A spinal cord injury (SCI) damages the communication pathways between the brain and body. This often impacts bladder control, leading to urinary incontinence. The injury level significantly determines the type and severity of bladder dysfunction.
The Spinal Cord’s Role in Bladder Control
Bladder control relies on complex communication within the nervous system. The brain, spinal cord, and peripheral nerves manage urine storage and elimination. During filling, stretch receptors in the bladder wall send signals up the spinal cord to the brain, indicating fullness. The brain, including higher cortical structures and the pontine micturition center (PMC) in the brainstem, processes these signals, inhibiting bladder contraction and promoting sphincter closure to prevent leakage.
When a person decides to urinate, the brain sends signals down the spinal cord to initiate voiding. The PMC coordinates bladder contraction (detrusor muscle) and the relaxation of the urethral sphincters. Parasympathetic nerves (S2-S4) stimulate the detrusor muscle to contract. Sympathetic nerves (T11-L2) help relax the bladder and contract the internal sphincter during storage.
Somatic nerves, like the pudendal nerve (S2-S4), control the voluntary external urethral sphincter. This intricate neural coordination allows for both involuntary reflex control and voluntary regulation of urination.
General Impact of Spinal Cord Injury on Bladder Function
A spinal cord injury disrupts the neural control over the bladder, leading to various forms of bladder dysfunction, collectively known as neurogenic bladder. The specific pattern of dysfunction depends on where the injury occurs along the spinal cord. SCI interrupts signals between the brain and bladder, preventing proper communication. This can result in either an overactive bladder that contracts involuntarily or an underactive bladder that struggles to empty.
Two broad categories of bladder dysfunction are commonly observed after SCI: spastic (reflex) and flaccid (areflexic) bladder. Spastic bladder occurs with injuries above the sacral micturition center, causing uncontrolled contractions due to disrupted inhibitory signals. Flaccid bladder results from injuries at or below the sacral micturition center, damaging nerves responsible for bladder contraction, causing the bladder to overfill without emptying. These patterns help predict the types of urinary incontinence.
Urinary Incontinence and Specific Spinal Cord Injury Levels
The level of spinal cord injury influences the characteristics of urinary incontinence. Injuries above the sacral micturition center (T12 and above) often cause spastic bladder. The bladder fills and reflexively contracts without voluntary control due to lost connection to brain inhibitory centers. This can lead to frequent, involuntary urine leakage, known as urge or reflex incontinence.
A common issue with spastic bladder is detrusor-sphincter dyssynergia (DSD), where the bladder muscle contracts while the external urethral sphincter fails to relax. This uncoordinated action creates high bladder pressure, potentially causing urine to back up towards the kidneys and increasing kidney damage risk. High thoracic and cervical injuries (e.g., T6 and above) are associated with DSD and can trigger autonomic dysreflexia, a sudden and dangerous rise in blood pressure.
Lower thoracic and lumbar injuries, particularly around the T12-L1 level, can present a mixed or transitional picture. While injuries above T12 lead to spasticity, lesions in this area might initially cause a flaccid bladder due to spinal shock before developing spastic characteristics. The impact depends on whether the injury affects sympathetic pathways (T11-L2) or the sacral reflex arc, resulting in a combination of storage and emptying issues.
Sacral, conus medullaris, or cauda equina injuries (S2-S4 and below) damage the sacral micturition center or peripheral bladder nerves. This causes a flaccid bladder, where the muscle loses its ability to contract. The bladder overfills without emptying, leading to overflow incontinence when bladder pressure exceeds urethral resistance. Damage to the external urethral sphincter can also cause stress incontinence (urine leakage during activities that increase abdominal pressure, such as coughing or sneezing).
Identifying Neurogenic Bladder Dysfunction
Recognizing neurogenic bladder dysfunction after a spinal cord injury involves a comprehensive medical evaluation. Initial assessment includes a detailed review of the patient’s symptoms, such as frequency, urgency, retention, or leakage, and a physical examination. Understanding the patient’s voiding patterns and any changes is important.
Diagnostic approaches include measuring post-void residual (PVR) volume, indicating urine remaining in the bladder after emptying. Imaging techniques like ultrasound assess the bladder and kidneys for structural changes or urine backup. Urodynamic studies are considered the gold standard for objectively evaluating bladder function. These tests measure bladder capacity, pressure during filling and emptying, and coordination between the bladder muscle and sphincters. These tools help understand incontinence mechanisms and guide management.