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Non-invasive Assessment of Changes in Corticomotoneuronal Transmission in Humans
Published on: May 24, 2017
H-reflex modulations during voluntary and automatic movements following upper motor neuron damage
C T Leonard1, P M Diedrich, T Matsumoto
1Physical Therapy Department, The University of Montana, Missoula 59812, USA.
Electroencephalography and Clinical Neurophysiology
|February 25, 1999
Summary
Individuals with upper motor neuron (UMN) syndrome experience impaired voluntary movement and postural responses. This study found a lack of reflex inhibition in these individuals, suggesting neural pathway deficits contribute to movement impairments.
Area of Science:
- Neuroscience
- Motor Control
- Neurology
Background:
- Spasticity, often resulting from upper motor neuron (UMN) syndrome, affects both voluntary movement and automatic postural responses.
- The underlying neural mechanisms responsible for these dual impairments are not fully understood.
Purpose of the Study:
- To investigate whether shared mechanisms underlie the deficits in voluntary movement and postural responses in individuals with UMN syndrome.
- To examine soleus H-reflex changes during voluntary and automatic postural tasks in individuals with and without UMN involvement.
Main Methods:
- The study involved 22 participants: 12 non-disabled, 4 with spastic-type cerebral palsy, and 6 with adult-onset cerebral vascular accident.
- Changes in soleus H-reflexes were measured during voluntary tibialis anterior (TA) muscle contraction and during postural perturbations.
- Data were analyzed using ANOVAs and Tukey HSD tests to compare H-reflex amplitude changes relative to TA activation onset.
Main Results:
- Individuals with UMN involvement showed no inhibition of soleus H-reflexes during voluntary TA activation.
- This lack of inhibition was also observed during automatic postural perturbations, irrespective of TA activation level.
Conclusions:
- Damage to the upper motor neuron pathways impairs both volitional movements and postural reflexes.
- Deficits in neural pathways responsible for reciprocal inhibition are implicated in the motor impairments seen in UMN syndrome.
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