Fingertip touch improves postural stability in patients with peripheral neuropathy.

The purpose of this work was to determine whether fingertip touch on a stable surface could improve postural stability during stance in subjects with somatosensory loss in the feet from diabetic peripheral neuropathy. The contribution of fingertip touch to postural stability was determined by comparing postural sway in three touch conditions (light, heavy and none) in eight patients and eight healthy control subjects who stood on two surfaces (firm or foam) with eyes open or closed. In the light touch condition, fingertip touch provided only somatosensory information because subjects exerted less than 1 N of force with their fingertip to a force plate, mounted on a vertical support. In the heavy touch condition, mechanical support was available because subjects transmitted as much force to the force plate as they wished. In the no touch condition, subjects held the right forefinger above the force plate. Antero-posterior (AP) and medio-lateral (ML) root mean square (RMS) of center of pressure (CoP) sway and trunk velocity were larger in subjects with somatosensory loss than in control subjects, especially when standing on the foam surface. The effects of light and heavy touch were similar in the somatosensory loss and control groups. Fingertip somatosensory input through light touch attenuated both AP and ML trunk velocity as much as heavy touch. Light touch also reduced CoP sway compared to no touch, although the decrease in CoP sway was less effective than with heavy touch, particularly on the foam surface. The forces that were applied to the touch plate during light touch preceded movements of the CoP, lending support to the suggestion of a feedforward mechanism in which fingertip inputs trigger the activation of postural muscles for controlling body sway. These results have clinical implications for understanding how patients with peripheral neuropathy may benefit from a cane for postural stability in stance.

Ankle and hip postural strategies defined by joint torques.

Previous studies have identified two discrete strategies for the control of posture in the sagittal plane based on EMG activations, body kinematics, and ground reaction forces. The ankle strategy was characterized by body sway resembling a single-segment-inverted pendulum and was elicited on flat support surfaces. In contrast, the hip strategy was characterized by body sway resembling a double-segment inverted pendulum divided at the hip and was elicited on short or compliant support surfaces. However, biomechanical optimization models have suggested that hip strategy should be observed in response to fast translations on a flat surface also, provided the feet are constrained to remain in contact with the floor and the knee is constrained to remain straight. The purpose of this study was to examine the experimental evidence for hip strategy in postural responses to backward translations of a flat support surface and to determine whether analyses of joint torques would provide evidence for two separate postural strategies. Normal subjects standing on a flat support surface were translated backward with a range of velocities from fast (55 cm/s) to slow (5 cm/s). EMG activations and joint kinematics showed pattern changes consistent with previous experimental descriptions of mixed hip and ankle strategy with increasing platform velocity. Joint torque analyses revealed the addition of a hip flexor torque to the ankle plantarflexor torque during fast translations. This finding indicates the addition of hip strategy to ankle strategy to produce a continuum of postural responses. Hip torque without accompanying ankle torque (pure hip strategy) was not observed. Although postural control strategies have previously been defined by how the body moves, we conclude that joint torques, which indicate how body movements are produced, are useful in defining postural control strategies. These results also illustrate how the biomechanics of the body can transform discrete control patterns into a continuum of postural corrections.

The timing of galvanic vestibular stimulation affects responses to platform translation.

We compared the effects of galvanic vestibular stimulation applied at 0, 0.5, 1.5 and 2.5 s prior to a backward platform translation on postural responses. The effect of the galvanic stimulation was largest on the final equilibrium position of the center of pressure (CoP). The largest effects occurred for the 0.5 and 0-s pre-period, when the dynamic CoP pressure changes in response to both the galvanic stimulus and the platform translation coincided. The shift in the final equilibrium position was also larger than the sum of the shifts for the galvanic stimulus and the platform translation alone for the 0.5 and 0-s pre-periods. The initial rate of change of the CoP response to the platform translation was not significantly affected in any condition. Changes in the peak CoP position could be accounted for by local interaction of CoP velocity changes induced by the galvanic and translation responses alone, but the changes in final equilibrium position could only be accounted for by a change in global body orientation. These findings suggest that the contribution of vestibulospinal information is greatest during the dynamic phase of the postural response, and that the vestibular system contributes most to the later components of the postural response, particularly to the final equilibrium position. These findings suggest that a nonlinear interaction between the vestibular signal induced by the galvanic current and the sensory stimuli produced by the platform translation occurs when the two stimuli are presented within 1 s, during the dynamic phase of the postural response to the galvanic stimulus. When presented at greater separations in time, the stimuli appear to be treated as independent events, such that no interaction occurs.

Role of vestibular information in initiation of rapid postural responses.

Patients with bilateral vestibular loss have difficulty maintaining balance without stepping when standing in tandem, on compliant surfaces, across narrow beams, or on one foot, especially with eyes closed. Normal individuals (with no sensory impairment) maintain balance in these tasks by employing quick, active hip rotation (a "hip strategy"). The absence of a hip strategy in vestibular patients responding to translations of a short support surface has previously been taken as evidence that the use of hip strategy requires an intact vestibular system. However, many tasks requiring hip strategy alter one or a combination of important system characteristics, such as initial state of the body (tandem stance), dynamics (compliant surfaces), or biomechanical limits of stability (narrow beams). Therefore, the balance deficit in these tasks may result from a failure to account for these support surface alterations when planning and executing sensorimotor responses. In this study, we tested the hypothesis that vestibular information is critical to trigger a hip strategy even on an unaltered support surface, which imposes no changes on the system characteristics. We recorded the postural responses of vestibular patients and control subjects with eyes closed to rearward support surface translations of varying velocity, in erect stance on a firm, flat surface. Subjects were instructed to maintain balance without stepping, if possible. Faster translation velocities (25 cm/s or more) produced a consistent pattern of early hip torque (first 400 ms) in control subjects (i.e., a hip strategy). Most of the patients with bilateral vestibular loss responded to the same translation velocities with similar torques. Contrary to our hypothesis, we conclude that vestibular function is not necessary to trigger a hip strategy. We postulate, therefore, that the balance deficit previously observed in vestibular patients during postural tasks that elicit a hip strategy may have been due to the sensorimotor consequences of the system alterations imposed by the postural tasks used in those studies. Preliminary results from two younger patients who lost vestibular function as infants indicate that age, duration of vestibular loss, and/or the timing of the loss may also be factors that can influence the use of hip strategy as a rapid postural response.

Effects of vestibular loss on head stabilization in response to head and body perturbations.

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.

Organizing sensory information for postural control in altered sensory environments.

Healthy human subjects can maintain adequate balance despite distorted somatosensory or visual feedback or vestibular feedback distorted by a peripheral vestibular disorder. Although it is not precisely known how this sensorimotor integration task is achieved, the nervous system coordinates information from multiple sensory systems to produce motor commands differently in different sensory environments. These different ways of coordinating sensory information and motor commands can be thought of as "sensorimotor states". The way the nervous system distributes the monitoring of postural sway among states is analysed in this paper as a logical structure of transitions between states. The form of the transition structure is specified and distinguished from a finite state machine. The hypothesis that the nervous system could use a transition structure to maintain balance is tested by developing transition structures which are consistent with a set of experimental observations of postural control in healthy subjects and three groups of patients with peripheral vestibular disease.

Effect of galvanic vestibular stimulation on human postural responses during support surface translations.

1. We investigated the role of the vestibular system in postural control by combining galvanic vestibular stimulation (0.2-0.5 mA) with platform translations in standing subjects. Vestibular stimulation delivered 500 ms before and continuously during the platform translation produced little change in the earliest center of pressure (COP) and center of mass (COM) movements in response to platform translations, but resulted in large changes during the execution of the postural movement and in the final equilibrium position. 2. Vestibular stimulation produced anterior or posterior shifts in the position of COP and COM, depending on the polarity of the galvanic current. These shifts were larger during platform translations than during quiet stance. The peak of these shifts in COP and COM occurred at 1.5-2.5 s after the onset of platform translation, and increased in magnitude with increasing platform velocity. The final equilibrium positions of COP and COM were also shifted, but these shifts were smaller and not dependent on platform velocity. 3. These results imply that a tonic step of galvanic current to the vestibular system can change the final equilibrium position for an automatic postural response. Furthermore, these results indicate that the vestibular system may play a larger role in interpreting sensory reafference during postural movements, and especially during fast postural movements, than in controlling quiet stance. Finally, these results indicate that the vestibular system does not play a critical role in triggering the earliest postural responses, but it may be critical in establishing an internal reference for verticality.

Hip sway associated with vestibulopathy.

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.

Vestibular and somatosensory contributions to responses to head and body displacements in stance.

The relative contribution of vestibular and somatosensory information to triggering postural responses to external body displacements may depend on the task and on the availability of sensory information in each system. To separate the contribution of vestibular and neck mechanisms to the stabilization of upright stance from that of lower body somatosensory mechanisms, responses to displacements of the head alone were compared with responses to displacements of the head and body, in both healthy subjects and in patients with profound bilateral vestibular loss. Head displacements were induced by translating two 1-kg weights suspended on either side of the head at the level of the mastoid bone, and body displacements were induced translating the support surface. Head displacements resulted in maximum forward and backward head accelerations similar to those resulting from body displacements, but were not accompanied by significant center of body mass, ankle, knee, or hip motions. We tested the effect of disrupting somatosensory information from the legs on postural responses to head or body displacements by sway-referencing the support surface. The subjects' eyes were closed during all testing to eliminate the effects of vision. Results showed that head displacements alone can trigger medium latency (48-84 ms) responses in the same leg and trunk muscles as body displacements. Nevertheless, it is unlikely that vestibular signals alone normally trigger directionally specific postural responses to support surface translations in standing humans because: (1) initial head accelerations resulting from body and head displacements were in opposite directions, but were associated with activation of the same leg and trunk postural muscles; (2) muscle responses to displacements of the head alone were only one third of the amplitude of responses to body displacements with equivalent maximum head accelerations; and (3) patients with profound bilateral vestibular loss showed patterns and latencies of leg and trunk muscle responses to body displacements similar to those of healthy subjects. Altering somatosensory information, by sway-referencing the support surface, increased the amplitude of ankle muscle activation to head displacements and reduced the amplitude of ankle muscle activation to body displacements, suggesting context-specific reweighting of vestibular and somatosensory inputs for posture. In contrast to responses to body displacements, responses to direct head displacements appear to depend upon a vestibulospinal trigger, since trunk and leg muscle responses to head displacements were absent in patients who had lost vestibular function as adults.(ABSTRACT TRUNCATED AT 400 WORDS)

The importance of somatosensory information in triggering and scaling automatic postural responses in humans.

To clarify the role of somatosensory information from the lower limbs of humans in triggering and scaling the magnitude of automatic postural responses, patients with diabetic peripheral neuropathy and age-matched normal controls were exposed to posterior horizontal translations of their support surface. Translation velocity and amplitude were varied to test the patients' ability to scale their postural responses to the magnitude of the translation. Postural response timing was quantified by measuring the onset latencies of three shank, thigh, and trunk muscles and response magnitude was quantified by measuring torque at the support surface. Neuropathy patients showed the same distal-to-proximal muscle activation pattern as normal subjects, but the electromyogram (EMG) onsets in patients were delayed by 20-30 ms at all segments, suggesting an important role for somatosensory information from the lower limb in triggering centrally organized postural synergies. Patients showed an impaired ability to scale torque magnitude to both the velocity and amplitude of surface translations, suggesting that somatosensory information from the legs may be utilized for both direct sensory feedback and use of prior experience in scaling the magnitude of automatic postural responses.

Effects of unilateral loss of vestibular function on the vestibulo-ocular reflex and postural control.

Long-term recovery from surgically induced unilateral loss of vestibular function was studied in 14 patients. Seven patients underwent surgical extirpation or section of the vestibular nerve, and seven patients underwent labyrinthectomy without vestibular nerve section. The vestibulo-ocular reflex (VOR) and postural control were evaluated preoperatively and monitored for up to 4 years postoperatively with use of pseudorandom rotation (combined sinusoidal frequencies from 0.009 to 1.5 Hz) and moving platform posturography. Immediately following surgery all patients showed minimal reductions in the VOR gain constant, but marked reduction in the time constant, and marked increase in slow eye velocity bias. Bias returned to normal values within about 10 days, but time constants never returned to normal values. Results of standard Romberg tests in these patients were normal throughout the preoperative and postoperative periods. However, all patients showed marked postural control abnormalities in tests of the ability to maintain balance in unusual sensory environments in the immediate postoperative period. Seventy-five percent of the patients eventually recovered normal postural control. Postural control returned to near baseline performance with a time course similar to that of the VOR bias. However, postural control also continued to improve after the recovery of VOR bias was complete.

Components of postural dyscontrol in the elderly: a review.

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.

Organization of posture controls: an analysis of sensory and mechanical constraints.

We analyse two components of posture control in standing human subjects: (1) the mechanical properties which constrain the body's ability to execute stabilizing postural movements and (2) the mechanical and neural properties which constrain the ability of the vestibular system to sense changes in body orientation. Rules are then proposed to describe the central organization of posture controls within the sensory and mechanical constraints. The organizational rules and knowledge of constraints are combined to predict the effects of selective semicircular canal and utricular otolith lesions on postural stability and the patterns of body and head movements used to maintain balance. Our analysis leads to the prediction that semicircular canal and otolith deficits destabilize patients at different frequencies, and force them to use different patterns of body and head movements. These predictions are compared to posture controls observed in patients with different types of vestibular deficits. The additional steps required to prove or disprove the theory are discussed.

Tachygastria and motion sickness.

Cutaneously-recorded electrogastrograms (EGGs) were obtained from 21 healthy volunteers who were seated within a drum, the rotation of which produced vection or illusory self-motion. Fourteen subjects developed symptoms of motion sickness during vection and in each the EGG frequency shifted from the normal 3 cpm to 5-8 cpm, tachygastria, an abnormal pattern. In 6 of 7 asymptomatic subjects, the 3 cpm EGG pattern was unchanged during vection. It was concluded that illusory self-motion produces tachygastria and motion sickness in susceptible subjects.

Spatial orientation mechanisms and their implications for falls.

Postural stability is only one function on a multisensory system that also subserves spatial orientation and gaze stability. The problem of falling is discussed in the context of understanding the nature and integration of these sensory loops, and the possibility of their modification is discussed. The characteristics of the visual system contributing to spatial orientation are analyzed. The role of gaze stability in postural balance and its modification as a function of age are also discussed. It is suggested that our understanding of the problem of falling will be enhanced by a research strategy that views the problem as a special case of spatial orientation.