Relevance of Sympathetic Dyssynergia in the Region of External Urethral Sphincter: Possible Mechanism of Voiding Dysfunction in the Absence of (Somatic) Sphincter Dyssynergia

Abstract

The genesis of the cystourethrographic appearance of external sphincter spasm in 11 paraplegics with complete lower motor neuron bladders was examined. By the demonstration of its close association with a postural increase in the urethral pressure and catecholamine release, and its responsiveness to alpha-adrenolytic drugs an external sphincter spasm was suggested to be a result of sympathetic dyssynergia in the region of the external sphincter. The smooth muscular component in this region is believed to be a responsible unit of this disorder, since its surgical ablation by means of radical transurethral resection of the prostate uniformly resulted in the relief of sympathetic dyssynergia. The clinical implication of this disorder in the management of vesical dysfunction of the lower motor neuron type is discussed.

Neurogenic Urethra: Clinical Relevance of Isolated Neuropathic Dysfunction of the Urethra, and the Denervation Supersensitivity of the Urethra Revisited

“…The urethra whose somatomotor innervation was completely deprived still fails to relax and even constricts on voiding attempts to give outflow obstruction as it responds supersensitively to catecholamines that are liberated during voiding ma neuvers. As has been discussed in case 1 this is a wellunderstandable phenomenon considering the current dogma concerning somatomotor innervation of the EUS [25,28,29], The mechanism of this phenomenon, the fact that only the denervated EUS, even after radical TURP, responds supersensitively to exogenously admin istered adrenergics (data not described here) [10,12], is again supportive of significant adrenergic involvement in the function of motor deprived EUS [29,31], As to whether (muscarinic) parasympathetic decentralization affects the urethral sphincter we do not believe it is pos sible since there was no change in profilometry to para sympathetic stimulation throughout our experience [1,10,11,31], although another study of the cauda equina lesion in cats recognizes its partial role [21]. dal or pelvic nerve [28]), the sympathetic nerve seems to be conveyed to the EUS with its somatomotor nerve ( fig.…”

“…In fact 1 patient with multisystem disease in our series was initially classified as being of unknown cause which, however, eventually evolved into a full-blown Shy-Drager syndrome during follow-up. Assessments of urethral function with pres sure profilometry [8, 9,12] and sphincter EMG [13] must be an integrated part of the approach to such an instance. Secondly the urodynamic data derived from Case 2 (BH, This 66-year-old man was referred to us for evaluation of void ing difficulty after a fall from a roof that resulted in cauda equina injury.…”

“…Urethral sphincteric function was evaluated statically as well as dynamically. Static examinations were urethral pressure pro-file study, followed by assessment of its response to postural (sitting) change and/or a-adrenergic stimulation in the manner described previously [1,11,12], In selected cases the urethral response to parasympathetic stimulation was also evaluated following Lapides' test. Denervation supersensitivity of the urethra was defined as a more than 10-mmHg rise in the maximal urethral pressure after sitting posture and/or a-adrenergic stimulation [ 1 ].…”

“…Why then was he unable to void and why was vigorous 'bladder training' not employed? The pathophysiology of voiding difficulty and the risk of blind 'bladder training' in such an instance have already been addressed in the discussion of 'sympathetic dyssynergia' of the urethral sphincter [12], This is an illustrative case. The urethra whose somatomotor innervation was completely deprived still fails to relax and even constricts on voiding attempts to give outflow obstruction as it responds supersensitively to catecholamines that are liberated during voiding ma neuvers.…”

Nicergoline in the treatment of neuropathic bladder dysfunction: a preliminary report

“…These effects are more evident in patients with a neuropathic bladder than in normal individuals (Rossier et al, 1982), possibly due to an urethral hypersensitivity to alpha stimulation when bladder denervation is present. Koyanagi (1982) report an increase in blood catecholamines in patients with lower motor neurone lesions when placed in the sitting position, leading to an 'urethral sym pathetic dyssynergia' that causes outflow obstruction in response to this postural discharge of catecholamines (Koyanagi et al, 1982). Nevertheless, Nordling, in histochemical studies of trigonal and bladder strips obtained from patients with neuropathic bladder, failed to demonstrate an increment in adrenergic fibres as an organic basis for urethral hyper sensitivity (Nordling et al, 1980).…”