Short- and long-latency contributions to reciprocal inhibition during various levels of muscle contraction of individuals with cerebral palsy.
Deficits in reciprocal inhibition likely contribute to excessive antagonist muscle cocontraction during voluntary movements of individuals with cerebral palsy. This study examined neural contributions to reciprocal inhibition of the soleus motoneurons of individuals with spastic, diplegic cerebral palsy and nondisabled individuals during various levels of voluntary tibialis anterior contraction. A condition-test H-reflex paradigm examined short- and long-latency contributions to reciprocal inhibition of soleus neural pools during changing levels of voluntary tibialis anterior contraction. Electrically induced short- and long-latency inhibition was similar between healthy, neurologically intact control subjects and subjects with cerebral palsy during rest. With increasing levels of tibialis anterior contraction, control subjects experienced increasing levels of soleus motoneuron inhibition, especially of long-latency inhibitory responses. In contrast, there was no evidence of modulation of short- or long-latency inhibition with increasing levels of tibialis anterior contraction among subjects with cerebral palsy. Deficits in long-latency (presynaptic) inhibition appear to contribute prominently to voluntary movement impairment of individuals with cerebral palsy.
Leonard
Charles T
CT
Physical Therapy Department, The Motor Control Research Laboratory, The University of Montana, Missoula, MT 59812, USA. charles.leonard@umontana.edu
Sandholdt
Daniel Y
DY
McMillan
James A
JA
Queen
Susan
S
D000328:Adult; D002547:Cerebral Palsy / Q000503:physiopathology*; D004558:Electric Stimulation / Q000379:methods; D004576:Electromyography / Q000379:methods; D006181:H-Reflex / Q000502:physiology; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation / Q000503:physiopathology; D009433:Neural Inhibition / Q000502:physiology; D011930:Reaction Time / Q000502:physiology; D012016:Reference Values; D013997:Time Factors