Failure of normal development of central drive to ankle dorsiflexors relates to gait deficits in children with cerebral palsy
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Failure of normal development of central drive to ankle dorsiflexors relates to gait deficits in children with cerebral palsy. / Petersen, Tue Hvass; Farmer, Simon F; Kliim-Due, Mette; Nielsen, Jens Bo.
In: Journal of Neurophysiology, Vol. 109, No. 3, 2013, p. 625-639.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Failure of normal development of central drive to ankle dorsiflexors relates to gait deficits in children with cerebral palsy
AU - Petersen, Tue Hvass
AU - Farmer, Simon F
AU - Kliim-Due, Mette
AU - Nielsen, Jens Bo
N1 - CURIS 2013 NEXS 010
PY - 2013
Y1 - 2013
N2 - Neurophysiological markers of the central control of gait in children with cerebral palsy (CP) are used to assess developmental response to therapy. Here we measure the central common drive to a leg muscle in children with CP. We recorded EMGs from the Tibialis Anterior (TA) muscle of 40 children with hemiplegic CP and 42 typically-developing age-matched controls during static dorsiflexion of the ankle and during the swing phase of treadmill walking. The common drive to TA motoneurones was identified through time and frequency domain cross-correlation methods. In control subjects, the common drive consists of frequencies between 1 and 60 Hz with peaks at beta (15-25 Hz) and gamma (30-45 Hz) frequencies known to be caused by activity within sensori-motor cortex networks: this drive to motoneurones strengthens during childhood. Similar to control subjects, this drive to the least affected TA in the CP children tended to strengthen with age, although compared to the control subjects it was slightly weaker. For CP subjects' of all ages the most affected TA muscle common drive was markedly reduced compared both to their least affected muscle and to controls. These differences between the least and most affected TA muscles were unrelated to differences in the magnitude of EMG in the two muscles but positively correlated with ankle dorsiflexion velocity and joint angle during gait. Time and frequency domain analysis of on-going EMG recruited during behaviourally relevant lower limb tasks provides a non-invasive and important measure of the central drive to motoneurones in subjects with CP.
AB - Neurophysiological markers of the central control of gait in children with cerebral palsy (CP) are used to assess developmental response to therapy. Here we measure the central common drive to a leg muscle in children with CP. We recorded EMGs from the Tibialis Anterior (TA) muscle of 40 children with hemiplegic CP and 42 typically-developing age-matched controls during static dorsiflexion of the ankle and during the swing phase of treadmill walking. The common drive to TA motoneurones was identified through time and frequency domain cross-correlation methods. In control subjects, the common drive consists of frequencies between 1 and 60 Hz with peaks at beta (15-25 Hz) and gamma (30-45 Hz) frequencies known to be caused by activity within sensori-motor cortex networks: this drive to motoneurones strengthens during childhood. Similar to control subjects, this drive to the least affected TA in the CP children tended to strengthen with age, although compared to the control subjects it was slightly weaker. For CP subjects' of all ages the most affected TA muscle common drive was markedly reduced compared both to their least affected muscle and to controls. These differences between the least and most affected TA muscles were unrelated to differences in the magnitude of EMG in the two muscles but positively correlated with ankle dorsiflexion velocity and joint angle during gait. Time and frequency domain analysis of on-going EMG recruited during behaviourally relevant lower limb tasks provides a non-invasive and important measure of the central drive to motoneurones in subjects with CP.
U2 - 10.1152/jn.00218.2012
DO - 10.1152/jn.00218.2012
M3 - Journal article
C2 - 23136346
VL - 109
SP - 625
EP - 639
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 3
ER -
ID: 41828751