The lower urinary tract serves two main functions: to store and empty urine. In the case of neurological disease, the disruption of these two main roles can be attributed to discommunication between neural micturition centers. Stroke is a devastating neurologic event that can have both short and long term urologic complications.Stroke survivors commonly develop symptoms of overactive bladder (OAB), reporting increased urinary urgency, frequency and urge incontinence. Patients with idiopathic OAB are known to exhibit distinct patterns of brain activity during urinary storage and voiding. Here we examined whether stroke survivors with severe OAB symptoms exhibited distinct patterns of micturition-related brain activity compared to those with mild symptoms.

Simulations have indicated that to identify typical activations at the individual voxel level, a minimum of 12 subjects would be needed to achieve 80% power.
This study has a prospective design. Our Institutional Review Board approved the study protocol, and all participants provided informed consent.
Twenty-five patients with a history of post-stroke OAB were recruited. OAB severity was
assessed using the ICIQ-OAB. Symptoms were categorized as severe if the ICIQ-OAB score was 11 or greater, those who failed to meet all inclusion criteria were removed from the study. Patients were placed within an MRI and micturition-related brain activity was assessed by simultaneous urodynamics and blood-oxygen-level-dependent (BOLD) fMRI. BOLD signal during the period of maximum urgency (10 seconds preceding a detrusor contraction) was compared between patients with severe and mild OAB using statistical parametric mapping (p < 0.01, cluster size ≥ 25 voxels). The models were adjusted for age, sex, and time since stroke.

Thirteen patients were categorized as having mild and 12 patients as having severe OAB
symptoms. Compared to those with mild symptoms, patients with severe symptoms exhibited increased BOLD signal in 22 clusters, including bilateral basal ganglia, bilateral supplementary motor area, bilateral anterior cingulate gyrus, bilateral precentral and postcentral gyri, bilateral frontal gyri (including dorsolateral prefrontal cortex), right amygdala, right precuneus, and left insula; and decreased BOLD signal in only 1 cluster corresponding to the left precuneus.

Compared to those with mild OAB symptoms, stroke survivors with severe OAB symptoms exhibit increased BOLD signal in multiple brain regions associated with LUT control. Interestingly, these findings intuitively contradict others, which suggest that cortical activity is necessary for proper functioning of the LUT. However, we hypothesize that those patients, who report worse symptoms, may actually have greater awareness of urgency and the LUT explaining their relatively higher brain activity. In the future, BOLD signal will be compared against objective measures of LUT dysfunction such as bladder diary data and urodynamic parameters.

We have conducted the first of its kind study with promising results, we believe this is the first time these differences have been brought to light. Comparing brain activity as a critical component in understanding the fundamental mechanism of bladder function has become crucial. As neuroimaging bladder related research has improved in the last years, BOLD studies of the brain have become a pragmatic reality.

Continence 7S1 (2023) 100762
DOI: 10.1016/j.cont.2023.100762