often hereditary condition (primary RLS), or in association with medical conditions (secondary RLS) including iron deficiency, uremia, and polyneuropathy. Current understanding of the pathophysiology of RLS points to the involvement of three interrelated components: dopaminergic dysfunction, impaired iron homeostasis, and genetic mechanisms. The diagnosis of RLS is made according to the consensus criteria by a National Institutes of Health panel: 1) an urge to move the legs, usually accompanied by uncomfortable sensations; 2) beginning or worsening during rest; 3) relieved by movement; and 4) worse, or only occurring, in the evening or at night. The differential diagnosis of RLS aims to: 1) distinguish RLS from other disorders with RLS-like symptoms and 2) identify secondary forms, with investigation of underlying diseases. The treatment of RLS demands a clinical evaluation to rule out and cure causes of secondary RLS, including iron supplementation when deficient, and to eliminate the triggering factors. The presence of neuropathy should be especially investigated in nonhereditary, late-onset RLS, in view of a possible treatment of the underlying disease. The first line treatment for idiopathic RLS is represented by dopamine agonists, in particular nonergot-derived ropinirole and pramipexole, whereas ergot dopamine agonists (cabergoline and pergolide) are no longer in first-line use given the risks of cardiac valvulopathy. Although no comparative trials have been published, a meta-analysis of pramipexole versus ropinirole suggests differences in efficacy and tolerability favoring pramipexole.Keywords: restless legs syndrome, pramipexole, dopamine, agonists, small fiber neuropath
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