The time course of changes in motor cortex excitability associated with voluntary movement

Citation
R. Chen et M. Hallett, The time course of changes in motor cortex excitability associated with voluntary movement, CAN J NEUR, 26(3), 1999, pp. 163-169
Citations number
80
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES
ISSN journal
03171671 → ACNP
Volume
26
Issue
3
Year of publication
1999
Pages
163 - 169
Database
ISI
SICI code
0317-1671(199908)26:3<163:TTCOCI>2.0.ZU;2-J
Abstract
The excitability of the motor cortex is modulated before and after voluntar y movements. Transcranial magnetic stimulation studies showed increased cor ticospinal excitability from about 80 and 100 ms before EMG onset for simpl e reaction time and self-paced movements, respectively. Following voluntary movements, there are two phases of increased corticospinal excitability fr om 0 to approximately 100 ms and from approximately 100 to 160 ms after EMG offset. The first phase may correspond to the frontal peak of motor potent ial in movement-related cortical potentials studies and the movement-evoked magnetic field I (MEFI) in magnetoencephalographic (MEG) studies, and like ly represents a time when decreasing output from the motor cortex falls bel ow that required for activation of spinal motoneurons, but is still above r esting levels. The second phase of increased corticospinal excitability may be due to peripheral proprioceptive inputs or may be centrally programmed representing a subthreshold, second agonist burst. This may correspond to t he MEFII in MEG studies. Corticospinal excitability was reduced below basel ine levels from about 500 to 1,000 ms after EMG offset, similar to the timi ng of increase in the power (event-related synchronization, ERS) of motor c ortical rhythm. Similarly, motor cortex excitability is reduced at the time of ERS of motor cortical rhythm following median nerve stimulation. These findings support the hypothesis that ERS represents an inactive, idling sta te of the cortex. The time course of cortical activation is abnormal in mov ement disorders such as Parkinson's disease and dystonia, reflecting abnorm alities in both movement preparation and in cortical excitability following movement.