Further Characterization of the External Urethral Sphincter in Spinal Cord Injury: Study during Spinal Shock and Evolution of Responsiveness to Alpha-Adrenergic Stimulation

Abstract

To shed further insight into its ever evolving concepts, we studied the activity of the external urethral sphincter in patients with spinal cord injury. Study during the phase of acute spinal shock revealed persistent electromyographic activity in the external urethral sphincter and no activity in the external anal sphincter, suggesting the presence of functional dissociation between the 2 sphincters from the onset of acute spinal injury. The genesis of dissociated activity was discussed by reference to recent experiments on the individual differences in motor neuron and muscle subtypes. Only the external urethral sphincter of chronic paraplegics demonstrated a uniformly increased electromyographic activity after alpha-adrenergic stimulation, while the response in the external anal sphincter was variable. The mechanism of increased response to alpha-adrenergic stimulation in the denervated external urethral sphincter appears to reside either in direct postsynaptic stimulation or recruitment of motor neurons other than the somatic pudendal system, since pre-treatment with competitive muscle relaxant failed to block this increased response in the external urethral sphincter.

Activation of the external urethral sphincter central pattern generator by a 5-HT1A receptor agonist in rats with chronic spinal cord injury

“…This is due mostly to a spinal reflex, given that it survives spinal cord injury even acutely in rats (27,38) and humans (18,24), and in that setting is presumably the basis for simultaneous contractions of bladder and EUS (bladder-sphincter dyssynergia). The pathway controlling this spinal tonic EUS reflex is schematized in Fig.…”

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

“…On pres sure profile study the urethra responded supersensitively to both a-adrenergic stimulation and sitting posture with a rise in the max imal pressure of 22 and 26 mm Hg, respectively, while there was no change to parasympathetic stimulation. On sphincter EMG the EUS was absolutely silent and no change was evoked after a-adrenergic stimulation [14]. There was no opening of the vesical neck on void ing cystourethrography.…”

“…5). Conjoining these data and the recent experimen tal study by Elbadawi and Atta [29], who convincingly demonstrated autonomic reinnervation and even hyper innervation of rhabdosphincter (EUS) following its so matic denervation by bilateral sacral ventral rhizotomy, the phenomenon of a-activation of the EUS whose mo tor efferents are deranged would not be an enigma any more [14,30],…”

“…Much controversy re mains here, and yet our study indicates the complex nature of urethral innervation where the old dogma fails to prevail. a-Activation of motor-deprived urethral sphincter (synonymous to denervated urethra) is suppor tive of the ever-accumulating basic data concerning sym pathetic involvement in urethral innervation [19,25,29], Furthermore the denervation supersensitivity of the urethra, albeit its mechanism [10,14,32], offers a clue as to why urinary flow is obstructed in the neurogenic ure thra. Finally a few comments concerning its manage ment.…”

“…The dynamic aspects of ure thral function were assessed with electromyography (EMG) of the external urethral sphincter (EUS) in the same manner as reported elsewhere and hence the sphincter was thought to be dyssynergic when there was either a failure of suppression or rather augmenta tion of its electroactivity with the voiding attempt [13]. Specifically the response of EUS to a-adrenergic stimulation was evaluated by analyzing its single motor units, and it was thought to be supersensitively responding when the electroactivity of EUS was augmented either by an increase in the amplitude and frequency of preexisting motor units and/or by the appearance of newly recruited units after adrenergic stimulation [14]. If the isolated neurogenic dysfunction of the urethra is defined urodynamically as a supersensitive re sponse in the urethral pressure study and/or the EUS activated by a-adrenergic stimulation, without evidence of vesical denervation as seen from the negative response to Lapides' test, then we have found a total of 21 such cases.…”