Proceedings of The Physiological Society
King's College London (2009) Proc Physiol Soc 14, PC6
Frequency domain analysis of abnormal cortical drive in individuals with congential mirror movements
S. F. Farmer1,2, L. M. James2,3, J. A. Stephens3, D. M. Halliday4
1. Institute of Neurology, University College London, London, United Kingdom. 2. Neurology, Imperial College Healthcare NHS Trust, London, United Kingdom. 3. Department of Physiology, University College London, London, United Kingdom. 4. Department of Electronics, University of York, York, United Kingdom.
The mechanisms of congenital mirror movements (MM) are not fully understood. We examined two contrasting hypotheses of MM production using EEG-EMG coherence and partial coherence analysis. Hypothesis 1: MM are produced by the same area of the motor cortex providing via aberrant corticospinal pathways synchronizing drive to the motoneuron pools on left and right sides of the spinal cord during attempted unilateral voluntary muscle activation. Hypothesis 2: during attempted unilateral voluntary activation there is bilateral co-activation of left and right motor cortices and it is this co-activation that produces mirrored EMG activity. We postulated that if a single cortical area is responsible for mirrored EMG activity then use of partial coherence analysis will differentiate this from a scenario in which both motor cortices activate to produce the common descending drive. We studied 6 subjects with congenital MM and 8 normal control subjects. We recorded simultaneously the EEG and right and left 1DI EMGs. During unilateral voluntary contraction in 6 MM subjects coherence was calculated between EEG contralateral to the activated hand and EMGs from the voluntarily activated and the mirroring hand. In MM subjects ~20 Hz coherence and tri-phasic cumulant was present between the motor cortex EEG and both EMGs. Using the mirroring EMG as predictor the partial coherence between the EEG and the activated hand EMG was calculated. In 5/6 MM subjects the partial coherence at ~20 Hz was less than the coherence-indicating that the mirroring EMG receives coherent drive from the ipsilateral motor cortex and that this drive is shared with the voluntary EMG. In 8 controls we calculated EEG-EMG coherence during bilateral activation. In controls the ~20 Hz coherence was detected between the EEG and the contralateral EMG. Calculation of the partial coherence with the ipsilateral EMG as predictor did not show a reduction. No components of the ipsilateral EMG in normals were coherent with the EEG-contralateral EMG correlation. In 4/6 MM subjects during bilateral activation task there was reduction of the EEG-EMG coherence when using the other EMG as predictor. Finally in the MM subjects we calculated EEG-EMG coherence between the EEG contralateral to the voluntarily activated hand with the ipsilateral motor cortex EEG as predictor. In no cases was the coherence reduced. Thus in the MM subjects there was no evidence for abnormal left-right EEG synchronization as a cause of MM. We conclude that the dominant mechanism underlying congenital MM is the delivery of abnormal synchronizing drive from a single area of the motor cortex that projects to the left and right motoneurone pools via contralateral and ipsilateral corticospinal pathways.
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