In dystonic and spastic movement disorders, however different in their pathophysiological mechanisms, a similar impairment of sensorimotor control with special emphasis on afferentation is assumed. Peripheral intervention on afferent inputs evokes plastic changes within the central sensorimotor system. Intramuscular application of botulinum toxin type A (BoNT-A) is a standard evidence-based treatment for both conditions. Apart from its peripheral action on muscle spindles, a growing body of evidence suggests that BoNT-A effects could also be mediated by changes at the central level including cerebral cortex. We review recent studies employing electrophysiology and neuroimaging to investigate how intramuscular application of BoNT-A influences cortical reorganization. Based on such data, BoNT-A becomes gradually accepted as a promising tool to correct the maladaptive plastic changes within the sensorimotor cortex. In summary, electrophysiology and especially neuroimaging studies with BoNT-A further our understanding of pathophysiology underlying dystonic and spastic movement disorders and may consequently help develop novel treatment strategies based on neural plasticity.

• Keywords
• botulinum toxin, dystonia, electrophysiology, functional magnetic resonance imaging, neural plasticity, spasticity,
• MeSH
• Botulinum Toxins, Type A adverse effects   therapeutic use   MeSH
• Dystonia diagnosis   drug therapy   physiopathology   MeSH
• Muscle, Skeletal innervation   MeSH
• Humans MeSH
• Magnetic Resonance Imaging MeSH
• Brain Mapping MeSH
• Cerebral Cortex diagnostic imaging   drug effects   physiopathology   MeSH
• Neuromuscular Agents adverse effects   therapeutic use   MeSH
• Neuronal Plasticity drug effects   MeSH
• Recovery of Function MeSH
• Motor Activity drug effects   MeSH
• Treatment Outcome MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Botulinum Toxins, Type A MeSH
• Neuromuscular Agents MeSH