Most patients with multiple sclerosis report bowel symptoms, but the underlying pathophysiology is unclear.
We hypothesize that rectal dysfunction in multiple sclerosis is secondary to involvement of the spinal cord by the disease and that this can be measured by assessing rectal compliance.
This was a case-control study.
The study took place in a neurogastroenterology clinic and tertiary referral center.
Forty-five patients with multiple sclerosis, 19 with a spinal cord injury above T5, and 25 normal control subjects were included in this study. Patients with multiple sclerosis were subdivided into 2 groups according to the Expanded Disability Status Scale, below 5 (multiple sclerosis minor disability, n = 25) or above 5 (multiple sclerosis major disability, n = 20), as a reflection of spinal cord involvement.
Rectal compliance, Wexner constipation, and Wexner incontinence scores were measured.
Data are presented as mean and SD. Expanded Disability Status Scale correlated with rectal compliance but not with Wexner constipation or Wexner incontinence scores. Post hoc analysis showed no significant difference in Wexner constipation and Wexner incontinence between the 2 multiple sclerosis groups.
Limitations to this study include the lack of an asymptomatic group with multiple sclerosis and the small sample size to evaluate bowel symptoms.
Rectal compliance correlates with disability, and observed alterations in the rectal properties are secondary to spinal cord involvement. Our findings suggest that, in patients with neurologic impairment, rectal compliance is a surrogate of reflex activity of the spinal cord regulating rectal function and both a potential predictor of outcome and target for treatment. Multiple sclerosis patient subgroups had similar symptom burden, arguing that bowel dysfunction is multifactorial.
1Gastrointestinal Physiology Unit, University College London Hospitals, London, United Kingdom
2Division of Surgery and Interventional Science, University College London, London, United Kingdom
3Department of Uro-Neurology, National Hospital for Neurology and Neurosurgery, London, United Kingdom
4Division of General Surgery, University College London, London, United Kingdom
5University College London Institute of Neurology, London, United Kingdom
Funding/Support: Dr Preziosi was supported with a research grant from the MS Society of Great Britain and Northern Ireland (grant 902–08). This includes costs for salary, equipment, and consumables.
Financial Disclosure: None reported.
Presented at the meeting of the British Society of Gastroenterology, Birmingham, United Kingdom, March 16, 2011.
Poster presentation at the meeting of the European Federation of Gastroenterology, Barcelona, Spain, October 23 to 27, 2010.
Poster presentation at the meeting of the European Committee for Research and Treatment in Multiple Sclerosis, Gothenburg, Sweden, October 13 to 16, 2010.
Correspondence: Anton Emmanuel, B.Sc., M.D., F.R.C.P., Gastrointestinal Physiology Unit, Lower Ground Floor, EGA Wing, University College Hospital, 235 Euston Rd, London, NW1 2BU United Kingdom. E-mail: email@example.com