Investigation of urinary storage symptoms in Parkinson's disease utilizing structural MRI techniques

Background Lower urinary tract symptoms occur in 27% to 86% of patients with Parkinson's disease (PD), however, the mechanisms responsible for bladder dysfunction are not fully understood. This study utilized magnetic resonance imaging (MRI) to test the hypothesis that key brainstem bladder con...

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Published inNeurourology and urodynamics Vol. 38; no. 4; pp. 1168 - 1175
Main Authors Roy, Holly A., Griffiths, Derek J., Aziz, Tipu Z., Green, Alexander L., Menke, Ricarda A. L.
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.04.2019
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Summary:Background Lower urinary tract symptoms occur in 27% to 86% of patients with Parkinson's disease (PD), however, the mechanisms responsible for bladder dysfunction are not fully understood. This study utilized magnetic resonance imaging (MRI) to test the hypothesis that key brainstem bladder control areas (including the pontine micturition center and the pontine continence center (PCC) and their links with the basal ganglia are important in the development of urinary storage symptoms in PD. Methods Seventeen patients with PD completed a “bladder symptom questionnaire” and underwent diffusion‐weighted MRI (1.5 T). Storage symptom severity and MRI measures of white matter microstructural integrity were correlated using tract‐based spatial statistics. Results Mean diffusivity in the ventral brainstem correlated significantly with the bladder symptom severity in areas close to the predicted anatomical co‐ordinates of the PCC. Tracts seeded from these regions passed via areas involved in pelvic floor musculature control and urinary voiding including the cerebellum, pallidum, and precentral gyrus. Conclusion We used diffusion‐weighted MRI to investigate the role of the brainstem and its structural connections in the development of urinary storage symptoms in PD. Our data suggest that the brainstem degenerative change in the vicinity of the PCC may be implicated in the pathogenesis of storage symptoms in these patients.
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ISSN:0733-2467
1520-6777
DOI:10.1002/nau.23976