Sensory pathways mediating the neck muscle response in rear-end impacts

The goal of this study was to examine whether the vestibulocollic (VCR) and cervicocollic (CCR) reflexes play a primary or secondary role in the activation of neck muscles to transient perturbations simulating a rear-end collision. To achieve this goal, we exposed subjects to transient surge perturbations and compared the onset and amplitude of their neck muscle responses to the onset and amplitude of their torso and head accelerations. We hypothesized that neck muscle activation times and response amplitudes would correlate to the onset and amplitude of either i) torso acceleration, if the CCR was a primary mediator of the neck muscle response, or ii) head acceleration, if the VCR was a primary mediator of the neck muscle response. Thirty subjects (15F, 15M) underwent 36 consecutive forward horizontal perturbations consisting of three different peak accelerations (7.8, 14.7, and 21.7 m/s2) and three different final velocities (0.25, 0.50, and 0.75 m/s). Onset and amplitude of the sternocleidomastoid (SCM) and cervical paraspinal (PARA) muscle responses were measured using surface electromyography. Onset and amplitude of the torso and head acceleration were measured using accelerometers on the torso (manubrium) and head. Weak correlations between the onset of muscle activation and the onset of both torso and head accelerations suggested that neither the cervicocollic nor vestibulocollic pathways were primarily responsible for activation of the neck muscles. INTRODUCTION o counter the inherent instability of a large head mass atop a multi-articulated neck, reflexes such as the vestibulocollic reflex (VCR), cervicocollic reflex (CCR), and longer-latency polysynaptic reflexes have developed. This actively-controlled system of reflexes manages to balance the competing demands of voluntary head movement and head stability – both in space and relative to the torso – during both familiar body movements and novel perturbations. In addition to the knowledge gained from studying the head/neck system dynamics, insight into the neck neuromusculature has also been gained by studying the onset latencies and amplitude of the human neck muscle responses to transient perturbations in standing, supine and seated postures. In studies of perturbed standing, neck muscles have been observed to activate at or before abdominal muscles (Keshner et T Sensory pathways mediating the neck muscle response in rear-end impacts al., 1988). Although this deviation from a sequential upward muscle activation pattern could suggest that the VCR triggered the neck muscle response (Woollacott et al., 1988), a comparison between normal and avestibular subjects demonstrated only minor differences in neck muscle onset latencies and response amplitudes (Keshner et al., 1988) and thus indicated that the VCR was not primarily responsible for neck muscle activation in perturbed standing. During head drop tests in supine subjects, short onset latencies (24 ± 3 ms after onset of head acceleration) were observed in the sternocleidomastoid (SCM) muscles of normal subjects, whereas longer onset latencies (67 ± 7 ms) were observed in avestibular subjects (Ito et al., 1995, 1997; Bisdorff et al., 1999). These studies showed that the VCR could activate neck muscles at very short latencies. The longer onset latencies observed in the avestibular subjects, however, were still about 40 ms shorter than voluntary SCM activation times (Mazzini and Schieppati, 1992; Siegmund, 2001). This suggested that other reflexive pathways, possibly polysynaptic in nature, also mediate neck muscle activation. In seated subjects exposed to transient perturbations, Gresty (1989) reported bursts of neck muscle activity 25 to 50 ms after torso acceleration onset during surge perturbations and Kanaya et al. (1995) reported onset of neck muscle activity as short as 25 ms after onset of angular head acceleration in two of seven subjects exposed to pitch perturbations. Various other groups have reported neck muscle activation times of 69 to 82 ms in seated subjects during surge perturbations (Forssberg and Hirschfeld, 1994; Brault et al., 2000; Vibert et al., 2001; Siegmund et al., 2002), although these latencies were reported relative to platform motion and thus likely overestimated the time between mechanoreceptor stimulation and neck muscle activation. Based on similarly short neck muscle onset latencies in seated normal and avestibular subjects exposed to transient surge perturbations, Gresty (1989) concluded that the neck muscle response was mediated by the CCR rather than the VCR. Using consecutive transient pitch and surge perturbations, Forssberg and Hirschfeld (1994) also excluded a major vestibular component to the postural response of the neck muscles, but rather than the CCR, these researchers suggested that pelvic rotation relative to the support surface triggered the neck muscle response. Based on a shortening of the sternocleidomastoid muscle during their pitch perturbations, Kanaya et al. (1995) eliminated a homonymous stretch reflex as a likely trigger for neck muscle activation. Instead, these authors concluded that the neck muscle response was likely mediated by the VCR in normal subjects, and by an unloading response or trunk-based mechanoreceptors in avestibular patients. These perturbation studies in standing, supine, and seated postures have shown that the VCR can operate quick enough to trigger the observed neck muscle responses, though it apparently does not do so under all circumstances. When the perturbation is isolated to the head (e.g., head drop tests), the VCR plays a dominant role in triggering the muscle response; whereas, under other circumstances (e.g., standing or seated perturbations), the VCR appears to be less consistent. To further examine whether the VCR and CCR play a primary or secondary role in the activation of neck muscle responses to transient perturbations, we compared the onset and amplitude of neck muscle responses to the onset and amplitude of the torso and head accelerations in subjects exposed to transient surge perturbations. To generate the necessary stimulusresponse data, seated subjects were exposed to abrupt transient surge perturbations of different accelerations and velocities. It was hypothesized that neck muscle activation times and response amplitudes would correlate to the onset and amplitude of either i) torso acceleration if the CCR was a primary mediator of the neck muscle response, or ii) head acceleration if the VCR was a primary mediator of the neck muscle response.