Modulation of the rectoanal inhibitory reflex (RAIR): qualitative and quantitative evaluation in multiple sclerosis.

Int J Colorectal Dis

Service de Neuro-Urologie et Explorations Périnéales, Unité de Recherche Er6 UPMC, Université Pierre et Marie Curie Paris VI, Hôpital Tenon, APHP, 4, Rue de Chine, 75970, Paris Cedex 20, France.

Published: April 2011

Background: Rectoanal inhibitory reflex (RAIR) is a physiological modulated reflex involved in anorectal continence and defined by a relaxation of internal anal sphincter following rectal distension. Its existence depends on intramural autonomic ganglions and its modulation on the integrity of the autonomic nervous system (ANS).

Aims: The aim of this study was to analyse RAIR modulation in terms of amplitude and duration in multiple sclerosis (MS) patients.

Methods: Twenty-one patients with MS and 40 control patients had anorectal manometry. Qualitative assessment (presence or absence) of RAIR was evaluated together with its modulation in amplitude and in duration.

Results: All patients had present RAIR for each volume of rectal distension (10-50 ml). Seven patients (33.3%) in the MS group had abnormal RAIR modulation in amplitude (odds ratio (OR) = 2.78, compared to control group, p = 0.11). Nine patients (42.9%) in the MS group had abnormal RAIR modulation in duration (p = 0.14, OR = 2.54, compared to control group). Alteration of RAIR modulation was not correlated with Expanded Disability Status Scale, faecal incontinence and constipation (p > 0.05). Course of MS (relapsing-remitting MS or secondary progressive form) seems to be correlated to alteration of modulation in amplitude and in duration (OR = 1.31 and 1.07).

Conclusion: Even if our results do not have the required statistical significance (p > 0.05), they are interesting. If RAIR is always present in MS, its modulation seems to be altered. A hypothesis for this lack of RAIR modulation could be the alteration of ANS, often involved in MS besides somatic nervous system lesions.

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http://dx.doi.org/10.1007/s00384-010-1109-0DOI Listing

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