Intra Detrusor Botulinum Toxin and Lower Limbs Motor Deficit: About 2 Clinical Cases
- *Corresponding Author:
- Hichem Khenioui
Physical Medicine and Rehabilitation
Hospital Group in Lille
Catholic Institute, France
E-mail: [email protected]
Received January 02, 2016; Accepted April 12, 2016; Published April 17, 2016
Citation: Khenioui H, Le berre M, Massot C, Blanchard A, Marcelli C, et al. (2016) Intra Detrusor Botulinum Toxin and Lower Limbs Motor Deficit: About 2 Clinical Cases. J Clin Case Rep 6:761. doi:10.4172/2165-7920.1000761
Copyright: © 2016 Khenioui H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.