H-reflex modulations during voluntary and automatic movements following upper motor neuron damage.
OBJECTIVE
It is not known whether similar mechanisms account for the impairments of voluntary movement and automatic postural responses of individuals with spasticity secondary to damage to the sensorimotor cortex and its projections (i.e. upper motor neuron syndrome (UMN)).


METHODS
The present study examined changes in soleus H-reflexes preceding and during voluntary tibialis anterior (TA) muscle contraction of standing subjects and during balance platform induced postural perturbations that elicited similar TA muscle contractions. Twenty-two subjects (12 non-disabled; 4 with spastic-type cerebral palsy; 6 with adult-onset cerebral vascular accident) participated in the study. Data were analyzed using ANOVAs and Tukey HSD post-hoc comparison tests to assess the timing and magnitude of soleus H-reflex amplitude changes relative to the onset of TA muscle activation.


RESULTS
Results indicated that, regardless of the level of TA activation, soleus H-reflexes of subjects with UMN involvement did not demonstrate inhibition either. during voluntary movements or during automatic postural perturbations.


CONCLUSIONS
These findings indicate that postural reflexes, as well as volitional movements, are impaired following UMN damage and that deficits in neural pathways subserving reciprocal inhibition contribute to the impairments.
Leonard
C T
CT
Physical Therapy Department, The University of Montana, Missoula 59812, USA.
Diedrich
P M
PM
Matsumoto
T
T
Moritani
T
T
McMillan
J A
JA
D000328:Adult; D000368:Aged; D002547:Cerebral Palsy / Q000150:complications / Q000503:physiopathology*; D002561:Cerebrovascular Disorders / Q000503:physiopathology*; D004576:Electromyography; D005260:Female; D006181:H-Reflex / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology*; D009068:Movement / Q000502:physiology*; D009128:Muscle Spasticity / Q000150:complications / Q000503:physiopathology*; D011930:Reaction Time / Q000502:physiology