Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
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PMID:[The striated sphincter of the urethra. 3: Urodynamic and physiopathologic study of the striated sphincter]. 639 28

Eighteen women with the urethral syndrome were studied urodynamically with synchronous video-pressure flow studies and electromyography of the external urethral sphincter (EUS). When compared with an age and sex matched control group, the most striking finding was a significantly higher than normal maximum urethral closure pressure. Abnormal and low urinary flow rates, instability of the intraurethral pressure at rest, incomplete funnelling of the bladder neck, and distal urethral narrowing during voiding constitute other typical urodynamic findings in the female urethral syndrome. Detrusor-striated sphincter dyssynergia or primary striated sphincter spasm was not observed. Even though striated EUS spasticity cannot be excluded as a cause of this syndrome in some patients, an autonomically mediated spasm of the smooth muscle sphincter seems plausible to explain both our urodynamic findings and a favorable response of 4 patients treated with alpha-blocking agents.
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PMID:Female urethral syndrome: clinical and urodynamic perspectives. 653 53