[The striated sphincter of the urethra. 3: Urodynamic and physiopathologic study of the striated sphincter]

Dysfunction of the rhabdosphincter results from an increase (dyssynergia) or decrease in activity of either neurological or non-neurological origin. We have defined dyssynergia as the absence of urethral relaxation and/or sphincter contraction during and/or before detrusor muscle contraction. Non-invasive exploratory methods include flowmetry, anal contact EMG and an abdominal pressure or EMG examination. Invasive techniques are of various types: urethro-cystometry with EMG, via the perineum in males and the endo-urethral approach in females, provides quantitative data on extent of altered function and relative involvement of either smooth or striated muscle sphincters. An essential complement to urodynamic exploration is a conventional mictional cystogram. We have proposed an etiologic classification of dyssynergia: tonic dyssynergia is pathognomonic of supra-sacral medullary lesions while clonic dyssynergia reflects the bladder-sphincter conflict, whether it be of neurologic or other origin. Clonic dyssynergia in patients with neurologic affections is seen mainly in those with supra-sacral medullary lesions at whatever level, and with a 50 to 100% frequency. Its serious nature is not related to the bladder-sphincter equilibrium but to the high pressures developed by the system. The neurologic rhabdosphincter presents characteristic persistent reflex activity at the spinal shock phase and a possible course leading to fibrosis. In patients without neurologic disease the terms dyssynergia or pseudodyssynergia are used depending on whether the sphincter contraction during bladder contraction is involuntary or voluntary. To explain this non-neurologic pseudodyssynergia, Lapides suggested as a basis the theory of the evolution of sphincter control, Tanagho that of sphincter spasticity. In reality it involves a vicious circle centered on the bladder-sphincter conflict, entry being possible at various levels: bladder instability, urethral instability, urethral hypersensitivity, rhabdosphincter spasticity. These disturbed functions induce the urethral syndrome, repeated urinary infections, reflux and sometimes even renal stasis. Deficient sphincter activity of neurologic origin presents pathognomonic electromyographic signs; from a functional point of view valid data can be obtained from measurement of variations in maximum urethral pressure during a retention effort. Among the neurologic etiologies, the rhabdosphincter is only rarely affected by poliomyelitis or amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)