Angular Acceleration Of Head Research Articles

Encoding of head acceleration in vestibular neurons. I. Spatiotemporal response properties to linear acceleration

1. Extracellular recordings were made in and around the medial vestibular nuclei in decerebrated rats. Neurons were functionally identified according to their semicircular canal input on the basis of their responses to angular head rotations around the yaw, pitch, and roll head axes. Those cells responding to angular acceleration were classified as either horizontal semicircular canal-related (HC) or vertical semicircular canal-related (VC) neurons. The HC neurons were further characterized as either type I or type II, depending on the direction of rotation producing excitation. Cells that lacked a response to angular head acceleration, but exhibited sensitivity to a change in head position, were classified as purely otolith organ-related (OTO) neurons. All vestibular neurons were then tested for their response to sinusoidal linear translation in the horizontal head plane. 2. Convergence of macular and canal inputs onto central vestibular nuclei neurons occurred in 73% of the type I HC, 79% of the type II HC, and 86% of the VC neurons. Out of the 223 neurons identified as receiving macular input, 94 neurons were further studied, and their spatiotemporal response properties to sinusoidal stimulation with pure linear acceleration were quantified. Data were obtained from 33 type I HC, 22 type II HC, 22 VC, and 17 OTO neurons. 3. For each neuron the angle of the translational stimulus vector was varied by 15, 30, or 45 degrees increments in the horizontal head plane. In all tested neurons, a direction of maximum sensitivity was identified. An interesting difference among neurons was their response to translation along the direction perpendicular to that that produced the maximum response ("null" direction). For the majority of neurons tested, it was possible to evoke a nonzero response during stimulation along the null direction always had response phases that varied as a function of stimulus direction. 4. These spatiotemporal response properties were quantified in two independent ways. First, the data were evaluated on the basis of the traditional one-dimensional principle governed by the "cosine gain rule" and constant response phase at different stimulus orientations. Second, the response gain and phase values that were empirically determined for each orientation of the applied linear stimulus vector were fitted on the basis of a newly developed formalism that treats neuronal responses as exhibiting two-dimensional spatial sensitivity. Thus two response vectors were determined for each neuron on the basis of its response gain and phase at different stimulus directions in the horizontal head plane.(ABSTRACT TRUNCATED AT 400 WORDS)

Chapter 30 Synergies and strategies underlying normal and vestibulary deficient control of balance: implication for neuroprosthetic control

Future developments of neuroprosthetic control will probably permit locomotion and posture to be maintained without the aid of crutches and will therefore require some form of balance control. Three fundamental questions will arise. First, the question of the location of imbalance-sensing transducers must be assessed. Secondly, the synergy, which is the relative amplitude and timing of muscle activity, and/or the strategy of joint torques required to re-establish a stable posture for different types of balance disturbances must be addressed. Thirdly, the control laws that map either trunk muscle activity or imbalance-sensing transducer outputs into multi-joint postural control of standing by paraplegic individuals must be generated. The most appropriate means of gathering the relevant information applicable to neuroprosthetic control systems is through the detailed analysis of normal and non-normal human models. In order to gain such detailed insights into normal balance control and its dependence on head angular and linear accelerations, the synergy and strategy of balance corrections in normal subjects or patients with vestibular deficits were investigated for two types of support surface perturbation, a dorsiflexion rotation (ROT) and a rearward translation (TRANS). These experimentally induced perturbations to upright stance were adjusted to cause equal amplitudes of ankle dorsiflexion, thus providing additional information about the role of lower leg proprioception on balance control. Synergies defined on the basis of peak cross-correlations of each recorded muscle's EMG to that of the largest muscle response were significantly different for TRANS and ROT. Translation synergies consisted of a sequential coactivation at several levels (soleus and abdominals some 30 msec before hamstrings, and trapezius some 15 msec before paraspinals), whereas the sequential activation of paraspinals and tibialis anterior dominated the balance synergy to ROT. Likewise, response strategies, defined using cross-correlations of joint torques, differed. That for TRANS was organised as a multi-link strategy with neck torques leading those of all other joints by 40 msec or more; hip joint lead ankle torques by 30 msec. That for ROT was organised around hip and ankle torques without a major correlation to neck torques. Vestibulary deficient subjects developed weaker synergies with respect to subjects with normal balance systems under eyes-open conditions and there was no clear synergy with eyes closed. Consequently, hip torques were delayed some 180 msec with respect to ankle torques, and correlations to neck torques were completely out of phase under eyes-closed conditions. Fundamental changes in TRANS synergies and strategies also occurred in vestibulary deficient subjects for eyes-open and eyes-closed conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

A Postural Model of Balance-Correcting Movement Strategies

The patterns of joint torques and movement strategies underlying human balance corrections were examined using a postural model. Two types of support-surface perturbation, dorsiflexion rotation (ROT) and rearward translation (TRANS), were employed. These two perturbations were adjusted to produce similar profiles of ankle dorsiflexion in order to obtain information on the role of lower leg proprioceptive inputs on triggering balance corrections. In addition, the dependence of balance control on head angular and linear accelerations was investigated by comparing the responses of normal and vestibularly deficient subjects under eyes-closed and eyes-open conditions. Differences in ROT and TRANS movement strategies were examined in three ways First, the amplitude and polarity of active joint torques were analysed. These were obtained by altering joint torques applied to a postural model until movements of the model accurately duplicated those of measured responses. Second, the pattern of body-segment angular movements depicted by stick figures moving in response to the computed joint torques was investigated. Third, the peak amplitude and patterns of crosscorrelations between joint torques were measured. Active ankle, knee, and hip joint torques computed for normal subjects rotated the body forward for ROT. In the case of TRANS, computed active torques in normals were of opposite polarity to those of ROT and reversed the forward motion of the body. Subjects with vestibular deficits had lower amplitude torques for ROT and failed to counter the platform rotation. Hip torques for TRANS in vestibular deficient subjects were of opposite polarity to those of normal subjects and resulted in excessive forward trunk rotation. Normally, neck torques acted to stabilize the head in space when trunk angular velocity peaked. Vestibular deficient subjects displayed head movements in response to ROT similar to those generated when neck torques were absent. For TRANS, these same subjects exhibited overcompensatory neck torques. Stick figures of normal responses indicated a stiffening of the body into a leg and a trunk-head link for ROT and a flexible multilink motion for TRANS. Likewise, normal response strategies, defined by using crosscorrelations of joint torques, differed for ROT and TRANS. All joint torque crosscorrelations were significant for TRANS. Neck torques led those of all other joint torques by 40 ms or more, and hip joint led ankle torques by 30 ms. Joint torque correlations for ROT were organised around hip and ankle torques without a major correlation to neck torques. Fundamental changes in all torque crosscorrelations occurred for vestibularly deficient subjects under both eyes-open and eyes-closed conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptive suppression of biodynamic interference in helmet-mounted displays and head teleoperation

This paper addresses errors caused by vibration or turbulence in airborne helmet displays and teleoperation. It is shown by analysis and computer simulations that a modified version of the least-mean-squares adaptive noise suppression algorithm facilitates the separation of the large voluntary head movements from the vibrationinduced small nonvoluntary head motion. Thus, the effects of the biodynamic interference can be essentially removed. The results also indicate that errors in head-tracking teleoperated devices can essentially be suppressed. Extensive man-in-the-loop laboratory simulations that validate the method are described. YSTEM teleoperation by pilot head motion and presentation of computer-gene rated symbols and flight information in helmet-mounte d displays is emerging as a promising technology in modern avionic systems. Head teleoperation is potentially an effective method for instinctive and rapid aiming of radar antennas, missile seeker heads, or laser designators. In addition, it relieves the hands of the pilot for other vital manual tasks in increasingly complex airborne environments. Helmet-mounted displays (HMD) can, in principle, be the ultimate solution in merging computer-generated displays with the outside scene, thus embracing the entire field of view available to the pilot. Therefore, the HMD potentially relieves the pilot from the troublesome need to share his attention between the all-aspect outside scene and a restrictive cockpitmounted panel or head-up display. However, a potential shortcoming of head teleoperation and HMDs is their vulnerability to biodynamic interference resulting from vibration, atmospheric turbulence, or self-induced vehicle motion. These interferences can cause substantial random aiming errors and apparent display blurring that may seriously impair pilot performance. Two kinds of biodynamic interference exist, namely, 1) additive interferences due to nonvoluntary limb motions caused by, and correlated with, vibration,1'2 and 2) nonadditive interferences resulting from the disturbances in the central nervous system caused by the body and head vibrations, uncorrelated with them, but monotonically increasing with their intensity.3'4 Head vibration causes relative angular motion of the HMD with respect to the line of sight of the eye, which is inertially stabilized by the vestibular system. Consequently, as a result of the apparent display shift, image blurring occurs, resulting in substantial degradation of reading speed and probability of correct character recognition.5'6 This neuromotor stabilization, known as the vestibulo-ocular reflex (VOR), is effective in the frequency range of 2-10 Hz.7 Wells and Griffin6'8 conducted experiments to cancel this blurring by shifting the display in the opposite direction with an amplitude equal to the measured head motion which was determined by an approximate double integration of head angular acceleration. They succeeded in demonstrating the effectiveness of the concept, but the imperfection of the integration caused substantial transients in the display position in the presence of large angular head motion.

Human Otolithic Function Before and After Unilateral Vestibular Neurectomy1

One index of otolith function is the so-called oculogravic “illusion” that during centrifugal stimulation a small luminous bar, fixed with respect to the observer, appears to be roll-tilted by the same amount that the observer feels to be roll-tilted. Many patients undergoing therapeutic unilateral vestibular nerve section show the illusion symmetrically for left and right roll-tilts prior to the operation, but at testing one week after vestibular nerve section show a large asymmetry: they perceive the illusion when the resultant force is directed toward their intact ear, but they perceive a much reduced illusion when the force is directed toward their operated ear. This roll-tilt perceptual response asymmetry appears similar to the asymmetrical horizontal semicircular canal vestibulo-ocular responses for symmetrical but opposite head accelerations that these same patients exhibit for values of head angular accelerations in the natural range (Ewald’s second law), and the present paper suggests that a version of Ewald’s second law may apply to the otolithic system: specifically, that there is a response asymmetry for linear accelerations. Anatomical and physiological evidence concerning such an otolithic asymmetry is reviewed.

Compensation of horizontal canal related activity in the medial vestibular nucleus following unilateral labyrinth ablation in the decerebrate gerbil

The spontaneous activity and dynamic responses to two frequencies (1.3 and 0.13 Hz) of sinusoidal angular horizontal head acceleration of type I neurons in the medial vestibular nucleus were recorded bilaterally in decerebrate Mongolian gerbils (Meriones unguiculatus) under three experimental conditions; normal labyrinth intact, acutely following unilateral labyrinthine lesion, and four to seven weeks following labyrinthine lesion. The mean spontaneous activity and number of detected type I neurons decreased immediately ipsilateral to the lesion but recovered significantly with time. In contrast, spontaneous activity on the contralateral side increased during compensation following hemilabyrinthectomy. The mean response gains at both frequencies of head oscillation were depressed bilaterally and asymmetrically acutely following the lesion such that the response gain of cells on the intact side exceeded that of the neurons recorded on the injured side. After compensation the number of detected type I neurons on the side ipsilateral to the injury increased but remained below normal levels. The mean gains remained depressed but became symmetric with compensation as a result of improvement in the response of ipsilateral neurons. The phase of responses were significantly advanced in the compensated animals. Although response gain is not fully restored, the linearity of the dynamic modulation in compensated animals is improved as evidenced by a continuous modulation of the increased spontaneous activity of neurons contralateral to the hemilabyrinthectomy. It is proposed that this effect is related to the concurrent improvement in the linearity of the horizontal vestibulo-ocular response. Electrical cathodal polarization of the vestibular nerve ipsilateral to the ablated labyrinth was utilized to investigate the relationship between recovery of spontaneous activity and dynamic function. Acutely following hemilabyrinthectomy, cathodal polarization restored activity in second-order type I neurons to near normal levels but their response gain to head rotation remained depressed. Similar galvanic stimulation in compensated animals also elevated ipsilateral spontaneous activity. As in the acute preparation, such stimulation did not modify the response gain or phase. Thus, the improvement in response of type I neurons in the compensated gerbil was not a direct consequence of restoration of spontaneous activity on the side of the injury.

Compensation of horizontal canal related activity in the medial vestibular nucleus following unilateral labyrinth ablation in the decerebrate gerbil

The spontaneous activity and dynamic responses to sinusoidal horizontal head angular acceleration of type II horizontal semicircular canal related neurons in the medial vestibular nucleus (MVN) were recorded bilaterally in decerebrate Mongolian gerbils (Meriones unguiculatus) under three experimental conditions: normal labyrinths intact, acutely following unilateral labyrinthine lesion, and four to seven weeks following labyrinthine lesion. The number of type II neurons detected contralateral to the lesion was greatly reduced both in the acutely hemilabyrinthectomized animals and following compensation. The gain of the responses was depressed bilaterally acutely following the lesion. A greater reduction in response gain was noted in cells contralateral to the lesion. The gain of the contralateral type II responses increased with time such that in the compensated animal bilaterally symmetric gains were recorded. While the significant changes which occur in the gain of type II neurons with recovery from peripheral vestibular lesions can largely be attributed to type I neurons on the other side of the midline, changes in type I neurons were not entirely reflected in the type II population. The spontaneous activity of type II neurons did not undergo any significant changes following the labyrinthine lesion. We present a model utilizing the dynamic responses to estimate the functional recovery of commissural connections in compensated animals. The overall gain of the contralateral type I to ipsilateral type I commissural polysynaptic pathway appears to improve, while the efficacy in the reverse direction remains depressed, suggesting that modifications in commissural connections, particularly involving the type II to type I connections within the MVN on the injured side, mediate aspects of behavioral recovery.

Influence of static head position on the horizontal nystagmus evoked by caloric, rotational and optokinetic stimulation in the squirrel monkey

We studied the influence of static head position on the horizontal nystagmus produced by caloric, rotational and optokinetic stimulation in alert squirrel monkeys. Caloric nystagmus is stronger for nose up (NU) than for nose down (ND) pitches; so, for example, slow-phase eye velocity is four times larger in supine than in prone positions. A similarly directed asymmetry occurs in the horizontal vestibulo-ocular (HVOR) responses to long-duration, constant angular-head accelerations, but not to midband (0.1 Hz) sinusoidal head rotations. Consistent with a first-order model of the HVOR, the low-frequency or acceleration gain of the reflex (GA) is equal to the product of the midband velocity gain (GV) and a time constant (TVOR). GV is proportional to the cosine of the angle between the horizontal-canal plane and the plane of rotation, from which it is concluded that signals from the horizontal, but not from the vertical canals contribute to the HVOR. TVOR can be as much as twice as large in NU than in ND positions. GA is proportional to TVOR and it, too, shows a NU-ND asymmetry. The time constant of optokinetic after nystagmus (TOKAN) was also studied. Since TVOR and TOKAN are modified in similar ways by static tilts, it is concluded that head position affects the time constants by way of velocity-storage mechanisms. Evidence is presented that the position-dependent modification of velocity storage is otolith-mediated. The results are used to analyze the mechanisms of caloric nystagmus. The caloric response consists of a convective component (CC), as originally envisioned by Bárány (1906), and a nonconvective component (NC). CC accounts for 75% of the caloric response in the conventional supine testing position. Both components can be affected by the position-dependent modification of TVOR or, equivalently, of GA. It has been suggested that two mechanisms might contribute to NC: 1) a direct thermal effect on hair cells or afferents; or 2) a thermal expansion of labyrinthine fluids that results in a cupular displacement. Both theoretical and experimental evidence indicates that only the first of these mechanisms could result in the steady-state caloric response that is observed in the absence of convection (e.g., in spaceflight and after canal plugging) and that contributes to the prone-supine asymmetry seen in caloric testing.

Anthropomorphic dummy neck modeling and injury considerations

This study investigates the modeling of the Hybrid III dummy head and neck system and its response under impulsive loading. Two neck models were proposed, one rigid, one flexible; both give satisfactory head kinematics upon comparing to minisled test results. The flexible neck model provides a more detailed understanding of the Hybrid III neck structure behavior. It indicates that the Hybrid III neck has a torque response similar to a human neck but has higher shear response. During flexion whiplash, the torque at the occipital condyle reverses its direction at about 25 ms after impact. Since concussion may be related to the head angular acceleration, which reaches its peak value in the first 25 ms. it might be necessary to extend the existing human torque-rotation corridor to include the neck response in this region. For flexion whiplash impact, simulation results indicated that the neck injury threshold is reached before exceeding the head injury threshold as the impact velocity is increased.

Stability of the head in pitch (neck flexion-extension): studies in normal subjects and patients with axial rigidity.

The dynamic stability of the head in pitch during normal upright posture has been studied in normal subjects and patients with neurological disease affecting neck muscle tone by examining angular head acceleration responses to unpredictable linear motion of the trunk in the direction of surge. Within the frequency range of natural head movements the transfer function between head and trunk for both normal subjects and patients approximated a second-order linear differential equation involving inertia and coefficients of viscosity and elasticity. The degree of neck rigidity was determined by the damping ratio (viscosity:elasticity), which averaged .35 for normal subjects and ranged from 0.6 to 0.96 for patients with rigid syndromes. A patient with absent labyrinthine function and a "floppy" head had a damping ratio 0.18. The technique gives a numerical measurement of neck rigidity, which could be of value in characterising severity of disorder and response to therapy.

Computer Simulation of Head Impact: Estimation of Head-Injury Risk during Soccer Heading

With a validated mathematical model of the head-neck consisting of nine rigid bodies (skull, seven cervical vertebrae, and torso), we simulated head impacts to estimate the injury risk associated with soccer heading. Experimental data from head-linear accelerations during soccer heading were used to validate the nine-body head-neck model for short duration impact loading of the head. In the computer simulations, the mass ratios between head mass and impacting body mass, the velocity of the impacting body, and the impact elasticity were varied. Head-linear and angular accelerations were compared to standard head-injury tolerance levels, and the injury risk specifically related to soccer heading was estimated. Based on our choice of tolerance levels in general, our simulations showed that injury risk from angular head accelerations was greater than from linear head accelerations, and compared to frontal impacts, lateral impacts had greater angular and less linear head accelerations. During soccer heading, our simulations indicated an unacceptable injury risk caused by angular head accelerations for frontal and lateral impacts at relatively low impact velocities for children, and at medium range impact velocities for adults. For linear head accelerations, injury risk existed for frontal and lateral impacts at medium range to relatively larger impact velocities for children, while no injury risk was shown for adults throughout the entire velocity range. For injury prevention, we suggest that head-injury risk can be reduced most substantially by increasing the mass ratio between head and impacting body. In soccer with children, the mass of the impacting body has to be adjusted to the reduced head mass of a child, that is, it must be clearly communicated to parents, coaches, and youngsters to only use smaller soccer balls.

頭振後眼振と頭部角加速度および温度眼振との比較

A head-shaking test in generally used to provoke vestibular nystagmus. We tried two types of head-shaking tests. One is head-shaking by the examiner and the other is head-shaking by the patient. The elicited head-shaking nystagmus (HSN) was recorded on an electronystagmograph. At the same time acceleration of the patient's head was recorded by an accelerometer attached to the forehead with a headband and converted into acceleration. We studied 36 patients who had complained of vertigo.We found the angular acceleration of the patient's head ranged from 3000°/s2 to 11500°/s2, but there was no correlation between the appearance of HSN and the angular acceleration of the patient's head. There was no correlation between the slow phase velocity of HSN and the angular acceleration, either.Next, we investigated the correlation between canal paresis and the slow phase velocity of HSN. The coefficient of correlation was only 0.53, but there was a tendency that the severer the canal paresis was, the larger was the slow phase velocity of the elicited nystagmus.

Indicators of the influence a peripheral vestibular deficit has on vestibulo-spinal reflex responses controlling postural stability.

For a controlled sway stabilization task, the areas underlying EMG responses in ankle and neck muscles, as well as amplitudes of ankle torque responses, were shown to be significantly correlated with the clinically defined extent of a patient's peripheral vestibular deficit. The responses, elicited by ankle dorsiflexion of the support surface on which the subject stood, were statistically examined in order to select those measurements which would best indicate differences between a normal, a patient with a unilateral deficit, or one with a bilateral deficit. For this purpose, a stepwise discriminant analysis was performed on measurements of head and trunk angular accelerations in addition to muscle EMG and ankle torque signals. The primary measurements selected to optimally assign a subject to a population were the periods of ankle torque and neck extensor activity associated with correcting for the imposed body displacement backwards and maintaining upright head position respectively. The resulting division into populations was 100% correct. However, within the population of unilateral deficit patients, the technique failed to correctly identify those with acute from those with compensated deficit. This technique of investigating vestibulo-spinal reflex responses is more specific and sensitive than Romberg tests, because it will quantify and specify the underlying cause of the patient's balance and ambulatory disorder.

Visual and vestibular contributions to pitch sway stabilization in the ankle muscles of normals and patients with bilateral peripheral vestibular deficits.

Vestibular, visual, and proprioceptive influences on muscle activity correcting for backwards body tilt were investigated in normals and patients with bilateral peripheral vestibular deficits. Body tilt was induced by a dorsi-flexion rotation of the feet about the ankle joints while the subject stood on a force measuring platform. Ankle muscle activity and torque were monitored as upright stance was reestablished, and correlated with head angular accelerations and neck muscle activity. In normals with eyes closed, soleus stretch reflex activity at 50-80 ms was followed by two bursts of tibialis anterior (TA) EMG activity at ca 80 and 125 ms from the onset of 36 deg/s, 3 deg amplitude platform rotations. Neck muscle activity rotated the head backwards at the same time as TA activity rotated the body forwards about the ankle joints. Under the influence of vision, i.e. eyes open, slight increases in the second burst of TA activity, and ankle torque were observed. When the subjects sat, and were instructed to activate TA rapidly on onset of the platform movement, TA EMG activity increased gradually at ca. 150 ms and not as a burst. In patients with long-lasting bilateral vestibular deficits, both bursts of TA activity were significantly less than normal with eyes closed. Consequently sway correcting torques were abnormally low and all but one of the patients fell over backwards. With eyes open, TA activity was slightly less than, and ankle torques were approximately equal to normal values. In contrast to normals, TA responses obtained in standing and sitting positions were not significantly different. Neck EMG activity varied from normal, consisting of a long burst 100 ms in duration. The present data indicate that a coordinated pattern of ankle, and neck muscle activity occurs during the first 150 ms following induced backward tilt. Ankle muscle activity corrects for the body sway, and neck muscle activity attempts to stabilise the head with respect to earth fixed coordinates. It is proposed that the vestibulo-spinal reflex system predominantly underlies the genesis and coordination of this muscle activity.

Responses of semicircular canal and otolith afferents to small angle static head tilts in the Gerbil

The discharge activity of first-order vestibular neurons was recorded in anesthetized or decerebrated gerbils from the post-ganglionic fibers of the vestibular nerve. Semicircular canal afferents were distinguished from otolith afferents on the basis of their responses to linear and angular head acceleration. In decerebrated preparations, canal afferents exhibited significantly faster discharge activity (average= 87.8impulses/s) than that of canal afferents in anesthetized preparations (average= 66.2impulses/s), when the head was held to position the lateral semicircular canals coplanar with the earth horizontal plane (standard position). The effects of changes in linear forces on vestibular afferent activity were determined by statically tilting the head ± 10° about either the fore-aft and/or left-right head axes. A change in activity, from that recorded in the standard position, of 10% or greater was considered significant. Using this criterion, significant changes in the tilt response in anesthetized animals were observed in both anterior (23 of 48 neurons, 48%) and lateral (22 of 31, 71%) canal afferents as well as otolith (18 of 25, 72%) afferents. In decerebrated preparations for tilts around the pitch (left-right) axis, comparable effects were measured in (19 of 36, 53%) anterior and (17 of 30, 57%) lateral canal afferents. Neurons with irregular firing activity were more likely than regularly firing canal afferents to change their average discharge rate during static tilt. No significant differences in response magnitude to ± 10° head tilt were found between canal and otolith afferents in anesthetized animals. Mechanisms to account for the responses to linear acceleration of canal afferents are discussed.

A comparison of nonfatal motor vehicle occupant injuries in crash versus noncrash events

The description of cervical spine motion and the risk to sustain a cervical spine injury is mainly based on cadaver studies. As the active influence of soft tissue is neglected in cadaver studies, our understanding of the kinematic model for whiplash is limited. Therefore the objective of this study was, to describe the in vivo cervical spine motion and acceleration during rear-end sled collisions to identify sequences of motion in which the risk of injury to the cervical spine is increased.A rear-end collision with a speed change (ΔV) of 6.3 km/h was simulated in a sled test with eight female subjects with no history of prior injury or pain of the cervical spine. A high-speed camera was used to document motion data. Acceleration data were recorded using accelerometers. Acceleration input to the cervical spine was assessed by the simultaneous analysis of the head angle and angular head acceleration as well as the simultaneous analysis of the relative motion and the relative acceleration between the head and T1 to define intervals of increased risk of cervical spine injuries during rear-end collision.The motion sequence is characterized by the same phases that have already been described for male volunteers. Increasing angular head acceleration can explain facet joint injuries during the extension movement (100–120 ms) and hence occur about 50 ms later than shown in cadaver models. In the late rebound the combination of maximal ventral head acceleration and head movement is underestimated and can be responsible for soft tissue injuries.The study shows that during the extension phase and the late rebound phase, acceleration and movement pattern occur that could lead to cervical spine injuries.

Characteristics of responses of medial brain stem neurons to horizontal head angular acceleration and electrical stimulation of the labyrinth in the cat

Characteristics of responses of medial brain stem neurons to horizontal head angular acceleration and electrical stimulation of the labyrinth in the cat

On the kinematics of the head using linear acceleration measurements

The paper deals with an application of the nine accelerometer scheme proposed by Padgaonkar et al. (1975) to the analysis of the head kinematics including the head angular acceleration and velocity using linear acceleration measurements. The computed results have been compared with the film analysis and with the actual measured quantities in the case of the dummy experiments. The study reveals an excellent agreement among these results and indicates the feasibility of the application of the method to biomechanical studies.

Mathematical simulation of gliding contusions

A gliding contusion in the acute phase is characterized by a streaklike hemorrhage of venous origin situated subcortically in a paramedial convolution. In later stages perivascular necrosis may develop. This type of injury is caused by head angular acceleration and is often seen in traffic casualties when the head has hit the steering wheel, the dashboard or the windshield. The deformation of the brain matter close to the superior sagittal sinus has been simulated by means of a mathematical viscoelastic model in order to clarify the genesis of the gliding contusions. The blood vessels in the brain matter will be strained as a consequence of the brain deformation which results from head angular acceleration. The highest values of the strain occur subcortically where the blood vessels are injured first. The tolerance levels for gliding contusions have been deter- mined. The calculations which were based on experiments regarding the dynamic properties of the superior cerebral veins and on two alternative injury criteria proposed, indicate that a gliding contusion is not likely to arise if the maximal angular acceleration does not exceed 4500 rad/sec' or the change in angular -velocity does not exceed 70_rad/sec. INTRODUCHON Lindenberg and Freytag (1960) have described exten- sive hemorrhages of traumatic origin which were sit- uated subcortically in the paramedial parts of the cer- ebral hemispheres. The hemorrhages were of venous nature and were considered to be caused by deforma- tion of the brain matter when the head was subjected to angular acceleration. The lesions were designated as gliding contusions. For consecutive autopsy mater- ial Voigt and Lawenhielm (1974) have demonstrated similar injuries in 25% of traffic casualties. Also in these cases a head angular acceleration had occurred. The hemorrhages were however not always as exten- sive as in the description by Lindenberg and Freytag (1960). They appeared 'as streaklike perivascular bleedings mostly found in the back aspect of the fron- tal superior gyrus and in the upper part of the anter- ior central convolution. The hemorrhages seemed to originate from intracerebral portions of the superior cerebral veins. In victims surviving more than one week areas with necrosis or perivascular glial scars often running deeply into the white matter could be found. Remarkably the peripheral layers of the brain cortex remained intact in spite of sometimes extensive injuries. Brain injuries due to head impact can be very com- plex. The gliding contusion may be part of such an injury pattern but may as well not be present. On the other hand gliding contusions can occur alone. Different mechanisms of origin probably account for these differences. Although lesions of the gliding con- tusion type are quite common in traffic accidents they have attracted little attention in the literature. There- fore an investigation to clarify the genesis of the glid- ing contusion and thereby make it possible to predict threshold levels was needed. * Received 15 Jffrzuury 1975.

Neural pathways from the vestibular labyrinths to the flocculus in the cat.

In decerebrate, unanesthetized cats, responses in the flocculus were evoked by electric stimulation of the vestibular nerves and by natural stimulation of horizontal head angular acceleration. Field potentials in the flocculus and intracellular recording from Purkinje cells following vestibular nerve stimulation indicated that the responses were produced by mossy fiber inputs. Field potentials evoked from the contralateral labyrinth were as large as those from the ipsilateral one. There was considerable convergence of bilateral labyrinthine mossy fiber inputs to a Purkinje cell. In view of the effects of incision at the midline of the cerebellum and the brain stem, inputs from the contralateral labyrinth were mainly conveyed through the midline of the brain stem and partly through the midline of the cerebellum. Primary vestibular afferents were involved in the transcerebellar crossed pathway. Fibers of the secondary vestibular neurons projecting to the contralateral flocculus were implicated in the brain stem-mediated pathway and, in part, presumably in the transcerebellar crossed pathway. About one-third of the axon spikes examined in the flocculus responded to horizontal head angular acceleration. Commissural inhibition was observed in more than half of the axon spikes in the flocculus which were presumed to be mono- or polysynaptically activated from the vestibular nerve.