A physiologically compliant detrusor muscle and a competent urethral sphincter are both necessary to maintain urinary function and continence. Normal micturition has a storage phase and a voiding phase. The storage phase consists of a passive filling of the bladder while voiding needs careful coordination between the detrusor contraction and relaxation of both external and internal sphincters. This complex micturition process is under the control of the central nervous system, which coordinates the activity of the autonomic and somatic nervous systems to guarantee normal urinary continence and micturition. Detrusor sphincter dyssynergia (DSD) is the urodynamic term for variable lower urinary tract symptoms due to detrusor muscle contraction with concomitant and inappropriate involuntary urethral sphincter contraction.

Detrusor sphincter dyssynergia is believed to occur due to neurological lesions of the suprasacral spinal cord. The lesions might be due to spinal cord injury (traumatic), myelodysplasia, multiple sclerosis, congenital anomalies like neural tube defects, spina bifida, and spinal dysraphism, stroke, infections of the spinal cord, and transverse myelitis. Of these, spinal cord injuries, spinal bifida, and multiple sclerosis are most commonly associated with DSD.

DSD is categorized into 3 types. Type 1 describes the condition where, initially, there is a simultaneous detrusor contraction and sphincter tightening. As the detrusor contraction peaks, the sphincter relaxes suddenly, resulting in urination. In type 2 DSD, the external urethral sphincter contracts sporadically across the entire detrusor contraction. Type 3 DSD is characterized by a crescendo-decrescendo pattern of sphincter contraction that results in obstruction of the urethra throughout the entire detrusor contraction.

While in the storage phase, urine is contained in the bladder by the tone of sphincter complexes. The internal urinary sphincter, an elongation of the trigone/detrusor muscle, encircles the neck of the bladder. As the bladder is filling up with urine, sympathetic activation contracts the internal sphincter and closes the bladder neck. The external sphincter, however, is a muscle that is under voluntary control and is situated more distal than the internal sphincter. The external urinary sphincter (EUS) functions under the control of pudendal nerve fibers and is situated in Onuf’s nucleus between S2–S4.

During urine storage, the proximal urethral pressure must exceed the pressure within the bladder to ensure continence. While the bladder is filling, urethral pressure increases progressively through the stimulation of internal and external sphincters via the hypogastric and pudendal nerve, respectively. This is known as “the guarding reflex.” When there is an urge for voiding, inhibition from the midbrain and prefrontal cortex is reduced, and the guarding reflex is suppressed by the pontine micturition center through the spinobulbospinal tracts. There is inhibition of the sympathetic nervous system, a decrease in the stimulation of Onuf’s nucleus and the pudendal nerve, causing relaxation of the external sphincter muscle that result in decreased urethral pressures. Micturition then occurs with the activation of the parasympathetic nervous system (S2–S4). However, in DSD, the detrusor contracts against a closed bladder outlet as there is an 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 increased urethral closure pressures during detrusor contractions.

Hydronephrosis and renal deterioration have been associated with sustained, elevated detrusor pressures over 40 cm of water. This represents an elevated detrusor leak point pressure, which is often found in DSD, particularly the continuous type. The potential for progressive kidney damage and renal failure is an important reason to properly diagnose and treat this condition.

There may also be an association between DSD and autonomic dysreflexia, but this has been difficult to document as diagnosing these two conditions has not been standardized.

CONCLUSION

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