Background : In addition to inhibition of muscle and glandular hyperactivity, botulinum neurotoxin (BoNT) type A also interferes with pain processing. Previously, in a rat model of paclitaxel-induced polyneuropathy, abobotulinumtoxinA (aboBoNT-A) elicited analgesic effects not only in the injected paw, but also in the contralateral, non-injected paw. Methods : Here, we assessed bilateral analgesic effects of unilateral aboBoNT-A in several chronic pain models in Sprague-Dawley rats. Effects of aboBoNT-A on the paw withdrawal threshold in response to mech. pressure was assessed in models of streptozotocin-induced diabetic polyneuropathy, chronic constriction injury (CCI)-associated mononeuropathy, and bilateral carrageenan-induced inflammatory pain. Results : In diabetic polyneuropathy, aboBoNT-A (15, 20 U/kg) reversed hyperalgesia in the toxin-injected and non-injected paws. Discussion : These results suggest that unilateral administration of aboBoNT-A results in bilateral reduction in mech. hyperalgesia across neuropathic and inflammatory pain conditions, bilateral activation of sensory neurons being prerequisite for its expression. Significance : The results expand evidence on bilateral analgesic effects of aboBoNT-A following unilateral administration across pain modalities, as the phenomenon is seen in more than one model of polyneuropathy as well as in a model of chronic inflammatory pain when the latter is rendered bilateral.