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Botulinum a Toxin Treatment for Detrusor-Sphincter Dyssynergia in Spinal Cord Disease

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Botulinum a Toxin Treatment for Detrusor-Sphincter Dyssynergia in Spinal Cord Disease Spinal Cord (1998) 36, 91 ± 94 1998 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/98 $12.00 Botulinum A toxin treatment for detrusor-sphincter dyssynergia in spinal cord disease H Petit1, L Wiart2, E Gaujard3, F Le Breton1, JM FerrieÁ re4, A Lagueny5, PA Joseph1 and M Barat1 1Service de reÂeÂducation fonctionnelle, HoÃpital Pellegrin, Bordeaux, France, 2Centre de reÂeÂducation fonctionnelle La Tour de Gassies, Bruges, 3Centre de reÂeÂducation fontionnelle Les Grand CheÃnes, Bordeaux, 4Service d'urologie, HoÃpital Pellegrin, Bordeaux, 5Service de neurologie, HoÃpital Haut-LeÂveÃque, Pessac We studied the ecacy of endoscopic injection of Botulinum A toxin (150 I.U. Dysport1)in the treatment of detrusor-sphincter dyssynergia in 17 patients with spinal cord disease. One month after the injection, the postvoiding residual urine volume (7176 ml, P50.001), the bladder pressure on voiding (719 cm water, P50.01), and the urethral pressure (724 cm water, P50.001) were signi®cantly decreased. The modality of voiding was improved in 10 patients (ie micturition by suprapubic tapping was easier to induce, discontinuation of indwelling catheter use, or decrease in frequency of intermittent catheterizations). The tolerance of the treatment was excellent. The therapeutic eect lasted 2 to 3 months on the average. The low doses used in this study probably explain in part why the treatment sometimes failed. Botulinum A toxin could become an alternative treatment for detrusor- sphincter dyssynergia in certain patients, notably in those who are refractory to sphincterotomy or in patients, such as those who are tetraplegic, and who are incapable of performing intermittent self-catheterization. Keywords: spinal cord disease; detrusor-sphincter dyssynergia; botulinum toxin Introduction Detrusor-sphincter dyssynergia (DSD) represents a evaluated as a treatment for DSD by Dykstra et al8,9 major cause of voiding dysfunction in those who have in 16 patients, then by Schurch et al10,11 in 24 patients. an upper motor neuron bladder abnormality. This These studies showed that BTx relaxes the external dyssynergia can lead to chronic urinary retention, high urethral sphincter (EUS) and reduces DSD in intravesical pressure, chronic infections, vesicoureteral approximately 80% of cases. However, these authors re¯ux and renal damage. used iterative injections (between one and ®ve with an Oral treatments (adrenergic alpha antagonists, interval of 1 week between injections for Dykstra, and antispastic agents) for DSD have little eect.1 1 month for Schurch) with various doses of BTx Intermittent self-catheterisation (ISC) is the principal (between 100 and 720 I.U. of Botox1 BTx and treatment in selected patients, but remains impossible 750 I.U. of Dysport1 BTx) making comparisons and in tetraplegic patients, or in those with altered assessment of the cost/ecacy ratio of this expensive cerebellar function ± which is frequently present in treatment dicult. We wished to determine if a lower patients with multiple sclerosis. ISC may also be dose of BTx would provide a therapeutic eect in poorly tolerated locally (hematuria, urethral stricture) certain patients, so that the cost might be reduced as or psychologically.2 Sphincterotomy is eective but much as possible. Thus, the object of our study was to permanent incontinence may be induced and a high assess the ecacy of a single cytoscopic injection of reoperation rate and long term failure has been 150 I.U. BTx (Dysport1) for DSD in patients with described.3,4 Sacral anterior root stimulators and spinal cord disease. posterior rhizotomy are mainly indicated for patients 5 with complete neural de®cits. Thus, there remain Methods patients in which known treatments for DSD are insucient or excessively invasive. The inclusion criteria were a stable neurological status, Botulinum A toxin (BTx) is an inhibitor of the presence of an upper motor neuron type of bladder acetylcholine release at the neuromuscular junction dysfunction, the existence of DSD de®ned as and is used principally in the management of focal `inappropriate contractions of the external urethral dystonia, spasms and spasticity.6,7 It was ®rst sphincter (EUS) coincident with detrusor contrac- tions'12 and diagnosis by a urodynamic examination and by voiding cystourethrography, a postvoiding Correspondence: Dr H Petit, M.D. urine volume (PRUV) greater than 100 ml, and failure Botulinum A toxin treatment of detrusor-sphincter dyssynergia HPetitet al 92 of oral treatment by adrenergic alpha-antagonists (voluntary or by suprapubic tapping). Once in (alfuzosin) and antispastic agents (baclofen, dantro- position, the urodynamic catheter was retained in lene). Enlightened oral consent was obtained from each place by external adhesive tape and the location of the subject. microtransducers was veri®ed by measuring pressures Exclusion criteria were pregnancy, allergy to the during coughing. Three urethral pressure pro®les were toxin, hemocoagulation abnormalities, myasthenia, also recorded. A transperineal electromyogram of the treatment by aminoglycosides (the aminoglycosides EUS was coupled with a urodynamic examination in have an eect on the myoneural junction and may be seven of the patients before and 1 month after actually facilitating to BTx), in¯ammation or infection injection, the other 10 did not have an electromyo- of the injection site, or alterations of the proximal gram. The principle parameters analyzed were the urinary tract. bladder pressure during inhibited bladder contractions Endoscopic injection into the external urethral or during voiding, urethral pressure pro®les, and sphincter at three or four points was performred in PRUV. Urine cultures were performed before each all patients by the same coauthor of this report (JMF). assessment. If infection was present, the urodynamic This injection was performed under general anaesthe- examination was performed after antimicrobial ther- sia in patients with incomplete cord lesions (to avoid apy. painful phenomena when pain sensation was con- Other therapeutic means that may have interfered served) and under simple sedation (diazepam) in those with bladder functioning were discontinued during the with complete cord lesions. For the 24 h following the trial except in four patients in whom antispastic or injection, the patients had an indwelling Foley antidepressive medication was maintained at a catheter. All patients had an initial injection of constant dose throughout the study (60 mg: day 150 I.U. BTx (Dysport1), diluted to 4 ml with 0.9% baclofen in three cases, 6 mg/day clonazepam in one saline solution (ie 1 ml for each of the four points of case, 50 mg/day clomipramine in one case). No search injection into the striated urethral sphincter). We for anti-BTx antibodies was carried out. chose a procedure similar to that of Dykstra9 diluting Statistical analysis was performed using the non- BTx more than is generally recommended because we parametric Wilcoxon test to compare values before aimed to avoid excessive loss of the toxin linked to the and after injection of BTx. technical constraints of the injection site (losses in the relatively long tubing of the cystoscope, and the Results possibility of toxin leakage into the urethral lumen by bleeding). Seventeen patients were included between January and The pretherapeutic work-up included a complete September 1995. All were male. Their average age was medical history, a physical examination, a micturition 35+13 years (range: 22 to 63). Eight were tetraplegic diary, three PRUV measurements, a sample of the and three paraplegic, resulting from trauma. Six urine for culture, a voiding cystourethrography and a patients had nontraumatic myelopathies: four idio- urodynamic examination. pathic, one bilharzial and one by impingement. Seven Assessment was performed as follows. On day 15, patients had complete motor lesions. The average PRUV was measured. On day 30, PRUV and a period of time between the occurrence of spinal cord micturition diary were recorded, the patient's personal lesions and inclusion in this trial was 36.4+56.5 opinion was quanti®ed on two analogue visual scales: months. Do you ®nd this treatment to be ecacious? from 0 Before treatment, ®ve patients used an indwelling (no ecacy) to 10 (maximal ecacy), Have you Foley catheter or had suprapubic drainage because of tolerated this treatment well? from 0 (very poor complete urinary retention or diculties with inter- tolerance) to 10 (very good tolerance), side eects, mittent catheterization; six others practised intermit- when present, were noted, and a urodynamic tent self-catheterization but wished to stop, two had examination was performed. On day 60 and the intermittent catheterization, three voided using supra- subsequent assessment dates, PRUV was measured pubic tapping, and one voided using suprapubic and a urodynamic examination carried out once a tapping and Crede's manoeuvre. In our study, the month until the reappearance of the former condi- three types of goal for treatment with BTx were thus tions. If the ®rst injection failed, a second injection of discontinuation of indwelling drainage, discontinua- 250 I.U. was administered under the same conditions 2 tion or diminution of intermittent catheterization, or months later. If the therapeutic eect persisted longer improvement of tapping ecacy. Initial PRUV and than 4 months, PRUV and a urodynamic examination urodynamic parameters are shown in Table 1. were recorded at 6 months and 1 year. After BTx
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