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Neurophysiological and Clinical Effects
of Botulinum Toxin Type A
Dr. Alfredo Berardelli
Posted: October 2005  
Presented at the 5th International Conference on Basic
and Therapeutic Aspects of Botulinum and Tetanus Toxins
Denver, CO; June 23-25, 2005


In his opening clinical lecture, Dr. Berardelli highlighted the interactive relationship between the basic science of botulinum and tetanus toxins and their potential clinical uses. As noted by Dr. Berardelli, botulinum toxin acts peripherally by inhibiting the release of acetylcholine from the presynaptic neuromuscular terminals, thereby weakening muscle contraction, and produces its clinical benefit primarily through its peripheral action. There is no conclusive evidence to demonstrate that BoNT-A acts directly on the central nervous system (CNS) structures in humans; a number of animal and human studies provide strong evidence suggesting that BoNT-A affects the functional organization of the CNS indirectly through peripheral mechanisms.

According to Dr. Berardelli, further neurophysiologic studies support a more complicated interaction of botulinum toxin in the peripheral and central nervous system.

Dr. Berardelli concluded that BoNT-A has complex mechanisms of action above and beyond the traditional neuromuscular junction. In addition to direct action at the neuromuscular junction, BoNT-A may also alter sensory inputs to the CNS by indirectly inducing secondary changes in the CNS. As we learn more about the intricate interaction of the peripheral and central nervous system and the effect of botulinum toxin treatment it is possible that we will find that some of the long-term clinical benefits of BoNT-A therapy are due to resultant plasticity in the CNS.