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Biomedical subjects

André Reitz

Publications and source records attributed to André Reitz.

18 recordsLinked to original sources
PubMed2006

Persistence of therapeutic effect after repeated injections of botulinum toxin type A to treat incontinence due to neurogenic detrusor overactivity.

OBJECTIVES: To study the effect of repeated botulinum toxin type A injections into the detrusor in patients with neurogenic detrusor overactivity and incontinence to determine the safety of repeated injections, the persistence of the clinical and urodynamic treatment efficacy, and potential changes in bladder compliance. METHODS: Seventeen patients with neurogenic detrusor overactivity who had received three or more botulinum toxin type A injections into the detrusor were studied. The clinical and urodynamic data were analyzed at baseline (before the first injection), after the first injection, and after the last repeated injection. RESULTS: No systemic side effects were observed for the total of 91 injections. The mean number of injections per patient was 5.4 (range 3 to 9). The mean number of incontinence episodes per day decreased from 2.6 at baseline to 0 after the first injection, and remained at 0 after the last injection. The maximal cystometric bladder capacity and reflex volume increased significantly after the first and last injection compared with at baseline. The maximal detrusor pressure decreased significantly after the first and last injection compared with at baseline. No difference in compliance was found from baseline to the first or last injection. CONCLUSIONS: Repeated injections of botulinum toxin A into the detrusor muscle are a safe and valuable treatment option for neurogenic detrusor overactivity. After repeated injections, the effect on the clinical and urodynamic parameters remained constant. Also, repeated injections did not decrease bladder compliance.

Botulinum Toxins, Type A↗
PubMed2006

Topographic anatomy of a new posterior approach to the pudendal nerve for stimulation.

OBJECTIVES: To describe a new approach to the pudendal nerve from a dorsal direction in terms of topographic anatomy and to discuss pudendal nerve neurophysiology in light of the rationale behind pudendal nerve stimulation to treat lower urinary tract disorders. MATERIALS AND METHODS: Cadavers of four women aged 78-87 yr were studied. After placing the cadavers in prone position with a 40 degrees -60 degrees flexion of the hips and determining anatomic landmarks, a 20-G insulated needle was inserted close to the pudendal nerve. Then the topographic relationships of the puncture with the pudendal canal were explored by dissection. RESULTS: The mean points of insertion of the needle were 14 cm inside the great trochanter, 9 cm above the ischiatic tuberosity, and 6 cm outside the gluteal fold. If the needle was inserted 6.5 cm under the previous with an orifice of 60 degrees and this route was followed, the needle could have a contact area with the pudendal nerve larger, leading to a greater stimulation efficacy with less stimulation intensities. The rectum was so far away that a rectal injury with the needle seemed unlikely. No vascular structure was at the contact of the nerve. CONCLUSIONS: The described new puncture technique to reach the pudendal nerve provides easy and safe accessibility of the nerve for stimulation. In light of our increasing understanding of the rationale behind neuromodulative stimulation, the pudendal nerve could be a promising target for continuous lower urinary tract neuromodulation by implant.

Aged↗
PubMed2006

Systemic nitric oxide augmentation leads to a rapid decrease of the bladder outlet resistance in healthy men.

OBJECTIVE: We examined the immediate effect of a systemic nitric oxide augmentation on the bladder outlet resistance in healthy men. METHODS: Eleven healthy male volunteers with a mean age of 25.5 yr were included in the study. They were prepared for a standard urodynamic study, and a baseline pressure-flow study was obtained. The subjects were then given 20 mg isosorbide dinitrate sublingually, and after refilling their bladder a second pressure-flow study was done after 20 min. The pressure-flow studies were then compared in regard to the average flow rate, the average detrusor pressure during micturition, and the detrusor pressure at maximum flow rate. RESULTS: One of the subjects was unable to void and had to be excluded from the study. In the remaining 10 men, the mean average flow rate increased from 16.7 ml/s before to 20.2 ml/s after the intake of the NO donor (P=0.013). Concomitantly, the average detrusor pressure during micturition decreased from a mean of 57 to 52 cm H2O (P=0.004) and the mean detrusor pressure at maximum flow rate decreased from 60 to 52 cm H2O (P=0.013). CONCLUSIONS: Systemic NO augmentation can lower the functional bladder outlet resistance very rapidly in men. Our results support the concept that the NO-cGMP pathway may be a promising target for medical treatment of lower urinary tract symptoms.

Administration, Sublingual↗
PubMed2006

Histologic features in the urinary bladder wall affected from neurogenic overactivity--a comparison of inflammation, oedema and fibrosis with and without injection of botulinum toxin type A.

OBJECTIVES: To study histological features and morphological differences in bladder wall specimen from patients with and without botulinum toxin A injections and to compare those issues in responders and non-responders to the toxin therapy. MATERIAL AND METHODS: Bladder wall specimen obtained from cystectomy in 45 patients with neurogenic overactive bladders with and without injection of botulinum toxin A into the detrusor muscle for treatment of neurogenic incontinence were evaluated concerning the histological criteria inflammation, oedema and fibrosis of the bladder wall. RESULTS: Bladder wall specimen obtained from patients suffering from neurogenic detrusor overactivity showed important histological alterations. Generally, inflammatory infiltration, oedema and fibrosis of the bladder wall were frequently observed. When comparing specimen from patients who had received botulinum toxin injection to those from patients who had not, there was no difference concerning inflammation and oedema. However, patients who had received botulinum toxin injection showed significantly less fibrosis of the bladder wall than those who had not received the toxin injection (p<0.00073). When comparing specimen from responders and non-responders to the botulinum toxin therapy, there was no difference in inflammation. Although not significant, a trend was observed that responder to the toxin therapy had less fibrosis and oedema of the bladder wall than non-responder. CONCLUSION: In our study injection of botulinum toxin into the detrusor muscle did not lead to increased fibrotic activity within the bladder wall, on the contrary patients with previous botulinum toxin injection revealed significant less fibrosis than patients without toxin injection.

Adult↗
PubMed2006

Facilitatory neuromodulative effect of duloxetine on pudendal motor neurons controlling the urethral pressure: a functional urodynamic study in healthy women.

OBJECTIVE: The aim of this functional urodynamic experiment in healthy women was to study the effect of duloxetine, which is a combined serotonin and norepinephrine (5-HT/NE) reuptake inhibitor, on urethral resting pressure, excitability of pudendal motor neurons, and urethral sphincter contractility. METHODS: In 11 healthy female subjects three baseline urethral pressure profiles (UPPs) were obtained to study resting pressure. Afterward the individual motor threshold (MT) for external urethral sphincter (EUS) contraction in response to transcranial magnetic stimulation (TMS) was determined to study the excitability of pudendal motor neurons. Another three UPPs were recorded while sacral root magnetic stimulation (SMS) was performed to evoke reproducible urethral contractions to study urethral sphincter contractility. Then the women received 40 mg duloxetine and the protocol was repeated 4 h after drug administration. The resting pressure values, MT values following TMS, and the EUS pressure amplitudes in response to SMS obtained at baseline were statistically compared to the corresponding values at follow-up after duloxetine. RESULTS: Oral administration of duloxetine significantly lowered MT for EUS contraction in response to TMS (p=0.013). In addition, duloxetine significantly increased EUS pressure amplitudes in response to SMS (p=0.0007, 5 of 11 subjects evaluated) but did not change urethral resting pressures. CONCLUSIONS: This is the first functional, urodynamic controlled study to show that the combined 5-HT/NE reuptake inhibitor duloxetine has a significant effect on the excitability of pudendal motor neurons and on urethral sphincter contractility in healthy women in vivo but no significant effect on urethral resting tone. Our data confirm a facilitatory neuromodulative effect of duloxetine on sphincter motor neurons in humans.

Blood Pressure↗
PubMed2006

Systemic augmentation of nitric oxide: is there an immediate effect on the urinary flow rate in healthy men?

INTRODUCTION: Nitric oxide (NO) is an important neurotransmitter in the lower urinary tract. Data from experimental studies in animals and humans suggest that NO donors like isosorbide dinitrate could be used to lower the infravesical resistance. Despite the potentially significant clinical benefit of such an effect, it has hardly been studied in vivo in men. We investigated the immediate effect of isosorbide dinitrate on the urinary flow rate and the functional bladder capacity in healthy young men. PATIENTS AND METHODS: A free urinary flow was measured in 20 healthy male volunteers on two consecutive micturitions. 15-25 min prior to the second micturition, 10 mg of the NO donor isosorbide dinitrate was administered sublingually. RESULTS: We found no significant difference between baseline measurement and the micturition after NO administration with regard to the totally voided volume, the maximal or the average flow rate as well as the flow rate corrected for the voided volume. CONCLUSION: Systemic augmentation of NO does not produce a relevant immediate effect on the urinary flow rate or the functional bladder capacity in healthy men.

Adult↗
PubMed2005

Conditioning stimulus can influence an external urethral sphincter contraction evoked by a magnetic stimulation.

AIMS: To study the effect of a conditioning stimulus on an external urethral sphincter (EUS)contraction evoked by a magnetic stimulation at different time intervals. METHODS: Seven healthy male volunteers underwent EUS pressure measurement. At baseline, magnetic stimulation of the lumbosacral spinal cord above the motor threshold was performed and evoked EUS pressure responses were recorded. The lumbosacral magnetic stimulation was repeated with same intensity, while a selective electrical dorsal penile nerve stimulation below the bulbocavernosus reflex (BCR) threshold was preceding at five different intervals (10, 20, 30, 50, 100 msec). The protocol was performed with empty and full bladder (BLA), and baseline responses were statistically compared to those with combined stimulation. RESULTS: When the dorsal penile nerve electrical stimulation preceded the lumbosacral magnetic stimulation by 20 msec (P=0.0048), 50 msec (P=0.0039), or 100 msec (P=0.0002), the amplitudes of the EUS pressure response with empty BLA were significantly reduced compared to lumbosacral magnetic stimulation alone. With a filled BLA, the amplitudes of the EUS were significantly reduced only at an interval of 50 msec (P<0.0001). CONCLUSIONS: A conditional sensory pudendal stimulation seems to have the capacity to inhibit the external urethral sphincter contraction induced by a magnetic stimulation. The inhibitory effect seems to depend on the latency between the peripheral and lumbosacral stimulation as well as on the degree of BLA filling. It remains to be proved if the neuromodulative effect of the conditional stimulus occurs at a spinal or supraspinal level.

Adult↗
PubMed2005

A case of undiagnosed tethered cord syndrome aggravated by transurethral prostate resection.

BACKGROUND: A 68-year-old man presented with a history of significant urinary urge incontinence, pollakiuria, and weak bladder sensation. He also reported mild fecal incontinence and a hypotrophic and slightly weaker left leg. At 63 years of age he had presented to a urologist for treatment of irritative lower urinary tract symptoms and incontinence. A transurethral resection of the prostate had been performed. After the operation, the symptoms had persisted and the incontinence seriously worsened. INVESTIGATIONS: Clinical neurologic examination, videourodynamic examination, neurophysiologic examination, and MRI of the spinal cord. DIAGNOSIS: Neurogenic bladder dysfunction caused by adult tethered cord syndrome with myelon up to S2 level, spina bifida occulta, and lipoma infiltrating the conus medullaris. MANAGEMENT: Conservative anticholinergic treatment failed, and injection of botulinum-A toxin is planned.

Aged↗
PubMed2005

Adherens junctions of the human detrusor.

OBJECTIVE: To immunohistochemically identify the protein composition of adherens junctions, which couple smooth muscle cells mechanically, and to confirm their decrease in different bladder dysfunctions, as studies in geriatric bladder dysfunction show fewer such junctions in patients with detrusor overactivity (DO) and bladder outlet obstruction (BOO). MATERIAL AND METHODS: Detrusor biopsies were obtained from video-urodynamically evaluated patients with neurogenic DO (NDO, 31 patients), BOO (six patients) and from six patients with stress urinary incontinence (SUI) with stable, unobstructed detrusors (serving as controls). Specimens were fixed, paraffin-embedded, sectioned, stained with a polyclonal pan-cadherin antibody, monoclonal alpha-, beta- and gamma-catenin antibodies, and a monoclonal integrin-beta1 antibody. All antibodies were known to react with proteins of adherens junctions. Two examiners unaware of sample origin evaluated the sections qualitatively and using a semiquantitative scale. The results were correlated with the patient groups. RESULTS: Specific immunohistochemical staining of pan-cadherin, alpha-, beta- and gamma-catenin could not be detected in any detrusor smooth muscle compartment, but was present in the urothelium. There was integrin-beta1 reactivity in the basement membranes of bladder smooth muscle cells in 38 of 43 detrusor biopsies. There were no differences among the three groups. CONCLUSION: The known proteins of cell-cell adherens junctions are not part of the cell-cell junctions of detrusor smooth muscle. The specific staining of integrin-beta1 indicates either the presence of cell-matrix junctions or of cell-cell junctions within the human detrusor. Further studies are needed to identify the complete protein composition of adherens junctions within smooth muscle cells.

Adherens Junctions↗
PubMed2004

The effect of nitric oxide on the resting tone and the contractile behaviour of the external urethral sphincter: a functional urodynamic study in healthy humans.

AIMS: This functional urodynamic study assessed the effect of the nitric oxide donor isosorbide dinitrate on the external urethral sphincter and hypothesised first that nitric oxide could lower the resting sphincter pressure, second that nitric oxide could influence the sphincter contractility during magnetic stimulation, and third that nitric oxide could induce a faster external urethral sphincter fatigue during continuous magnetic stimulation. METHODS: Eight healthy males gave their written informed consent and were included. A 2-channel microtip pressure transducer catheter was inserted into the urethra measuring the bladder and the external urethral sphincter pressure. Magnetic stimulation of the sacral roots was performed to evoke reproducible contractions of the external urethral sphincter. The baseline protocol included six single pulse stimulations and three stimulations 10sec in duration each for two frequencies 5Hz and 50Hz with intensities at the motor threshold of the pelvic floor. Then the subjects received 10 mg of isosorbide nitrate sublingually and the protocol was repeated 5min, 20min, 40min and 60min after drug administration. RESULTS: The sublingual administration of isosorbide dinitrate could significantly reduce the resting pressure of the external urethral sphincter for at least one hour. The maximal contractile strength measured as the maximal urethral pressure during single pulse and continuous magnetic stimulation of the sacral roots also decreased significantly. Nitric oxide did not induce a significantly faster fatigue of the external urethral sphincter during continuous magnetic stimulation of the sacral roots. CONCLUSIONS: This study shows a functionally relevant effect of nitric oxide on the resting tone and the contractile behaviour of the human external urethral sphincter in vivo while the fatigue properties did not changed significantly. Nitric oxide donors could offer a new pharmacological approach to treat urinary retention due to overactive or non-relaxing external urethral sphincter.

Adult↗
PubMed2004

Oral nitric oxide donors: a new pharmacological approach to detrusor-sphincter dyssynergia in spinal cord injured patients?

PURPOSE: Detrusor-sphincter dyssynergia is a common cause of bladder outlet obstruction in spinal cord injured patients and leads to poor bladder emptying and high bladder pressures, which if left untreated might cause renal failure. In this study, we tested the recently published hypothesis that oral administration of a nitric oxide donor could be a new pharmacological approach to treat detrusor-sphincter dyssynergia in humans with spinal cord injury. METHODS: 12 male spinal cord injured patients presenting with neurogenic detrusor overactivity and detrusor-sphincter dyssynergia were studied. 6 performed clean intermittent catheterisation and 6 used suprapubic tapping for bladder emptying. During cystometry the bladder was filled until the first overactive bladder contraction accompanied by detrusor-sphincter dyssynergia occurred while bladder and external urethral sphincter pressures were continuously recorded. Then the bladder was emptied and the patients received 10 mg of isosorbide dinitrate sublingually. Resting pressures were recorded and cystometry was repeated starting 15 min after drug administration. Maximal and mean values for bladder and external urethral sphincter pressures were calculated in both fillings and statistically compared by analysis of variance for repeated measurements (level of significance p < 0.05). RESULTS: Nitric oxide significantly reduced external urethral sphincter pressures at rest (p < 0.05) and during dyssynergic contraction (p < 0.05) while bladder pressures at rest and during contraction as well as the reflex volume remained unchanged. In the patients who used suprapubic tapping for bladder emptying the mean post triggering residual volume was significantly reduced (p < 0.05). CONCLUSIONS: Oral administration of nitric oxide donors significantly reduced bladder outlet obstruction due to detrusor-sphincter dyssynergia suggesting a role for nitric oxide in inhibitory neurotransmission to the urethral sphincter. This new approach could offer a potential pharmacological option to treat detrusor-sphincter dyssynergia in spinal cord injured patients.

Administration, Oral↗
PubMed2004

European experience of 200 cases treated with botulinum-A toxin injections into the detrusor muscle for urinary incontinence due to neurogenic detrusor overactivity.

OBJECTIVES: To present a comprehensive experience with botulinum-A toxin (BTA) injected into the detrusor muscle in patients with spinal cord injuries/diseases causing neurogenic incontinence. METHODS: Ten European medical centers provided the results of 231 patients with neurogenic detrusor overactivity who were treated with BTA. 300 units of Botox (Allergan Inc.) were injected cystoscopically into the detrusor muscle at 30 different locations, while sparing the trigonum. Urinary continence status, concomitant anticholinergic medication use and patient satisfaction were recorded. Key urodynamic parameters (reflex volume, maximum detrusor pressure during voiding, detrusor compliance and maximum cystometric bladder capacity) at baseline and at the first and second urodynamic follow-up examinations were analyzed. RESULTS: By the time of the initial (mean 12 weeks after injection) as well as at the second urodynamic follow-up examinations (mean 36 weeks after injection), the mean cystometric bladder capacity (p < 0.0001) and the mean reflex volume (p < 0.01) increased significantly, while the mean voiding pressure (p < 0.0001) decreased significantly. The mean bladder compliance had increased significantly (p < 0.0001) by the first follow-up examination and non-significantly by the time of the second follow-up. No injection related complications or toxin related side effects were reported. The patients considerably reduced or even stopped taking anticholinergic drugs without recurrence of reflex incontinence and were satisfied with the treatment. CONCLUSIONS: This retrospective European multicenter study presents the most extensive experience to date with BTA injections into the detrusor muscle to treat neurogenic incontinence due to detrusor overactivity and confirms that this new treatment is safe and valuable. Significant improvement of bladder function corresponds with continence and the subjective satisfaction indicated by the treated patients.

Botulinum Toxins, Type A↗
PubMed2004

The effect of tamsulosin on the resting tone and the contractile behaviour of the female urethra: a functional urodynamic study in healthy women.

AIMS: The aim of this functional urodynamic experiment was to study the effect of the selective alpha1(A)-blocker tamsulosin on the urethral pressure in healthy human females and assessed first the resting urethral pressure and second the urethral contractility in response to magnetic stimulation of the sacral roots. METHODS: 11 healthy female subjects gave their written informed consent and were included. A microtip pressure transducer catheter was inserted into the bladder and three baseline urethral pressure profiles were obtained. Another three urethral pressure profiles were recorded while magnetic single pulse stimulation of the sacral roots was performed above the motor threshold of the pelvic floor to evoke reproducible urethral contractions. Then the subjects received 0.4 mg of tamsulosin and the entire protocol was repeated 6 hours after drug administration. Cardiovascular monitoring was obtained during the baseline and follow-up measurements. Mean and maximal urethral pressure values calculated over the entire urethra, mean pressure values calculated over the proximal, middle and distal third of the urethra and the pressure amplitudes to magnetic stimulation at baseline were statistically compared to the follow-up measurements with tamsulosin. RESULTS: The oral administration of tamsulosin did not change the systemic blood pressure, but did significantly reduce the mean and maximal urethral pressure acquired over the entire urethra. When the proximal, middle and distal third of the urethra were analysed separately, there was a significant pressure reduction in all three segments. Amplitudes of the urethral contractions evoked by sacral magnetic stimulation remained unchanged after tamsulosin. CONCLUSIONS: These data show a significant relaxing effect of tamsulosin on the resting urethral tone in healthy females in vivo. These results may suggest tamsulosin as a new pharmacological approach to treat urinary retention due to overactive or non-relaxing urethra in women.

Adrenergic alpha-Antagonists↗
PubMed2004

Intravesical therapy options for neurogenic detrusor overactivity.

STUDY DESIGN: Review article. SETTING: Neuro-Urology, Spinal Cord Injury Center, Balgrist University Hospital, Zurich, Switzerland. OBJECTIVES: This review considers intravesical treatment options of neurogenic detrusor overactivity and discusses the underlying mechanism of action, clinical safety and efficacy, and the future trends. METHODS: The available literature was reviewed using medline services. RESULTS: Oral anticholinergic drugs are widely used to treat detrusor overactivity, but they are ineffective in some patients or cause systemic side effects such as blurred vision or dry mouth. As an alternative, topical therapy strategies have been suggested to achieve a profound inhibition of the overactive detrusor and to avoid high systemic drug levels. Currently available intravesical treatment options either act on the afferent arc of the reflex such as local anaesthetics or vanilloids or on the efferent cholinergic transmission to the detrusor muscle such as intravesical oxybutynin or botulinum toxin. Although an established and effective therapy, intravesical oxybutynin is not widely used. Evidence for clinical significance of intravesical atropine and local anaesthetic is missing. Intravesical capsaicin has been shown to improve clinical and urodynamic parameters, but cause pain in some patients. The intravesical instillation of resiniferatoxin and the injection of botulinum-A toxin into the detrusor muscle are promising new options; however, randomised placebo-controlled studies to prove their safety and efficacy are still missing. CONCLUSION: Intravesical treatment strategies in patients with neurogenic detrusor overactivity may provide alternatives to established therapies such as oral anticholinergics. The selectivity of the intravesical treatment and the reduction or even the absence of side effects are major advantages of this topical approach.

Administration, Intravesical↗
PubMed2003

Afferent fibers of the pudendal nerve modulate sympathetic neurons controlling the bladder neck.

AIMS: Pudendal nerve stimulation is known to have a potential modulative effect on bladder function. However, even if its efficiency has been established for various neurogenic and non-neurogenic bladder dysfunctions, the underlying neuronal mechanism, and the involved pathways in humans remain unknown. In this prospective study we focused on the effects of pudendal nerve stimulation in complete spinal cord injured patients to identify neuromodulative processes that occur on spinal level. METHODS: Twenty complete spinal male presenting with upper motor neuron lesion and neurogenic incontinence underwent pudendal nerve stimulation. Bladder, bladder neck (BN), and external urethral sphincter (EUS) pressures were continuously recorded with a three channel microtip pressure transducer catheter. Fifty six pudendal stimulations using biphasic rectangular impulses (0.2 ms, 10 Hz) with intensities up to 100 mA were applied to the dorsal penile nerve. In six patients, 18 stimulations were repeated after intravenous (i.v.) administration of 7 mg phentolamine. RESULTS: Mean BN and EUS pressure increased during stimulation significantly (P < 0.001). The latencies to the EUS responses range between 27 and 41 ms and those to the BN responses between 188 and 412 ms. Phentolamine decreased initial BN pressure and reduced the pressure rise during stimulation significantly (P < 0.05). CONCLUSIONS: Pudendal nerve stimulation evoked somatic responses in the EUS and autonomic responses in the smooth muscle sphincter controlling the BN. Longer latencies of the BN responses and the sensitivity to the alpha-blocking agent phentolamine suggest that sympathetic alpha-adrenergic fibers are involved. Somatic afferent fibers of the pudendal nerve are supposed to project on sympathetic thoracolumbar neurons to the BN and modulate their function. This neuromodulative effect works exclusively at the spinal level and appears to be at least partly responsible for BN competence and at least continence.

Adrenergic Fibers↗
PubMed2003

Botulinum toxin as a new therapy option for voiding disorders: current state of the art.

Botulinum toxin is a presynaptic neuromuscular blocking agent inducing selective and reversible muscle weakness up to several months when injected intramuscularly in minute quantities. Different medical disciplines have discovered the toxin to treat mainly muscular hypercontraction. In urology, indications for botulinum-A toxin have been neurogenic detrusor overactivity, detrusor-sphincter dyssynergia, motor and sensory urge and, more recently, chronic prostatic pain. The available literature was reviewed using Medline Services. The keywords "botulinum-A toxin", "detrusor-sphincter dyssynergia", "neurogenic bladder", "spinal cord injury", "denervation", "chronic prostatic pain", "chronic urinary retention" were used to obtain references. A toxin injection is effective to treat detrusor-sphincter dyssynergia when injected either transurethrally or transperineally. After treatment, external urethral sphincter pressure, voiding pressure and post-void residual volume decreased. The effect lasts between 2 to 9 months depending on the number of injections. Best indications seem to be multiple sclerosis and incomplete spinal cord injury patients suffering from neurogenic detrusor overactivity and detrusor-sphincter dyssynergia. According to the previous results, the use of botulinum-A toxin injections into the external urethral sphincter has been extended to a variety of bladder obstructions and to decrease outlet resistance in patients with acontractile detrusor. In cases of successful treatment, spontaneous voiding re-occurs and catheterization can be resumed. Injections of the toxin into the external urethral sphincter also seem to have a beneficial effect on chronic prostatic pain, presumably by reducing hypertonicity and hyperactivity of the external urethral sphincter. Injections of botulinum-A toxin into the detrusor muscle has first been tested to treat neurogenic detrusor activity in spinal cord injured patients and in myelomeningocele children. Long lasting (mean 9 months) detrusor relaxation occurs after injection of usually 300 units of Botox). Continence is restored in about 95% of the patients and anticholinergic drugs can be markedly reduced or even stopped. Excellent results of botulinum-A toxin injections into the detrusor in neurogenic detrusor overactivity have lead to an expansion of this treatment to incontinence due to idiopathic detrusor overactivity. Although preliminary results are promising, adequate dosage of the toxin required for this indication is not yet known. In conclusion, it appears that botulinum toxin injection into either the external urethral sphincter or the detrusor offers new promising treatment options for many different urological dysfunctions. However, large controlled trials are absolutely required to establish the role of botulinum-A toxin injections in the fields of urology and neurourology on evidence based medicine.

Animals↗
PubMed2002

Sympathetic sudomotor skin activity in human after complete spinal cord injury.

Spinal cord injury (SCI) causes serious disturbances in autonomic innervation and malfunction of the sympathetic nervous system that controls the pelvic organs, blood pressure, skin temperature and sweating. We studied sympathetic sudomotor pathways in 6 healthy subjects and 14 patients with sensory and motor complete SCI on cervical, thoracic and lumbar level. Sympathetic skin responses (SSRs) were provoked by auditory bursts and electrical stimulation of median, pudendal and tibial nerve and recorded from the palmar and plantar skin. The SSRs in healthy subjects occurred generally with the same pattern and with similar latencies suggesting a common sudomotor pathway mediating the SSR. Appearance or absence of the SSRs in SCI following stimulation above the lesion depend on the spinal level of lesion and on the location of stimulation. Lesions below T3 show palmar and lesions below T12 palmar and plantar SSR. Pudendal nerve stimulation evoked plantar SSRs in patients with complete cervical and thoracic SCI. No SSRs were obtained in patients with lesions at L1 and more caudal. SSRs following pudendal nerve stimulation in complete SCI above the level L1 are mediated by sacral somatic afferents and a sympathetic pathway originating at the upper lumbar level. The underlying sacro-lumbar reflex circuit is organized on spinal level and requires intact lumbar segments. Tibial nerve stimulation was not found to elicit SSRs below a SCI lesion and we suppose that this type of electrical stimulation cannot activate the spinal sudomotor reflex circuit.

Adrenergic Fibers↗