Neurogenic Bladder Due to Hypoxic-Ischemic Demyelination

  1. Sindhu Ramchandren MD,
  2. David S. Liebeskind MD

Article first published online: 22 OCT 2007

DOI: 10.1111/j.1552-6569.2007.00167.x

Issue

Journal of Neuroimaging

Journal of Neuroimaging

Volume 18, Issue 2, pages 198–201, April 2008

Additional Information

How to Cite

Ramchandren, S. and Liebeskind, D. S. (2008), Neurogenic Bladder Due to Hypoxic-Ischemic Demyelination. Journal of Neuroimaging, 18: 198–201. doi: 10.1111/j.1552-6569.2007.00167.x

Author Information

  1. University of Michigan Health System, Neurology, Ann Arbor, MI (SR); and UCLA Stroke Center—University of California, Los Angeles, CA (DSL).

*Correspondence: Address correspondence to Sindhu Ramchandren, MD, Department of Neurology, University of Michigan at Ann Arbor, 300 North Ingalls St, #3D06, Ann Arbor, MI 48109. E-mail: sindhur@med.umich.edu.

  1. Conflict of Interest: The authors have reported no conflicts of interest.

Publication History

  1. Issue published online: 22 OCT 2007
  2. Article first published online: 22 OCT 2007
  3. Acceptance: Received October 6, 2006, and in revised form May 24, 2007. Accepted for publication June 18, 2007.

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Keywords:

  • Hypoxia;
  • ischemia;
  • demyelination;
  • neurogenic bladder;
  • Wallerian degeneration

ABSTRACT

BACKGROUND AND PURPOSE

Hypoxia is commonly known to target neuronal cell bodies. Although myelin is a non-infrequent target, posthypoxic demyelination is a rarely described entity. We describe the case of a man who developed neurogenic bladder following a motor vehicle accident.

CASE REPORT

Following a severe motor-vehicle accident involving massive blood loss, a 46-year-old man developed urinary urgency requiring catheterization, with hyperactive reflexes and bilateral Babinski signs on exam.

RESULTS

Magnetic resonance imaging of the brain and cervical cord revealed diffuse, isolated white matter signal abnormality in a symmetric, confluent distribution, extending inferiorly into the spinal cord, with changes consistent with bilateral Wallerian degeneration. Serologic and CSF evaluations were normal.

CONCLUSIONS

Unlike previous reports of hypoxic-ischemic demyelination, our patient lacked any cortical abnormalities, presumably due to isolated white matter changes. This report alerts physicians to the possibility of hypoxic-ischemic demyelination due to global hypoxia-ischemia as an etiologic factor for neurogenic bladder.

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