 Botulinum toxin type A has been reported to inhibit the release of various pain neurotransmitters SP, CGRP, glutamate responsible for neurogenic inflammation, a process that results from the sensitization of C-fiber nociceptors peripheral sensitization. This action is probably responsible for the analgesic effect of botulinum toxin type A recently demonstrated in patients with neuropathic pain of peripheral origin.In those studies, patients had been suffering for years. The investigators can hypothesizes that earlier administration of Botox in the course of neuropathic pain might prevent central sensitization, that is secondary to peripheral sensitization. The investigators can hope to increase efficacy of Botulinum toxin type A injections and to prevent chronification of pain. 