Introduction: Intramuscular administration of botulinum toxin type A (BoNT-A) is used to treat hyperkinetic disorders such as dystonia and spasticity. Our research suggests that BoNT-A, in addition to its primary peripheral action, also exerts effects on the central nervous system, which could explain its prolonged effect. Methods: Studies were conducted on Wistar Han rats and primary cultures of rat cerebellar neurons. Peripheral and central effects of BoNT-A were assessed using motor tests, electromyography, intrathecal administration of antitoxin, and latrotoxin (LTX). The protease activity of the toxin was analyzed using the Western blot method. Results: The antispastic effect of BoNT-A was dose-dependent in the later phase, with higher doses preventing spasm and improving motor performance. Intrathecal antitoxin accelerated the recovery of muscle weakness. BoNT-A reduced muscle tone induced by tetanus toxin (TeNT) without affecting the monosynaptic reflex. Central transsynaptic activity contributed to the late antispastic effect, with the presence of BoNT-A enzymatic activity in muscles and the spinal cord. LTX accelerated the recovery of neuroparalysis and reduced the late antispastic effects of BoNT-A. Conclusion: Peripheral and central activities of BoNT-A act synergistically, with the later central effect dependent on the reduction of intense peripheral action. This is also confirmed by the initial dominance of the flaccid neuroparalytic effect of TeNT on peripheral NMJ, in relation to the central disinhibitory effect and the occurrence of spasms in cephalic tetanus.