What causes post-stroke incontinence?

Causes of Post-Stroke Incontinence

Post-stroke incontinence results from three primary mechanisms: disruption of cortical bladder control pathways causing detrusor overactivity (most common), cognitive/functional impairments preventing appropriate toileting despite normal bladder function, and concurrent conditions or medications causing bladder hyporeflexia with overflow incontinence. 1

Primary Pathophysiological Mechanisms

Neurogenic Detrusor Overactivity (Most Common)

• Stroke disrupts cortical inhibitory control over the pontine micturition center while preserving afferent sensory pathways from the bladder, resulting in preserved sensation but loss of voluntary control 2
• Detrusor overactivity (hyperreflexia) is the most common urodynamic finding, occurring in approximately 37% of incontinent stroke patients, manifesting as urgency, frequency, and urge incontinence 2, 1
• Suprapontine lesions typically cause bladder storage dysfunction by removing cortical inhibition of the micturition reflex 3
• The disruption of neuromicturition pathways represents a physiological disinhibition of the micturition reflex 4

Cognitive and Functional Impairments

• Approximately 37% of incontinent stroke patients have completely normal urodynamic studies but cannot maintain continence due to stroke-related cognitive deficits, aphasia, or severe functional impairment 1
• Impaired cognitive awareness of the need to void or having voided creates functional incontinence and correlates with increased mortality and need for nursing home care at 3 months post-stroke 5, 2
• Behavioral control deficits are closely related to severity of urinary incontinence, independent of bladder dysfunction 4
• Communication difficulties from aphasia prevent patients from requesting toileting assistance despite intact bladder sensation 5
• Mobility impairments create difficulty reaching the bathroom in time despite awareness of need to void 5

Concurrent Bladder Hyporeflexia (Overflow Incontinence)

• Bladder hyporeflexia accounts for approximately 21% of post-stroke incontinence cases 1
• All patients with hyporeflexic bladders in one study had underlying diabetes mellitus or were taking anticholinergic medications, indicating this mechanism is typically due to concurrent conditions rather than stroke itself 1
• Overflow incontinence from urinary retention can mimic primary incontinence and must be distinguished through post-void residual assessment 6

Risk Factors for Post-Stroke Incontinence

Stroke-Related Factors

• Large infarct size is significantly associated with incontinence (p < 0.05) 1
• Frontoparietal lesions are specifically associated with urinary incontinence, while insular lesions are associated with urinary retention 3
• Brainstem lesions can cause various urinary symptoms depending on location relative to the pontine micturition center 3

Patient Characteristics

• Age is a significant risk factor for both bladder and bowel incontinence 5, 2
• Cognitive impairment is significantly associated with incontinence (p < 0.05) 1
• Motor impairments and functional disability are significant risk factors (p < 0.05) 5, 1
• Aphasia is significantly associated with incontinence (p < 0.05) 1

Fecal Incontinence Mechanisms

• Age and functional impairment are the primary risk factors for fecal incontinence on admission for stroke 5
• Cognitive deficits, immobility, and inability to perceive bowel signals are major contributors to fecal incontinence 7
• Constipation with fecal impaction is actually more common than true fecal incontinence post-stroke, and overflow incontinence from impaction mimics primary incontinence 7
• Fecal impaction independently worsens both bowel and urinary incontinence 7

Clinical Implications and Natural History

• Approximately 40-60% of stroke patients have urinary incontinence during acute admission, falling to 25% by hospital discharge and 15% at one year 5
• Fecal incontinence prevalence is approximately 40% acutely but diminishes to 20% by discharge from rehabilitation 5
• Most patients recover continence after stroke, indicating that neural recovery occurs over time 5
• 29% of acute stroke patients develop urinary retention initially, decreasing to 15-20% by hospital discharge as neural recovery occurs 2

Critical Pitfalls to Avoid

• Failing to distinguish between detrusor overactivity, functional incontinence with normal bladder function, and overflow incontinence from retention, as each requires different management approaches 1
• Overlooking impaired cognitive awareness of voiding needs as a contributing mechanism, which correlates with poor outcomes 5, 2
• Not assessing for urinary retention through bladder scanning or post-void residual measurement, as overflow incontinence mimics urge incontinence 5
• Neglecting to evaluate for constipation and fecal impaction, which can worsen both bowel and urinary incontinence 7
• Attributing all incontinence to stroke when concurrent conditions (diabetes, medications) may be responsible for bladder hyporeflexia 1