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Disorders of the vesico-sphincteral system are due to multiple causes (urological, gynaecological, neurological, psycho-behavioural, iatrogenic) which may be associated. By providing information on the type and evolution of these disorders and on the circumstances in which they developed, questioning is fundamental for the diagnosis. Completed by physical examination, it must precede all exploratory methods, including urodynamic, electrophysiological and radiological examinations. It allows these examinations to be graded and, compared with the results, it gives a better understanding of the physiopathology and aetiology of micturition disorders and therefore ensures their better treatment.

For many years, perineal neurogenic abnormalities associated with stress urinary incontinence have been described using electromyography examination, evoked potentials or neuromuscular biopsy. It has been suggested that the progressive denervation of the striated pelvic sphincter musculature that occurs in genuine stress incontinence is due to repeated stretch injury of the innervation of these muscles when the pelvic floor diaphragm is weak. New investigations such as perineal nerve motor latency confirmed this hypothesis. A real "perineal stretch neuropathy" may be described. It is very important to know about this neurogenic factor before considering rehabilitation therapy.

Continence in women, ensured by a constantly positive urethral closing pressure, is the result of two phenomena: purely passive factors (urethral pressure and compliance, transmission of bladder pressure to the urethra) and active factors mediated by a voluntary and reflex neuromuscular mechanism (contraction, reflexivity, sphincter endurance). In order to define these active forces of continence, we simultaneously studied the quantitative electromyographic activity of the striated sphincter and the bulbocavernosus muscle and variations in the urethral and vesical pressure under various conditions (rest, coughing, stimulation of the pudendal nerve). During coughing, the urethral pressure peak occurred earlier (100 milliseconds) than the vesical peak, associated with hypertransmission of 20%, the bulbocavernosus muscle contracted first, followed by contraction of the striated urethral sphincter (150 ms delay) and this electrical activity preceded the rise in vesical and urethral pressures. Stimulation of the pudendal nerve eliminated the possibility of an artefact related to coughing and induced the same sequence of events.

Fluorine-18-setoperone PET imaging was used to investigate serotonergic 5-HT2-specific binding in unlesioned cerebral cortex in stroke patients.Seventeen stroke patients (mean age 50 +/- 31 yr) with right (n = 9) or left (n = 8) chronic stroke (middle or anterior cerebral artery territory) underwent [18F]setoperone PET and MR imaging. The distribution volume of the 5-HT2-specific binding at equilibrium (DVSe) was determined in the unlesioned cortical regions. The results were compared with those obtained in 14 age-matched controls. In addition, we investigated the effect of the side of the stroke, lesion volume and its localization.After removing the age effect by covariance analysis, we found a significant DVSe decrease in the temporal (p0.05) and frontal (p0.05) unlesioned cortices ipsilateral to the stroke. The changes were similar in patients with left and right stroke and did not correlate with the volume of the stroke. However, the localization of the stroke affected the topography of DVSe abnormalities. When the lesion did not extend more medially than the internal capsule, DVSe was significantly reduced in the temporal lobe (-30%, p0.05) but not in the frontal lobe (-21%, p = ns). Conversely, when the lesion extended subcortically in the anteromedial region, close to the midline, DVSe was reduced in both temporal (-40%, p0.05) and frontal (- 49%, p0.05) lobes.This study confirms that stroke may alter 5-HT2 receptors in large unlesioned cortical areas and that the changes depend on the subcortical extent of the lesion.

Results of flowmeter studies in 145 patients before and then immediately after urodynamic exploration were unchanged in 80% of women and 72% of men. Abnormal results on flowmetric examination, detected in 18% of cases prior to urodynamic studies, were assessed as normal during follow-up urodynamic tests. These findings raise the question of the validity of flowmeter parameters determined during urethrocystometric exploration.

Two hundred and twenty-five patients with multiple sclerosis and bladder dysfunction were evaluated. 72% had urinary incontinence, 46% dysuria and 24% urinary retention. Detrusor hyperreflexia was the most common finding on cystometry (70%) and 9% of patients had areflexia. Coaxial needle electromyography was performed on all patients and 82% had detrusor-sphincter dyssynergia. Cortical evoked potentials following stimulation of the pudendal nerve were delayed in 72% and sacral evoked latency in 16% especially in patients with incontinence secondary to overactive bladder (25%), suggesting a conus medullaris lesion in these cases. Urologic complications were noted in 40%, with benign lesions in 24% (diverticula, urinary infections) and serious lesions in 16% (hydronephrosis, pyelonephritis, renal reflux). The most common treatment was anticholinergic drugs (efficacy in 92%), alphablockers agents (efficacy in 60%) and autocatheterism in 28%.

The progressive denervation of the striated pelvic sphincter musculature is due to repeated stretch injury of the innervation of these muscles when the pelvic floor diaphragm is weak. Electromyography examination, evoked potentials and perineal nerve motor latency confirmed perineal neurogenic abnormalities. This real "perineal stretch neuropathy" can be determine stress urinary incontinence, fecal incontinence and sexual disorders. Rehabilitation therapy may be tried in the treatment of the neuropathy.

Eight cases of vesico-sphincteric disorders (dysuria and chronic retention of urine) observed after spinal anaesthesia are reported. These symptomatic disorders were caused by a peridural haematoma in 3 cases and by lack of bladder contraction due to an "exhausted detrusor muscle" in 5 cases. The mechanism of the disorders (predominant vesical hypoactivity with sensory disorders) is discussed. The usefulness of urodynamic investigation in determining the physiopathological mechanism(s) and that of electrophysiological exploration in the search for a neurogenic disease is emphasized, as is the need for a preventing treatment (intermittent catheterization) in case of forced bladder detected by systematic recording of postoperative micturitions.

The bulbocavernosus reflex (BCR) was evaluated before, during and after micturition in 35 patients. All the 19 patients with upper motor neuron lesions had a positive BCR during micturition. By comparison, 11/16 of the patients with a lower motor neuron lesion or with urogynecologic diseases did not have a BCR during micturition. The persistence of BCR during voiding seems to be a loss of central inhibition and maybe represent a good sign of upper motor neuron bladder dysfunction.

Congenital indifference to pain (CIP) is a rare condition in which patients have severely impaired pain perception, but are otherwise essentially normal. We identified and collected DNA from individuals from nine families of seven different nationalities in which the affected individuals meet the diagnostic criteria for CIP. Using homozygosity mapping and haplotype sharing methods, we narrowed the CIP locus to chromosome 2q24-q31, a region known to contain a cluster of voltage-gated sodium channel genes. From these prioritized candidate sodium channels, we identified 10 mutations in the SCN9A gene encoding the sodium channel protein Na v 1.7. The mutations completely co-segregated with the disease phenotype, and nine of these SCN9A mutations resulted in truncation and loss-of-function of the Na v 1.7 channel. These genetic data further support the evidence that Na v 1.7 plays an essential role in mediating pain in humans, and that SCN9A mutations identified in multiple different populations underlie CIP.