Introduction: Stroke often leads to the development of storage lower urinary tract symptoms (LUTS) by damaging brain centers involved in micturition control or interrupting communication between them. Yet, little is known about how brain activity changes after a stroke to result in the development of these symptoms. To address this question, we compared micturition-related brain activity in patients with mild and severe stroke-related LUTS.
Methods: Fifteen patients who developed LUTS after a stroke were recruited and completed the International Consultation on Incontinence Overactive Bladder (ICIQ-OAB) questionnaire. Symptoms were categorized as mild if symptom score on the ICIQ-OAB was less than 11, and severe if the score was 11 or greater. Functional magnetic resonance imaging (fMRI) was used to assess brain activity in each subject. In a task-based block design, blood-oxygen-level-dependent (BOLD) signal was detected during rest, active bladder filling, and bladder voiding. In total, four cycles of the micturition sequence were acquired while urodynamics were simultaneously performed. Following standard fMRI preprocessing, statistical analysis using first level generalized linear modeling estimated BOLD signal intensity for each condition and 2nd level group differences between patients with mild and severe LUTS were calculated by 2-sample, 2-sided t-test, including covariates for age, gender and time since stroke. We report results for differences immediately before detrusor contraction (DC) and during initiation of DC.
Results: Compared with patients with mild post-stroke LUTS, patients with severe symptoms exhibited higher BOLD signal in the insula, dorsolateral prefrontal cortex (DLPFc), and frontal cortex (FC) immediately prior to DC, and in the supplementary motor area, posterior cingulate cortex and postcentral sulcus during initiation of DC.
Conclusions: In our cohort, patients with severe post-stroke LUTS demonstrated increased cortical activation immediately prior to and during voiding initiation compared to patients with mild symptoms. Areas found to exhibit increased activation are known to be involved in LUT interoception (insula), and volitional (DLPFc and FC) and involuntary (cingulate cortex) inhibition of LUT activity. These results suggest that more severe subjective LUTS after stroke may be due to increased awareness of urgency and detrusor overactivity events.
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