Fay B. Horak

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 Parkinsons 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.

Postural strategies associated with somatosensory and vestibular loss

SummaryThis study examines the roles of somatosensory and vestibular information in the coordination of postural responses. The role of somatosensory information was examined by comparing postural responses of healthy control subjects prior to and following somatosensory loss due to hypoxic anesthesia of the feet and ankles. The role of vestibular information was evaluated by comparing the postural responses of control subjects and patients with bilateral vestibular loss. Postural responses were quantified by measuring 1) spatial and temporal characteristics of leg and trunk EMG activation; 2) ankle, knee, and hip joint kinematics, and 3) surface forces in response to anterior and posterior surface translations under different visual and surface conditions. Results showed that neither vestibular nor somatosensory loss resulted in delayed or disorganized postural responses. However, both types of sensory deficits altered the type of postural response selected under a given set of conditions. Somatosensory loss resulted in an increased hip strategy for postural correction, similar to the movement strategy used by control subjects while standing across a shortened surface. Vestibular loss resulted in a normal ankle strategy but lack of a hip strategy, even when required for the task of maintaining equilibrium on a shortened surface. Neither somatosensory nor vestibular loss resulted in difficulty in utilizing remaining sensory information for orientation during quiet stance. These results support the hypothesis that cutaneous and joint somatosensory information from the feet and ankles may play an important role in assuring that the form of postural movements are appropriate for the current biomechanical constraints of the surface and/or foot. The results also suggest that vestibular information is necessary in controlling equilibrium in a task requiring use of the hip strategy. Thus, both somatosensory and vestibular sensory information play important roles in the selection of postural movement strategies appropriate for their environmental contexts.

Postural inflexibility in parkinsonian subjects.

In order to identify the types of postural deficits seen in parkinsonian patients with postural instability, we compared the performance of parkinsonian subjects with young and old control subjects in 3 aspects of postural control: (1) the use of sensory information for postural orientation, (2) the coordination of postural movement patterns in response to surface displacements, and (3) the flexible modification of postural response patterns to changes in support conditions. Parkinsonian subjects had very small sway, even under altered sensory conditions. Postural response latencies to displacements were also normal. Postural instability was associated with abnormal patterns of postural responses including excessive antagonist activity and inflexibility in adapting to changing support conditions. Some parkinsonian subjects appeared to have difficulty sequencing motor programs for postural correction. The parkinsonian subjects appeared stiffer since the rate-of-change of sway in response to displacements was reduced. Levodopa improved postural coordination but not the flexible adaptation to changing support conditions.

The Balance Evaluation Systems Test (BESTest) to Differentiate Balance Deficits

Background: Current clinical balance assessment tools do not aim to help therapists identify the underlying postural control systems responsible for poor functional balance. By identifying the disordered systems underlying balance control, therapists can direct specific types of intervention for different types of balance problems. Objective: The goal of this study was to develop a clinical balance assessment tool that aims to target 6 different balance control systems so that specific rehabilitation approaches can be designed for different balance deficits. This article presents the theoretical framework, interrater reliability, and preliminary concurrent validity for this new instrument, the Balance Evaluation Systems Test (BESTest). Design: The BESTest consists of 36 items, grouped into 6 systems: “Biomechanical Constraints,” “Stability Limits/Verticality,” “Anticipatory Postural Adjustments,” “Postural Responses,” “Sensory Orientation,” and “Stability in Gait.” Methods: In 2 interrater trials, 22 subjects with and without balance disorders, ranging in age from 50 to 88 years, were rated concurrently on the BESTest by 19 therapists, students, and balance researchers. Concurrent validity was measured by correlation between the BESTest and balance confidence, as assessed with the Activities-specific Balance Confidence (ABC) Scale. Results: Consistent with our theoretical framework, subjects with different diagnoses scored poorly on different sections of the BESTest. The intraclass correlation coefficient (ICC) for interrater reliability for the test as a whole was .91, with the 6 section ICCs ranging from .79 to .96. The Kendall coefficient of concordance among raters ranged from .46 to 1.00 for the 36 individual items. Concurrent validity of the correlation between the BESTest and the ABC Scale was r=.636, P<.01. Limitations: Further testing is needed to determine whether: (1) the sections of the BESTest actually detect independent balance deficits, (2) other systems important for balance control should be added, and (3) a shorter version of the test is possible by eliminating redundant or insensitive items. Conclusions: The BESTest is easy to learn to administer, with excellent reliability and very good validity. It is unique in allowing clinicians to determine the type of balance problems to direct specific treatments for their patients. By organizing clinical balance test items already in use, combined with new items not currently available, the BESTest is the most comprehensive clinical balance tool available and warrants further development.

Cortical control of postural responses

SummaryThis article reviews the evidence for cortical involvement in shaping postural responses evoked by external postural perturbations. Although responses to postural perturbations occur more quickly than the fastest voluntary movements, they have longer latencies than spinal stretch reflexes, suggesting greater potential for modification by the cortex. Postural responses include short, medium and long latency components of muscle activation with increasing involvement of the cerebral cortex as latencies increase. Evidence suggests that the cortex is also involved in changing postural responses with alterations in cognitive state, initial sensory-motor conditions, prior experience, and prior warning of a perturbation, all representing changes in “central set.” Studies suggest that the cerebellar-cortical loop is responsible for adapting postural responses based on prior experience and the basal ganglia-cortical loop is responsible for pre-selecting and optimizing postural responses based on current context. Thus, the cerebral cortex likely influences longer latency postural responses both directly via corticospinal loops and shorter latency postural responses indirectly via communication with the brainstem centers that harbor the synergies for postural responses, thereby providing both speed and flexibility for pre-selecting and modifying environmentally appropriate responses to a loss of balance.

Effects of deep brain stimulation and levodopa on postural sway in Parkinson's disease

Objective: To quantify postural sway in subjects with Parkinsons disease and elderly controls, and determine the effects of Parkinsons disease, deep brain stimulation, levodopa, and their interactions on postural control during quiet stance. Methods: Centre of foot pressure (CoP) displacement under each foot was measured during three 60 s trials of quiet stance with eyes open in 11 controls and six patients with Parkinsons disease. Subjects with Parkinsons disease were tested in four treatment conditions: off both deep brain stimulation and levodopa (off condition); on deep brain stimulation; on levodopa; and on both deep brain stimulation and levodopa. The variables extracted from CoP included: root mean square distance (rms), mean velocity, 95% power frequency (f95%), area of the 95% confidence ellipse (ellipse area), direction of its major axis (mdir), and postural asymmetry between the feet. Results: rms and area of postural sway were larger than normal in subjects with Parkinsons disease in the off condition, increased further with levodopa, and significantly decreased with deep brain stimulation. Mean velocity and f95% were also larger than normal but were restored to normal by all treatments, especially by deep brain stimulation. The combined effect of deep brain stimulation and levodopa resulted in a postural sway that was an average of the effect of each treatment individually. Levodopa increased sway more in the mediolateral than in the anterior-posterior direction. Subjects with Parkinsons disease had asymmetrical mean velocity and f95% between the feet, and this asymmetry increased with levodopa but decreased with deep brain stimulation. The f95% of the CoP correlated with tremor, posture, and gait subcomponents of the unified Parkinsons disease rating scale. Conclusions: Subjects with Parkinsons disease have abnormal postural sway in stance. Treatment with levodopa increases postural sway abnormalities, whereas treatment with deep brain stimulation improves postural sway. Quantitative evaluation of static posturography may be a useful adjunct to clinical measures in patients with Parkinsons disease.

Direction-specific postural instability in subjects with Parkinson's disease

The purpose of this study was to determine whether and why subjects with Parkinsons disease (PD) have greater instability in response to specific directions of perturbations than do age-matched control subjects and how instability is affected by stance width. This study compared postural responses to 8 directions of surface translations in PD subjects and age-matched control subjects while standing in a narrow and wide stance. PD subjects were tested in their practical OFF state. A postural stability margin was quantified as the difference between peak center of pressure (CoP) and peak center of mass (CoM) displacement in response to surface translations. The control subjects maintained a consistent stability margin across directions of translations and for both narrow and wide stance by modifying rate of rise of CoP responses. PD subjects had smaller than normal postural stability margins in all directions, but, especially for backwards sway in both stance widths and for lateral sway in narrow stance width. The reduced stability margin in PD subjects was due to a slower rise and smaller peak of CoP in the PD subjects than in control subjects. Lateral postural stability was compromised in PD subjects by lack of trunk flexibility and backwards postural stability was compromised by lack of knee flexion, resulting in excessive displacements of the body CoM. Stability margins in PD subjects were related to their response on the pull test in the Unified Parkinsons Disease Rating Scale. Thus, PD patients have directionally specific postural instability due to an ineffective stiffening response and inability to modify their postural responses for changing postural demands related to direction of perturbation and initial stance posture. These results suggest that the basal ganglia, in addition to regulating muscle tone and energizing postural muscle activation, also are critical for adapting postural response patterns for specific biomechanical conditions.

iTUG, a Sensitive and Reliable Measure of Mobility

Timed Up and Go (TUG) test is a widely used clinical paradigm to evaluate balance and mobility. Although TUG includes several complex subcomponents, namely: sit-to-stand, gait, 180° turn, and turn-to-sit; the only outcome is the total time to perform the task. We have proposed an instrumented TUG, called iTUG, using portable inertial sensors to improve TUG in several ways: automatic detection and separation of subcomponents, detailed analysis of each one of them and a higher sensitivity than TUG. Twelve subjects in early stages of Parkinsons disease (PD) and 12 age matched control subjects were enrolled. Stopwatch measurements did not show a significant difference between the two groups. The iTUG, however, showed a significant difference in cadence between early PD and control subjects (111.1 ± 6.2 versus 120.4 ± 7.6 step/min, p <; 0.006) as well as in angular velocity of arm-swing (123 ± 32.0 versus 174.0 ± 50.4°/s, p <; 0.005), turning duration (2.18 ± 0.43 versus 1.79 ± 0.27 s, p <; 0.023), and time to perform turn-to-sits (2.96 ± 0.68 versus 2.40 ± 0.33 s, p <; 0.023). By repeating the tests for a second time, the test-retest reliability of iTUG was also evaluated. Among the subcomponents of iTUG, gait, turning, and turn-to-sit were the most reliable and sit-to-stand was the least reliable.

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 agematched 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 distalto-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.

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 bodys 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.