Rigi10™ Malleable Penile Prosthesis
Also Known As
Detrusor sphincter dyssynergia (DSD), Bladder sphincter dyssynergia, Neurogenic detrusor-sphincter dyscoordination, Detrusor-striated sphincter dyssynergia, Vesicourethral dyssynergia
Definition
Detrusor-external sphincter dyssynergia (DESD) is a neurologically induced urodynamic condition characterized by the simultaneous and uncoordinated contraction of the detrusor muscle and the external urethral sphincter during attempted micturition.1 This pathological dyssynergy creates bladder outlet obstruction as the detrusor contracts against a closed urethral sphincter, preventing efficient bladder emptying.2 The condition occurs due to disruption of the spinobulbospinal tract between the pontine micturition center and Onuf’s nucleus, resulting in elevated urethral closure pressures during detrusor contractions.3 DESD is exclusively associated with neurological pathologies affecting the central nervous system, particularly those involving the suprasacral region of the spinal cord.4
Clinical Context
Detrusor-external sphincter dyssynergia occurs exclusively in patients with neurological disorders affecting the central nervous system.1 The condition is most commonly associated with spinal cord injuries (particularly suprasacral injuries), multiple sclerosis, and spina bifida.2 During urodynamic testing, approximately 75% of patients with suprasacral spinal cord injuries demonstrate DESD, while about 35% of patients with multiple sclerosis and up to 50% of infants with spina bifida may exhibit this disorder.1
DESD is classified into three distinct types based on sphincter behavior during detrusor contraction: Type 1 features initial sphincter tightening followed by relaxation at peak detrusor contraction; Type 2 involves sporadic sphincter contractions throughout detrusor contraction; and Type 3 presents with a crescendo-decrescendo pattern of sphincter contraction that obstructs the urethra throughout the entire detrusor contraction.1 Type 1 DESD is commonly associated with incomplete neurological lesions, while complete neurological lesions often lead to Types 2 and 3.1
Patients typically present with lower urinary tract symptoms including chronic urinary retention, intermittent voiding, irregular small-volume voiding, or reflex incontinence.1 If left untreated, DESD can lead to serious complications including hydronephrosis, renal scarring, and progressive kidney damage due to sustained elevated detrusor pressures exceeding 40 cm of water.3 There is also an association between DESD and autonomic dysreflexia, though standardized diagnostic criteria for both conditions are lacking.1
Diagnosis requires urodynamic studies with EMG recordings, voiding cystourethrogram, and potentially urethral pressure monitoring.2 Treatment approaches include clean intermittent self-catheterization with antimuscarinics, alpha-blockers, botulinum toxin injections, and in severe cases, surgical interventions such as sphincterotomy or sacral neuromodulation.4 Regular clinical assessments and repeat urodynamic studies are essential to monitor treatment effectiveness and prevent upper urinary tract damage.5