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Introduction It's in the wake of Brigitte Schurch's work that the indication of Botulinum Toxin (BoNT) developed in the treatment of Detrusor Hyperactivity (DH). DH treatment by BoNT injection is considered to be well tolerated. However, in two patients treated with intradetrusor BoNT injections, a motor deficit located at the root of lower limbs was noticed. That observation raises questions about its diffusion beyond the injection site. Observations They are two women with Secondary Progressive Multiple Sclerosis (SPMS) receiving BoNT as a treatment for DH. On several occasions in post injection, an aggravation of the proximal motor deficit on the hip flexors was observed, which justified the realization of a SOLUMEDROL bolus in the event of relapses. Discussion Ramirez-Castaneda et al. [1] describe three means of dissemination of the BoNT: migration by systemic or neuronal transport, propagation and diffusion. Migration by systemic transport: it has been established by electromyography (EMG) analysis. These subclinical manifestations are not correlated by EMG [2] . This mechanism can’t account for an isolated motor deficit. Migration by axonal transport Animal experiments confirm the axonal transport of BoNT. On human subjects, Marchand-Pauvert et al. suggest its existence: reduction of the reciprocal inhibition exercised by Renshaw cells after BoNT injections [3] . Local dissemination of BoNT by diffusion and propagation In the absence of direct connection between the iliopsoas and the bladder, this hypothesis looks compromised. Synthesis A retrograde migration of BoNT via hypogastric nerves seems to prevail. It could be followed by axonal anterograde transport causing a deficit on the hip flexors via the L2 nerve root.