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Using acoustic stimuli to inhibit the startle response triggered by whiplash collisions : implications.. Mang, Daniel 2010

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 USING ACOUSTIC STIMULI TO INHIBIT THE STARTLE RESPONSE TRIGGERED BY WHIPLASH COLLISIONS: IMPLICATIONS FOR INJURY PREVENTION  by  DANIEL MANG  B.Sc, Boston University, 2007    A THESIS SUBMITED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE DEGRE OF  MASTER OF SCIENCE  in  THE FACULTY OF GRADUATE STUDIES (Human Kinetics)   THE UNIVERSITY OF BRITISH COLUMBIA (Vancouver)      April 2010  © Daniel Mang, 2010   ii Abstract Introduction: In British Columbia, whiplash injuries and its asociated disorders are serious economical and social burdens to society. Despite afecting les than 1 percent of the population, whiplash injuries costs of over 850 milion dollars annualy (ICBC 2007). In recent studies, the startle response was shown to form part of the neuromuscular response to whiplash-like perturbations (Blouin et al. 2006a and b). In non-whiplash experiments, a weak or startling pre-stimulus tone presented before a subsequent startling stimulus can inhibit the startle response (Ison and Krauter 1974; Vals-Sole et al. 2005). The objective of the present study was to investigate how diferent pre-stimulus tones (weak and startling) afected the amplitude of muscle responses and the peak magnitude of head kinematics observed in human volunters during whiplash-like perturbations. Methods: Twenty healthy subjects experienced five consecutive whiplash-like perturbations presented simultaneously with a loud collision sound (109 decibels (dB). The thre experimental conditions difered with the intensity of pre-stimuli tone presented 250 miliseconds prior to the onset of the perturbation: 1.) no pre-stimulus tone (Control), 2.) a weak pre-stimulus tone (85dB) and 3.) a startling pre-stimulus tone (105dB). Electromyography (EMG) of neck and distal limb muscles, and kinematics of the head and trunk were simultaneously collected. Mixed model ANOVAs and post-hoc Tukey’s honest significant diference test were used to analyze each EMG and kinematic variable (alpha=0.05).   iii Results: Presenting a startling pre-stimulus tone before the whiplash-like perturbation decreased muscular (sternocleidomastoid: !16%, C4 paraspinal: !26%, biceps brachii: !66%, triceps brachii: !62%, first dorsal interosseous: !68%, and rectus femoris: 78%) and kinematic (peak retraction: !17%, peak horizontal aceleration of the head: !23%, and peak head angular aceleration in extension: !23%) responses from Control condition (p<0.05). A weak pre-stimulus tone decreased only the muscular responses of triceps brachii (!38%), first dorsal interosseous (!48%) and rectus femoris (!57%) from Control condition (p<0.01). Conclusion: A startling tone presented prior to a whiplash-like perturbation alters the head-neck responses in ways that are consistent with reducing neck tisue strains. This study is an initial step in the development of preventive devices to decrease the whiplash injury potential during low-speed, rear-end automotive collisions.    iv Table of Contents Abstract .........................................................................................................................ii!Table of Contents.........................................................................................................iv!List of!List of Figures..............................................................................................................vii!Acknowledgements.....................................................................................................vii!1!Literature Review....................................................................................................1!1.1!Epidemiology.....................................................................................................1!1.2!Whiplash Injury Mechanism to the Zygapophysial Joint...............................3!1.3!Low-Velocity Human Volunter Whiplash Experiments................................7!1.3.1!Biomechanics and Kinematics of Whiplash-Like Perturbations...................................7!1.3.2!Electromyography of Muscle Responses during Whiplash-Like Perturbation.............8!1.3.3!Factors Affecting the Human Response to Whiplash-Like Perturbations...................10!1.4!Startle Response..............................................................................................12!1.4.1!The Neurophysiology of the Startle Response..............................................................13!1.4.2!The Neurophysiology of Whiplash Colisions..............................................................14!1.4.3!Atenuation of Neck Muscle Activity: Habituation of a Startle Response?................17!1.4.4!Prepulse and Paired-Pulse Inhibition of the Startle Response.....................................20!1.4.5!Prepulse and Paired-Pulse Inhibition in Human Volunteers........................................23!2!Objective and Hypotheses.....................................................................................26!2.1!Rationale..........................................................................................................26!2.2!Hypotheses.......................................................................................................27   v  3!Methods.................................................................................................................28!3.1!Subjects...........................................................................................................28!3.2!Instrumentation..............................................................................................28!3.2.1!Electromyography...........................................................................................................28!3.2.2!Kinematics.......................................................................................................................29!3.3!Test Procedure................................................................................................30!3.4!Reference Frames............................................................................................34!3.5!Data Analysis...................................................................................................35!3.6!Statistical Analysis..........................................................................................37!4!Results....................................................................................................................38!5!Discusion..............................................................................................................45!6!Conclusion.............................................................................................................55!References....................................................................................................................56!Appendices...................................................................................................................69!Appendix A: Graphical Figures of Individual Subject Data.................................69!Appendix B: Research Ethics Board Certification of Approval............................90!   vi List of Tables Table 4.1   Mean (SD) of normalized RMS amplitudes and onsets of EMG for Control, WK-PREP and ST-PREP conditions...............................41 Table 4.2   Mean (SD) of the initial head angle, onsets of head movement, peak linear and angular kinematics for Control, WK-PREP and ST-PREP conditions....................................................42 Table 5.1   Comparison between habituation and pre-stimulus inhibition experiments during repeated whiplash-like perturbations..................47   vii List of Figures Figure 1.1   Ilustration of the zygapophysial joint....................................................3 Figure 1.2  Schematic drawings ilustrating atachment sites of the cervical multifidus.............................................................................6 Figure 1.3  Neural circuit for acoustic, vestibular and trigeminal startle responses...................................................................14 Figure 1.4  Estimated averaged coherence between left and right SCM muscles recorded during exposure to  1.8 km/h forward perturbation.............................................................19 Figure 1.5  Comparison of paired-pulse inhibition on the startle response in rats at various inter-stimulus intervals.............................................22 Figure 3.1  Photographs of experimental set up of the car seat  on the moving platform.........................................................................30 Figure 3.2  A sample of the acceleration profile used to simulate rear-end whiplash-like perturbations...................................................32 Figure 4.1  Sample muscular and kinematic responses from a single subject for Control, WK-PREP, and ST-PREP conditions..............................40 Figure 4.2  Group means and standard deviations of muscular responses for Control, WK-PREP, and ST-PREP conditions..............................43 Figure 4.3   Group means and standard deviations of head kinematic responses for Control, WK-PREP, and ST-PREP conditions.............44   vii Acknowledgements I would like to expres my sincerest gratitude to my supervisors, Drs. Jean-Sebastien Blouin and Gunter Siegmund, for their continued support throughout the duration of the Master of Science (MSc) program. Without their vision, guidance, and enthusiasm, this thesis would not have been possible.  Throughout the writing period of my thesis, they helped me with my writing technique, provided encouragement, and most of al, were patient with the gradual learning proces. To the both of you, thank you for always having your doors open to answer questions, providing the fredom to grow as an independent researcher and making my MSc thesis a memorable experience. I would also like to thank my commite member Dr. Tim Inglis, for his humourous, yet insightful, comments and questions. Thank you once again for al your vast knowledge and asistance at al levels of this thesis project. Thank you to Mr. Jef Nickel and Mr. Mircea Oala-Florescu of MEA Forensic Engineers and Scientist for helping me operate, maintain and modify the perturbation sled used in this experiment. I would also like to thank my friends, felow graduate students and colleagues in the Sensorimotor Physiology Laboratory for their patience, words of encouragement and wilingnes to be subjects in my experiment. Lastly, I would like to thank my family for the support they provided me through my entire life. This acomplishment was only possible because of the many opportunities you provided me.1  1 Literature Review 1.1 Epidemiology  Whiplash injuries are the most common type of injuries in motor vehicle acidents and rear-end collisions pose the greatest risk of whiplash injury at 48% compared to frontal (20%) and side (14%) collisions (Jakobsson et al. 2000; ICBC 2006; ICBC 2007). Whiplash injuries acount for approximately 70% of al injury claims reported by the Insurance Corporation of British Columbia (ICBC) (ICBC 2000). In 2000, ICBC paid out over $500 milion—50% of al injury payouts—for whiplash injuries and whiplash-asociated disorders (WAD). Half of the money paid for medical treatment and the other half covered the lost wages and diminished earning capacity of drivers and occupants injured (ICBC 2000). In 2006, the estimated cost of whiplash injuries and WAD (excluding litigation costs) increased to approximately $850 milion (ICBC 2007).  The annual incidence of WAD in the western world ranges from 28 to 834 per 100,000 inhabitants (Otremski et al. 1989; Casidy et al. 2000; Holm et al. 2008). Women are 1.2 to 3 times more likely to suffer from whiplash injuries after a rear-end car collision as compared to men (Harder et al. 1998; Verstegen et al. 2000; Mordaka and Gentle 2003). Females between the ages 20 to 24 present the highest incidence rate of reported WAD with 965 cases per 100,000 people annualy (Quinlan et al. 2004). The greater susceptibility of younger females is hypothesized to be related to the gender diferences in anatomical, physiological, behavioural and sociological parameters 2  (Mordaka and Gentle 2003) as wel as the influence of seat properties on neck biomechanics and occupant dynamics (Viano 2003b). The whiplash injury, WADs and recovery times folowing whiplash collisions are greatly variable and depend on factors such as impact severity, seat position and stifnes, and subject initial posture (Suisa et al. 2001; Viano 2003a). The most common symptoms following whiplash injuries are neck pain (88-100% of patients) and headaches (54-66% of patients) (Todman 2007). Other symptoms of whiplash injuries include dizines, auditory symptoms (tinnitus – perceived ringing noise in the ears), paresthesias in the upper extremities, and back pain (Evans 1992; Spitzer et al. 1995; Mordaka and Gentle 2003; Sterner and Gerdle 2004). The recovery time from whiplash injuries depends on the initial whiplash injury severity, but 26% of subjects recover within the first week and the median recovery time is approximately 32 days (Suisa et al. 2001). However, 12% of patients do not fully recover within six months (Suisa et al. 2001) and 5 to 8% of patients do not return to work within a year following the acident (Evans et al. 2001; Buitenhuis et al. 2009). Between 14 and 42% of individuals develop chronic neck pain and approximately 10% are left with permanent severe pain and disability (Barnsley et al. 1994). Due to the high cost per claim in British Columbia (les than 1 percent of the population valuing over 850 milion dollars) and the persistence of chronic symptoms of whiplash injuries and its asociated disorders, these injuries are a serious economical and social burden to society. Therefore, it is important to reduce the risk and number of whiplash injury per year. 3  1.2 Whiplash Injury Mechanism to the Zygapophysial Joint Although the exact aetiology of whiplash remains unclear, the cervical zygapophysial joints have been identified as a possible source for pain (Barnsley et al. 1995). In a double-blind clinical study, the cervical zygapophysial joint was the most common source of neck pain in approximately 40-68% of patients with whiplash injuries (Barnsley et al. 1995). The cervical zygapophysial joints (or cervical facet joints) are located between each pair of cervical vertebrae from C2 – C7. This joint is clasified as a synovial joint because it is enclosed by a thin capsular ligament, or facet joint capsule, which is lined by a synovial membrane as ilustrated in Figure 1.1. Fibro-adipose meniscoids or synovial folds, are found between the articular facets and function to Figure 1.1 Ilustration of the zygapophysial joint. Reprinted with permision from (Yoganandan et al. 201) 4  protect the articular cartilages during normal movement of the zygapophysial joint (Mercer and Bogduk 1993). The capsular ligament is innervated by both mechanoreceptors and nociceptors providing neural inputs responsible for proprioception and pain sensations, respectively (Wyke 1972; Wyke 1979; McLain 1994; Inami et al. 2000; Inami et al. 2001; Azar et al. 2009). The facet joints and capsular ligaments provide axial rotational, segmental shear strength and lateral bending stability, but contribute litle to flexion-extension stability of the cervical spine (Raynor et al. 1985; Onan et al. 1998).  Kinematics of the facets joints and capsular ligaments during simulated whiplash-like perturbations have been observed in human cadaver experiments (Yoganandan et al. 1998; Winkelstein and Myers 2000; Pearson et al. 2004; Stemper et al. 2005) and volunter studies (Kaneoka et al. 1999). As a result, two mechanisms of injury to the cervical zygapophysial joint have been proposed: pinching of the synovial fold and excesive strain to the facet capsule. The sudden flexion and extension of the neck following a rear-end impact causes abnormal motions of the cervical spine and zygapophysial joints (Kaneoka et al. 1999; Luan et al. 2000). Kaneoka et al. (1999) observed that whiplash motion may shift the instantaneous axis of rotation (IAR) of the cervical vertebra bodies superior causing the posterior facet surfaces to compres together and pinch of the synovial fold (Kaneoka et al. 1999). Consequently, nociceptive fibers found in the synovial fold may be inflamed and could be a possible source of cervical zygapophysial joint pain. 5  The second possible injury mechanism to the zygapophysial joint is excesive strain to the capsular joint ligament during whiplash motion. Failure testing of the joint capsules has determined mean maximum capsular strain at sub-catastrophic and catastrophic failure threshold to be between 35–65% and 94–104%, respectively (Winkelstein et al. 2000; Siegmund et al. 2001). Pearson et al. (2004) observed capsular ligament strains in the sub-catastrophic range at whiplash-like perturbation acelerations of 6.5 g measure at the thoracic vertebrae T1 and were largest in the lower cervical spine (C6-C7: 39.9%). Peak capsular ligament strains were determined to occur between 200 to 225 ms after the onset of thoracic vertebrae T1 aceleration  (Pearson et al. 2004). During whiplash motions, activation of the cervical multifidi spinae muscle coincided with the timing of peak capsular ligament strain and, in about half the subjects (55.6%), the muscle activity was greater than their recorded maximum voluntary contraction (MVC) level (Siegmund et al. 2008a). The cervical multifidi muscles, part of the transversospinal muscle group, insert directly on the cervical capsular ligaments and can be divided into two layers based on their atachment locations: superficial and deep fascicles as shown in Figure 1.2. (Anderson et al. 2005). Both the superficial and deep fascicles span two to five vertebral levels in length but difer in their sites of origin and insertion (Malanga and Nadler 2002; Anderson et al. 2005). Most fascicles of the superficial cervical layer originate directly from the lateral to posterolateral aspect of the cervical facet capsules of C4-C7 to insert on the spinous proces of the superior vertebrae. Whereas, most of the deep cervical fascicles originate from the cervical facet capsule, more posterior and medial than the superficial layers to insert on the laminae of superior vertebrae. The forces generated by the multifidi during whiplash collisions will 6  cause the muscle to pull directly on the cervical facet capsular ligament. Increased muscle activity may occur at a moment when the ligament is vulnerable and exacerbate peak strain on the capsular ligament (Winkelstein et al. 2000; Siegmund et al. 2001; Siegmund et al. 2008a). In some subjects, the peak capsular ligament strain may be increased into the sub-catastrophic failure range and result in whiplash injury.    Figure 1.2 Schematic drawings ilustrating atachment sites of thre fascicular subgroups for a.) superficial cervical multifidus and b.) dep cervical multifidus. Reprinted with permision from (Anderson et al. 205). 7  1.3 Low-Velocity Human Volunter Whiplash Experiments 1.3.1 Biomechanics and Kinematics of Whiplash-Like Perturbations The biomechanics of human subjects during a low-speed rear-end collision are quite variable and depend on the magnitude and shape of the aceleration pulse, seat back properties (stifnes and angle) and subject’s initial posture. The biomechanical movements of the torso, head and neck can be divided into two phases to help understand whiplash injuries: retraction and rebound phases (Brault et al. 2000; Pearson et al. 2004; Vasavada et al. 2007). The retraction phase is defined from onset of head movement to peak head retraction; whereas, the rebound phase is defined from peak head retraction to peak forward head extension relative to the torso. During the retraction phase, the torso is acelerated faster than the head in the horizontal direction and causes the head to lag behind the torso (McConnel et al. 1995; Luan et al. 2000). The forward aceleration causes the torso to ramp up against the seat back compresing the cervical spine. As a consequence of the shear and compresive forces, the cervical spine forms a non-physiological “S”-shaped curve, in which the lower cervical vertebrae are in extension and the upper cervical vertebrae are in flexion. Neck extension begins at the lower cervical vertebrae and progreses upwards generating a net extension moment of the neck. Shear forces are generated as the inferior facet of a vertebra slides posteriorly along the superior facet of lower adjacent vertebra and the resulting shear motion between facet joints stretches the capsular ligament (Luan et al. 2000; Pearson et al. 2004).  8  After peak head retraction, the head is acelerated forward relative to the torso due to the internaly generated forces of the neck (McConnel et al. 1995) and rebound from the head restraint. As the torso pulls on the lower cervical vertebrae, the head is acelerated forward faster than the torso and the neck changes from extension to flexion. Since the head rebounded forward at a greater velocity than the torso, the neck actively decelerates and stops the head at maximum forward excursion with respect to the torso.  After the head reaches maximum forward excursion, the subject’s head and torso return back to their pre-perturbation position.  1.3.2 Electromyography of Muscle Responses during Whiplash-Like Perturbation Anterior and posterior neck muscles have the potential to be injured or to cause injury to other cervical structures because they are active during the whiplash-like perturbation (Brault et al. 2000; Hernandez et al. 2006; Vasavada et al. 2007; Siegmund et al. 2008a). The sternocleidomastoid (SCM) muscle is a key landmark of the anterior neck and is a powerful flexor of the neck when contracted bilateraly (Hiat and Gartner 1987). Computerized simulations modeled from previous whiplash studies determined peak lengthening of the SCM to occur during the retraction phases and peak shortening of the muscle to occur during the rebound phase (Vasavada et al. 2007). Conversely, posterior neck muscles shortened as the head retracted and experienced peak lengthening as the head rebounded. When the recorded muscle activity data (electromyography (EMG)) were superimposed on to the muscle strain curves, both the anterior and posterior muscles were ecentricaly contracting – active during muscle lengthening. Ecentric muscle contractions have been shown to damage muscle fibers, resulting in temporary 9  loss of the ability to generate force (McCully and Faulkner 1985; McCully and Faulkner 1986; Lieber and Friden 1993). In some subjects, the peak lengthening strains for both anterior and posterior muscles (SCM: 15%, splenius capitis (SPL): 37%, and semispinalis capitis (SEMI): 50%) (Vasavada et al. 2007), in combination with the ecentric muscular contractions were observed to exced the injury threshold between 15–20% and may potentialy cause muscle injury (McCully and Faulkner 1985; McCully and Faulkner 1986; Macpherson et al. 1996; Vasavada et al. 2007). Vasavada et al. (2007) modeled from previous whiplash data that lengthening fascicle strains were greater in posterior neck muscles (SPL and SEMI); therefore, these muscles are more likely to be injured than the SCM. However, direct injury to the neck muscles usualy persists up to nine days before subsiding and is unlikely to explain the chronic symptoms observed in some patients (Evans et al. 1986; Scott and Sanderson 2002). In addition to being injured, neck muscles can indirectly cause injury to other anatomical structures of the neck. During whiplash-like perturbations, neck muscle activity may afect the neck kinematics and spinal tisue strains. One example of this interaction is the direct atachment of the cervical multifidus to the capsular ligament (Winkelstein et al. 2001; Anderson et al. 2005). Siegmund et al. (2008a) observed that the early activation of the multifidus muscle following a whiplash-like perturbation may potentialy coincide with the peak capsular ligament strain caused by the impact-induced head and neck kinematics. The additional multifidus activity may potentialy injure the cervical facet capsular ligament by increasing peak capsular ligament strain beyond the sub-catastrophic threshold. 10  1.3.3 Factors Affecting the Human Response to Whiplash-Like Perturbations The muscular and kinematic responses of humans experiencing a whiplash-like perturbation are afected by multiple factors such as state of awarenes and gender diferences. A subject’s state of awarenes to an iminent perturbation, or event, can be divided into thre components: amplitude, temporal and event awarenes (Frank 1986; Siegmund 2001). Amplitude awarenes describes whether a subject knows the amplitude of a perturbation, temporal awarenes describes whether a subject knows the exact timing of when a perturbation wil occur, and event awarenes describes whether a subject knows a perturbation wil occur.  Siegmund (2001) observed that amplitude awarenes did not afect the muscular and kinematic responses at low speeds (< 1.26g); however, it stil remains unclear whether a subject’s response would be afected by knowing the amplitude of more intense whiplash-like perturbations. Likewise, temporal awarenes did not afect the muscular and kinematic responses between subjects who received a countdown to the onset of the perturbation and those who did not (p > 0.05) (Siegmund et al. 2003a). In the same study, Siegmund et al. (2003a) deceived subjects and surprised them with an unexpected perturbation to investigate the efects of event awarenes. The muscular and kinematic responses of subjects who were deceived had larger rearward retraction and peak head angular aceleration in flexion (p < 0.05) than subjects who were aware of the iminent perturbation. Despite the significant efects of event awarenes, it is impossible to maintain the initial awarenes level of subjects deceived to the first perturbation during repeated perturbation studies.  Thus, event awarenes may 11  be a potential limitation of repeated whiplash-like perturbation studies and may not acurately represent the responses of unprepared individuals in real rear-end collisions.  Epidemiological data have shown that females are 1.2 to 3 times more at risk to suffer whiplash injuries after a car collision as compared to males (Harder et al. 1998; Verstegen et al. 2000; Mordaka and Gentle 2003). Female necks are not simply scaled versions of male necks but in fact have smaler external neck and vertebral dimensions and  lower overal neck strength than males (Vasavada et al. 2008). Gender diferences have been observed in the neck muscles responses and the head and neck kinematic responses during whiplash-like perturbations and may possibly be a consequence of the anthropometric and anatomical diferences between males and females.  Males were observed to have larger normalized muscle response amplitudes of the SCM (p < 0.0001) and PARA (p < 0.01) muscles than females (Siegmund et al. 2003a). For kinematic responses, females on average exhibited greater (> 10%) peak head forward (horizontal x-direction) aceleration, larger head extension angle (15%) and increased rearward head retraction (~29%) than males (Siegmund et al. 2003a; Linder et al. 2008).  These gender diferences in muscular and kinematic responses may lead to increased capsular ligament strain in females and may explain the greater potential of whiplash injury previously reported in females.   12  1.4 Startle Response Recent work on whiplash simulations in healthy volunters has shown that a startle response forms part of the neuromuscular response to whiplash injuries and may play a role in the aetiology of whiplash injuries (Blouin et al. 2006a). The startle response is a complex reflex which is elicited by a sudden intense tactile stimulus (e.g. displacement of the skin, hair on skin or muscles), acoustic stimulus (e.g. activation of hair cels in the cochlea), vestibular stimulus (e.g. aceleration of the head) or any combination of these stimuli. This response has been described as a protective mechanism found in virtualy al mamalian species (Landis and Hunt 1939; Davis 1984). The startle response elicits a sudden excesive agonist and antagonist muscle contraction throughout the body such as blinking of the eyes, facial expresions, abduction of the upper arms and bending of the knees (Landis and Hunt 1939). In humans, the bilateral muscle activation of the SCM has been described as the most consistent indicator of a startle response (Brown et al. 1991). However, the activation of cervical multifidi has also been observed during the perturbation evoked startle response (Siegmund et al. 2008a).  If the startle response elicits excesive muscular responses during the whiplash motion, the increased posterior neck muscle activity may potentialy increase strain in the cervical facet capsular ligament. Reducing the startle component of the neuromuscular response to whiplash-like perturbations may decrease neck muscle activity and capsular ligament strain to find an efective way of to prevent or mitigate whiplash injuries. 13  1.4.1 The Neurophysiology of the Startle Response Researchers have conducted numerous studies to understand the neurophysiology underlying the startle response and a simple neurophysiological pathway has been proposed (Figure 1.3) (Fox 1979; Le et al. 1996; Koch 1999; Yeomans et al. 2002; Grosse and Brown 2003). Sudden vestibular, acoustic, and tactile stimuli activate fast mechanoreceptors that detect diferent mechanical stimuli applied to the body. Primary sensory neurons of each modality then activate large secondary neurones in the primary sensory nuclei found in the caudal pons and rostral medulla (Yeomans et al. 2002). Vestibular signals activate large vestibular nucleus neurons that utilize the vestibulospinal tract to evoke muscle responses. On the other hand, auditory aferent inputs activate central cochlear nucleus and nuclei of the lateral lemniscus that relay to the giant neurons of the ventrocaudal pontine reticular formation (PnC). The large axon of a giant neuron branches on to hundreds of motorneurons in the brain stem and spinal cord to evoke rapid muscle responses throughout the body (Mitani et al. 1988; Lingenhohl and Friauf 1994). Signals from tactile mechanoreceptors may use either the reticulospinal tract, vestibulospinal tract or both (Yeomans et al. 2002). Both reticulospinal and lateral vestibulospinal tract terminate on interneurons at al spinal levels (Shamboul 1980). Cross-modal summation of the thre stimuli has been shown to be stronger than temporal summation of just one modality and the PnC has been suggested to be the summation point (Lingenhohl and Friauf 1994; Le et al. 1996; Yeomans et al. 2002).  14   1.4.2 The Neurophysiology of Whiplash Collisions A car collision is a complex, multi-sensorial perturbation that stimulates the visual, vestibular, somatosensory, and auditory systems. Litle is known about the exact neurophysiological pathways responsible for the triggering and modulation of neck muscle responses during whiplash-like perturbations. However, results from previous perturbation studies have methodologicaly shifted the importance between each sensory modality. For instance, vision is one of the most important senses to alow people to gain information regarding the orientation of the head throughout the whiplash motion. Figure 1.3 Neural circuit for acoustic, vestibular and trigeminal (tactile) startle responses. This model shows convergence of information in the caudal pontine reticular formation (PnC) and spinal cord. Reprinted with permision from (Yeomans et al. 202). 15  However, Siegmund and Blouin (2009) observed that vision (eyes open vs. eyes closed) has litle efect on neck muscle responses during whiplash-like perturbations with various levels of aceleration and jerk – the time rate change of aceleration at the leading edge of the collision pulse. Since diferences in visual conditions produced the same muscle response, the visual system appears to play a minimal role in the amplitude of the neurophysiology response to whiplash-like perturbations. The vestibulocollic reflex (VCR) is a compensatory muscle response designed to counteract head movement and keep the head stationary in space. Aferent inputs from the vestibular system (semicircular canals and otolith organs) are activated by movements of the head to evoke responses in the muscles of the neck (Wilson and Schor 1999). Gresty (1989) compared seated normal and avestibular subjects to a transient perturbation and observed similar neck muscle onset latencies. Therefore, the VCR does not contribute to the triggering of the neck muscle responses because subjects with intact and damaged vestibular systems had similar activation times. Additionaly, Forsberg and Hirschfeld (1994) compared the postural response of seated subjects to a forward translation and to a legs-up rotation. They observed similar muscle response amplitudes despite the head rotating in two diferent directions and provided compeling evidence that the VCR does not contribute to the amplitude of neck muscle responses. Based on these two studies, it was suggested that the VCR has a secondary role in the onset and amplitude of the neurophysiology of whiplash response.   During whiplash collisions, somatosensory aferent pathways from the trunk and pelvis are the first detectors of the physical movement of the vehicle as these body parts 16  are in contact with the car seat. Forsberg and Hirschfeld (1994) proposed that somatosensory aferents derived from the backwards rotation of the pelvis were responsible for the postural responses during siting (Forsberg and Hirschfeld 1994). Based on nerve conduction velocities and distances between the pelvis and brainstem, it is possible for the somatosensory aferent signals from the trunk to elicit SCM onset latencies of about 70 ms (Siegmund et al. 2008c). Although there is support for trunk/pelvic somatosensory aferents to be responsible for the onset and amplitude of neck muscle responses, there remains questions as to which aferent mechanoreceptor is responsible. In addition to the uncertainty of the aferent mechanoreceptors, litle is known about the spinal pathways (i.e. reticulospinal, vestibulospinal, corticospinal, or bulbospinal) involved with transmision of neck muscle responses and further investigation is required. The acoustic startle reflex (ASR) can be evoked by very loud (over 85 dB) acoustic stimuli comprising of any frequencies within the normal audible range (Yeomans and Frankland 1995). The primary excitatory ASR neural pathway includes the auditory nerve, central cochlear nucleus, nuclei of the lateral lemniscus, PnC, and reticulospinal tract (Davis et al. 1982; Yeomans et al. 2002). However, direct recordings of the reticular structures are inacesible in awake human subjects. Grosse and Brown (2003) used correlation techniques in the frequency domain (Haliday et al. 1998; Haliday and Rosenberg 2000) on ASR-evoked muscle responses to identify markers of reticulospinal activity. Increased synchronized muscle activity of bilateral homologous upper limb muscles in the 10 – 20 Hz range was observed in response to an auditory startle stimulus (Grosse and Brown 2003). This increase in coherence was not observed following either 17  a sham startle or a voluntary contraction, suggesting the 10 – 20 Hz bandwidth may represent a surrogate marker of increased reticulospinal activity (Grosse and Brown 2003). Blouin et al. (2006a) compared the muscular and kinematic responses between subjects who were simultaneously exposed to both a whiplash-like perturbation and a loud auditory stimulus (40 ms, 124 dB, 1kHz tone) and subjects who were exposed to only the perturbation. The addition of a loud auditory stimulus increased posterior neck muscle activity and advanced the activation onset times of al muscle (Blouin et al. 2006a). This study revealed strong evidence that suggests the ASR may be a primary pathway of neck muscles responses to whiplash-like perturbations. 1.4.3 Attenuation of Neck Muscle Activity: Habituation of a Startle Response? In human volunters, the kinematic and muscular responses during the whiplash motion are greatest during the first exposure to a startling stimulus (Blouin et al. 2003; Siegmund et al. 2003b). In response to a novel startling whiplash-like perturbations, subjects initialy co-contract the neck muscles (SCM and PARA) in what has been described as a “strap down” strategy (Nashner 1976). This co-activation appears to be a protective startle response causing the head/neck complex to stifen with the torso. After repeated exposures to the same whiplash-like perturbation, atenuation, or habituation, of the reflexive muscle responses causes the amplitudes of neck muscles to decrease and, consequently, causes the stifnes of the head/neck complex to decrease. A reduction of muscle response and neck stifnes after habituation are observed to change the kinematic properties of the head by increasing peak angular acelerations of the head in extension (!1), retraction (rx) and peak head extension angle (") as wel as decreasing peak linear 18  aceleration of the head (ax) (Siegmund et al. 2003b).  Previous studies have shown that habituation changes a subject’s response and may be a major confounder during repeated whiplash-like perturbation experiments utilizing human volunters (Blouin et al. 2003; Siegmund et al. 2003b; Blouin et al. 2006b; Blouin et al. 2006a; Siegmund et al. 2008b). The use of habituated response compromises the external validity of a study if the objective was to test human responses during unexpected rear-end collisions. However, the exaggerated neck muscle responses observed in the first trial suggest that a startle response may form part of the neuromuscular response to whiplash injuries.   To further investigate the presence of the startle response during whiplash-like perturbations, Blouin et al. (2006b) utilized Grosse and Brown’s (2003) coherence analysis on EMG data from human repeated rear-end perturbation experiments (Figure 1.4) (Brault et al. 2000; Siegmund et al. 2003a; Blouin et al. 2006a). Thre experimental datasets were analyzed: 1.) the initial perturbation (EMGfirst, no auditory stimulus), 2.) the atenuated, or habituated, startle response after multiple repeated- perturbation trials (EMGhab, no auditory stimulus), and 3.) the atenuated startle response presented simultaneously with a startling auditory stimulus (EMGstartle). Blouin et al (2006b) observed a peak in coherent synchronous EMG activity between 10 – 20 Hz following the initial perturbation (EMGfirst), but not in the atenuated trials (EMGhab). This suggests that the first trial contains a startle response that significantly decreased during the atenuated trials (Blouin et al. 2006b). When the atenuated trials were presented simultaneously with a startling stimulus (EMGstartle), the local peak in synchronize EMG activity between 10 and 20 Hz reappeared, similar to EMGfirst. Thus, the startle response was shown to form part of the neuromuscular response to low-speed whiplash-like 19     perturbations and may play a role in the aetiology of whiplash injuries (Blouin et al. 2006b; Blouin et al. 2006a). The whiplash-like perturbation and startling stimulus increased the amplitude of posterior muscle responses (Blouin et al. 2006a) and extended to the deep multifidus muscles (Siegmund et al. 2007; Siegmund et al. 2008a). By reducing the startle response during the whiplash-like perturbation, the amplitude of the posterior muscles wil be decreased.  Consequently, this may reduce the potential of posterior neck muscles to afect other cervical structures such as the capsular ligament and ligament strains during whiplash-like perturbations. Figure 1.4 Estimated averaged coherence betwen left and right SCM muscles recorded during exposure to 1.8 km/h forward perturbation. The first perturbation (EMGfirst), atenuated perturbations (EMGhab), and atenuated perturbations simultaneously with a acoustic startle (EMGstartle). The horizontal doted lines represent the 95% confidence limit for the coherence estimates (black = EMGfirst & grey = EMGhab and EMGstartle). Reprinted with permision from (Blouin et al. 206b) 20  One method to minimize the efects of habituation during whiplash experiments is to increase the inter-perturbation time interval (IPI) between subsequent trials. Brault et al. (1998) used an IPI of at least seven days between their two whiplash-like perturbation conditions (impact speed: 4 km/h and 8 km/h). However, this duration is not practical and too long for experiments with more than two experimental conditions. During a pilot experiment conducted for the proposed study (n = 10), whiplash-like perturbations (peak aceleration: 2.060 ± 0.005g) presented simultaneously with loud collision stimuli (109dB) at IPIs between 15-20 minutes did not show any significant efects of habituation on the muscle and kinematic responses (p > 0.05) (Mang et al. 2009). As a result, we suggest that for future repeated whiplash-like perturbation studies, an IPI of 15-20 can efectively minimized the efects of habituation and increase the external validity of the experiment. 1.4.4 Prepulse and Paired-Pulse Inhibition of the Startle Response Apart from being habituated by a series of repeated stimuli, the startle response is strongly suppresed by preceding the startling stimulus with a weak or startling prepulse stimulus (visual, acoustic or tactile) (Hoffman and Searle 1968; Ison and Krauter 1974; Fendt et al. 2001; Vals-Sole et al. 2005). The suppresion by a weak prepulse stimulus is known as “Prepulse Inhibition (PI)” and is a salient, wel-studied feature of the startle response in rats (Yeomans et al. 2006) and in humans (Filion et al. 1998; Fendt et al. 2001; Vals-Sole et al. 2005; Bitsios et al. 2006). PI exhibits the following characteristics on the startle response: increases in inhibition with increased prepulse intensity (Hoffman and Searle 1968), increases in inhibition with an increased prepulse 21  duration (Blumenthal 1995), and decreases in inhibition with increased background noise (Hoffman and Searle 1968).  In addition, the inter-stimulus time interval (ISI) between the prepulse and the startle stimuli has been shown to influence the efectivenes of PI (Plappert et al. 1999). Prepulse Facilitation (PF), facilitation of the startle response produced by a prepulse stimulus, was observed at ISIs below 37.5 ms; whereas, PI occurred for ISIs greater than 37.5 ms but inhibition decreased as the ISI increased to values greater than 400 ms (Plappert et al. 2004). The most important characteristic of PI is that the prepulse stimulus must be weak enough to not evoke a muscle response distinguishable from resting muscle activity, yet strong enough to modify the response to a subsequent suprathreshold stimulus (Vals-Sole et al. 2008). The strongest inhibition of startle is observed to occur with a prepulse duration of 10 – 20 ms (Reijmers et al. 1995), prepulse intensity up to, but not exceding, the startle threshold (Hofman and Searle 1968; Li et al. 1998), and an ISI between 60 and 120 ms (Braf et al. 1978; Ison and Pinckney 1983).  In contrast to prepulse inhibition, paired-pulse inhibition uses a startling prepulse stimulus (visual, acoustic or tactile) to inhibit a subsequent startling stimulus (Ison and Krauter 1974). Paired-pulse inhibition exhibits the same characteristics as PI such as increasing the inhibition of the startle response with increased paired-pulse intensity (Hoffman and Searle 1968) and decreasing inhibition with longer ISI (Wilson and Groves 1973). Ison and Krauter (1974) compared the efects of paired-pulse inhibition from an intense and weak startling stimulus in rats (Figure 1.5). A 95 dB, 20ms 10 kHz tone was used as the weak paired-pulse tone (s1) and a 125 dB, 20 ms 10 kHz tone was used as both the intense paired-pulse tone (S1) and startling stimulus (S2). Larger inhibition of 22  the startle response was observed from paired-pulse inhibition (S1S2) than PI (s1S2) for ISIs of 0.5, 1, 2, and 4 seconds (Figure 1.5). In addition, prepulse and paired-pulse appear to have greater inhibition efects for smal ISI (~0.5 seconds) (Ison and Krauter 1974). The early prepulse and paired-pulse inhibition studies were primarily based on rat studies and have repeatedly been generalized to humans. Therefore, due to the inter-species diferences in the paterns of neural circuit connectivity and nerve conduction velocities (Koch 1999), further research is required to determine the optimal parameters and efects of PI and paired-pulse inhibition in humans.      Figure 1.5 Comparison of paired-pulse inhibition on the startle response in rats at various inter-stimulus intervals: 0.5, 1, 2, and 4 seconds. Startle reflexes in response: to an intense acoustic stimulus (S1), to a weak acoustic stimulus (s1), to an intense stimulus when preceded by an equaly intense stimulus (S1-S2), and to an intense stimulus when preceded by a weak stimulus. Reprinted with permision from (Ison and Krauter 1974)   23   1.4.5 Prepulse and Paired-Pulse Inhibition in Human Volunteers  In an experimental pilot study, we conducted a two part experiment to determine the efects of paired-pulse and prepulse inhibition of the ASR in human volunters (Mang et al. Unpublished Observations).  For clarification purposes, the term “Pre-Stimulus” wil be operationaly defined as any auditory tone (prepulse or paired-pulse) presented prior to a startle-eliciting sound. Thus, pre-stimulus inhibition refers to the inhibitory efects of the pre-stimulus on the subsequent startle tone. In the first study, the objective was to determine the efects of pre-stimulus on the ASR in humans for diferent ISIs – the time between the pre-stimulus and startling stimuli – while keeping the sound presure level of the stimuli constant. After determining an optimal ISI for pre-stimulus inhibition, the next study characterized the influence of varying the pre-stimulus sound presure level at the optimal ISI. In the first experiment (n = 14), the pre-stimulus and startle stimuli were paired startle tones (124 dB, 40 ms 1 kHz sine waves). We selected ISIs of 100, 250, 500 and 1000 ms to determine the efects of ISI on the ASR and the ISI with the greatest level of inhibition. EMG was recorded from the left and right SCM (L and R SCM), right cervical paraspinals at the level of C4 (RPARA) and right orbicularis oculi (ROOc). ROOc was not further analysed in the study due the large inter-subject variability. Pre-stimulus tones presented at al ISI conditions inhibited the startle responses in al muscles (p < 0.05). However, no statisticaly significant diferences were observed in the level percent inhibition between the various ISIs conditions (F(3,52) = 1.512, p = 0.222). For 24  some subjects, muscle activity elicited by the pre-stimulus response lasted greater than 100 ms and contaminated the startle-evoked response for the 100 ms ISI condition making it dificult to diferentiate the two responses.  Thus, we propose that an ISI of 250 ms is optimal for future research because this ISI elicits two distinct responses for analysis, yet stil cause significant inhibition of the startle response.  In the second experiment, we kept the ISI constant at 250 ms and varied the intensity of the pre-stimulus tone to characterize the influences of sound presure level (i.e. comparing prepulse to paired-pulse). The startle tone (40 ms 1 kHz sine waves) had an intensity of 124 dB, whereas, the sound presure levels of the pre-stimulus tones (40 ms, 1 kHz sine waves) were set at 80, 85, 95, 105 and 124 dB. All intensities of pre-stimulus tones significantly inhibited the startle responses in bilateral SCM (p > 0.05), but only pre-stimulus tone intensities of 95 dB or greater produced inhibition in the RPARA. Post-hoc Tukey’s Honest Significant Diference (HSD) test revealed a significant diference between pre-stimulus tone conditions 80 dB and 105 dB in the RPARA muscle(F(4,65) = 3.180, p < 0.05). To clasify the sound presure level of pre-stimulus tones, we utilized the same characteristic guidelines as prepulse and paired-pulse tones. A weak pre-stimulus tone had a sound presure level that did not evoke muscle responses distinguishable from resting muscle activity (prepulse); whereas, a startling pre-stimulus tone evoked an independent startle response (paired-pulse). A paired t-test confirmed that the 105 dB pre-stimulus generated a startle response significantly diferent from background noise levels (ambient room sound presure level: ~59 dB) (p < 0.0001); whereas, the response to the 80 dB pre-stimulus did not difer from background noise (p = 0.3001). Similar to the 80 dB pre-stimulus the 85 dB pre-stimulus tone did not vary 25  from background noise (RSCM: p = 0.1432, LSCM: p =0.4598, and ROOc: p = 0.2214; with the exception of RPARA: p = 0.0172). Thus, we propose that pre-stimulus tone intensities of 85 dB and 105 dB presented 250 ms prior to a startling stimulus are efective intensities to inhibit the startle response representing a weak pre-stimulus tone (WK-PREP) and a startling pre-stimulus tone (ST-PREP), respectively. 26  2 Objective and Hypotheses 2.1 Rationale Whiplash injuries are the most common injury asociated with low-speed rear end collisions and are serious economical and social burdens to society.  Blouin et al. (2006b) suggested that a startle response may form part of the neurophysiological response to a whiplash-like perturbation and may be an important factor in the genesis of whiplash injuries. One characteristic of the startle response is the ability to be strongly inhibited when a stimulus is presented prior to the startling stimulus (Hoffman and Searle 1968; Ison and Krauter 1974; Fendt et al. 2001; Vals-Sole et al. 2005). Preliminary research has shown that in humans the practical parameters for a pre-stimulus to inhibit the ASR in seated subjects are an 85 dB prepulse tone or a 105 dB paired-pulse tone presented with an ISI of 250 ms (Mang et al. Unpublished Observations).  If we can inhibit the startle response during low-speed rear-end collisions, we may be able to decouple the startle response from the postural response during the whiplash motion. Reducing the startle component of the neuromuscular response to the whiplash motion should decrease neck muscle activity, decrease head angular and linear acelerations and increase peak head retraction. Increasing peak head retraction may increase the physical strain applied to the capsular ligament, whereas decreasing neck muscle activity and forces acting on the capsular ligament may reduce the capsular ligament strain. Overal, pre-stimulus inhibition could prove to be an efective way to mitigate or prevent whiplash injuries in the future. 27  The objectives of the present research are to investigate the influences of two diferent pre-stimulus tones (weak and startling) on the 3-D head kinematic and muscle responses observed in human volunters during the whiplash-like perturbations. 2.2 Hypotheses We hypothesize that presenting a pre-stimulus auditory tone prior to the startle stimulus wil reduce the amplitude of neck muscle activity, which wil directly influence the kinematics of the head and neck. More specificaly, we hypothesize that reducing neck muscle responses wil decrease peak linear forward and angular aceleration in flexion, and increase peak angular aceleration in extension, extension angle and head rearward retraction. We also hypothesize that a startling pre-stimulus tone would have greater efect on the kinematic and muscular responses than a weak pre-stimulus tone. In particular, the startling pre-stimulus tone wil generate a larger reduction of muscle amplitudes during whiplash-like perturbations than the weak pre-stimulus tone.  28  3 Methods 3.1 Subjects Twenty subjects (10 males/10 females; Age: 26 ± 6 years; Height: 169.2 ± 11.1 cm; Weight: 63.3 ± 11.2 kg) with no history of whiplash injury were recruited. All subjects provided writen informed consent and were paid a nominal fe for their participation. The research protocol was approved by the UBC linical Ethics Review Board (H07-01281) and conformed to the Declaration of Helsinki. 3.2 Instrumentation 3.2.1 Electromyography For each subject, surface electromyography (EMG) electrodes (Ambu Blue Sensors: M and N type, Balerup, Denmark) were placed bilateraly on the sternocleidomastoid (SCM: L and R) and cervical paraspinal muscles at the level of C4 (PARA: L and R) as wel as biceps brachii (BIC), triceps brachii (TRI), first dorsal interosseous (FDI) and rectus femoris (RF) on the left side of the body. In addition, two reference electrodes were positioned bilateraly on the acromia (due to equipment requirements). The term cervical paraspinal muscles was used to describe al posterior muscles at the level of C4 due to the dificulty of distinguishing individual muscles in the neck with surface EMG. EMG recording sites were shaved with a disposable razor to remove hair and dead skin cels, cleansed with alcohol and lightly abraded with an abrasive skin prepping gel (NuPrep, D.O. Weaver and Co., Aurora, CO, USA) prior to the placement of surface recording electrodes. All EMG signals were amplified using an 29  eight-channel Neurolog EMG system (Digitimer: NL 900D with NL844 pre-amp, England, UK) and bandpas filtered from 10 Hz to 1000 Hz. 3.2.2 Kinematics Head acelerations were measured using a nine acelerometer aray (8 Kistler 8302B20S1; ± 20 g, Amherst, NY, USA. and 1 Silicon Design Inc 2220-010; ± 10 g. Isaquah, WA, USA) aranged in a 3-2-2-2 configuration (Padgaonkar et al. 1975). The nine acelerometers were rigidly mounted on an aluminum pyramidal frame and securely fastened to the subject’s head by an adjustable headgear device. Torso acelerations and angular velocities were measured respectively with a tri-axial linear acelerometer (summit 34103A; ±7.5 g, Akron, OH) and tri-axial angular rate sensor (DynaCube; ±100 rad/s. ATA-Sensors, Albuquerque, NM). These sensors were fixed to an aluminum plate and strapped tightly to the chest directly below the sternal notch. Sled aceleration was measured with a uni-axial acelerometer (Silicon Design Inc 2220-100; ± 100 g. Isaquah, WA, USA) mounted horizontaly to the sled along the axis of motion. A motion capture system (Optotrak Certus System; Northern Digital, Waterloo, ON, Canada) was used to measure head, torso and sled displacements. A total of 12 Optotrak infrared (IRED) markers (four markers per structure) were afixed to the head acelerometer aray, trunk chest plate, and car seat/sled platform. All EMG, acelerometer, and angular rate sensor data were simultaneously sampled at 2000 Hz using a National Instrument Data Acquisition (DAQ) system and Labview program, (National Instruments Corporation, Austin, Texas, USA). Optotrak data were acquired at 200 Hz per marker using the same computer.  30  3.3 Test Procedure Subjects were instrumented with EMG electrodes and acelerometer arays before siting on a custom-fabricated moving platform system, or sled, equipped with a 2005 Honda Accord front driver automobile seat (Figure 3.1). The sled was powered by fedback-controlled linear induction motors (Kollmorgen IC55-100A7, Kommack, NY) that alowed for repeatable perturbations to stimulate whiplash motions. This moving platform system generated no audible or mechanical pre-perturbation signals that could have helped subjects predict the onset of a perturbation. The head restraint was removed from the top of the seat back to prevent any head-to-head-restraint interaction that may afect the kinematics of the head and neck or generate additional sensory inputs. To Figure 3.1 Photographs of experimental set up of the car seat on the moving platform. Location of head and torso acelerometer arays, horn speaker and laboratory reference frame (X, Z) are also included. Inset: Close-up view of the nine acelerometer aray on the headgear device. (Electromyography (EMG) electrodes are not shown)  "!#!$%&!’(%)*!31  eliminate possible habituation efects, subjects were provided neither practice nor demonstration trials (Blouin et al. 2003; Siegmund et al. 2003b), and an inter-perturbation time interval between 15 and 20 minutes was used (Mang et al. 2009). Subjects were aware of the number of trials presented, but were not told the magnitude or the timing of the perturbation. Once on the sled, subjects were instructed to sit facing forward, adopt a comfortable seated posture, rest their forearms on their lap and relax their head and neck muscles.   The experiment consisted of thre diferent experimental conditions as subjects underwent five forward whiplash-like perturbation trials (Figure 3.2) that replicated the initial aceleration profile of an 8 km/h vehicle-to-vehicle collision.  For each condition, a collision sound was presented time-locked with the whiplash-like perturbations to simulate a realistic rear-end collision. Based on our previous studies in the lab (over 150 subjects tested), the aceleration pulse (Figure 3.2) was sufficient to evoke a startle response in the neck muscles and was reported to be neither painful nor noxious by participants. To further replicate a real rear-end collision, we used a collision sound (109 dB, time-to-peak 34.2 ± 0.2ms) recorded from an 8 km/h frontal crash of a 1987 Ford Mustang into a barier. The sound was recorded with a microphone and a dB sound meter placed at the driver’s ear level with the windows up. 32    The thre experimental conditions difered with the type of pre-stimuli tone occurring 250 ms prior to the onset of perturbation and collision sound: 1.) no pre-stimulus tone (Control), 2.) a weak pre-stimulus tone (WK-PREP) and 3.) a startling pre-stimulus tone (ST-PREP) (Figure 4.1). WK-PREP was a weak auditory tone (85 dB, 1 kHz sine wave, 40 ms duration) delivered 250 ms before the onset of the perturbation.  This weak pre-stimulus tone was audible above the background noise (~63.7 dB) from the sled and room, but not loud enough to evoke an independent startle response (se preliminary results). The startling pre-stimulus tone (ST-PREP) (105 dB, 1 kHz sine wave, 40 ms duration) was also sent 250 ms before the onset of the perturbation and this tone was capable of eliciting an auditory startle response (se preliminary results). The Figure 3.2 A sample of the aceleration profile and pulse properties used to simulate a 2.7 km/h rear-end whiplash-like perturbations. The dashed line shows an 8 km/h vehicle-to-vehicle colision pulse recorded during previous experiments (Siegmund et al. 197). 33  WK-PREP and ST-PREP tones were delivered through a horn speaker (MG Horn Speaker HS17T, Hauppauge, NY, USA) located directly above the subject’s head. In addition to the horn speaker, the collision sound was played through a stereo speaker (Yamaha NS-66, Shizuoka, Japan) and an automotive subwoofer (JL Audio 10” subwoofer, Miramar, FL, USA) surrounding the subject.  Before each perturbation trial, the location of the head and torso acelerometers, and IRED markers relative to anatomical landmarks were digitized using the thre-dimensional (3D) digitizer function of Optotrak and a digitization probe tool. The digitized anatomic landmarks (upper incisors, bilateral lower rims of the orbit, external acoustic meati, glabela, vertex, opisthocranion, occiput, manubrium and spinous proces of C7) determined the Frankfort plane and alowed resolution of head kinematics to anatomicaly relevant locations (i.e. atlanto-occipital joint and head centre of mas). Subjects were seated on the sled for between 15 – 20 minutes before the first perturbation to alow sufficient time for both the subject to adopt a comfortable posture and the digitization proces. Subjects were informed to expect the iminent perturbation within the next five minutes after the digitization proces – subjects became aware of the event, but remained unaware of the exact timing of when the perturbation would occur. After each perturbation, subjects remained seated on the sled in their initial position until the next trial. The head acelerometer aray was loosened and retightened between trials to reduce the compresion of the head caused by the tight headgear. Consequently after retightening the headgear, the subject’s anatomical landmarks were redigitized prior to the subsequent perturbation to establish proper position and orientation of the head 34  acelerometers with respect to the Frankfort plane. Once again, after each digitization proces, subjects were informed to expect a perturbation within 5 minutes to acount for potential efects of diferent awarenes levels. Subjects had no auditory, tactile or visual cues that could have aided in predicting the onset of the perturbation. To reduce the efects of habituation on the kinematic and muscle responses, a IPI between 15 – 20 minutes was used and muted episodes of BC television series ‘The Blue Planet” was shown to distract subjects during the experiment. Of the five trials performed, the first, middle and last trials (Control 1, Control 3, and Control 5) in the series were Control trials to control and determine the potential efects of habituation during the experiment and to provide a comparative scale for the inhibition caused by the pre-stimulus tone. The two pre-stimulus conditions (WK-PREP and ST-PREP) were randomly distributed into the two remaining test trials (Trial 2 and Trial 4) to investigate the efects of pre-stimuli on th9e startle response evoked by whiplash-like perturbations. 3.4 Reference Frames Data from the head aceleration aray were transformed into the head reference frames with the origin at the atlanto-occipital joint (AOJ), which was estimated to be 24 m posterior and 37 m inferior to the head’s center of mas (Siegmund et al. 2007). The head’s center of mas was estimated to lie in the mid-sagital plane, rostral to the interaural axis by 17% of the distance between the vertex and the interaural axis (NASA 1978). The Frankfort plane was defined as the plane pasing through the external acoustic meatus and lower rim of the orbit (Pozzo et al. 1990). All kinematic responses were transformed into, and subsequently reported in, the global reference frame with the x-axis 35  horizontal and positive in the forward direction of the sled, the y-axis horizontal and positive to the right of the subject, and the z-axis vertical and positive downwards in the direction of gravity (Figure 3.1). All head, trunk, and sled acelerometers were corrected for the efects of earth’s gravitational field prior to data analysis (Blouin et al. 2006b).  3.5 Data Analysis   A subject’s initial head position and orientation were determined from the average of position/orientation estimated over a 50 ms period preceding the onset of sled perturbation. Initial head angle in the sagital plane was reported as the relative angle between the Frankfort plane and the positive global X-axis (+": Extension, -": Flexion). The onset of vertical and horizontal head movements, peak head acelerations (linear and angular), and the time of peak head acelerations were determined directly from the transformed acelerometer data. Onsets of head movement in the vertical and horizontal directions were defined as the first point at which the linear Z- and X-axes acelerometer data reached 10 times the peak background noise amplitude. Peak linear head aceleration (x: first positive peak) was determined from the linear head forward (X-axis) aceleration data. Peak angular head acelerations were defined by two peaks: peak angular aceleration in extension (!1: first positive peak) and peak angular aceleration in flexion (!2: first negative peak). Peak retraction was estimated by the maximum relative horizontal displacement in the lab reference frame between the AOJ and the midpoint between the superior margin of the manubrium and the palpable aspect of the C7 spinous proces (Queiser et al. 1994) 36  All EMG muscle data were high-pas filtered (30 Hz) to remove any possible motion artefacts before calculating onsets of muscle activity and muscle response amplitudes. Onsets of muscle activity were determined to be when the root-mean-square (RMS) EMG amplitude (20 ms sliding window) reached 10 percent of the maximum value and was confirmed visualy (Siegmund 2001; Siegmund et al. 2003a; Siegmund et al. 2003b). The RMS amplitude of each muscle response to the perturbation (perturbation response) was calculated over the entire interval between muscle activation and peak head extension angle. The RMS muscle responses evoked by the pre-stimuli (pre-stimulus response) were calculated over the same time interval as the perturbation response, but the time interval was shifted to the onset of the pre-stimulus tone (#t = -250 ms) (i.e. from onset of muscle activity minus 250ms to peak head extension angle minus 250 ms). Visual inspections were performed to ensure that the pre-stimulus response did not contaminate the perturbation response. Pre-perturbation background RMS EMG offsets were quantified over the 50 ms time interval preceding the pre-stimulus tone and were subtracted from the perturbation responses. Only perturbation response RMS EMG data were normalized to the first control trial (Control 1) to represent each trial as a percentage of the initial startle trial. Normalizing al the trials to Control 1 helped to determine: 1.) whether habituation confounded the EMG responses during the experiment and 2.) whether the addition of a pre-stimulus tone afected the EMG response when compared to Control EMG responses. 37  3.6 Statistical Analysis For the EMG variables, normalized RMS EMG data from the left and right sides of SCM and PARA were averaged for subsequent analysis (Blouin et al. 2006b; Siegmund et al. 2003b ).   The amplitudes of the EMG and kinematic responses were first asesed with a one-way, repeated-measures analysis of variance (ANOVA) for al Control trials (Control 1 vs. Control 3 vs. Control 5) to determine if the responses were significantly afected by habituation. After confirming that there were no statisticaly significant muscular and kinematic response diferences betwen the thre Control trials, the thre trials were averaged to calculate a mean Control variable. To determine whether WK-PREP or ST-PREP generated an independent startle response, we used a Paired T-Test to compare the pre-stimulus response to the pre-perturbation background noise level. For each EMG and kinematic variable, diferences between gender (males vs. females) and pre-stimulus conditions (Control vs. WK-PREP vs. ST-PREP) were tested using a mixed model (2 Group $ 3 Condition) ANOVAs with repeated measures on the Condition factor. Post-hoc comparisons for the ANOVAs were performed using a Tukey’s honest significant diference (HSD) test. All statistical analyses were performed using the [R] statistic program (version 2.10.1) and the significance level was set at " = 0.05. 38  4 Results In response to a whiplash-like perturbation, al subjects exhibited stereotypical muscular and kinematic responses (Figure 4.1; Table 4.1 and 4.2). The unexpected forward perturbation evoked generalized muscle activity throughout the body from head to lower limbs (SCM, PARA, BIC, TRI, FDI and RF). All onsets of muscles activity occurred before the time-to-peak of any kinematic variables (Table 4.1). We observed the onsets of head movement appear first in the vertical direction before the horizontal direction. The subject’s heads experienced peak angular and linear aceleration before peak head retraction and head extension angle. Habituation of the muscular and kinematic responses was not observed over the duration of the experiment (p > 0.05). The addition of a pre-stimulus tone (WK-PREP and ST-PREP) before a subsequent, startling whiplash-like perturbation decreased the evoked normalized RMS EMG amplitudes in al muscles relative to the Control condition (Figure 4.1 and 4.2; Table 4.1). The ANOVAs determined that when a weak pre-stimulus tone (85 dB: WK-PREP) was presented, we observed decreases only in TRI (!38%), FDI (!48%) and RF (!57%) from Control conditions (p < 0.01). However, by increasing the pre-stimulus intensity to a startling pre-stimulus tone (105 dB: ST-PREP), we observed significant decreases (p <0.01) in al EMG amplitudes (SCM: !16%, PARA: !26%, BIC: !66%, TRI: !62%, FDI: !68%, and RF: !78%). Post-hoc analysis revealed that ST-PREP decreased the muscle responses of PARA, BIC, and TRI greater than WK-PREP (p <0.05). Thus, greater intensity of pre-stimulus tones produced greater inhibition of the muscle response evoked during whiplash-like perturbations.  39  The addition of pre-stimulus tones afected the peak kinematic variables of the head during whiplash-like perturbations (Figure 4.1 and 4.3; Table 4.2). The addition of the ST-PREP tone significantly decreased (p < 0.05) peak retraction (rx) by 5.7 m (!16.8%), peak horizontal aceleration of the head (ax) by 4.4 m/s2 (!22.8%), and peak head angular aceleration in extension (#1) by 37.0 rad/s2 (!23.0%). However, no significant efects were observed during the WK-PREP condition (p > 0.05). ANOVAs revealed that there were gender-related diferences in the initial head angle and peak head extension angles. On average, the initial head angles of female subjects were 4.7° les in extension than male subjects (p = 0.0045); whereas, the peak head extension angles of female subjects were 3.7° greater than male subjects (p = 0.0099). Therefore, female subjects had a greater angular range of motion of the cervical spine in extension than male subjects. ANOVAs determined that the RMS EMG amplitudes were unafected by diferences in gender.    40  Figure 4.1 A sample of muscular and kinematic responses from a single subject during Control, WK-PREP, and ST-PREP conditions. Labeled holow circles in the Control panel represent kinematic peaks used for analysis and are replicated on WK-PREP and ST-PREP panels to highlight the changes due to pre-stimulus tones. The vertical scale bars are aligned with the onset of pre-stimulus tones (-250 ms) and are consistent betwen conditions. The vertical doted line represents the onset of sled perturbation. Electromyographic data: left (L), right (R), sternocleidomastoid (SCM), cervical paraspinal (PARA), biceps brachi (BIC), triceps brachi (TRI), first dorsal interoseous (FDI), and rectus femoris (RF) muscles.  Kinematic data: subscript x refers to the x-direction, linear aceleration (a), head angular aceleration (#), and head angle ($). 41   Table 4.1 Mean (SD) of normalized RMS amplitudes and onsets of EMG for Control, WK-PREP and ST-PREP conditions (n = 20).  Data also grouped as a function of gender (Female and Male).   F-statistics and post-hoc Tukey’s HSD sumarized at right for mixed-model two-way ANOVAs using gender (G) and condition (C) as independent variables as wel as Control (Control), WK-PREP (WK), and ST-PREP (ST) as the thre conditions. Electromyographic data: sternocleidomastoid (SCM), cervical paraspinal (PARA), biceps brachi (BIC), triceps brachi (TRI), first dorsal interoseous (FDI), and rectus femoris (RF) muscles.  Control WK-PREP ST-PREP ANOVA Results (F; P) Post-Hoc Tukey's HSD Variable Female Male Female Male Female Males Gender Condition G x C Control-WK Control-ST WK-ST EMG RMS Amplitude               SCM 1.01 (0.07) 1.01 (0.14) 0.97 (0.12) 0.85 (0.2) 0.90 (0.16) 0.78 (0.27)  4.827; p = 0.018   ST<Control; p < 0.085    PARA 1.02 (0.17) 1.1 (0.30) 0.97 (0.28) 0.94 (0.31) 0.80 (0.30) 0.71 (0.23)  7.324; p = 0.015    ST<Control; p < 0.012 ST<WK; p = 0.0453   BIC 0.9 (0.38) 1.07 (0.38) 0.63 (0.47) 0.8 (0.8) 0.30 (0.23) 0.39 (0.42)  9.58; p = 0.003   ST<Control; p = 0.002 ST<WK; P = 0.0309   TRI 1.02 (0.26) 0.95 (0.17) 0.65 (0.38) 0.57 (0.28) 0.30 (0.1) 0.43 (0.38)  25.72; p < 0.00  WK<Control; p = 0.002 ST<Control; p < 0.00 ST<WK; p = 0.020   FDI 0.94 (0.40) 1.01 (0.30) 0.57 (0.75) 0.52 (0.46) 0.17 (0.18) 0.29 (0.26)  14.96; p < 0.00  WK<Control; p = 0.079 ST<Control; p < 0.00    RF 0.98 (0.12) 1.2 (0.89) 0.65 (0.42) 0.24 (0.15) 0.30 (0.23) 0.16 (0.14)  2.98; p < 0.00  WK<Control; p < 0.00 ST<Control; p < 0.00  Onset of EMG               SCM (ms) 54.9 (5) 54.8 (4) 49.8 (7) 48 (5) 53.3 (12) 50.3 (6)  3.503; p = 0.0371  WK<Control; p = 0.0282     PARA (ms) 59.7 (6) 56.1 (6) 50.0 (10) 50.2 (7) 54.9 (10) 49.6 (8)  4.871; p = 0.014  WK<Control; p = 0.0105     BIC (ms) 56.7 (12) 52.0 (13) 54.2 (11) 47.8 (11) 59.8 (23) 50.9 (21)       TRI (ms) 64.4 (10) 63.4 (11) 59.6 (8) 58.4 (14) 6.1 (15) 60.8 (14)      FDI (ms) 70.2 (16) 64.4 (24) 67.5 (23) 64.7 (32) 70.9 (33) 54.8 (24)      RF (ms) 82.0 (9) 81.5 (12) 85.7 (11) 74.6 (18) 8.8 (21) 71.8 (21) 5.456; p = 0.0232       42  Table 4.2 Mean (SD) of the initial head angle, onsets of head movement, peak linear and angular kinematics for Control, WK-PREP and ST-PREP conditions (n = 20).  Data also grouped as a function of gender (Female and Male).   F-statistics and post-hoc Tukey’s HSD sumarized at right for mixed-model two-way ANOVAs using gender (G) and condition (C) as independent variables as wel as Control (Control), WK-PREP (WK), and ST-PREP (ST) as the thre conditions. Kinematic peaks are labeled with holow circles in the left panel of Figure 9.1.  Onset of head movement X and Z refer to the x- and z-directions of the lab reference frame.   Control WK-PREP ST-PREP ANOVA Results (F; P) Post-Hoc Tukey's HSD Variable Female Male Female Male Female Males Gender Condition G x C Control-WK Control-ST WK-ST Initial Head Angle                Angle (deg) 10.6 (6.3) 15.9 (6.1) 9.7 (5.4) 14.2 (6.4) 10.7 (6.5) 14.9 (7.0) 8.801; p = 0.045      Onset of Head Movement               X (ms) 56 (12) 60 (8) 53 (15) 54 (19) 57 (17) 53 (15)         Z (ms) 37 (5) 38 (4) 33 (5) 37 (6) 33 (13) 35 (13)       Linear Kinematics                  ax (m/s2) 18.9 (4.7) 19.7 (6.1) 16.9 (4.6) 19.6 (6.6) 15.0 (4.0) 14.8 (4.0)  3.303; p = 0.044   ST<Control; p = 0.0218     ax (ms) 129 (6) 131 (8) 129 (11) 123 (11) 131 (9) 127 (11)         retraction (mm) -35.5 (5.4) -32.3 (7.3) -31.7 (4.6) -29.4 (6.5) -27.2 (8.5) -29.2 (7.5)  3.532; p = 0.0363   ST<Control; p = 0.0287  Angular Kinematics             !1(rad/s2) 169 (38) 153 (64) 147 (51) 168 (63) 130 (28) 118 (40)  3.429; p = 0.0396   ST<Control; p = 0.0526  !"1"(ms) 126 (7) 125 (11) 122 (14) 120 (10) 119 (11) 119 (11)       !2"(rad/s2) -188 (72) -235 (97) -187 (65) -208 (96) -179 (65) -173 (56)       !"2"(ms) 176 (9) 174 (10) 178 (5) 168 (12) 185 (8) 176 (16) 7.132; p = 0.010      # (deg) 23.4 (5.4) 18.2 (4.4) 20.9 (8.6) 19.1 (4.0) 21.3 (4.7) 17.1 (4.1) 7.142; p = 0.09      # (ms) 214 (21) 187 (15) 205 (15) 200 (22) 204 (18) 196 (20) 4.4279; p = 0.040      43   Figure 4.2 Group means and standard deviations of muscular responses for Control, WK-PREP, and ST-PREP conditions. Faded lines in the background depict response of individual subjects for both males (blue lines) and females (red lines). Solid bars above conditions denote that a significant diference was observed betwen the two indicated conditions (p < 0.05). 44         Figure 4.3 Group means and standard deviations of head kinematic responses for Control, WK-PREP, and ST-PREP conditions. Faded lines in the background depict response of individual subjects for both males (blue lines) and females (red lines). Solid bars above conditions denote that a significant diference was observed betwen the two indicated conditions (p < 0.05). * denotes a significant diference betwen gender (p < 0.05).  45  5 Discusion The human startle response has been suggested to form part of the neurophysiological response of seated subjects exposed to rear-end, whiplash-like perturbations (Blouin et al. 2006b). The objective of the current study was to investigate if presenting pre-stimulus tones (WK-PREP: 85 dB and ST-PREP: 105 dB) before a subsequent whiplash-like perturbation could inhibit the perturbation evoked startle response in human volunters. We initialy anticipated our muscular and kinematic responses to miic the responses of habituated subjects because habituation was shown to decrease neck muscle activity (Siegmund et al. 2003b; Blouin et al. 2006a; Mang et al. Unpublished Observations). Thus, we hypothesized that pre-stimulus inhibition would decrease the amplitude of whole-body muscle responses, decrease peak linear forward and angular aceleration in flexion, and increase peak angular aceleration in extension, extension angle and head rearward retraction. We observed the expected decrease in al muscle response amplitudes when we presented a startling pre-stimulus tone prior to a subsequent startling whiplash-like perturbation. Contrary to our hypothesis, pre-stimulus inhibition decreased certain peak kinematic variables (retraction, head linear aceleration and head angular aceleration in extension and flexion) during the retraction phase of the head movement (Figure 4.1).  46  When comparing the current study to previous habituation experiments, our results clearly suggested that pre-stimulus inhibition and habituation are two independent behavioural phenomena (Table 5.1) (Siegmund et al. 2003b; Blouin et al. 2006a). Despite a similar decrease in the ratio between the reduction of flexor and extensor muscle responses of the neck, the resulting changes in kinematic responses were considerably diferent between habituation and pre-stimulus inhibition (Table 5.1). In a habituation experiment, Siegmund et al. (2003b) suggested that habituated subjects became more familiar with the aceleration profile of subsequent repeated perturbations and responded more pasively. Consequently, a decreased co-activation of the neck muscles caused a reduction in stifnes of the connection between the torso and head. The decrease in neck stifnes may have contributed to decreased linear forward head aceleration and angular head aceleration in flexion, and increased rearward head displacements, extension angle and angular head aceleration in extension (Siegmund et al. 2003b). Interestingly, we observed that pre-stimulus inhibition decreased most peak kinematic variables including linear forward head aceleration, angular head aceleration in extension and rearward head displacement. Some possible explanations for the deceased kinematic responses caused by pre-stimulus inhibition may be due to changes to the active component of neck and torso muscle activity.    47   Table 5.1 Comparison betwen habituation and pre-stimulus inhibition experiments during repeated whiplash-like perturbations. Al variables represent a percentage change from first perturbation trial variables. Electromyographic data: sternocleidomastoid (SCM), cervical paraspinal (PARA); Kinematic data: peaks are labeled with holow circles in the left panel of Figure 9.1. Variables Siegmund et al. (203b) Blouin et al. (206a) Mang et al. (2010) Type of Experiment Habituation Habituation Startling Pre-Stimulus EMG Amplitude    SCM !48% !28% !16% PARA !56% !45% !26% Linear Kinematics (AOJ)    ax (m/s2) !9%† !21% !23% retraction (m) "11% "4%‡ !17% Angular Kinematics (AOJ)    #1 (rad/s2) "8% "15%‡ !23% #2 (rad/s2) !8% !11%‡ !17%‡ $ (deg) "17% "22% !8%‡ Note: †: ax at the mastoid proces; ‡: not significantly diference (p > 0.05)  As the whole body responds to the pre-stimulus inhibition, changes to the muscle responses of the neck and torso may explain the decreased neck muscle and peak kinematic responses observed (Table 5.1).  Changes to the stifnes of the neck may have afected the dynamics of the head because decreasing the stifnes of the neck was previously shown to decrease linear head forward acelerations (Siegmund et al. 2003b; Blouin et al. 2006a). The smaler co-contractions of the neck muscles suggest that neck 48  stifnes may potentialy afect the kinematic responses. Alternatively, if a pre-stimulus tone can decrease the muscle responses and the stifnes of the torso, there may be les force transfered from the upper torso to the base of the neck. Decreasing the forces applied to the base of the neck would cause the neck to respond as if it was perturbed by a lower intensity whiplash-like perturbation (Siegmund et al. 2004). Further analysis of muscular and kinematic responses of the torso would be needed to support this explanation. Although the exact cause of the observed kinematic changes remain uncertain, decreasing the peak kinematics of the head and neck would be beneficial in preventing whiplash injury. One proposed whiplash injury mechanism is excesive strain to the cervical facet capsular joint ligament during the whiplash-like perturbations (Winkelstein et al. 2000; Siegmund et al. 2001; Winkelstein et al. 2001). Increased neck muscle activity during the whiplash motion may increase the capsular ligament strain at a moment when the ligament is vulnerable. Angular and linear head acelerations have been suggested to be proportional to the internal reaction forces of the neck; whereas, changes to peak head retraction have been suggested to be proportional to neck tisue strains (Blouin et al. 2003; Siegmund et al. 2003b). Reducing the acelerations applied to the head would decrease the internal forces generated by the neck muscles on the facet capsule and may reduce the capsular ligament strain (Winkelstein et al. 2001). On the other hand, limiting head displacement would decrease head rearward retraction and also reduce strains in the cervical facet capsular ligament (Winkelstein et al. 2000; Siegmund et al. 2001). The results from the current study observed a reduction in both the (linear and angular) 49  acelerations and rearward displacement of the head. Therefore, pre-stimulus inhibition demonstrated multiple mechanisms that can potentialy reduce the capsular ligament strain during whiplash-like perturbations and may be applicable in the prevention or reduction of whiplash injuries. Further research is required to determine the exact efects of pre-stimulus inhibition on facet capsular ligament stain; however, direct calculations of capsular ligament strain in human volunters are currently very dificult and may require the extensive use of mathematical models. In the current study, the secondary objective was to compare the efectivenes of two pre-stimulus tones with diference auditory intensities on the inhibition of the human startle response. We observed that the muscle responses evoked by a whiplash-like perturbation could be significantly inhibited by a startling pre-stimulus tone (ST-PREP: 105 dB) (Figure 4.1). ST-PREP decreased the amplitude of al muscle responses (p < 0.01); whereas, WK-PREP decreased the normalized RMS EMG amplitudes from Control for only TRI, FDI and RF muscles (p < 0.01). When comparing the efects of diferent pre-stimulus tone intensity on the peak kinematic response variable, only ST-PREP significantly (p < 0.05) decreased peak head retraction (rx), peak linear head forward aceleration (ax) and peak angular head aceleration during extension (!1). Thus, pre-stimulus tone with greater auditory intensities (105 dB vs. 85 dB) produced greater inhibition of the startle responses evoked during whiplash-like perturbations.  The largest inhibition of muscle amplitudes during the ST-PREP condition were observed in the distal and proximal limbs (greater than 60%); whereas, SCM decreased by 16% and PARA decreased by 26%. These results suggest that not only did the startle 50  response elicit whole-body muscle contractions in seated subjects, but pre-stimulus inhibition afected the whole-body and had greater inhibitory efects on appendicular muscles than neck muscles. Greater inhibition of appendicular muscles may have occurred because these muscles were not as important as the neck muscles in maintaining upright seated posture during the perturbation-induced motion. In contrast, neck muscles could not be inhibited as much as appendicular muscles because the co-activation of the neck muscles was required to increase neck stifnes and maintain upright head position. Vibert et al. (2001) observed that the neck of some subjects responded in a “floppy” manner when the neck muscles were not consistently activated during transient perturbations. Those subjects appeared to rely on the pasive biomechanical properties of their head and neck to maintain upright head position. Some “floppy” subjects activated reflex muscular synergies that exaggerate the inertial kinematic response to the perturbation and may potentialy cause injury to the neck (Vibert et al. 2001). If pre-stimulus inhibition completely inhibited the startle component of neck muscle responses, the observed amplitudes of neck muscle responses would represent the minimum amplitudes required to maintain upright head position. Alternatively, we propose that at least 16% of SCM and 26% of PARA muscle responses contribute to the startle response evoked during whiplash-like perturbations. The mamalian neurophysiology of pre-stimulus inhibition from an auditory pulse is mediated by nuclei located in the brainstem and share similar neural pathways as the startle response (Davis et al. 1982; Davis 1984; Koch et al. 1993; Yeomans et al. 1993; Yeomans and Frankland 1995). A commonly acepted pre-stimulus inhibition 51  circuit includes the folowing neuroanatomical structures: inferior colliculus (IC), superior colliculus (SC), pedunculopontine tegmental nucleus (PTg) and ventrocaudal pontine reticular formation (PnC) (Koch and Schnitzler 1997; Koch 1999; Fendt et al. 2001; Leumann et al. 2001). It is believed that maximum pre-stimulus inhibition occurs when the inhibitory circuit produces maximum inhibition of the PnC (the summation site for the startle response and pre-stimulus inhibition) at the moment that the excitatory startle response arives (Hoffman and Ison 1980). The level of inhibition has been shown to increase with increased intensity of the pre-stimulus tone (Blumenthal 1996) and to decrease with increased pre-stimulus ISI (pre-stimulus facilitation occurred at 30 ms or les (Vals-Sole et al. 1999) and pre-stimulus inhibition was stil efective after 1000 ms (Mang et al. Unpublished Observations). Thus, this model may explain the diferent intensities of pre-stimulus inhibition observed between WK-PREP and ST-PREP in the current study. The only diference between WK-PREP and ST-PREP was the diferent sound presure level of the pre-stimulus tone because the ISI was held at a constant 250 ms. Thus, the non-significant decreases of muscular and kinematic responses observed in WK-PREP, suggested that the intensity of WK-PREP tone did not surpas a threshold to elicit a significant inhibition efect on the subsequent startle response. In the current study, we observed gender-related diferences more predominantly in the kinematic responses than in the muscular responses (Table 4.1 and 4.2). Female subjects started with a more flexed initial head angle and reached greater peak head extension angle than male subjects. This increased range of angular motion may be a result of females having significantly smaler geometry of the vertebrae in the anterior-52  posterior dimension (Vasavada et al. 2008). Overal, females have a lower head mas and smaler neck geometry than males, but female necks and heads are not equaly proportionaly smaler than males (Vasavada et al. 2008). In previous studies, female subjects were found to activate their neck muscles 3 to 8 ms earlier than male subjects (Brault et al. 2000; Siegmund et al. 2003a); however, Blouin et al. (2006a) and our results did not observe this diference. The efect of pre-stimulus inhibition and fewer subjects used in the current study may potentialy hide the gender–related diference between the onsets of muscle activity. Regardles, the absence of significant interaction between gender and condition observed in the current study suggested that pre-stimulus inhibition afected males and females equaly. The rapid habituation of muscle and kinematic responses had been quantified for sequential whiplash-like perturbations with short inter-perturbation time intervals (IPI) (< 10 minutes) and, potentialy, confounded the results of many previous whiplash studies. The current protocol utilized a longer IPI (15-20 minutes) that was previously shown to minimize the habituation of muscle and kinematic response during the series of five sequential whiplash-like perturbations (Mang et al. 2009). To ensure corect positioning and orientation of al acelerometers and angular rate sensors throughout the experiment, we re-digitized al anatomical landmarks and IRED markers imediately prior to the perturbation. Statistical analysis of the thre Control trials positioned in the first, middle and last trials found no significant diferences (p > 0.05) between the muscular and kinematic responses of the thre Control trials. The present observations for the two pre-stimulus conditions were unlikely to be limited by habituation between trials, but a direct 53  result of pre-stimulus inhibition on the startle response during whiplash-like perturbations. Another limitation of the current study was the amplitude of the whiplash-like perturbation (speed change: 2.7 km/h, peak aceleration: 2.060 ± 0.005g; !t: 53.2 ± 0.05ms; !v: 0.7500 ± 0.0003m/s) used in the curent study as compared to many actual whiplash inducing collisions. Other studies have implemented greater speed changes between 4 to 16 km/h resulting in peak acelerations up to 6.0 g (Matsushita et al. 1994; Szabo et al. 1994; McConnel et al. 1995; Brault et al. 1998; Brault et al. 2000), but the muscular and kinematic response have been shown to exhibit a graded response proportional to perturbation intensity (Siegmund et al. 2004). Despite subjects having larger muscle responses to more intense perturbations, we would expect pre-stimulus tones to evoke inhibition of the muscular and kinematic responses similar to the observed results of this study. Our goal for future research would be to implement pre-stimulus inhibition techniques in experiments exposing subjects to more intense perturbation amplitudes (> 2.7 km/h). These studies would alow us to beter understand how pre-stimulus inhibition would influence the muscular and kinematic responses and, hopefully, reduce the risk of whiplash injuries during real-life low-speed rear-end collisions. The results from the proposed studies would help to lay the foundation for developing new preventive devices used in cars to mitigate whiplash injuries. These preventive devices would be easily implemented into vehicles because existing car audio systems are capable of reaching a startling sound presure level of 105 dB (Mang et al., Unpublished Observations). These 54  new devices would rely on pre-collision warning systems already instaled in many new vehicles to trigger a startling pre-stimulus tone to cause the inhibition of the startle response elicited by the iminent automotive collision. 55  6 Conclusion The results of this experiment showed that presenting a pre-stimulus tone (85 dB weak: WK-PREP or 105 dB startling: ST-PREP) before a startling whiplash-like perturbation could inhibit the muscular responses and decrease peak kinematic response variables evoked by the perturbation. The use of a startling pre-stimulus tone was shown to be more efective than a weak pre-stimulus tone and, consequently, should be used in future pre-stimulus research. A startling pre-stimulus tone significantly reduced the amplitudes of al muscle responses and decreased peak kinematic variables such as peak head acelerations and rearward head retraction. 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Cervical spine vertebral and facet joint kinematics under whiplash. J Biomech Eng 120(2): 305-7.   69  Apendices Apendix A: Graphical Figures of Individual Subject Data  The following figures ilustrate the muscular and kinematic responses for each subject during Control, WK-PREP, and ST-PREP conditions, similar to Figure 4.1. Labeled hollow circles in the Control panel represent kinematic peaks used for analysis and are replicated on WK-PREP and ST-PREP panels to highlight the changes due to pre-stimuli tones. The vertical scale bars are aligned with the onset of pre-stimulus tone (!250 ms) and are consistent between conditions. The vertical doted line represents the onset of sled perturbation. Kinematic data: subscript x refers to the x-direction, linear aceleration (x), head angular aceleration ("), and head angle (#). Electromyographic (EMG) data: left (L), right (R), sternocleidomastoid (SCM), cervical paraspinal (PARA), biceps brachii (BIC), triceps brachii (TRI), first dorsal interosseous (FDI), and rectus femoris (RF) muscles. Please note that the EMG data are limited to ±1 volt and may appear clipped in the figures. During the data analysis proces, al EMG data were visualy confirmed to ensure no actual data was lost due to clipping.  70  Subject 01  71  Subject 02  72  Subject 03  73  Subject 04  74  Subject 05  75  Subject 06  76  Subject 07  77  Subject 08  78  Subject 09  79  Subject 10  80  Subject 11  81  Subject 12  82  Subject 13  83  Subject 14  84  Subject 15  85  Subject 16  86  Subject 17  87  Subject 18  88  Subject 19   89  Subject 20  90  Apendix B: Research Ethics Board Certification of Aproval 91   92   


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