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DOI 10.1016/j.clinph.2012.01.006

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2012

Coactivation of ankle muscles during stance phase of gait in patients with lower limb hypertonia after acquired brain injury.

Chow John W, Yablon Stuart A, Stokic Dobrivoje S

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

OBJECTIVE

Examine (1) coactivation between tibialis anterior (TA) and medial gastrocnemius (MG) muscles during stance phase of gait in patients with moderate-to-severe resting hypertonia after stroke or traumatic brain injury (TBI) and (2) the relationship between coactivation and stretch velocity-dependent increase in MG activity.

METHODS

Gait and surface EMG were recorded from patients with stroke or TBI (11 each) and corresponding healthy controls (n=11) to determine the magnitude and duration of TA-MG coactivation. The frequency and gain of positive (>0) and significant positive (p<0.05) EMG-lengthening velocity (EMG-LV) slope in MG were related to coactivation parameters.

RESULTS

The magnitude of coactivation was increased on the more-affected (MA) side, whereas the duration was prolonged on the less-affected (LA) side of both stroke and TBI patients. The difference reached significance during the initial and late double support. The magnitude of coactivation positively correlated with the gain of significant positive EMG-LV slope in TBI patients.

CONCLUSIONS

Increased coactivation between TA and MG during initial and late double support is a unique feature of gait in stroke and TBI patients with muscle hypertonia.

SIGNIFICANCE: Increased coactivation may represent an adaptation to compensate for impaired stability during step transition after stroke and TBI.

Для цитирования: Chow John W, Yablon Stuart A, Stokic Dobrivoje S. Coactivation of ankle muscles during stance phase of gait in patients with lower limb hypertonia after acquired brain injury.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2012. DOI: 10.1016/j.clinph.2012.01.006.

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