Botulinum toxin type B for Type A resistant bladder spasticity

Urinary dysfunction is one of the main problems afflicting patients with spinal cord injury. In particular, detrusor hyperreflexia causes urinary incontinence, which decreases quality of life, and high bladder storage pressures with secondary renal damage. Available therapies are intermittent self-catheterization and oral anticholinergic drugs, which are associated with a high frequency of side effects. Botulinum toxin (BTX) selectively blocks the release of acetylcholine from nerve endings and accordingly blocks neural transmission in cholinergic synapses. The long-term experience of treatment for dystonia and blepharospasm has demonstrated that approximately 16% of patients undergoing repeated treatments become resistant to this drug. It is supposed that an immunological mechanism is responsible for drug resistance, and in many resistant subjects antibodies to the toxin can be detected. Recordings of the compound muscle action potentials (CMAPs) elicited by electrical stimulation of the peroneal nerve before and after botulinum toxin injection in the extensor digitorum brevis show a correspondence between antibody seropositivity and absence of toxin responsivity. 1 As botulinum toxin type B (BTX-B) has an antigenic specificity different from type A (BTX-A), type A resistant subjects affected by cervical dystonia have been treated successfully with BTX-B. BTX-A used in the treatment of bladder detrusor hyperreflexia causes increased bladder capacity and post-void residual urine volume, decreased mean maximum detrusor voiding pressure and resolution of autonomic dysreflexia. No significant side effects have been detected. BTX-B injection was introduced recently, and only 1 report of its effect in neurogenic bladder dysfunction has been published previously. 3 In that instance a good therapeutic effect was noted without significant side effects in a patient without previous treatments. We report our experience with botulinum toxin type B injection for the management of bladder spasticity in a subject resistant to BTX-A