Head-trunk movement coordination in the standing posture.
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Biomedical subjects
Publications and source records attributed to F B Horak.
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Vestibular status and motor proficiency of 30 hearing-impaired and 15 motor-impaired learning-disabled children were documented to determine whether vestibular loss can account for deficits in motor co-ordination. Vestibular loss was differentiated from sensory organization deficits by means of VOR and postural orientation test results, which were compared with those of 54 normal seven-to 12-year-olds. Reduced or absent vestibular function in 20 hearing-impaired children did not affect development of motor proficiency, except in specific balance activities. However, sensory organization deficits in the learning-disabled group and in three of the hearing-impaired children were associated with widespread deficits in motor proficiency.
1. The role of sensory information in shaping muscle activation patterns to postural perturbations in humans was investigated by varying velocity, amplitude, or duration of the perturbing stimulus. Ten normal subjects were exposed to 120 backward translations of the support surface under conditions of varying velocities (10-35 cm/s, constant amplitude), varying amplitudes (1.2-12 cm, constant velocity), or varying durations (40-800 ms). The effects of perturbation parameters on movement kinematics and EMG latencies, patterns, and integrated areas in six trunk and leg muscles were examined. Integrated EMG activity was normalized across subjects and the early (first 75 ms), middle (second 75 ms), and late (last 350 ms) components were analyzed separately. 2. Ankle, knee, and hip angle trajectories and surface reactive forces suggest that a relatively consistent movement strategy was scaled to the perturbation velocities and amplitudes applied. 3. Short-duration perturbations (75 ms) evoked a single burst of muscle activity (75-100 ms duration) in gastrocnemius, hamstrings, paraspinal, and rectus abdominis muscles at latencies too long to be explained by simple stretch reflexes. EMG latencies, patterns, and integrated areas were independent of the velocity and amplitude of the short-duration perturbations, suggesting a minimal time to incorporate peripheral velocity information into the triggered response. 4. For translations lasting longer than 75 ms, the integrated areas of the early agonist EMG bursts were positively correlated with stimulus velocity. The integrated area of later, more tonic EMG components were best correlated with stimulus amplitude. These relationships were found in both distal (stretched) muscles and in proximal muscles. Absolute latencies (94-145 ms), intersegmental latencies (18-29 ms), and burst durations (75-100 ms) were not influenced by the velocity or amplitude of the stimulus. 5. These results suggest that the spatial and temporal organization of automatic postural responses may be organized independently of response intensity. Within a particular spatial-temporal pattern, the amount of muscle activation appears to be adjusted by sensory information, which specifies velocity and amplitude of the perturbation.
The purpose of this study was to investigate the relationship of vestibular function to motor proficiency, including balance, in children with hearing impairments. Thirteen children with normal hearing and 29 children with hearing impairments, ranging in age from 7 to 13 years, were classified into categories based on vestibular function using neuro-otologic measures (ie, vestibulo-ocular reflex function and posturography). Children in each category were tested for motor proficiency using clinical assessment measures (eg, balance, muscle tone, and coordination). The test results indicated that the children with hearing impairments and normal peripheral vestibular function (n = 7) exhibited normal motor proficiency, including balance. The children with hearing impairments and loss of peripheral vestibular sensitivity (n = 19) also demonstrated normal motor proficiency, except for balance ability. The children with hearing impairments and sensory organization deficits (n = 3), however, exhibited motor deficits in many areas. The results of this study indicate that motor proficiency in children with hearing impairments depends on vestibular function. Interventions for motor deficits in children with hearing impairments, therefore, must consider vestibular function as well as motor performance.
Postural control is the ability to maintain equilibrium and orientation in a gravitational environment. Effective approaches for clinical measurement of postural control remain to be developed. This article summarizes important neurophysiological and clinical considerations for developing measurement tools to assess postural control in adults. The postural control system is divided into three basic functional components for assessment: 1) biomechanical components, 2) motor coordination components, and 3) sensory organization components.
The transition among hominids from quadrupedalism to bipedalism resulted in modifications in their musculoskeletal morphology. It is unclear, however, whether changes in the circuitry of the CNS were also necessary in order to accommodate the unique balance requirements of two-limb support. This study addresses the issue of modifications in control strategies by investigating the rapid, automatic postural responses of feline and human subjects to sudden disturbances of balance in the anteroposterior (AP) direction while they stand quadrupedally and bipedally on movable platforms. Postural responses are characterized in terms of segmental adjustments, generated AP shear forces, and electromyographic activity. Feline and human subjects correct posture similarly when standing quadrupedally. Furthermore, both species correct stance primarily with their hindlimbs and use their forelimbs as supportive struts. In contrast, both species use completely different correctional strategies when standing bipedally. Morphological restrictions, however, prevent cats from adopting the pillar-like plantigrade posture of human beings. Thus, the correctional strategies of bipedal cats are distinct from those of bipedal human subjects. It is concluded that 1) automatic postural response patterns of quadrupedal Felis and bipedal Homo reflect the different biomechanical characteristics of the initial postures rather than species differences in CNS circuitry controlling stance; 2) hindlimb-dominated posture control is probably a common and relatively ancient pattern; and 3) reorganization of hominid CNS circuitry was probably unnecessary because hindlimb control was already a feature of the system.
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We studied the extent to which automatic postural actions in standing human subjects are organized by a limited repertoire of central motor programs. Subjects stood on support surfaces of various lengths, which forced them to adopt different postural movement strategies to compensate for the same external perturbations. We assessed whether a continuum or a limited set of muscle activation patterns was used to produce different movement patterns and the extent to which movement patterns were influenced by prior experience. Exposing subjects standing on a normal support surface to brief forward and backward horizontal surface perturbations elicited relatively stereotyped patterns of leg and trunk muscle activation with 73- to 110-ms latencies. Activity began in the ankle joint muscles and then radiated in sequence to thigh and then trunk muscles on the same dorsal or ventral aspect of the body. This activation pattern exerted compensatory torques about the ankle joints, which restored equilibrium by moving the body center of mass forward or backward. This pattern has been termed the ankle strategy because it restores equilibrium by moving the body primarily around the ankle joints. To successfully maintain balance while standing on a support surface short in relation to foot length, subjects activated leg and trunk muscles at similar latencies but organized the activity differently. The trunk and thigh muscles antagonistic to those used in the ankle strategy were activated in the opposite proximal-to-distal sequence, whereas the ankle muscles were generally unresponsive. This activation pattern produced a compensatory horizontal shear force against the support surface but little, if any, ankle torque. This pattern has been termed the hip strategy, because the resulting motion is focused primarily about the hip joints. Exposing subjects to horizontal surface perturbations while standing on support surfaces intermediate in length between the shortest and longest elicited more complex postural movements and associated muscle activation patterns that resembled ankle and hip strategies combined in different temporal relations. These complex postural movements were executed with combinations of torque and horizontal shear forces and motions of ankle and hip joints. During the first 5-20 practice trials immediately following changes from one support surface length to another, response latencies were unchanged. The activation patterns, however, were complex and resembled the patterns observed during well-practiced stance on surfaces of intermediate lengths.(ABSTRACT TRUNCATED AT 400 WORDS)
Monkeys were trained to make a visually triggered arm-reaching movement to a lighted button in a simple reaction-time paradigm, during which the reaction time (RT) and movement time (MT) were measured. Stimulus trains of varying duration were applied at various times before and during the movement at locations in the globus pallidus where application of long stimulus trains caused increased MTs. A critical stimulus period was identified during which stimulus application effectively prolonged MTs. The activity of pallidal neurons was examined during performance of the same behavioral task. More than 60% of the neurons examined showed task-related changes in activity that began before or during the reaching movement. For 45% of these cells, the initial change in firing occurred during the critical stimulus period, 50-150 ms before mechanically detected movement. Comparison of the critical stimulus period, the time of task-related changes in the discharge of pallidal neurons, and the time of EMG activity in muscles acting at the back, shoulder, elbow, and wrist revealed that both the critical stimulus period and changes in neuronal discharge occurred at or after initial muscle activation and during the buildup of EMG activity. These data are consistent with a model in which the globus pallidus plays a role in scaling the magnitude of muscle activity that determines movement velocity without affecting the initiation or sequential organization of the programmed motor output.
The activation times for trunk and leg muscles were examined in normal and left hemiplegic subjects who raised their right arms at different velocities in self-paced or reaction time conditions. Activity in these postural muscles preceded arm displacement, and they were activated in a similar sequence during all types of rapid movements. The presence and sequencing of associated postural adjustments were more variable during slow movements.
The role of basal ganglia output via the globus pallidus (GP) was examined in monkeys trained to make rapid arm-reaching movements to a visual target in a reaction-time task. When neurons in the globus pallidus were destroyed by injection of kainic acid (KA) during task execution, contralateral arm movement times (MT) were increased significantly, with little or no change in reaction times (RT). The slowed movements were associated with a generalized depression in the amplitude and rate of rise of electromyographic (EMG) activity in all the contralateral muscles studied at the wrist, elbow, shoulder, and back, but there was no change in the sequential activation of these muscles. The most profound and persistent increases in movement time occurred when neurons were destroyed in the ventrolateral and caudal aspects of the internal as well as external pallidal segment. These results suggest a role for globus pallidus output in scaling the magnitude and/or buildup of EMG activity without affecting the initiation or the sequential organization of the programmed motor output.
The effect of changing basal ganglia activity with electrical stimulation in and around the globus pallidus (GP) was studied in monkeys trained to make rapid arm-reaching movements to a visual target in a reaction time task. As was the case following kainic acid (KA) lesions of the globus pallidus (30), stimulation changed movement times (MT) without affecting the pattern of sequential activation of muscles involved in the task or, in most cases, the reaction times (RT). Stimulation in the ventrolateral internal segment of the globus pallidus (GPi) or in the ansa lenticularis reduced movement times, whereas stimulation at many sites in the external pallidal segment (GPe), dorsal GPi, and putamen increased movement times for the contralateral arm. These results are consistent with the hypothesis that arm movements are speeded up when the critical output of GPi is increased and arm movements are slowed down when critical GPi output is reduced, either by an inhibitory process (via stimulation-induced activation of inhibitory elements presynaptic to GPi) or by destroying GPi neurons (via kainic acid). The influence of the basal ganglia on the scaling of electromyographic (EMG) amplitude, as opposed to the spatiotemporal organization of EMG activation, is discussed.
The concept of a generalized aging effect on a generalized balance mechanism is discussed, and an alternative, multicomponent approach to understanding the heterogeneity of postural dyscontrol in the elderly is presented. Neural sensorimotor components of normal postural control mechanisms are identified and discussed. The effects of Parkinson's disease, hemiplegia, cerebellar degeneration, peripheral vestibular loss, and other disorders on the components of postural control are summarized. Quantitative posturography is advocated to detect preclinical manifestation of multiple musculoskeletal and neuromuscular pathologies and reduced compensatory abilities in posturally unstable elderly adults.
Patients with panic disorder and patients with vestibular disorders often share symptomatology, such as dizziness, spatial disorientation, and anxiety in particular environments. Because of the similar clinical presentations, it is not always apparent whether these symptoms are due primarily to a vestibular disorder or to panic disorder. Depending on where and how these patients enter the medical system, their symptoms may be remedied by treatment from behavioral therapists or physical therapists trained in vestibular rehabilitation. Although vestibular rehabilitation developed independently of behavioral treatment for anxiety disorders, there are remarkable similarities in treatment conceptualization and implementation. For example, both use exposure procedures designed to produce habituation of dizziness and disorientation, as well as enhancing functional compensation. Furthermore, there appears to be a subset of individuals with panic disorder who also have vestibular pathology and thus, may benefit from both interventions. In this paper, similarities and differences in the clinical presentation, treatment goals, and specific interventions for patients with panic disorder or vestibular pathology is examined, and future implications are discussed.
Twelve subjects, 6 bilateral vestibular-loss (3 well compensated and 3 poorly compensated) and 6 controls, attempted to maintain balance during anterior-posterior sinusoidal surface translation at 6 different frequencies. For frequencies or= 0.75 Hz, these subjects fixed their head/upper-trunk in space. Poorly compensated vestibular subjects showed large head and center of mass variability and were unable to balance at frequencies requiring a head fixed in space pattern. All vestibular subjects were less stable with vision than the controls. Without vision, vestibular subjects experienced more falls than the controls at all frequencies, with falls observed in 61% of the vestibular subjects trials and 16% of the control subjects trials. Vestibular information is important in stabilizing head and upper-trunk motion in space. Visual and somatosensory information can compensate, in part, for vestibular-loss. The results are discussed in light of models that characterize postural control in a vestibular/visual top-down and somatosensory bottom-up manner.
We identify a population of patients with vestibular complaints who show excessive hip sway and center of gravity movement during clinical balance testing. To determine the postural control strategy used by these patients, the body movement and muscle activation patterns of 9 patients responding to backward support surface translations were studied. Patients' responses were compared to those of normal subjects tested both under the same conditions and while using hip sway to balance across a narrow beam. Unlike normal subjects responding to translations of a flat support surface, all patients showed hip movement patterns that kinematically resembled the movements of normal subjects balancing across a beam. Although all patients showed the same body movement patterns, they showed two different muscle activation patterns, neither of which was similar to those of normal subjects responding to flat support surface translations. Four patients showed bursts in abdominal and/or quadriceps muscles characteristic of active hip flexion to move the center of mass, although the timing of these bursts was variable. The remaining 5 patients showed minimal activation of any proximal muscles, suggesting a failure to control upper body motion resulting from activation of ankle muscles. To determine whether the excessive hip sway observed in these patients could be a voluntary response to platform translation, the patients' responses were compared to those of a second group of normal subjects voluntarily responding to backward support surface translations with hip sway. Unlike the patients, all normal subjects responding voluntarily consistently activated abdominal muscles slightly later than ankle muscles. It is therefore unlikely that the patients' responses to platform translations were simply voluntary responses. Thus, vestibular deficits can result in abnormally coordinated postural movement strategies that result in excessive hip sway.
Control of head position during postural responses is important to facilitate both the interpretation of vestibular signals and the stabilization of gaze. In these experiments, we compared head stabilization for two different postural tasks: 1) in response to perturbations at the head, and 2) in response to perturbations induced at the support surface, which perturb both body and head position. To determine whether normal vestibular function is necessary for head stabilization in these two tasks, responses to forward and backward mechanical perturbations of the head and body were compared for 13 normal subjects and 4 patients with profound bilateral vestibular loss (two with vestibular loss in adulthood and two in infancy). Normal subjects showed little neck muscle activity for body perturbations, but large, early activations in both neck extensors and flexors for head perturbations. In contrast, vestibular patients showed excessive neck muscle activation for body perturbations and reduced or absent neck muscle activity for head perturbations. Patients with vestibular loss in adulthood also showed increased head acceleration in response to both head and body perturbations, but patients with vestibular loss in infancy showed more normal head accelerations. For body perturbations, the differences in head acceleration between patients and normals were greater for later head acceleration peaks, indicating poor head control during the execution of the postural response. Trunk angle changes were also higher in the patients for forward body perturbations, indicating that poorer control of trunk position could have contributed to their poorer head stabilization. These results indicate that the vestibular system plays an important role in head and trunk stabilization for both head and body perturbations. However, the more normal head accelerations of the patients with infant vestibular loss also indicate that other mechanisms, possibly involving neck reflexes, can at least partially substitute for the vestibular system to provide head and trunk stabilization.