Group I nonreciprocal inhibition in primary restless legs syndrome.
Identifieur interne : 001E97 ( Ncbi/Merge ); précédent : 001E96; suivant : 001E98Group I nonreciprocal inhibition in primary restless legs syndrome.
Auteurs : Cesa Scaglione [Italie] ; Roberto Vetrugno ; Giuseppe Plazzi ; Giovanni Rizzo ; Federica Provini ; Pasquale Montagna ; Paolo MartinelliSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Electrophysiology, H-Reflex (physiology), Humans, Intralaminar Thalamic Nuclei (physiopathology), Motor Neurons (physiology), Nerve Net (physiopathology), Neural Inhibition (physiology), Questionnaires, Restless Legs Syndrome (diagnosis), Restless Legs Syndrome (physiopathology), Reticular Formation (physiopathology), Spinal Nerves (physiopathology).
- MESH :
- diagnosis : Restless Legs Syndrome.
- physiology : H-Reflex, Motor Neurons, Neural Inhibition.
- physiopathology : Intralaminar Thalamic Nuclei, Nerve Net, Restless Legs Syndrome, Reticular Formation, Spinal Nerves.
- Electrophysiology, Humans, Questionnaires.
Abstract
Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P = 0.043), 5 (P = 0.007), and 6 ms (P = 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS.
DOI: 10.1002/mds.21794
PubMed: 17987650
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pubmed:17987650Le document en format XML
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<author><name sortKey="Montagna, Pasquale" sort="Montagna, Pasquale" uniqKey="Montagna P" first="Pasquale" last="Montagna">Pasquale Montagna</name>
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<term>Intralaminar Thalamic Nuclei (physiopathology)</term>
<term>Motor Neurons (physiology)</term>
<term>Nerve Net (physiopathology)</term>
<term>Neural Inhibition (physiology)</term>
<term>Questionnaires</term>
<term>Restless Legs Syndrome (diagnosis)</term>
<term>Restless Legs Syndrome (physiopathology)</term>
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<front><div type="abstract" xml:lang="en">Electrophysiological investigations of restless legs syndrome (RLS) have found spinal circuits impinging on motoneurones. We evaluated the H reflex threshold, latency, the Hmax/Mmax ratio, and the short latency autogenic inhibition in 7 patients with RLS and 10 age-matched controls by testing the excitability changes in soleus H reflex Ib interneuron function. A significant reduction in Ib inhibition at 4 (P = 0.043), 5 (P = 0.007), and 6 ms (P = 0.001) of H reflex conditioning interstimulus interval was found in RLS patients. Data support the hypothesis that altered group I nonreciprocal inhibition is implicated in enhancing the spinal circuitry excitability of RLS, and are consistent with the view of an abnormal supraspinal drive to spinal interneurons in RLS.</div>
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