Patients with DSD usually present with lower urinary tract symptoms (LUTS), frequently complaining about problems with voiding and/or storage. Symptoms generally include chronic urinary retention, intermittent voiding, and irregular small volume voiding or incontinence without an associated urge to void (reflex incontinence). Neurological symptoms may be predominant and lead to neurological workup initially. DSD is only likely to be found if there is some neurologic disorder affecting the central nervous system.

The history and physical examination aim are to discover the etiology and pattern of bladder dysfunction, to search for complications, and to evaluate for changes in bowel and bladder habits together with any associated neurological symptoms. Clinicians should screen for unseen neurological disease and investigate unexplained vision problems, back or neck pain, weakness, numbness, dysesthesia, and unexplained urinary or bowel symptoms. An abdominal examination is necessary to look for a palpable bladder, retained fecal matter, tenderness, and evidence of past surgeries. Examine the genitalia for any pathology and skin irritation. A digital rectal examination should be done to assess the anal tone at rest and also during voluntary contraction. Perineal sensation should be noted, and various other perineal reflexes should be noted.[14]

The ultimate aim of an evaluation is to make an accurate diagnosis of the nature of bladder dysfunction and identify the underlying cause as well as any associated complications. The general approach to the diagnosis begins with a basic investigation of lower urinary tract symptoms to rule out common causes. Urine culture and sensitivity should be done if there is a suspicion of UTI. Besides serum electrolytes, urea & creatinine should also be measured. A 24-hour urine voiding diary will help characterize the voiding dysfunction. Ultrasonography and computed tomography (CT) scan imaging can be helpful for the assessment of hydronephrosis, reflux, urinary calculi, and post-void residual urine volumes, although they will not specifically help diagnose DSD.

The diagnosis of DSD is made through a urodynamic study with or without fluoroscopy via electromyography (EMG), voiding cystourethrogram, video urodynamics, or urethral pressure profile measurements. Cystoscopy is often recommended to rule out any urethral strictures which might affect these studies.[1] The diagnosis of DSD by electromyography requires finding increased EMG sphincter activity during a detrusor contraction, in the absence of Valsalva or Crede maneuvers. Typical voiding cystourethrogram findings include a closed bladder neck during filling with subsequent dilation of the bladder neck and proximal urethra to the level of the external urinary sphincter during micturition.

DSD may be suggested by the finding of a plateau level of voiding detrusor pressure, but this is not diagnostic by itself without 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 with the urethral sensors at the point of maximal sphincter pressure in the proximal urethra. DSD is then defined as an acute urethral pressure rise >20 cm of water during or immediately prior to a voluntary or involuntary detrusor contraction.[1][16]

First, clinicians and patients should agree on the primary goals of treatment before initiating therapy. Protecting renal function, improving patient safety, and optimizing the quality of life are the three typical goals that need to be prioritized. In general, the specific goals of initiating treatment for DSD are achieving adequate storage and bladder emptying without high intravesical pressures, preserving the upper urinary tracts, controlling infections, and achieving social acceptability. After treatment is initiated, patients should be followed with frequent clinical assessments and repeat urodynamic studies to evaluate continuing treatment efficacy. Educating the patient and family by providing them with a clear, basic understanding of the anatomy and physiology of the condition can greatly assist in improving outcomes.

Type 1 DSD is usually managed conservatively (watchful waiting), with the exception of those patients complicated by hydronephrosis, renal cortical loss, vesicoureteric reflux, or autonomic dysreflexia. Types 2 and 3 DSD should be treated when diagnosed to avoid complications.

Pharmacotherapy alone has a relatively limited role in the management of DSD.[17] Alpha-blockers such as tamsulosin have shown some activity in reducing post-void residual volumes and increasing voided volumes.[18] Diazepam has also been used alone or together with alpha-blockers, and while there are anecdotal reports of reasonable success, there are no controlled studies to justify its use. Oral baclofen has long been used for skeletal muscle spasticity, but it does not penetrate the blood-brain barrier well and therefore has little effect on DSD unless direct intrathecal delivery is performed. This has been shown to work well for DSD, although there are no long term or randomized trials, and intrathecal delivery is labor-intensive as well as invasive.[19][20][21][22] 

Other pharmacotherapies have also been tried, including nitric oxide donors (glyceryl trinitrate), benzodiazepines, and dantrolene sodium, but none are currently recommended. Intravesical oxybutynin has also been used for DSD. It would theoretically reduce uninhibited contractions while increasing bladder storage capacity. There is currently insufficient clinical data or trials to support its use intravescially, although it appears to a helpful adjunct when taken orally.[23]

Sacral neuromodulation may be very useful in treating DSD, although randomized and long term studies are lacking. It appears able to improve bladder function while lowering average detrusor voiding pressures and avoids the development of detrusor sphincter dyssynergia in some experimental spinal cord injury animal models.[24]

Clean intermittent self-catheterization (CISC), combined optimally with antimuscarinics as needed to reduce detrusor contractions and pressures, is the most successful and commonly used treatment for DSD. But this modality might not be suitable for all patients. CISC treatment permits the bladder to be drained and emptied of urine despite the dyssynergic sphincter, while antimuscarinic therapy lowers the detrusor pressure and minimizes contractions.[1] Side effects of antimuscarinics include dry eyes, dry mouth, constipation, nausea, headache, and cognitive effects. Renal ultrasound can be used to track the effectiveness of treatment on reducing hydronephrosis. Indwelling catheters, especially suprapubic tubes, are recommended when patients are unable to do self-catheterization.[25][26]

There are three methods of self-catheterization. "Clean" technique is typically used at home as the other two methods are primarily used in hospitals, nursing homes, and rehab centers during early management. Then, patients are taught the clean technique. No therapy is exempt from complications. When done without proper care, attention, and manual dexterity, self-catheterization carries the risk of a urethral injury as well as the always present risk of infection.

When conservative treatments fail, botulinum toxin injections to the urethra or bladder appears to be a reasonable primary treatment strategy. Botulinum toxin cleaves synaptosomal-associated proteins, which normally move these vesicles to the presynaptic membrane resulting in inhibition of acetylcholine release. Botulinum toxin administration causes flaccid paralysis of the affected muscle. When injected directly into the sphincter muscle, either cystoscopically or via transperineal ultrasonography, the treatment appears to be effective with a reported duration from 2 to 13 months.[27][28][29] The technique involves 2 to 4 injections on the dorsal portion of the sphincter between the 9, 12, and 3 o'clock positions using a total of 100 units of botulinum toxin A.[30] Although the toxin may take 24 to 48 hours to exert its effects, it's binding to the presynaptic membrane is irreversible, and it produces a longlasting paralysis.[30][31]

Historically, external sphincterotomy (therapeutic destruction of the external sphincter at the 12 o'clock position) was the standard treatment, but this may be associated with significant complications such as uncontrollable incontinence, recurrent infections and epididymitis, stones, urethral diverticula, bladder neck stenosis, strictures, hemorrhage, erectile dysfunction, persistent hydronephrosis, and recurrent epididymitis. Minimally invasive techniques such as balloon dilatation and urethral stents (temporary and permanent) seem to be safe and efficacious, but long-term data are lacking. One obvious advantage of the urethral stent is potential reversibility, but it can migrate or cause bladder neck obstruction.[32][33]

Since DSD patients present with symptoms of lower urinary tract symptoms, more common causes need to be investigated before diagnosing DSD. More common etiologies of these symptoms include non-neurogenic causes like bladder neck obstruction, external sphincter spasticity, bladder neck, and urethral strictures, dysfunctional voiding, and pseudodyssynergia. Pseudodyssynergia is the presence of an external urethral sphincter contraction occurring during micturition that may be easily misinterpreted as DSD. Causes of pseudodyssynergia include abdominal straining with Valsalva, pain response, or attempting to block a detrusor contraction.[11]

Detrusor sphincter dyssynergia results in high bladder pressure leading to renal reflux effects, bladder damage, and various types of dysfunctional voiding. Up to 50% of patients with DSD suffer complications if no intervention is done. A metanalysis revealed varying success rates for different treatment modalities: botulinum A injections into the external sphincter (reported success rates = 64% to 100%) or bladder (44% to 76%), urethral stents (9% to 91%), sphincterotomy (48% to 85%), transurethral incision of the bladder neck (82%), pharmacologic therapy (44% to 76%), and sacral neuromodulation (60%).

Up to 50% of patients with untreated detrusor sphincter dyssynergia (DSD) can develop serious urologic complications, which are much less common in females because of the lower detrusor pressures generated compared to men with DSD. If left untreated, DSD can result in urinary tract infection/urosepsis, vesicoureteric reflux, hydronephrosis, upper urinary tract deterioration, renal insufficiency, urolithiasis, and bladder damage. In addition, patients may also suffer complications from the treatment received.

Since patients have symptoms of the lower urinary tract, which might affect social adaptability, proper education about the disease course and condition with patient-centered treatment modalities helps patients refrain from such social problems.

It is not unreasonable to try oral medications, such as alpha-blockers like tamsulosin, along with diazepam if the symptoms and intensity of the DSD are not too severe.

Sacral neuromodulation may be an effective early therapy even if still mostly unproven. Consider it if the technology is available. 

Sphincterotomy protects the bladder and kidneys, but the resulting incontinence is severe and irreversible.

It might be quite difficult for clinicians to diagnose DSD since the disease presentation mimics a myriad of other conditions. A high index of clinical suspicion with the relevant investigation is the key to diagnosis. Involving nurses, physiotherapists, pharmacists, and patients themselves is crucial for a holistic management approach. When possible, patients should be encouraged to perform clean intermittent self-catheterization, which requires them to have sufficient motivation and dedication as well as adequate manual dexterity, cognitive function, compatible body size and shape, and a psychological acceptation of the technique. If the patient is treated at home, community nurses and social workers should be involved to monitor patients and make referrals when needed.