Neurogenic detrusor overactivity (NDO) is a type of bladder dysfunction caused by a problem within the nervous system. NDO involves the detrusor muscle, the smooth muscle layer within the bladder wall. Normally, this muscle relaxes to allow the bladder to fill with urine. However, in NDO, impaired communication between the central nervous system and the bladder causes the detrusor to contract involuntarily and prematurely. This loss of coordinated bladder control is a manageable health issue.
Defining Neurogenic Detrusor Overactivity
The bladder’s two main functions—storage and emptying—rely on a coordinated system regulated by the central and peripheral nervous systems. The detrusor muscle normally remains relaxed while the bladder fills, allowing it to store up to 600 milliliters without a significant pressure rise. Urination is initiated when the nervous system signals the detrusor to contract and the sphincters to relax.
NDO occurs when neurological damage disrupts the regulatory signals traveling between the brain, spinal cord, and bladder. Inhibitory signals from the brain, which prevent untimely contraction, are lost or diminished. This loss of inhibition causes the detrusor muscle to contract unexpectedly and uninhibitedly, even when the bladder contains only a small volume of urine. These involuntary contractions characterize the filling phase.
Neurological Conditions That Cause NDO
NDO is caused by damage to the central nervous system, particularly lesions above the sacral level of the spinal cord. Damage in these upper regions interrupts the descending inhibitory pathways that keep the detrusor relaxed during storage. This interruption releases the lower urinary tract from conscious control, allowing primitive voiding reflexes to take over.
A variety of neurological diseases and injuries are associated with NDO. Spinal cord injury (SCI) is a frequent cause, especially with lesions in the thoracic or cervical spine, affecting up to 90% of patients. Multiple Sclerosis (MS) also commonly leads to NDO by causing lesions in the brain and spinal cord, affecting about half of those with the condition.
Other supraspinal lesions, located above the brainstem, also result in this dysfunction. These conditions include stroke, Parkinson’s disease, and brain tumors, all of which damage the higher brain centers responsible for conscious control over urination.
Symptoms and Associated Health Risks
The involuntary contractions of the detrusor muscle result in disruptive lower urinary tract symptoms. Patients experience urinary urgency, a sudden, compelling need to urinate that is difficult to defer, often accompanied by urinary frequency.
The most impactful symptom is urge incontinence, the involuntary loss of urine that accompanies the sudden, unmanageable urge. Because the bladder contracts prematurely, the volume of urine released during each voiding episode is typically low.
NDO presents long-term health risks primarily due to high intravesical pressure during the storage phase. Forceful contractions can create high pressures inside the bladder, sometimes exceeding 40 cm of water pressure. This sustained pressure can force urine backward into the ureters and toward the kidneys, a condition known as vesicoureteral reflux. This backward flow, combined with recurrent urinary tract infections, can ultimately lead to irreversible kidney damage and failure if NDO is not managed.
Management and Treatment Pathways
The primary goals of managing NDO are to restore low-pressure urine storage, prevent kidney damage, and improve continence. Treatment follows a hierarchical approach, beginning with conservative methods. Behavioral strategies involve fluid management and timed voiding schedules to prevent the bladder from reaching volumes that trigger involuntary contractions.
Pharmacological interventions are the first-line medical treatment, aiming to relax the detrusor muscle and increase the bladder’s storage capacity. Anticholinergic medications (antimuscarinics) are commonly prescribed, as they block the nerve signals that cause the detrusor to contract. Beta-3 agonists are an alternative class of drugs that help the detrusor relax during filling.
When oral medications are ineffective or cause intolerable side effects, advanced procedural treatments are considered. Intradetrusor injections of Botulinum Toxin type A (Botox) are a highly effective second-line therapy. The toxin is injected directly into the bladder muscle to temporarily paralyze the detrusor, suppressing involuntary contractions and significantly increasing bladder capacity. The effects typically last for several months, requiring repeat injections.
For select patients, sacral neuromodulation, a form of electrical stimulation, may be an option. In severe, refractory cases where high pressures cannot be controlled, major surgical procedures like augmentation cystoplasty may be performed. This involves surgically enlarging the bladder with a segment of the intestine to provide a low-pressure reservoir for urine storage.