Literature DB >> 7969975

Recurrent inhibition is decreased in patients with amyotrophic lateral sclerosis.

E M Raynor1, J M Shefner.   

Abstract

Recurrent inhibitory pathways are powerful modulators of motor neuron excitability. Renshaw cell activation can both inhibit homologous motor neurons and disinhibit antagonists. In spastic spinal-cord-injured patients, recurrent inhibition is consistently increased, and clinical reductions in spasticity are associated with reduced recurrent inhibition. In this study, we evaluated 12 spastic patients with amyotrophic lateral sclerosis (ALS) to see whether a similar mechanism was operating. In contrast to spinal-cord-injured patients, spastic patients with ALS showed strikingly reduced recurrent inhibition, as assessed by a conditioned H-reflex technique, which produces a response (H') whose amplitude is inversely correlated with activity in recurrent inhibitory pathways. The mean ratio of the maximum H' response to the maximum H-reflex response (H'/H ratio) was 0.55, significantly greater than the ratio seen in normal subjects. Amplitude of the H' correlated with amplitude of the Achilles tendon reflex. Thus, in patients with classical ALS, recurrent inhibition appears to be abnormally reduced compared with control subjects, suggesting a different physiology for spasticity in this setting than in spinal cord transection.

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Year:  1994        PMID: 7969975     DOI: 10.1212/wnl.44.11.2148

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  15 in total

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Authors:  Lee J Martin; Qing Chang
Journal:  Mol Neurobiol       Date:  2011-11-10       Impact factor: 5.590

2.  Physiology of the fasciculation potentials in amyotrophic lateral sclerosis: which motor units fasciculate?

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3.  Motor units as tools to evaluate profile of human Renshaw inhibition.

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4.  Enhancement of single motor unit inhibitory responses to transcranial magnetic stimulation in amyotrophic lateral sclerosis.

Authors:  Annie Schmied; Shahram Attarian
Journal:  Exp Brain Res       Date:  2008-05-22       Impact factor: 1.972

5.  Glycinergic innervation of motoneurons is deficient in amyotrophic lateral sclerosis mice: a quantitative confocal analysis.

Authors:  Qing Chang; Lee J Martin
Journal:  Am J Pathol       Date:  2008-12-30       Impact factor: 4.307

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7.  The puzzling case of hyperexcitability in amyotrophic lateral sclerosis.

Authors:  Jong Seok Bae; Neil G Simon; Parvathi Menon; Steve Vucic; Matthew C Kiernan
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8.  Spasticity mechanisms - for the clinician.

Authors:  Angshuman Mukherjee; Ambar Chakravarty
Journal:  Front Neurol       Date:  2010-12-17       Impact factor: 4.003

9.  Early interneuron dysfunction in ALS: insights from a mutant sod1 zebrafish model.

Authors:  Alexander McGown; Jonathan R McDearmid; Niki Panagiotaki; Huaxia Tong; Sufana Al Mashhadi; Natasha Redhead; Alison N Lyon; Christine E Beattie; Pamela J Shaw; Tennore M Ramesh
Journal:  Ann Neurol       Date:  2012-12-31       Impact factor: 10.422

10.  Early presymptomatic cholinergic dysfunction in a murine model of amyotrophic lateral sclerosis.

Authors:  Caty Casas; Mireia Herrando-Grabulosa; Raquel Manzano; Renzo Mancuso; Rosario Osta; Xavier Navarro
Journal:  Brain Behav       Date:  2013-02-17       Impact factor: 2.708

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