Urodynamic characteristics of voiding dysfunction in patients with a cerebrovascular accident

Abstract

Cerebral vascular disease is the sudden onset brain tissue damage and subsequent loss of brain function due to ischemia (white infarct) or hemorrhage (red infarct). Voiding dysfunction is a common sequela after a cerebrovascular accident (CVA). Urinary incontinence occurs in 43.5% of CVA patients within 3 months of the event.1 Incontinence is not life-threatening, and the degree of morbidity often declines over time. Twelve months after CVA, 37.7% of patients continue to have symptoms of urge incontinence.1 The severity and trend of incontinence are dependent on the severity of the stroke and the patient’s age.1 Lower urinary tract symptoms (LUTSs), especially storage symptoms such as frequency and urgency with or without urge incontinence, are commonly present in the 3 months following a CVA.2e4 Pathophysiological conditions other than CVA can cause LUTSs in old age, such as bladder outlet obstruction (BOO), and might lead to confusion in diagnosing and treating voiding dysfunction in older men with a history of CVA.5,6 Foley catheter insertion is the most common method of addressing this problem. Involuntary detrusor muscle contractions are the most common urodynamic finding in patients after a CVA; however, patients with chronic CVA may have both detrusor overactivity (DO) during the storage phase and loss of coordination of urethral sphincter relaxation during voiding that causes urinary incontinence or difficult urination.7,8 Detrusor underactivity (DU) and detrusor hyperreflexia with impaired contractility (DHIC) are other problematic issues that can occur in elderly patients with multiple CVAs or in the acute