Lower urinary tract dysfunction following stroke: From molecular mechanisms to clinical anatomy

Abstract

Bladder dysfunction is a common clinical problem in stroke patients and a strong prognostic factor of disability and exerts an enormous impact on health and economy. The aim of this narrative review was tο examine the pathophysiological mechanisms of lower urinary tract symptoms after stroke, as well as the relevant clinical anatomy. Normal micturition is achieved through complex coordination between brain regions, spinal cord, and peripheral nerves, and anatomic brain connectivity is crucial to lower urinary tract physiology. The most important neurotransmitters involved in bladder control include γ-aminobutyric acid, opioids, glutamate, dopamine, norepinephrine, acetylcholine, and nitric oxide. The precise correspondence between brain damage and relevant urinary symptoms is not well understood. Urodynamic changes after stroke include detrusor overactivity, dyssynergia, and uninhibited sphincter relaxation. Several brain regions could be implicated in post-stroke urinary dysfunction. Brainstem lesions can cause various urinary symptoms. A lesion superiorly to the pontine micturition center (PMC) results in an uninhibited bladder, whereas a lesion between the sacral spinal cord and PMC leads to either a spastic bladder or sphincter-detrusor dyssynergia. Supra-pontine lesions usually cause bladder storage dysfunction. Frontoparietal lesions have been associated with urinary incontinence and insular lesions with urinary retention. Understanding the mechanisms underlying the dysfunction of the lower urinary tract following stroke can aid in the development of new therapeutic strategies for these patients.