Loud acoustic stimulation reveals an online reticulospinal contribution to long-latency reflexes in humans

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Abstract

The long-latency reflex (LLR), the fastest feedback response that recruits supraspinal pathways, is an important model for understanding how descending motor pathways shape rapid corrective responses in humans. While the corticospinal tract’s contribution to the LLR has been well established, that of the reticulospinal tract, the other major descending motor pathway, remains purely speculative. To address this online contribution to the generation of the LLR, we used loud acoustic stimulation (LAS), which can strongly engage brainstem circuits including the pontomedullary reticular formation. By delivering LAS at nine timings (0–80 ms in 10-ms steps) relative to perturbation onset, we tested whether LAS selectively facilitates the LLR but not the short-latency reflex (SLR), and whether the facilitated epoch shifts systematically with LAS timing. In twelve healthy participants, elbow extension perturbations were applied to evoke stretch reflexes in the biceps brachii muscle. LAS produced significant supralinear facilitation in the LLR but not in the SLR. Moreover, at LAS timings of 50 ms or more after perturbation onset, LLR facilitation shifted progressively later with LAS, remaining at an approximately fixed delay of 30 ms after LAS onset. This fixed delay indicates that LAS-evoked descending input from the same origin facilitates the ongoing LLR. Together with the lack of significant SLR facilitation, this temporal pattern supports an online reticulospinal contribution to the human LLR, alongside the established corticospinal contribution. This approach provides a new, non-invasive means to investigate the physiological role of the reticulospinal tract in human motor control.

Key Points

  • The long-latency reflex is a rapid muscle response to sudden stretch. Unlike faster spinal reflexes, it is shaped by commands descending from the brain and adjusts to the task.

  • Though the corticospinal tract is known to shape this reflex, whether the reticulospinal tract also contributes to the reflex has not been tested in humans.

  • We stretched the arm and, at various delays, played a loud sound that engages the brainstem origin of the reticulospinal tract. The sound significantly enhanced the long-latency reflex, whereas no significant enhancement was detected in the faster spinal reflex.

  • When the sound came 50 milliseconds or more after the stretch, the enhancement followed the sound at a stable delay, indicating that sound-evoked descending signals interacted with the ongoing reflex response.

  • These findings support a real-time contribution of the reticulospinal tract to the human long-latency reflex and provide a non-invasive way to study this pathway.

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