By CIBA Foundation Symposium
Incontinence is a truly universal and infrequently devastating challenge, yet person who is going principally unacknowledged. with a purpose to elucidate the underlying mechanisms of this significant scientific , this symposium introduced jointly neuroscientists engaged on the elemental biology of the bladder and bowel and clinicians facing some of the manifestations of urinary and fecal incontinence. The ensuing assurance is extensive and contains papers at the innervation and useful anatomy of the urinary tract and anorectal zone, and the important neural keep an eye on of those components. different contributions speak about the sensible overview of the anorectum and bladder, tension incontinence and the neurogenic speculation of incontinence, detrusor-external sphincter dyssynergia, and pharmacological and surgical methods to therapy.
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Extra resources for Ciba Foundation Symposium 151 - Neurobiology of Incontinence
Normally, peptidergic innervation is centred in the lower third of the bladder, but this might change during outflow obstruction. There are clinical correlates to the occurrence of hyperactivity of the bladder and sensitivity t o atropine. Dr Blaivas and his coworkers (Blaivas et a1 1980) did some interesting trials in which they titrated the dose of propantheline in patients with bladder hyperactivity and found that most patients responded well to this anticholinergic drug; so in many cases hyperactivity of the bladder is mediated through muscarinic cholinergic receptors.
Morrison refers to ‘pressure’ and shows a graded stimulation response due to increasing pressure, but I don’t know how that could be achieved in the whole bladder model. Is the implication that when you fill the bladder, it elicits afferent impulses, and the greater the pressure, the greater the impulse? Normally, when you fill the bladder, in an animal, you don’t get a graded pressure response; you get very little rise in pressure at all. Are you talking about tension in the wall of the bladder, or pressure?
At this point, increased afferent firing from tension receptors in the bladder reverses the pattern of efferent outflow, producing firing in the sacral parasympathetic pathways and inhibition of sympathetic and somatic pathways. The expulsion phase consists of an initial relaxation of the urethral sphincter (Fig. 1A) followed in a few seconds by a contraction of the bladder, an increase in bladder pressure and flow of urine. Secondary reflexes elicited by the passage of urine through the urethra reinforce the bladder contraction and facilitate bladder emptying (Kuru 1965, Wein & Barrett 1988).