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Updated: Nov 5, 2025

Detrusor Underactivity Model in Rats by Conus Medullaris Transection
Published on: August 28, 2020
[A case of lower urinary tract dysfunction due to acute hemorrhage in the lateral medulla oblongata]
Futoshi Eto1, Masahito Takagi1, Kanta Tanaka2
1Department of Cerebrovascular Medicine, National Cerebral and Cardiovascular Center.
A 67-year-old woman was transported to our hospital with abnormal sensation in the left temporal region and unstable gait. She had a history of increased urinary frequency without medication. Head CT showed intracerebral hemorrhage in the left dorsal medulla oblongata. On the day of admission, she became aware of difficulty in urination and the volume of residual urine was 100 ml. Cystometry revealed normal voiding sensation and relatively lower intravesical pressure during voiding effort. The maximum cystometric capacity was also mildly decreased. The lower urinary tract dysfunction in this patient was diagnosed as detrusor underactivity. An α1-adrenoreceptor antagonist, urapidil, was started and her residual urine was decreased. Urapidil was terminated on the 14th day of onset, but her lower urinary tract symptoms did not recur thereafter. The brain MR imaging with magnetization-prepared 2 rapid acquisition gradient-echoes (MP2RAGE) clearly demonstrated a small hematoma in the dorsolateral medulla with surrounding edema. The perihematomal edema initially spread to involve the left lateral tegmentum of the medulla, but it almost disappeared in the follow-up MP2RAGE imaging on the 21st day. At the medulla level, the descending tract from the pontine micturition center is assumed to lie lateral tegmentum. The lower urinary tract dysfunction in this case was presumed to be caused by damage to the descending tract from the pontine micturition center, and the disappearance of perihematomal edema and the compensation by the contralateral tract would have contributed to the early improvement of symptoms.
A 67-year-old woman was transported to our hospital with abnormal sensation in the left temporal region and unstable gait. She had a history of increased urinary frequency without medication. Head CT showed intracerebral hemorrhage in the left dorsal medulla oblongata. On the day of admission, she became aware of difficulty in urination and the volume of residual urine was 100 ml. Cystometry revealed normal voiding sensation and relatively lower intravesical pressure during voiding effort. The maximum cystometric capacity was also mildly decreased. The lower urinary tract dysfunction in this patient was diagnosed as detrusor underactivity. An α1-adrenoreceptor antagonist, urapidil, was started and her residual urine was decreased. Urapidil was terminated on the 14th day of onset, but her lower urinary tract symptoms did not recur thereafter. The brain MR imaging with magnetization-prepared 2 rapid acquisition gradient-echoes (MP2RAGE) clearly demonstrated a small hematoma in the dorsolateral medulla with surrounding edema. The perihematomal edema initially spread to involve the left lateral tegmentum of the medulla, but it almost disappeared in the follow-up MP2RAGE imaging on the 21st day. At the medulla level, the descending tract from the pontine micturition center is assumed to lie lateral tegmentum. The lower urinary tract dysfunction in this case was presumed to be caused by damage to the descending tract from the pontine micturition center, and the disappearance of perihematomal edema and the compensation by the contralateral tract would have contributed to the early improvement of symptoms.
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