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At least 1,243 records · Page 69Linked to original sources
PubMed2004

Sacral nerve stimulation.

The current concept of recruiting residual function of an inadequate pelvic organ by electrostimulation involves stimulation of the sacral spinal nerves at the level of the sacral canal. The rationale for applying SNS to fecal incontinence was based on clinical observations of its effect on bowel habits and anorectal continence function in urologic patients (increased anorectal angulation and anal canal closure pressure) and on anatomic considerations: dissection demonstrated a dual peripheral nerve supply of the striated pelvic floor muscles that govern these functions. Because the sacral spinal nerve site is the most distal common location of this dual nerve supply, stimulating here can elicit both functions. Since the first application of SNS in fecal incontinence in 1994, this technique has been improved, the patient selection process modified, and the spectrum of indications expanded. At present SNS has been applied in more than 1300 patients with fecal incontinence limited.

Electric Stimulation Therapy↗
PubMed1976

Early detection of diabetic visceral neuropathy. An electrophysiologic study of bladder and urethral innervation.

The segmental and supraspinal innervation of the detrusor muscle and periurethral striated musculature was studied in 27 patients with diabetes mellitus by gas cystometry, integrated sphincter electromyography, and spinal evoked-response latency measurements. Slowing of neural conduction velocities was a consistent finding in all the patients, even when cystometry did not show abnormalities. Thus, neuropathy in the segmental innervation of the bladder and urethra was documented.

Adolescent↗
PubMed1984

Long term results of superselective sacral nerve resection for motor urge incontinence.

Eight female patients suffering from severe urge incontinence not manageable by conservative treatment were subjected to superselective sacral nerve resection in the period 1974-1977. The aim of the resection was a complete parasympathetic decentralization of the bladder. The resection was carried out according to the results of pre-operative sacral nerve blockade and per-operative electrical nerve stimulation. Post-operatively all cystometrograms were shifted to the right and four patients had bladder areflexia. At six months follow-up, three patients were continent, four were improved and one patient had an indwelling catheter for persistent retention. However, incontinence and detrusor instability returned in all the patients within one year. After seven to eight years follow-up one patient had died, two patients had had a urinary diversion operation and three had an indwelling urethral catheter. Only two patients were permanently improved. The surgical procedure was complicated by wound necrosis in one patient, by persistent dysesthesia in two and hypesthesia in three.

Adult↗
PubMed1997

Entrapment neuropathy of the internal pudendal nerve. Report of two cases.

Entrapment neuropathy of the internal pudendal nerve in the Alcock canal is a rare entity and literature on the subject is lacking. The pathogenesis of this disease is probably related to repeated microtraumatisms of the perineal region acting on the Alcock canal or dysmetabolic diseases favouring compression of the pudendal nerve inside the Alcock canal. In this article two new cases which have come to our attention are described and literature on the topic, with special regard to diagnosis and treatment, is reviewed.

Autonomic Nerve Block↗
PubMed1992

Retrograde labeling of lumbosacral interneurons following injections of red and green fluorescent microspheres into hindlimb motor nuclei of the cat.

In order to map the laminar and segmental positions of lumbosacral interneurons that project to L7 motor nuclei, red and green fluorescent latex microspheres ("beads") were pressure-injected through micropipettes into the deep peroneal or posterior biceps-semitendinosus motoneuron pools of cats. Micropipette tips were positioned by recording the antidromic field potentials evoked by electrical stimulation of the muscle nerves. Projecting interneurons were identified by the presence of retrogradely transported beads. Small bead injections labeled large numbers of neurons. These were observed in all the spinal segments examined, L1-S2, and were most densely concentrated within laminae VI and VII ipsilateral to the injections and lamina VIII contralaterally. In addition, significant numbers of labeled cells were observed in lateral lamina V ipsilaterally and in lamina X. A few cells with bilateral projections were double-labeled following injections of red and green beads on opposite sides of the cord. These were most often observed in midlumbar segments (L3-L5) in medial regions of the gray matter. The results suggest that the intermediate zone (laminae V-VIII and X) of the lumbosacral spinal cord is a major source of interneuronal projections to the L7 ventral horn. This is true for both lateral and medial areas of the intermediate zone, as the fluorescent microspheres labeled neurons in medial regions of the cord largely undetected in previous studies in which other methodologies were employed.

Animals↗
PubMed1999

Glycemic modulation of insulin/IGF-1 mediated skeletal muscle blood following sympathetic denervation in normal rats.

Both insulin and IGF-1 decrease vascular resistance and increase blood flow in skeletal muscle, and it has been suggested that the mechanistic action for insulin may be by increasing autonomic vasodilatory activity. In this study we evaluated the effects of insulin and IGF-1 on blood flow to denervated and non-denervated skeletal muscle as part of a continuing investigation into the mechanism of regulation of cardiovascular responses by these hormones. Normal rats were prepared for measurements of mean arterial pressure (MAP), heart rate (HR) and vascular flow in the left and right iliac artery. Resection of the left lumbar sympathetic chain increased flow (expressed as conductance, flow/MAP) in the denervated left iliac but not in the intact right artery. Subsequent insulin infusion where hypoglycemia was allowed to occur increased conductance in both arteries, but more so in the denervated artery. Similarly, IGF-1 infusion increased conductances in both intact and denervated iliac arteries, and the effect was slightly greater in the denervated artery. Insulin infusion when euglycemia was maintained increased conductance to a similar extent in denervated and intact iliac arteries. Contrastingly, IGF-1 infusion under euglycemic conditions resulted in a much greater increased conductance in the intact iliac. We conclude that both insulin and IGF-1 increase conductance directly and that glycemic status and sympathetic nerve activity modulate these responses. The insulin-induced increase in conductance in the denervated limb under hypoglycemic conditions suggest that hypoglycemic-stimulated epinephrine release may enhance the dilatory response. while the greater response to IGF-1 in the intact vessel under euglycemic conditions may be due to IGF-1 capacity to decrease sympathetic activity leading to an enhanced conductance.

Animals↗