Lower urinary tract dysfunction in the central nervous system neurogenic bladder and the real-life treatment outcome of botulinum toxin A

Abstract

Neurogenic lower urinary tract dysfunction (NLUTD) is common in patients with central nervous system (CNS) lesions. Cases of cerebrovascular accidents (CVA), Parkinson's disease, dementia, and other intracranial lesions develop poor bladder control with or without urinary difficulty due to loss of cortical perception of bladder filling sensation and poor coordination of urethral sphincter relaxation during reflex micturition. Patients with CNS lesions usually have overactive bladder (OAB) symptoms, including urgency, frequency, incontinence, voiding symptoms of dysuria, large postvoid residual volume, and retention. In elderly patients with severe CNS disease the OAB symptoms are usually difficult to adequately relieve by medical treatment, and thus, their quality of life is greatly. Botulinum toxin A (BoNT-A) is currently licensed and has been applied in patients with idiopathic and neurogenic OAB due to spinal cord injury or multiple sclerosis. However, the application of BoNT-A in the treatment of urinary incontinence due to NLUTD in chronic CNS lesions has not been well-documented. Although cohort studies and case series support BoNT-A treatment for neurogenic OAB, chronic urine retention after intravesical BoNT-A injection for OAB and exacerbated urinary incontinence after urethral BoNT-A injection for voiding dysfunction have greatly limited its application among patients with NLUTD due to CNS lesions. This article reviews the pathophysiology and clinical characteristics of NLUTD in patients with CNS lesions and the clinical effects and adverse events of BoNT-A injection for patients with NLUTD. A flowchart was created to outline the patient selection and treatment strategy for neurogenic OAB.

Keywords: Botulinum toxin A; Dysfunctional voiding; Lower urinary tract dysfunction; Neurogenic bladder; Overactive bladder.

Figure 1

Video urodynamic study of patients with central nervous system lesion. (a) Urgency urinary incontinence in a patient with cerebrovascular accident (CVA). Involuntary detrusor contraction occurs at bladder capacity with coordinated urethral sphincter relaxation (arrow 1). A tight bladder neck and low detrusor contractility cause incomplete bladder emptying (arrow 2). (b) Pseudodyssynergia in a patient with CVA, urinary incontinence and difficult urination. Uninhibited detrusor contraction occurs with increased urethral sphincter activity during urination (arrow). (c) Uninhibited detrusor contraction occurs at the bladder capacity (arrow 1) in a CVA patient. The urethral sphincter does not relax adequately (arrow 2), resulting in incomplete bladder emptying. (d) A patient with Parkinson’s disease. Uninhibited detrusor contraction occurs at the bladder capacity (arrow 1), and the urethral sphincter contracts concomitantly, resulting in pseudodyssyneria (arrow 2) and incomplete voiding. (e) A patient with Parkinson’s disease. Uninhibited detrusor contraction occurs when the bladder capacity is reached (arrow 1), and pelvic floor guarding is noted (arrow 2). (f) Urinary incontinence in a patient with dementia. The patient does not sense bladder filling or urgency until urination starts when the bladder capacity is reached (arrow 1). No bladder outlet obstruction was noted (arrow 2)

Figure 2

A treatment algorithm for patients with central nervous system lesions and neurogenic overactive bladder. CVA: Cerebrovascular accident, PD: Parkinson’s disease, DHIC: Detrusor hyperreflexia and inadequate contractility, BOO: Bladder outlet obstruction, OAB: Overactive bladder, PVR: Postvoid residual, UTI: Urinary tract infection