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StartReact during gait initiation reveals differential control of muscle activation and inhibition in patients with corticospinal degeneration.

Bas J H Van LithMilou J M CoppensJorik NonnekesBart P C van de WarrenburgAlexander C H GeurtsVivian Weerdesteyn
Published in: Journal of neurology (2018)
Corticospinal lesions cause impairments in voluntary motor control. Recent findings suggest that some degree of voluntary control may be taken over by a compensatory pathway involving the reticulospinal tract. In humans, evidence for this notion mainly comes from StartReact studies. StartReact is the acceleration of reaction times by a startling acoustic stimulus (SAS) simultaneously presented with the imperative stimulus. As previous StartReact studies mainly focused on isolated single-joint movements, the question remains whether the reticulospinal tract can also be utilized for controlling whole-body movements. To investigate reticulospinal control, we applied the StartReact paradigm during gait initiation in 12 healthy controls and 12 patients with 'pure' hereditary spastic paraplegia (HSP; i.e., retrograde axonal degeneration of corticospinal tract). Participants performed three consecutive steps in response to an imperative visual stimulus. In 25% of 16 trials a SAS was applied. We determined reaction times of muscle (de)activation, anticipatory postural adjustments (APA) and steps. Without SAS, we observed an overall delay in HSP patients compared to controls. Administration of the SAS accelerated tibialis anterior and rectus femoris onsets in both groups, but more so in HSP patients, resulting in (near-)normal latencies. Soleus offsets were accelerated in controls, but not in HSP patients. The SAS also accelerated APA and step reaction times in both groups, yet these did not normalize in the HSP patients. The reticulospinal tract is able to play a compensatory role in voluntary control of whole-body movements, but seems to lack the capacity to inhibit task-inappropriate muscle activity in patients with corticospinal lesions.
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