Photo Credit: Tharakorn

Neural mechanisms are tied to urinary incontinence after a stroke, with differences in brain activity during volitional versus involuntary bladder contractions.

New research using functional MRI (fMRI) showed the neural mechanisms that contribute to urinary incontinence, a common condition affecting stroke survivors that significantly impacts their quality of life. The findings were published in Stroke.

Urinary incontinence impacts up to 79% of patients shortly after a stroke and persists in up to 38% of survivors a year later. The condition usually results from involuntary bladder contractions and uncontrolled urine release, leading to distressing symptoms like urgency, frequent urination, and leakage. Despite its prevalence, the condition is often undertreated. Furthermore, it is linked to worse long-term outcomes, including elevated mortality rates and greater levels of disability.

Because the underlying neural mechanisms remain poorly understood, researchers examined the brain activity patterns associated with volitional (voiding on command) and involuntary bladder contractions in stroke survivors.

The observational study included 15 stroke survivors with documented urinary incontinence and healthy patients. The cohorts underwent simultaneous blood oxygen level–dependent fMRI of the brain and urodynamics, capturing 25 involuntary and 23 volitional bladder emptying events in patients with stroke and 35 volitional voiding events in the control group.

 Differences in Brain Activity During Bladder Contractions

The researchers observed different brain activity patterns that occur during volition compared with involuntary bladder contractions in patients with stroke.

During voluntary bladder emptying, healthy individuals and stroke survivors exhibited significant activation in brain regions associated with sensorimotor control and executive decision-making, such as the brainstem, cingulate, cortex, prefrontal cortex, and motor areas. However, involuntary bladder emptying in stroke survivors showed minimal cortical activation, indicating a failure to engage key brain networks necessary for urinary control, according to the study.

In both cohorts, bladder filling before voluntary urination activated a group of brain regions known as the salience network (insula, anterior cingulate gyrus). In contrast, during bladder filling that preceded involuntary urination, this network remained inactive for stroke survivors experiencing incontinence.

“Our results suggest that the underlying mechanism of post-stroke incontinence may be the lack of salience network activity,” the study authors wrote. “Activating the salience network through pharmacological, electromagnetic, or ultrasonic neuromodulation techniques may hold promise for treating incontinence in stroke survivors.”