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November 24, 2020; 95 (21) Article

A clinico-neurophysiological study of urogenital dysfunction in MOG-antibody transverse myelitis

View ORCID ProfileVivien Li, Prasad Malladi, Sara Simeoni, Mahreen Pakzad, Rosie Everett, Chanjira Satukijchai, Maria Isabel Leite, Jacqueline Palace, Jalesh N. Panicker
First published October 12, 2020, DOI: https://doi.org/10.1212/WNL.0000000000011030
Vivien Li
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Prasad Malladi
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Sara Simeoni
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Mahreen Pakzad
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Rosie Everett
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Chanjira Satukijchai
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Maria Isabel Leite
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Jacqueline Palace
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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Jalesh N. Panicker
From the National Hospital for Neurology and Neurosurgery (V.L., P.M., S.S., M.P., J.N.P.), UCL Institute of Neurology, Department of Uro-Neurology; Queen Square MS Centre (V.L.), UCL Institute of Neurology, Department of Neuroinflammation, Queen Square, London; and Nuffield Department of Clinical Neurosciences (R.E., C.S., M.I.L., J.P.), John Radcliffe Hospital, University of Oxford, UK.
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A clinico-neurophysiological study of urogenital dysfunction in MOG-antibody transverse myelitis
Vivien Li, Prasad Malladi, Sara Simeoni, Mahreen Pakzad, Rosie Everett, Chanjira Satukijchai, Maria Isabel Leite, Jacqueline Palace, Jalesh N. Panicker
Neurology Nov 2020, 95 (21) e2924-e2934; DOI: 10.1212/WNL.0000000000011030

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This article has a correction. Please see:

  • A Clinico-Neurophysiological Study of Urogenital Dysfunction in MOG-Antibody Transverse Myelitis - February 01, 2022
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Abstract

Objective To assess the clinical, urodynamic, and neurophysiologic features of patients with persisting bladder, bowel, and sexual dysfunction after transverse myelitis in myelin oligodendrocyte glycoprotein antibody (MOG-Ab) disease.

Methods Patients with a history of MOG-Ab disease–related transverse myelitis seen prospectively in a tertiary center uro-neurology service between 2017 and 2019 were included. They received cross-sectional clinical assessment; completed standardized questionnaires on bladder, bowel, and sexual symptoms; and underwent urodynamic and pelvic neurophysiologic investigations.

Results Twelve patients (9 male) were included with a total of 17 episodes of transverse myelitis. Mean age at first attack was 26 (SD 9) years, and median follow-up duration was 50 (interquartile range 32–87) months. Acute urinary retention requiring bladder catheterization occurred in 14 episodes and was the first symptom in 10 episodes. Patients with lesions affecting the conus medullaris required catheterization for significantly longer durations than those without a conus lesion (median difference 15.5 days, p = 0.007). At follow-up, all patients had recovered full ambulatory function, but persisting bladder and bowel dysfunction moderately or severely affected quality of life in 55% and 36%, respectively, and 82% had sexual dysfunction. Pelvic neurophysiology demonstrated abnormal residual conus function in 6 patients. Urodynamic findings predominantly showed detrusor overactivity and/or detrusor-sphincter dyssynergia, indicative of a supraconal pattern of lower urinary tract dysfunction.

Conclusions Persisting urogenital and bowel dysfunction is common despite motor recovery. Although a proportion of patients had neurophysiologic evidence of residual conus abnormalities at follow-up, predominant urodyamic findings suggest that ongoing lower urinary tract dysfunction results from supraconal injury.

Glossary

ADEM=
acute disseminated encephalomyelitis;
AQP4-Ab=
aquaporin-4 antibody;
EDSS=
Expanded Disability Status Scale;
FSS=
functional system score;
IQR=
interquartile range;
LUT=
lower urinary tract;
MOG-Ab=
myelin oligodendrocyte glycoprotein antibody;
MS=
multiple sclerosis;
NMOSD=
neuromyelitis optica spectrum disorder;
ON=
optic neuritis;
PVR=
postvoid residual;
SEP=
sensory evoked potential;
TM=
transverse myelitis

Footnotes

  • Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

  • ↵* These authors contributed equally to this work.

  • CME Course: NPub.org/cmelist

  • Received January 30, 2020.
  • Accepted in final form June 26, 2020.
  • © 2020 American Academy of Neurology
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