Intra Detrusor Botulinum Toxin and Lower Limbs Motor Deficit: About 2 Clinical Cases

Hichem Khenioui,Morgane Le Berre

doi:10.4172/2165-7920.1000761

Abstract

Objective: To demonstrate how a single intra detrusor botulinum toxin injection could be responsible for lower limbs proximal motor deficit. Results: Two women-37 and 38 years old-presenting with secondary progressive multiple sclerosis, having received intra detrusor botulinum toxin injections (400 BOTOX® U and 750 DYSPORT® U) due to major neurogenic detrusor over activity with high-pressure and risks of uro-nephrologic complications despite an efficient-dose anticholinergic bi-therapy (DITROPAN®/CERIS®). Few days in post-injection they present heavy tiredness, instability of the pelvis, and a major reduction of the walking distance. Those symptoms last for several months. During the emergency neurology consultation set up in the event of a new relapse, an aggravation of the paraparesis at the proximal level is observed. This deficit accounts for the realization of a corticosteroids bolus, the effectiveness of which is questioned by the patient. A cerebral and medullary MRI is performed in order to certify the appearance of new lesions. The MRI doesn’t objectify any new lesions or any pathological contrast enhancement. Discussion: Ramirez-Castaneda et al. describe three means of dissemination of the BoNT: migration by systemic or neuronal transport, propagation/spread and diffusion. Conclusion: The retrograde migration of the botulinum toxin via hypo-gastric nerves seems to prevail. It could be followed by axonal anterograde transport causing a deficit on the hip flexors via the L2 nerve root.

Highlights

Multiple sclerosis is a chronic demyelinating and inflammatory disease of the central nervous system, characterised by a spatiotemporal dissemination of the lesions, source of a polymorphous clinical presentation
During the emergency neurology consultation set up in the event of a new relapse, an aggravation of the paraparesis at the proximal level is observed, with an iliopsoas rated at 0/5 on both sides. This deficit accounts for the realization of a corticosteroids bolus on 3 occasions, the effectiveness of which is questioned by the patient
Systemic manifestations in the migration of BoNT are many and most often subclinical: asthenia, global muscle fatigue. They are not always associated with the injected dose [13]. They are confirmed in the striated skeletal muscle by single-fiber electromyography (SFEMG) that reveals the presence of a reversible conduction delay in the distant muscles [14]

Summary

Introduction

Multiple sclerosis is a chronic demyelinating and inflammatory disease of the central nervous system, characterised by a spatiotemporal dissemination of the lesions, source of a polymorphous clinical presentation. It’s the first cause of non-traumatic handicap in France. Bladder disorders are extremely frequent in MS (prevalence of 87% with an average occurrence around 6 years in the evolution of the disease). They can be inaugural in 0-10% of the cases. Over activity and obstruction symptoms can be associated in 1 patient out of 2, with little clinical and urodynamical correlation. The most often found cystomanometric board is a neurogenic detrusor over activity (NDO) (median of 65 %) [3]

Results

Discussion

Conclusion