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The importance of the pontine tegmentum as the micturition centre responsible for urinary voiding has been well established from animal studies.1 A cliniconeuroradiological study showed that the nuclei involved are the pontine reticular nucleus and the reticular formation, located adjacent to the locus ceruleus and the medial parabrachial nucleus.2 This micturition centre, which is thought to coordinate detrusor sphincter activity during micturition, probably conveys its efferent fibres through the bulbospinal pathway to the spinal parasympathetic nucleus.
We describe a patient with suspicion of mild viral rhombencephalitis presenting with acute urinary retention because of a lesion affecting the dorsal tegmentum of the medulla and the pontomedullary junction bilaterally. Reports on urinary retention caused by bulbar lesions other than stroke and tumours are rare but emphasise the importance of this often neglected association.
A 34 year old Nepali construction worker, with no past medical history, presented with suprapubic pain because of acute urinary retention and was admitted for observation. In the weeks before admission he had complained of mild headache and dizziness. The headache responded well to paracetamol. There was no history of orogenital ulcers, and he had received no recent vaccinations.
On admission, he was conscious and alert, with normal cognitive examination. There was no neck stiffness. Fundoscopy, pupil reflexes, accommodation, and vertical and horizontal eye movements were normal. Bulbar function was intact. There was generalised hyperreflexia, including the jaw jerk, with equivocal plantar responses. There was no indication of spinal cord or cauda equina syndrome on sensory examination. Coordination and gait were normal. He had urinary retention (550 ml), which was managed with an indwelling catheter. General examination revealed an afebrile patient with normal vital signs. Skin testing for tuberculosis was negative. Peripheral blood analysis showed normal findings: the erythrocyte sedimentation rate was 4 mm/h and the white blood cell count was 8500/μl (60% neutrophils and 27% lymphocytes). Magnetic resonance imaging (MRI) of the spinal cord including the cauda equina was normal. However, MRI of the brain stem revealed a symmetrical bilateral abnormal high signal on T2 weighted images in the medulla and pontomedullary junction (fig 1). Cerebrospinal fluid (CSF) analysis revealed features of aseptic meningitis (105 cells/mm3 with 96% lymphocytes and 4% neutrophils, and normal protein, glucose, and IgG). Serum autoantibody, viral serology tests, and CSF smear and cultures did not contribute to the diagnosis. Neurophysiological investigations (visual evoked and somatosensory evoked potentials) were normal. A urogram showed an atonic bladder. Organic obstructive urological disease was excluded radiologically, and no urological cause for the urinary retention could be identified. On the basis of the neurological findings, there was involvement of the pyramidal tracts and the micturition centre or its efferent pathways. The differential diagnoses included mild viral rhombencephalitis, acute demyelinating disorder (multiple sclerosis or acute disseminated encephalomyelitis), or an underlying autoimmune disorder (for example, neuro-Behçet disease). Three weeks after admission, the neurological symptoms gradually disappeared. Repeat CSF analysis and spinal MRI were normal. MRI of the brain stem revealed regression of the hyperintense lesions on the T2 weighted images.
Although this patient was likely to have suffered from a mild, probably viral rhombencephalitis, the true diagnosis remains unclear. We speculate that parainfectious demyelination or direct viral invasion was likely to have been the cause of the patient’s neurological presentation. Intriguingly, a similar case was reported by Komiyama et al, in which a 30 year old man had urinary retention, mild horizontal gaze paresis, and hypaesthesia around the mouth and fingers.3 In their case, the MRI findings revealed several amorphous lesions in the pons and cerebellum, in addition to a well defined lesion in the right dorsolateral tegmentum of the upper pons. CSF analysis showed a mild increase in protein but only 3 cells/mm3. In contrast to their patient, the lesions in our case were bilateral and extended from the medulla to the pontomedullary junction, but showed a similar rate of disappearance (four weeks).
Brain stem control of micturition has been reviewed by Sakakibara and Fowler.4 Urinary retention is extensively described in patients with brain stem tumours or strokes. In the series of patients with brain stem tumours, the majority of the lesions were located in the pons and medulla, while in patients with brain stem strokes the lesions were exclusively located in the pontine tegmentum. Therefore it is likely that the efferent pathways originating from the pontine micturition centre were affected at the level of the medulla in our patient. This case shows that transient urinary retention with minimal neurological symptoms can be associated with medullary lesions, and is probably caused by direct viral infection or by parainfectious demyelination.
Competing interests: none declared
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