Botulinum toxine of Ty A (BT-A) is indicated in disorders primary connected to increased spastics of muscular structures, but the focus of the most recent research is the effect of the neurotoxin to pain. The BT A presents an extremely favourable pharmaco therapeutic profile with long lasting antinociceptive action and small number of side effects, making it different from other appr oved analgetics. It was deemed that the BT A shows its antinocicptive effects by inhibiting the release of anti inflammatory mediators at the peripheral ends of the sensor nerve fibres, but the positive outcomes in pain killing of inflammatory and neuropat hic origin indicate to the central place of the BT A action. The behavioral results obtained by models of visceral and mirror pain, in which bilateral analgesic effect of the BT A after unilateral peripheral and intraecal, but not central intracerebroventi cular and intracisternal application has been observed, have served as a fondation of the hypothesis on central segmental analgesic action of the BT A at spinal level. Immunohystochemically, the presence of a cracked SNAP 25 protein (indirect market of BT A activity) has been detected, predominantly in dorsal spinous processes of the back spinal cord segments. However, by applying axonal transport blocker, no presence has been observed, assuming that the BT A after the axonal back transport from the periphe ry is showing an anticiceptive effect by modulating the transport of the painful impulse by means of sensor fibres at the first synapsis level in the dorsal spine. The behaving of BT-A after supraspinal application to lateral brain chambers (i.c.v.) and c isterna magna (i.c.) has been tested. Although the cracked SNAP 25 was detected in further regions of the brain after the i.c.v. application of the BT a, the number of c Fos (the nociceptive activity marker) positive neurons has not decreased. After the i. c. application of BT A, the presence of cracked SNAP 25 in particular fibres of dorsal spinous processes of the back spinal cord has been observed, but the analgesic effect was absent. It is deemed that the BT-A performs action against pain by inhibiting t he release of anti inflammatory mediators from the ends of sensor fibres at the first synapsis level in the spinal cord, as well as interacting with the neuro transmission by means of endogenic GABA and opinoide system, resulting in modulation of the pain impulse transmission from the periphery to centres.