Abstract
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.
Highlights
Therapy with botulinum toxin type A (BoNT-A) is currently used in a wide range of medical conditions, including disorders characterised by muscle hyperactivity
These changes were observed in various forms of focal dystonia, including cervical dystonia, blepharospasm, and writer’s cramp, suggesting more global abnormalities in the processes mediating the long-term potentiation (LTP)-like and long-term depression (LTD)-like plasticity [56,57]
Spasticity was associated with decreased somatosensory evoked potentials (SEP) amplitude that increased after treatment, which is quite opposite to the effect reported in dystonia [39]
Summary
Therapy with botulinum toxin type A (BoNT-A) is currently used in a wide range of medical conditions, including disorders characterised by muscle hyperactivity. Reduced excitability of the spinal pathways indirectly modulates supraspinal motor control centres including the sensorimotor cortex [11] This is the presumed mechanism for how BoNT-A injected in the periphery may induce cortical reorganization [11]. It has been proposed that some of the clinical BoNT-A effects could be mediated (indirectly) by central structures [10,11,12] They are distinct conditions, dystonia and spasticity share common features such as involuntary movements, spasms, abnormal posturing and impaired movement performance resulting from muscle hyperactivity and co-contractions. We review evidence for the central effects of BoNT-A in dystonia and spasticity from both electrophysiology and functional neuroimaging studies, in an attempt to provide a comprehensive overview of the mechanisms triggered by BoNT-A that may possibly mediate its clinical effect. Positron emission tomography, SMA—supplementary motor area, TMS—transcranial magnetic stimulation
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