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The Journal of Neurophysiology Vol. 85 No. 5 May 2001, pp. 1858-1863
Copyright ©2001 by the American Physiological Society
1Department of Neurology, 2Department of Nuclear Medicine, and 3Division of Neuroradiology, Klinikum Rechts der Isar der Technischen Universität München, 81675 Munich, Germany
Weilke, Florian,
Sabine Spiegel,
Henning Boecker,
Helga Gräfin von
Einsiedel,
Bastian Conrad,
Markus Schwaiger, and
Peter Erhard.
Time-Resolved fMRI of Activation Patterns in M1 and SMA During
Complex Voluntary Movement. J. Neurophysiol. 85: 1858-1863, 2001. The aim of this study was to use
time-resolved functional magnetic resonance imaging (fMRI) to
investigate temporal differences in the activation of the supplementary
motor area (SMA) and the primary motor cortex (M1). We report data from
eight human volunteers who underwent fMRI examinations in a 1.5T
Philips Gyroscan ACS-NT MRI scanner. While wearing a contact glove,
subjects executed a complex automated sequence of finger movements
either spontaneously or in response to external auditory cues. Based on
the result of a functional scout scan, a single slice that included the
M1 and the SMA was selected for image acquisition (echo planar imaging, repetition time 100 ms, echo time 50 ms, 64 × 64 matrix,
1,000 images). Data were analyzed with a shifting cross-correlation approach using the STIMULATE program and in-house programs
written in Interactive Data Language (IDLTM). Time-course data
were generated for regions of interest in the M1 as well as in the
rostral and caudal SMA. Mean time between onset of the finger movement
sequence and half-maximum of the signal change in M1 was 3.6 s for
the externally cued execution (SD 0.5) and 3.5 s for the
spontaneous execution (SD 0.6). Activation in the rostral section of
the SMA occurred 0.7 s earlier than it did in the M1 during the
externally cued execution and 2.0 s earlier during the spontaneous
execution, a difference significant at the P < 0.01 level. Our results indicate that rostral SMA activation precedes
M1 activation by varying time intervals in the sub-second range that
are determined by the mode of movement initialization. By applying a
paradigm that exerts a differential influence on temporal activation,
we could ensure that the observed timing differences were not the
result of differences in hemodynamic response function.
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