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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
Michael P. Feloney ; Stephen W. Leslie .
Last Update: November 12, 2023 .
Bladder sphincter dyssynergia, also known as detrusor sphincter dyssynergia (DSD) or neurogenic detrusor overactivity (NDO), is a condition that causes lower urinary tract symptoms in patients with spinal cord injuries and neurological disorders. Diagnosing accurately and promptly is challenging due to overlapping symptoms with other clinical conditions. However, prompt identification and early intervention in the disease trajectory substantially enhance patient outcomes. Evidence-based interventions, encompassing pharmacological and non-pharmacological strategies, alleviate symptoms and improve the quality of life for patients. This activity reviews the evaluation and treatment of DSD, highlighting the interprofessional team approach in caring for patients with this condition.
Apply advanced urodynamic testing techniques, such as cystometry and pressure-flow studies, to aid in diagnosing and monitoring bladder sphincter dyssynergia.
Select and administer appropriate pharmacological treatments, such as alpha-blockers or antimuscarinics, based on individual patient needs and responses to manage bladder sphincter dyssynergia.
Implement evidence-based interventions, including pharmacological and non-pharmacological approaches, for managing bladder sphincter dyssynergia and improving patients' quality of life.
Collaborate with an interprofessional healthcare team, including physicians, nurses, pharmacists, and advanced care practitioners, to improve care coordination and deliver comprehensive care for patients with bladder sphincter dyssynergia.
Urinary function and continence depend on a physiologically compliant detrusor muscle and a competent urethral sphincter. Normal micturition consists of 2 phases—a storage phase and a voiding phase. The storage phase involves the passive filling of the bladder, whereas the voiding phase necessitates precise coordination between detrusor contraction and the relaxation of external and internal sphincters.
The central nervous system controls this complex micturition process. This process coordinates the activity of the autonomic and somatic nervous systems to ensure normal urinary continence and micturition. Detrusor sphincter dyssynergia (DSD) is the urodynamic term for variable lower urinary tract symptoms. This condition occurs due to detrusor muscle contraction with concomitant and inappropriate involuntary urethral sphincter contraction.[1]
DSD is believed to result from neurological lesions in the suprasacral region of the spinal cord. These lesions can be attributed to various causes, including traumatic spinal cord injury (SCI), myelodysplasia, multiple sclerosis, stroke, infections of the spinal cord, transverse myelitis, and congenital anomalies such as neural tube defects, spina bifida, and spinal dysraphism. DSD is most commonly associated with SCIs, spina bifida, and multiple sclerosis.
DSD is classified into 3 types. Type 1 DSD is characterized by the condition in which there is an initial simultaneous detrusor contraction and sphincter tightening. When the detrusor contraction reaches its peak, the sphincter relaxes abruptly, which results in urination. In type 2 DSD, the external urethral sphincter contracts sporadically during the entire detrusor contraction. Type 3 DSD is characterized by a crescendo-decrescendo pattern of sphincter contraction that obstructs the urethra throughout the entire detrusor contraction.[2][3]
Weld et al further classified DSD as either continuous or intermittent.[4] The type and extent of SCI lesions appear to correlate with the specific subtype of the corresponding DSD. Patients with lesions at the cervical level are more likely to develop DSD than those with lesions at lower levels of the spinal cord.[5] Type 1 DSD is commonly associated with patients who have incomplete neurological lesions. Complete neurological lesions can lead to the development of DSD types 2 and 3.
Although the exact incidence of DSD is unknown, it can occur in almost any significant neurological disease. SCI accounts for a substantial portion of all DSD cases. SCIs usually affect younger age groups and show a notable male predominance.[6] DSD is common in 75% of patients who have experienced suprasacral SCIs. During urodynamic testing, about 35% of patients with multiple sclerosis may exhibit DSD, whereas up to 50% of infants with spina bifida may also experience this disorder.[7][8]
During the storage phase, the tone of sphincter complexes keeps urine contained within the bladder. The internal urinary sphincter, an extension of the trigone region of the detrusor muscle, surrounds the neck of the bladder to retain the urine inside the bladder.[9] As the bladder fills with urine, sympathetic activation causes the contraction of the internal sphincter and closes the bladder neck. On the other hand, the external sphincter muscle is under voluntary control and located more distally than the internal sphincter. The external urinary sphincter functions under the control of pudendal nerve fibers and is situated in the Onuf’s nucleus between the S2 and S4 segments of the spinal cord.
To maintain continence during urine storage, the pressure in the proximal urethra must exceed the pressure within the bladder. As the bladder fills, urethral pressure gradually increases due to the stimulation of internal and external sphincters through the hypogastric and pudendal nerves. This phenomenon is referred to as the guarding reflex.
When there is an urge to void, inhibition from the midbrain and prefrontal cortex reduces. Subsequently, the pontine micturition center suppresses the guarding reflex through the spinobulbospinal tracts. Inhibition of the sympathetic nervous system results in reduced stimulation of the Onuf’s nucleus and pudendal nerve. This leads to the relaxation of the external sphincter muscle and decreased urethral pressures. Subsequently, micturition occurs with the activation of the parasympathetic nervous system, specifically in the S2 to S4 spinal segments.
However, in DSD, the detrusor contracts against a closed bladder outlet due to the involuntary contraction of the urinary sphincter. Pathophysiologically, this probably occurs from disruption of the spinobulbospinal tract between the pontine micturition complex and Onuf’s nucleus, resulting in elevated urethral closure pressures during detrusor contractions.[1]
Sustained elevated detrusor pressures exceeding 40 cm of water have been linked to hydronephrosis and renal deterioration.[10] This signifies an increased detrusor leak point pressure, a characteristic frequently observed in DSD, especially the continuous type. Recognizing and effectively treating this condition is crucial due to the potential for progressive kidney damage and renal failure.[11][12]
An association between DSD and autonomic dysreflexia has been suggested, although documenting this link has proven challenging because standardized diagnostic criteria for both conditions are lacking.[13]
Patients with DSD usually present with lower urinary tract symptoms and often report difficulties with voiding and/or storage. Common symptoms include chronic urinary retention, intermittent voiding, and irregular small-volume voiding or incontinence without an associated urge to void, which is referred to as reflex incontinence. Neurological symptoms may take precedence and prompt an initial neurological evaluation. DSD is likely associated with an underlying neurological disorder affecting the central nervous system.
The history and physical examination of patients can aid in identifying the cause and pattern of bladder dysfunction, searching for potential complications, and assessing any alterations in bowel and bladder habits and associated neurological symptoms. Clinicians should screen for underlying neurological diseases and investigate unexplained vision problems, back or neck pain, weakness, numbness, dysesthesia, and unexplained urinary or bowel symptoms. An abdominal examination is essential to assess for a palpable bladder, retained fecal matter, tenderness, and any indications of prior surgeries. The genitalia of patients should be examined for any signs of pathology or skin irritation. A digital rectal examination should be conducted to evaluate the anal tone both at rest and during voluntary contraction. Furthermore, it is essential to note the level of perineal sensation and document various other perineal reflexes.[14]
The main objective of evaluating bladder dysfunction is to diagnose the underlying cause and identify any possible complications accurately. The initial diagnostic approach involves a basic investigation of lower urinary tract symptoms to exclude the common causes. Urine culture and sensitivity should be ordered if there is a suspicion of a urinary tract infection (UTI). Along with serum electrolytes, measuring a patient's urea and creatinine levels is essential. A 24-hour urine voiding diary can be valuable in characterizing the nature of voiding dysfunction. Ultrasonography and computed tomography scan imaging techniques can help assess hydronephrosis, reflux, urinary calculi, and post-void residual urine volumes. However, it is noteworthy that the imaging results may not provide a specific diagnosis of DSD.
The diagnosis of DSD is established through a urodynamic study that is often accompanied by fluoroscopy and involves techniques such as electromyography (EMG), voiding cystourethrogram, video urodynamics, or urethral pressure profile measurements. A cystoscopy procedure is often recommended to rule out any urethral strictures in patients that might affect these studies.[1]
Diagnosing DSD using the EMG technique requires identifying heightened EMG sphincter activity during a detrusor contraction without using Valsalva or Crede maneuvers. During a voiding cystourethrogram, a closed bladder neck is observed during the filling phase, followed by the dilation of the bladder neck and proximal urethra up to the external urinary sphincter during micturition. A plateau in the detrusor pressure while voiding may indicate DSD. However, it is not a conclusive diagnostic criterion and needs confirmation.[15]
Urethral pressures are used as an adjunctive tool for diagnosing DSD. A 7-French urodynamic catheter with independent bladder and urethral pressure sensors is placed at the site of the highest sphincter pressure in the proximal urethra. DSD is subsequently defined as an abrupt increase in urethral pressure by more than 20 cm of water during or immediately preceding a voluntary or involuntary detrusor contraction.[1][16]
Before initiating the therapy, clinicians and patients should establish a consensus on the primary treatment objectives. The 3 typical clinical goals that should be emphasized are protecting renal function, enhancing patient safety, and optimizing the quality of life. The primary focus is attaining adequate storage and efficient bladder emptying without increased intravesical pressures, safeguarding the upper urinary tracts, preventing infections, and ensuring social adaptability. Following the initiation of treatment, patients should undergo regular clinical assessments and repeat urodynamic studies to assess the ongoing effectiveness of the treatment. Enhancing outcomes can be significantly aided by educating the patient and their family, providing them with a clear and fundamental understanding of the anatomy and physiology of the condition.
Type 1 DSD is usually managed conservatively through watchful waiting in patients, unless complicated by issues such as hydronephrosis, renal cortical loss, vesicoureteric reflux, or autonomic dysreflexia.
Pharmacotherapy by itself has a somewhat restricted function in the treatment of DSD.[17] Alpha-blockers such as tamsulosin have effectively reduced post-void residual volumes and increased voided volumes.[18] Diazepam has also been used either alone or in combination with alpha-blockers. Although anecdotal reports of reasonable success exist, no controlled studies substantiate its use.
Oral baclofen has traditionally been used to address skeletal muscle spasticity. However, its limited penetration of the blood-brain barrier results in minimal effectiveness in managing DSD unless direct intrathecal delivery is performed. This approach has demonstrated effectiveness in managing DSD. However, no long-term or randomized trials support its use, and intrathecal delivery is labor-intensive and invasive.[19][20][21][22]
Other pharmacotherapies have been experimented with, including nitric oxide donors such as glyceryl trinitrate, benzodiazepines, and dantrolene sodium. However, none of these are currently recommended as standard treatments. Intravesical oxybutynin has been used to treat DSD by, theoretically, reducing uninhibited contractions and increasing bladder storage capacity. There is inadequate clinical data or trials to support the intravesical use of oxybutynin presently, even though it seems to be a beneficial complement when administered orally.[23]
Sacral neuromodulation can potentially be highly beneficial in the treatment of DSD. However, randomized and long-term studies to confirm its efficacy are lacking. Sacral neuromodulation seems to enhance bladder function by reducing average detrusor voiding pressures and preventing the development of DSD in specific experimental SCI animal models.[24]
Clean intermittent self-catheterization (CISC), combined with antimuscarinics as necessary to reduce detrusor contractions and pressures, is the most effective and frequently used treatment for DSD. However, this modality might not be suitable for all patients. CISC treatment allows for the drainage and emptying of the bladder, even in the presence of a dyssynergic sphincter. Simultaneously, antimuscarinic therapy reduces detrusor pressure and minimizes contractions.[1] Antimuscarinics can lead to adverse effects such as dry eyes, dry mouth, constipation, nausea, headaches, and cognitive impairments. Renal ultrasound can be used to monitor the treatment's efficacy in reducing hydronephrosis. In cases where patients cannot perform self-catheterization, indwelling catheters, particularly suprapubic tubes, are advisable.[25][26]
There are 3 methods of self-catheterization, with the "clean" technique being the most appropriate for patients at home. The other 2 methods are primarily used in hospitals, nursing homes, and rehab centers during early management. Patients are instructed to use the "clean" technique, although it is noteworthy that no therapy exists without complications. Performing a "clean" self-catheterization procedure without proper care, attention, and manual dexterity poses the risk of urethral injury, scarring, bleeding, and the ever-present threat of infection.
When conservative treatments prove ineffective, using botulinum toxin injections in the urethra or bladder seems to be a reasonable initial treatment strategy. Botulinum toxin cleaves synaptosomal-associated proteins, which typically facilitate the movement of synaptic vesicles to the presynaptic membrane, inhibiting acetylcholine release. The administration of botulinum toxin induces flaccid paralysis in the targeted muscle. This treatment demonstrates efficacy when administered directly into the sphincter muscle through cystoscopy or transperineal ultrasonography, with reported durations ranging from 2 to 13 months.[27][28][29] The technique involves injecting 100 units of botulinum toxin A into the dorsal portion of the sphincter muscle at the 9-, 12-, and 3-o'clock positions.[30] Although the toxin may take 24 to 48 hours to exert its effects, its binding to the presynaptic membrane is irreversible, resulting in long-lasting paralysis.[30][31]
Historically, the standard treatment was the external sphincterotomy, which involved the therapeutic destruction of the external sphincter at the 12 o'clock position. However, this approach may be associated with significant complications, including uncontrollable incontinence, recurrent infections, epididymitis, stones, urethral diverticula, bladder neck stenosis, strictures, hemorrhage, erectile dysfunction, and persistent hydronephrosis.
Although there is a lack of long-term data to support their use, minimally invasive techniques, such as balloon dilatation and temporary and permanent urethral stents, are considered safe and effective. One obvious advantage of the urethral stent is potential reversibility. However, it carries the risk of migration or causing bladder-neck obstruction.[32][33]
As DSD patients exhibit a range of lower urinary tract symptoms, it is essential to explore more common causes before arriving at a diagnosis of DSD. More common etiologies of these urinary tract symptoms include non-neurogenic causes such as bladder neck obstruction, external sphincter spasticity, bladder neck and urethral strictures, dysfunctional voiding, and pseudodyssynergia. Pseudodyssynergia refers to the occurrence of an external urethral sphincter contraction during micturition, which can be mistakenly confused with DSD. Pseudodyssynergia can result from factors such as abdominal straining during the Valsalva maneuver, pain response, or voluntary efforts to block a detrusor contraction.[11]
DSD leads to elevated bladder pressures, resulting in renal reflux, bladder damage, and various types of dysfunctional voiding. If left untreated, up to 50% of patients with DSD can experience complications.
According to a meta-analysis, success rates differ across various treatment methods, some of which are listed below.
