The ipsilateral motor cortex does not contribute to long-latency stretch reflex amplitude at the wrist

A capacity for modulating the amplitude of the long-latency stretch reflex (LLSR) allows us to successfully interact with a physical world with a wide range of different mechanical properties. It has recently been demonstrated that stretch reflex modulation is impaired in both arms following monohemispheric stroke, suggesting that reflex regulation may involve structures on both sides of the motor system.

We examined the involvement of both primary motor cortices in healthy reflex regulation by eliciting stretch reflexes during periods of suppression of the motor cortices contra-and ipsilateral to the extensor carpi radialis in the nondominant arm.

LLSRs were significantly attenuated during suppression of the contralateral, but not ipsilateral, motor cortex. Modulation of the LLSR was not affected by suppression of either primary motor cortex.

Our results confirm the involvement of the contralateral motor cortex in the transmission of the LLSR, but suggest that the ipsilateral motor cortex plays no role in reflex transmission and that neither motor cortex is involved in stability-dependent modulation of the LLSR. The implications of these results for reflex impairments following stroke are discussed.