TURN-IT: a novel turning intervention program to improve quality of turning in daily life in people with Parkinson's disease.

BACKGROUND: People with Parkinson's disease (PD) have a high fall rate and many falls are associated with turns. Despite this, there is minimal research on effects of rehabilitation on the quality of turns. Further, quantifying turns in the home may have broader implications since rehabilitation of turns would ideally improve turning in real world mobility. METHODS: Sixty people with PD and a history of falls will be randomized to receive either a novel TURNing InTervention (TURN-IT) or no intervention (control group). The TURN-IT group will be seen for 6 weeks (18 visits) for an individualized, progressive program that is based on the specific constraints of turning in PD. Wearable sensors will be used to measure 7 days of mobility, including turns, before and after intervention or control period. In addition, blinded assessments of gait, mobility and turns will occur before and after intervention for both groups and falls will be monitored for twelve months post intervention with bimonthly email questionnaires. DISCUSSION: This study has the potential to change how we rehabilitate and assess turning in people with PD and falls. There are several novel aspects to our study including a comprehensive turning-focused intervention that is tailored to the underlying constraints that impair turning in people with PD. Further, our outcome measure of turning quality during 7 days of daily life is novel and has implications for determining real-life changes after rehabilitation. The ultimate goal of this rehabilitation intervention is to improve how patients turn in daily life and to reduce falls. TRIALS REGISTRATION: This protocol is registered at clinicaltrials.gov; #NCT04897256; https://clinicaltrials.gov/ct2/show/NCT04897256?term=Horak&cond=Parkinson+Disease&draw=2&rank=4 .

Case Studies in Neuroscience: A dissociation of balance and posture demonstrated by camptocormia.

Upright stance in humans requires an intricate exchange between the neural mechanisms that control balance and those that control posture; however, the distinction between these control systems is hard to discern in healthy subjects. By studying balance and postural control of a participant with camptocormia - an involuntary flexion of the trunk during standing that resolves when supine - a divergence between balance and postural control was revealed. A kinematic and kinetic investigation of standing and walking showed a stereotyped flexion of the upper body by almost 80° over a few minutes, and yet the participant's ability to control center of mass within the base of support and to compensate for external perturbations remained intact. This unique case also revealed the involvement of automatic, tonic control of the paraspinal muscles during standing and the effects of attention. Although strength was reduced and MRI showed a reduction in muscle mass, there was sufficient strength to maintain an upright posture under voluntary control and when using geste antagoniste maneuvers or "sensory tricks" from visual, auditory, and haptic biofeedback. Dual tasks that either increased or decreased the attention given to postural alignment would decrease or increase the postural flexion, respectively. The custom-made "twister" device that measured axial resistance to slow passive rotation revealed abnormalities in axial muscle tone distribution during standing. The results suggest that the disorder in this case was due to a disruption in the automatic, tonic drive to the postural muscles and that myogenic changes were secondary. NEW & NOTEWORTHY By studying an idiopathic camptocormia case with a detailed biomechanical and sensorimotor approach, we have demonstrated unique insights into the neural control of human bipedalism 1) balance and postural control cannot be considered the same neural process, as there is a stereotyped abnormal flexed posture, without balance deficits, associated with camptocormia, and 2) posture during standing is controlled by automatic axial tone but "sensory tricks" involving sensory biofeedback to direct voluntary attention to postural alignment can override, when required.

Consensus Paper: Neurophysiological Assessments of Ataxias in Daily Practice.

The purpose of this consensus paper is to review electrophysiological abnormalities and to provide a guideline of neurophysiological assessments in cerebellar ataxias. All authors agree that standard electrophysiological methods should be systematically applied in all cases of ataxia to reveal accompanying peripheral neuropathy, the involvement of the dorsal columns, pyramidal tracts and the brainstem. Electroencephalography should also be considered, although findings are frequently non-specific. Electrophysiology helps define the neuronal systems affected by the disease in an individual patient and to understand the phenotypes of the different types of ataxia on a more general level. As yet, there is no established electrophysiological measure which is sensitive and specific of cerebellar dysfunction in ataxias. The authors agree that cerebellar brain inhibition (CBI), which is based on a paired-pulse transcranial magnetic stimulation (TMS) paradigm assessing cerebellar-cortical connectivity, is likely a useful measure of cerebellar function. Although its role in the investigation and diagnoses of different types of ataxias is unclear, it will be of interest to study its utility in this type of conditions. The authors agree that detailed clinical examination reveals core features of ataxia (i.e., dysarthria, truncal, gait and limb ataxia, oculomotor dysfunction) and is sufficient for formulating a differential diagnosis. Clinical assessment of oculomotor function, especially saccades and the vestibulo-ocular reflex (VOR) which are most easily examined both at the bedside and with quantitative testing techniques, is of particular help for differential diagnosis in many cases. Pure clinical measures, however, are not sensitive enough to reveal minute fluctuations or early treatment response as most relevant for pre-clinical stages of disease which might be amenable to study in future intervention trials. The authors agree that quantitative measures of ataxia are desirable as biomarkers. Methods are discussed that allow quantification of ataxia in laboratory as well as in clinical and real-life settings, for instance at the patients' home. Future studies are needed to demonstrate their usefulness as biomarkers in pharmaceutical or rehabilitation trials.

Neural Control of Walking in People with Parkinsonism.

People with Parkinson's disease exhibit debilitating gait impairments, including gait slowness, increased step variability, and poor postural control. A widespread supraspinal locomotor network including the cortex, cerebellum, basal ganglia, and brain stem contributes to the control of human locomotion, and altered activity of these structures underlies gait dysfunction due to Parkinson's disease.

Compensatory stepping in Parkinson's disease is still a problem after deep brain stimulation randomized to STN or GPi.

The effects of deep brain stimulation (DBS) on balance in people with Parkinson's disease (PD) are not well established. This study examined whether DBS randomized to the subthalamic nucleus (STN; n = 11) or globus pallidus interna (GPi; n = 10) improved compensatory stepping to recover balance after a perturbation. The standing surface translated backward, forcing subjects to take compensatory steps forward. Kinematic and kinetic responses were recorded. PD-DBS subjects were tested off and on their levodopa medication before bilateral DBS surgery and retested 6 mo later off and on DBS, combined with off and on levodopa medication. Responses were compared with PD-control subjects (n = 8) tested over the same timescale and 17 healthy control subjects. Neither DBS nor levodopa improved the stepping response. Compensatory stepping in the best-treated state after surgery (DBS+DOPA) was similar to the best-treated state before surgery (DOPA) for the PD-GPi group and the PD-control group. For the PD-STN group, there were more lateral weight shifts, a delayed foot-off, and a greater number of steps required to recover balance in DBS+DOPA after surgery compared with DOPA before surgery. Within the STN group five subjects who did not fall during the experiment before surgery fell at least once after surgery, whereas the number of falls in the GPi and PD-control groups were unchanged. DBS did not improve the compensatory step response needed to recover from balance perturbations in the GPi group and caused delays in the preparation phase of the step in the STN group.

Do cognitive measures and brain circuitry predict outcomes of exercise in Parkinson Disease: a randomized clinical trial.

BACKGROUND: There is emerging research detailing the relationship between balance/gait/falls and cognition. Imaging studies also suggest a link between structural and functional changes in the frontal lobe (a region commonly associated with cognitive function) and mobility. People with Parkinson's disease have important changes in cognitive function that may impact rehabilitation efficacy. Our underlying hypothesis is that cognitive function and frontal lobe connections with the basal ganglia and brainstem posture/locomotor centers are responsible for postural deficits in people with Parkinson's disease and play a role in rehabilitation efficacy. The purpose of this study is to 1) determine if people with Parkinson's disease can improve mobility and/or cognition after partaking in a cognitively challenging mobility exercise program and 2) determine if cognition and brain circuitry deficits predict responsiveness to exercise rehabilitation. METHODS/DESIGN: This study is a randomized cross-over controlled intervention to take place at a University Balance Disorders Laboratory. The study participants will be people with Parkinson's disease who meet inclusion criteria for the study. The intervention will be 6 weeks of group exercise (case) and 6 weeks of group education (control). The exercise is a cognitively challenging program based on the Agility Boot Camp for people with PD. The education program is a 6-week program to teach people how to better live with a chronic disease. The primary outcome measure is the MiniBESTest and the secondary outcomes are measures of mobility, cognition and neural imaging. DISCUSSION: The results from this study will further our understanding of the relationship between cognition and mobility with a focus on brain circuitry as it relates to rehabilitation potential. TRIAL REGISTRATION: This trial is registered at clinical trials.gov (NCT02231073).

C-STIM: Protocol for a randomized, single-blind, crossover study of cerebellar repetitive transcranial magnetic stimulation (rTMS) for postural instability in people with progressive supranuclear palsy (PSP).

Background: Methods for modulating the cerebellum with transcranial magnetic stimulation (TMS) are well established, and preliminary data from our group and others has shown evidence of transient improvements in balance after cerebellar repetitive transcranial magnetic stimulation (rTMS) in progressive suprancuclear palsy (PSP). This study examines extensive posturography measures before and after 10 sessions of cerebellar rTMS and sham TMS in PSP. Methods: Thirty subjects with PSP and postural instability will undergo cerebellar active and sham rTMS in a single-blind, crossover design with a randomized order of a 10-day intervention. Primary outcomes will be changes in sway area and medio-lateral range of sway with eyes open while standing on a stationary force-plate, and safety, tolerability, and blindedness. Secondary outcomes will include posturography and gait analysis with body-worn, triaxial inertial sensors, clinical balance scales and questionnaires, and a bedside test of vestibular function. Exploratory outcomes are changes in functional near infrared spectroscopy (fNIRS) signal over the prefrontal, supplementary motor, and primary motor cortices while standing and walking, and speech samples for future analysis. Discussion: The C-STIM crossover intervention study adds a longer duration of stimulation and extensive posturography measures to more finely measure the improvements in balance and exploratory functional near-infrared spectroscopy (fNIRS) over the prefronal, supplementary motor, and primary motor cortices during balance assessments before and after 10 sessions of cerebellar rTMS and 10 sessions of sham cerebellar TMS. This project will improve our understanding of the importance of the cerebellum for control of postural stability in PSP.

Anticipatory postural adjustments prior to step initiation are hypometric in untreated Parkinson's disease: an accelerometer-based approach.

BACKGROUND AND PURPOSE: Anticipatory postural adjustments (APAs), prior to step initiation, are bradykinetic in advanced Parkinson's disease (PD) and may be one of the factors associated with 'start hesitation'. However, little is known about APAs in the early stage of PD. In this study, we determined whether body-worn accelerometers could be used to characterize step initiation deficits in subjects with early-to-moderate, untreated PD. METHODS: Eleven PD and 12 healthy control subjects were asked to take two steps. Postural adjustments were compared from center of pressure (COP) and from acceleration of the trunk at the center of mass level (L5). RESULTS: Our findings show that APAs measured from the peak COP displacement toward the swing leg and the peak trunk acceleration toward the stance leg were smaller in untreated PD compared with control subjects. The magnitude of APAs measured from peak COP displacements and accelerations were correlated. CONCLUSION: These results suggest that quantitative analysis of step initiation from one accelerometer on the trunk could provide useful information for the characterization of patients in early stages of PD, when clinical evidence of start hesitation may not be detectable. Ambulatory monitoring of step initiation is also promising for monitoring patient progression in the home environment, and eventually providing feedback for preventing freezing of gait episodes.

Compensatory postural adaptations during continuous, variable amplitude perturbations reveal generalized rather than sequence-specific learning.

We examined changes in the motor organization of postural control in response to continuous, variable amplitude oscillations evoked by a translating platform and explored whether these changes reflected implicit sequence learning. The platform underwent random amplitude (maximum +/- 15 cm) and constant frequency (0.5 Hz) oscillations. Each trial was composed of three 15-s segments containing seemingly random oscillations. Unbeknownst to participants, the middle segment was repeated in each of 42 trials on the first day of testing and in an additional seven trials completed approximately 24 h later. Kinematic data were used to determine spatial and temporal components of total body centre of mass (COM) and joint segment coordination. Results showed that with repeated trials, participants reduced their magnitude of COM displacement, shifted from a COM phase lag to a phase lead relative to platform motion and increased correlations between ankle/platform motion and hip/platform motion as they shifted from an ankle strategy to a multi-segment control strategy involving the ankle and hip. Maintenance of these changes across days provided evidence for learning. Similar improvements for the random and repeated segments, indicated that participants did not exploit the sequence of perturbations to improve balance control. Rather, the central nervous system may have been tuning into more general features of platform motion. These findings provide important insight into the generalizabilty of improved compensatory balance control with training.

Abnormal proprioceptive-motor integration contributes to hypometric postural responses of subjects with Parkinson's disease.

Subjects with Parkinson's disease exhibit abnormally short compensatory steps in response to external postural perturbations. We examined whether: (1) Parkinson's disease subjects exhibit short compensatory steps due to abnormal central proprioceptive-motor integration, (2) this proprioceptive-motor deficit can be overcome by visual-motor neural circuits using visual targets, (3) the proprioceptive-motor deficit relates to the severity of Parkinson's disease, and (4) the dysfunction of central dopaminergic circuits contributes to the Parkinson's disease subjects' proprioceptive-motor deficit. Ten Parkinson's disease subjects and 10 matched control subjects performed compensatory steps in response to backward surface translations in five conditions: with eyes closed, with eyes open, to a remembered visual target, to a target without seeing their legs, and to a target while seeing their legs. Parkinson's disease subjects were separated into a moderate group and a severe group based on scores from the Unified Parkinson's Disease Rating Scale and were tested off and on their dopamine medication. Parkinson's disease subjects exhibited shorter compensatory steps than did the control subjects, but all subjects increased their step length when stepping to targets. Compared with the other subject groups, the severe Parkinson's disease subjects made larger accuracy errors when stepping to targets, and the severe Parkinson's disease subjects' step accuracy worsened the most when they were unable to see their legs. Thus, Parkinson's disease subjects exhibited short compensatory steps due to abnormal proprioceptive-motor integration and used visual input to take longer compensatory steps when a target was provided. In severe Parkinson's disease subjects, however, visual input does not fully compensate because, even with a target and unobstructed vision, they still exhibited poor step accuracy. Medication did not consistently improve the length and accuracy of the Parkinson's disease subjects' compensatory steps, suggesting that degeneration of dopamine circuits within the basal ganglia is not responsible for the proprioceptive-motor deficit that degrades compensatory steps in Parkinson's disease subjects.

Somatosensory influence on postural response to galvanic vestibular stimulation.

We investigated how postural responses to galvanic vestibular stimulation were affected by standing on a translating support surface and by somatosensory loss due to diabetic neuropathy. We tested the hypothesis that an unstable surface and somatosensory loss can result in an increase of vestibulospinal sensitivity. Bipolar galvanic vestibular stimulation was applied to subjects who were standing on a force platform, either on a hard, stationary surface or during a backward platform translation (9 cm, 4.2 cm/s). The intensity of the galvanic stimulus was varied from 0.25 to 1 mA. The amplitude of the peak body CoP displacement in response to the galvanic stimulus was plotted as a function of stimulus intensity for each individual. A larger increase in CoP displacement to a given increase in galvanic current was interpreted as an increase of vestibulospinal sensitivity. Subjects with somatosensory loss in the feet due to diabetes showed higher vestibulospinal sensitivity than healthy subjects when tested on a stationary support surface. Control subjects and patients with somatosensory loss standing on translating surface also showed increased galvanic response gains compared to stance on a stationary surface. The severity of the somatosensory loss in the feet correlated with the increased postural sensitivity to galvanic vestibular stimulation. These results showed that postural responses to galvanic vestibular stimulus were modified by somatosensory information from the surface. Somatosensory loss due to diabetic neuropathy and alteration of somatosensory input during stance on translating support surface resulted in increased vestibulospinal sensitivity.

Effects of freezing of gait on postural motor learning in people with Parkinson's disease.

Protective postural responses, including stepping, to recover equilibrium are critical for fall prevention and are impaired in people with Parkinson's disease (PD) with freezing of gait (FoG). Improving protective postural responses through training may reduce falls in this population. However, motor learning, the basis of neurorehabilitation, is also impaired in people with PD and, in particular, people with PD who experience freezing. It is unknown whether people with PD who freeze can improve protective postural responses, and whether these improvements are similar to nonfreezers. Our goal was to assess whether people with freezing can improve protective postural responses and retain these improvements similarly to nonfreezers. Twenty-eight people with PD (13 freezers, 15 nonfreezers) were enrolled. Improvement in protective postural responses was assessed over the course of 25 forward and 25 backward support surface translations (delivered in pseudo-random order). Postural responses were re-assessed 24h later to determine whether improvements were retained. People who freeze did not improve or retain improvement in protective postural responses as well as nonfreezers in our primary outcome variable, center of mass (COM) displacement after perturbations (post hoc across group assessments: freezers- p=0.14 and nonfreezers- p=0.001, respectively). However, other protective stepping outcomes, including margin of stability, step length, and step time, improved similarly across groups. Significant improvements were retained in both groups. In conclusion, people with PD who freeze exhibited reduced ability to improve protective postural responses in some, but not all, outcome variables. Additional training may be necessary to improve protective postural responses in people with PD who freeze.

Supraspinal control of automatic postural responses in people with multiple sclerosis.

The neural underpinnings of delayed automatic postural responses in people with multiple sclerosis (PwMS) are unclear. We assessed whether white matter pathways of two supraspinal regions (the cortical proprioceptive Broadman's Area-3; and the balance/locomotor-related pedunculopontine nucleus) were related to delayed postural muscle response latencies in response to external perturbations. 19 PwMS (48.8±11.4years; EDSS=3.5 (range: 2-4)) and 12 healthy adults (51.7±12.2years) underwent 20 discrete, backward translations of a support surface. Onset latency of agonist (medial-gastrocnemius) and antagonist (tibialis anterior) muscles were assessed. Diffusion tensor imaging assessed white-matter integrity (i.e. radial diffusivity) of cortical proprioceptive and balance/locomotor-related tracts. Latency of the tibialis anterior, but not medial gastrocnemius was larger in PwMS than control subjects (p=0.012 and 0.071, respectively). Radial diffusivity of balance/locomotor tracts was higher (worse) in PwMS than control subjects (p=0.004), and was significantly correlated with tibialis (p=0.002), but not gastrocnemius (p=0.06) onset latency. Diffusivity of cortical proprioceptive tracts was not correlated with muscle onset. Lesions in supraspinal structures including the pedunculopontine nucleus balance/locomotor network may contribute to delayed onset of postural muscle activity in PwMS, contributing to balance deficits in PwMS.

Identification of Balance Deficits in People with Parkinson Disease; is the Sensory Organization Test Enough?

BACKGROUND AND PURPOSE: Balance deficits in people with Parkinson's disease can affect any of the multiple systems encompassing balance control. Thus, identification of the specific deficit is crucial in customizing balance rehabilitation. The sensory organization test, a test of sensory integration for balance control, is sometimes used in isolation to identify balance deficits in people with Parkinson's disease. More recently, the Mini-Balance Evaluations Systems Test, a clinical scale that tests multiple domains of balance control, has begun to be used to assess balance in patients with Parkinson's disease. The purpose of our study was to compare the use of Sensory Organization Test and Mini-Balance Evaluations Systems Test in identifying balance deficits in people with Parkinson's disease. METHODS: 45 participants (27M, 18F; 65.2 ± 8.2 years) with idiopathic Parkinson's disease participated in the cross-sectional study. Balance assessment was performed using the Sensory Organization Test and the Mini-Balance Evaluations Systems Test. People were classified into normal and abnormal balance based on the established cutoff scores (normal balance: Sensory Organization Test >69; Mini-Balance Evaluations Systems Test >73). RESULTS: More subjects were classified as having abnormal balance with the Mini-Balance Evaluations Systems Test (71% abnormal) than with the Sensory Organization Test (24% abnormal) in our cohort of people with Parkinson's disease. There were no subjects with a normal Mini-Balance Evaluations Systems Test score but abnormal Sensory Organization Test score. In contrast, there were 21 subjects who had an abnormal Mini-Balance Evaluations Systems Test score but normal Sensory Organization Test scores. DISCUSSION AND CONCLUSIONS: Findings from this study suggest that investigation of sensory integration deficits, alone, may not be able to identify all types of balance deficits found in patients with Parkinson's disease. Thus, a comprehensive approach should be used to test of multiple balance systems to provide customized rehabilitation.

Association of cognitive domains with postural instability/gait disturbance in Parkinson's disease.

INTRODUCTION: Research suggests an association between global cognition and postural instability/gait disturbance (PIGD) in Parkinson disease (PD), but the relationship between specific cognitive domains and PIGD symptoms is not clear. This study examined the association of cognition (global and specific cognitive domains) with PIGD symptoms in a large, well-characterized sample of individuals with PD. METHODS: Cognitive function was measured with a detailed neuropsychological assessment, including global cognition, executive function, memory, visuospatial function, and language. PIGD symptoms were measured using the Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Part III, Motor Examination subscale. Multiple linear regression analyses were performed to assess the relationship between cognition and PIGD symptoms with models adjusting for age, sex, education, enrollment site, disease duration, and motor symptom severity. RESULTS: The analysis included 783 participants, with mean (standard deviation) age of 67.3 (9.7) years and median (interquartile range) MDS-UPDRS Motor Subscale score of 26 (17, 35). Deficits in global cognition, executive function, memory, and phonemic fluency were associated with more severe PIGD symptoms. Deficits in executive function were associated with impairments in gait, freezing, and postural stability, while visuospatial impairments were associated only with more severe freezing, and poorer memory function was associated only with greater postural instability. DISCUSSION: While impairments in global cognition and aspects of executive functioning were associated with more severe PIGD symptoms, specific cognitive domains were differentially related to distinct PIGD components, suggesting the presence of multiple neural pathways contributing to associations between cognition and PIGD symptoms in persons with PD.

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.

Sensory organization for balance: specific deficits in Alzheimer's but not in Parkinson's disease.

BACKGROUND: The cause of frequent falling in patients with dementia of the Alzheimer type (AD) is not well understood. Distraction from incongruent visual stimuli may be an important factor as suggested by their poor performance in tests of shifting visual attention in other studies. The purpose of this study was to determine whether AD patients have difficulty maintaining upright balance under absent and/or incongruent visual and other sensory conditions compared to nondemented healthy elderly persons and individuals with Parkinson's disease (PD). METHODS: Seventeen healthy older adults, 15 medicated PD subjects, and 11 AD subjects underwent the Sensory Organization Test protocol. The incidence of loss of balance ("falls"), and the peak-to-peak amplitude of body center of mass sway during stance in the six sensory conditions were used to infer the ability to use visual, somatosensory, and vestibular signals when they provided useful information for balance, and to suppress them when they were incongruent as an orientation reference. Vestibular reflex tests were conducted to ensure normal vestibular function in the subjects. RESULTS: AD subjects had normal vestibular function but had trouble using it in condition 6, where they had to concurrently suppress both incongruent visual and somatosensory inputs. All 11 AD subjects fell in the first trial of this condition. With repeated trials, only three AD subjects were able to stay balanced. AD subjects were able to keep their balance when only somatosensory input was incongruent. In this condition, all AD subjects were able to maintain balance whereas some falls occurred in the other groups. In all conditions, when AD subjects did not fall, they were able to control as large a sway as the healthy controls, except when standing with eyes closed in condition 2: AD subjects did not increase their sway whereas the other groups did. In the PD group, the total fall incidence was similar to the AD group, but the distribution was generalized across more sensory conditions. PD subjects were also able to improve with repeated trials in condition 6. CONCLUSION: Patients with dementia of the Alzheimer type have decreased ability to suppress incongruent visual stimuli when trying to maintain balance. However, they did not seem to be dependent on vision for balance because they did not increase their sway when vision was absent. Parkinsonian patients have a more general balance control problem in the sensory organization test, possibly related to difficulty changing set.

Postural set for balance control is normal in Alzheimer's but not in Parkinson's disease.

BACKGROUND: It has been suggested that patients with dementia of the Alzheimer type have abnormalities in the basal ganglia, and thus, may have similar sensorimotor problems as patients with basal ganglia degeneration from Parkinson's disease. Whether the similarity extends to balance control is unknown. One distinguishing feature of balance disorder in Parkinson's disease is difficulty with changing postural set in terms of adapting the amplitude of leg muscle activity as a function of support condition. We, therefore, tested whether patients with Alzheimer's disease without extrapyramidal signs would show a similar problem in changing postural set as patients with Parkinson's disease. METHODS: The ability to quickly change postural set was measured by comparing leg muscle activity under two conditions of support (free stance, versus grasping a frame, or sitting) during backward surface translations, during toes up surface rotations, and during voluntary rise to toes. Results were compared among 12 healthy adults, 8 nondemented Parkinson's patients on their usual dose of medication, and 11 Alzheimer patients without extrapyramidal signs. RESULTS: Subjects with Alzheimer's, but not Parkinson's, disease performed similarly to the healthy control subjects. They changed postural set immediately, by suppressing leg muscle activity to low levels when supported. Parkinson subjects did not change postural set immediately. They did not suppress the tibialis anterior in voluntary rise to toes when holding, nor the soleus in perturbed sitting as much as the healthy control and Alzheimer subjects in the first trial. Instead, the Parkinson subjects changed set more slowly, over repeated and consecutive trials in both protocols. The onset latencies of soleus responses to backward surface translations and perturbed sitting, as well as tibialis anterior responses to toes up rotations, were the same for all three groups. CONCLUSION: Alzheimer patients without extrapyramidal signs, unlike nondemented Parkinson's disease patients, have no difficulty in quickly changing postural set in response to altered support conditions. Our results, therefore, do not support the hypothesis that Parkinson's and uncomplicated Alzheimer's diseases share common postural set problems that may contribute to disordered balance control.

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.