Vasoactive intestinal peptide (VIP) is a neuropeptide which previous studies showed be implicated in neuropathic pain. We hypothesized that VIP signalling is essential for sensitivity threshold after nerve injury. We used mice full knock out for VIP (VIP-/-) and the pain model of spared nerve injury (SNI) in which sciatic nerve, innervating hindpaw, is unilaterally lesioned. VIP-/- developed contralateral mechanical allodynia at the site of the not-affected hindpaw while wild type did not. At the level of lumbar spinal cord we recorded an higher inflammation an neuronal responsiveness in VIP-/- mice than VIP+/+. These observations suggest a central process involved in contralateral allodynia. Comprehension of the still unclear phenomenon of bilateral allodynia will help a future design of pharmacological treatment for this debilitating condition.