Botulinum Toxin Type A Injections for Treating Neurogenic Detrusor Overactivity Combined With Low-Compliance Bladder in Patients With Spinal Cord Lesions

Klaphajone J, Kitisomprayoonkul W, Sriplakit S. Botulinum toxin type A injections for treating neurogenic detrusor overactivity combined with low-compliance bladder in patients with spinal cord lesions. To evaluate botulinum toxin type A (BTX-A) for treating neurogenic detrusor overactivity in patie...

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Bibliographic Details
Published in:	Archives of physical medicine and rehabilitation Vol. 86; no. 11; pp. 2114 - 2118
Main Authors:	Klaphajone, Jakkrit, Kitisomprayoonkul, Wasuwat, Sriplakit, Supon
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 01-11-2005 Elsevier
Subjects:	Adolescent Adult Biological and medical sciences Bladder, neurogenic Botulinum toxin type A Botulinum Toxins, Type A - therapeutic use Cerebrospinal fluid. Meninges. Spinal cord Child Diseases of the osteoarticular system Diseases of the spine Female Humans Male Medical sciences Middle Aged Miscellaneous Muscle hypertonia Myelitis, Transverse - complications Nervous system (semeiology, syndromes) Neurology Neuromuscular Agents - therapeutic use Prospective Studies Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects) Rehabilitation Spinal cord diseases Spinal Cord Injuries - complications Treatment Outcome Urinary Bladder, Neurogenic - drug therapy Urinary Bladder, Neurogenic - etiology Urinary Incontinence - drug therapy Urinary Incontinence - etiology Rehabilitation Botulinum toxin type A Spinal cord diseases Bladder, neurogenic Muscle hypertonia Oxyphencyclimine Spinal cord Prognosis neurogenic; Botulinum toxin type A; Muscle hypertonia; Rehabilitation; Spinal cord diseases Diseases of the osteoarticular system Bladder Metalloendopeptidases Spine disease Contraction Functional capacity Cholinergic receptor Bontoxilysin Reeducation Antispasmodic agent Urinary bladder Antisecretory agent Detrusor muscle Secondary effect Clinical trial Overactive bladder Antagonist Human Nervous system diseases Urinary system disease Enzyme Hypertonia Urinary tract disease Compliance(volume pressure) Care High pressure Peptidases Treatment Orthopedics Central nervous system disease Hydrolases Bladder disease Spinal cord disease Parasympatholytic
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Summary:	Klaphajone J, Kitisomprayoonkul W, Sriplakit S. Botulinum toxin type A injections for treating neurogenic detrusor overactivity combined with low-compliance bladder in patients with spinal cord lesions. To evaluate botulinum toxin type A (BTX-A) for treating neurogenic detrusor overactivity in patients with spinal cord lesions, including those with abnormally low bladder compliance. Nonrandomized, before-after trial (9-mo follow-up). Hospitalized care. Ten patients with high detrusor contraction pressure and/or poor response to oxyphencyclimine with incontinence selected as a consecutive sample. BTX-A (Botox; 300U) was injected into the detrusor muscle. Urinary continence, functional bladder capacity, bladder compliance, detrusor contraction pressure, and volume at first reflex voiding. Measurements were taken before and 6, 16, and 36 weeks posttreatment. Six weeks after treatment, complete continence was restored in 7 patients without oxyphencyclimine. Mean functional bladder capacity ( P=.008), compliance ( P=.012), and reflex volume ( P=.045) significantly increased, whereas maximal detrusor contraction pressure significantly decreased ( P<.001). Urodynamic variables remained significantly improved at 16 weeks, but values were returning toward baseline levels by 36 weeks. The procedure was generally uneventful, without any serious side effects. BTX-A injections are an effective, well-tolerated treatment for neurogenic detrusor overactivity in patients with spinal cord lesions, even in patients with abnormally low bladder compliance. Patients may require repeat injections after 16 weeks to remain continent.
ISSN:	0003-9993 1532-821X
DOI:	10.1016/j.apmr.2005.06.008