Static and Dynamic Posturography in Patients
With Vestibular and Cerebellar Lesions
Robert W. Baloh, MD; Kathleen M. Jacobson, BA; Karl Beykirch, MS; Vicente Honrubia, MD
Objective:To assess the diagnostic usefulness of pos-turography in 2 well-defined patient groups with impaired balance.
Patients:Ten control subjects, 10 patients with bilat-eral vestibular loss, and 10 patients with cerebellar atrophy.
Outcome Measures:Amplitude, velocity, and
fre-quency of sway in the anteroposterior and medial-lateral directions on a static platform, on foam, and on a moving platform.
Results: Both patient groups consistently had
in-creased sway compared with controls, particularly when standing on foam or on a moving platform with eyes closed. Sway amplitude and velocity were increased about
the same amount. The Romberg ratio (sway with eyes closed/sway with eyes open) did not reliably differenti-ate patients from controls or the 2 patient groups from each other. Some patients with cerebellar atrophy ex-hibited a characteristic body tremor at about 3 Hz in the anteroposterior direction.
Conclusions:Although sway amplitude and velocity were consistently increased in patients with bilateral vestibu-lar loss and patients with cerebelvestibu-lar atrophy, none of the posturography measurements reliably distinguished the 2 patient groups. The finding of increased frequency of sway in the anteroposterior direction in patients with cer-ebellar atrophy was of limited value since the tremor was visible at the bedside.
Arch Neurol. 1998;55:649-654
BODY SWAYis a normal
phe-nomenon that occurs to some degree in everyone. Al-though sway can be esti-mated by several different methods, the most commonly used tech-nique is to record displacement of the cen-ter of pressure on a force-measuring plat-form (posturography). Numerous studies in patients with a variety of neurologic dis-orders suggest that posturography might be a useful clinical tool for evaluating balance problems in patients.1-8Since sway tends to be small when subjects stand on a stable platform, moving platforms (dynamic pos-turography) have been developed in an at-tempt to increase test sensitivity. The plat-form can be either tilted or linearly displaced and sway can be measured immediately af-ter the movement or during the move-ment. Furthermore, in an effort to dissect the different sensory contributions to the maintenance of balance, systems have been developed to selectively manipulate somato-sensation and vision.9With these devices, the angle of sway is fed back to a dynamic posture platform or to a movable visual sur-round so that movement about the ankle joint or movement of the visual surround
is “sway referenced.” Sway measured dur-ing sway-referencdur-ing conditions with eyes closed increases in patients with vestibular lesions because such patients are reliant on proprioceptive and visual input to com-pensate for the vestibular loss. Such an abnormality on posturography has been called a vestibular pattern, suggesting that it is specific for vestibular system disease.2,9
A wide range of stimulus-response pa-rameters have been measured with both static and dynamic posturography with-out any consensus having developed as to which measurements are most useful. Mea-surements of sway area or sway path are popular but such measurements com-bine sway in the anteroposterior (AP) and medial-lateral (ML) directions and may, therefore, miss important directional in-formation. For example, Maki et al10 re-ported that sway in the ML but not AP direction is a good indicator for the
This article is also available on our Web site: www.ama-assn.org/neuro. ORIGINAL CONTRIBUTION
From the Departments of Neurology (Dr Baloh and Ms Jacobson) and Surgery (Head and Neck) (Drs Baloh and Honrubia and Mr Beykirch), University of California–Los Angeles School of Medicine.
propensity to fall in older people. Mauritz et al11found that patients with cerebellar lesions, particularly those involving the anterior lobe, often have an increased fre-quency of sway in the AP direction. Although these and other reports1,2 suggest the possibility that posturo-graphic data might provide specific diagnostic informa-tion, most investigators have concluded that posturog-raphy is not useful for localizing lesions or for making specific diagnoses.12To further address these issues, we have performed static and dynamic posturography in 2 well-defined patient groups—one with bilateral periph-eral vestibular loss and the other with cerebellar atrophy— and compared the results with those of an age-matched control group. We measured the amplitude, velocity, and frequency of sway in both the AP and ML directions, with
eyes open and eyes closed, in each test condition. We also measured sway with subjects standing on foam to distort proprioceptive input and mimic a “sway-referenced” con-dition. Our goal was to define which measurements were most sensitive in separating patients from controls and to see whether any measurement or test condition could reliably separate the 2 patient groups.
As we16and others10,11have previously reported, sway in the AP direction was consistently greater than sway in the ML direction in the control subjects (both for
am-SUBJECTS AND METHODSSUBJECTS
Subjects consisted of 10 control subjects, 10 patients with bilateral peripheral vestibular loss, and 10 patients with cerebellar atrophy. All underwent quantitative visual-vestibular testing as previously described.13The control sub-jects (5 women and 5 men) had normal vestibulo-ocular reflex gain and time constant measurements, normal vi-sual tracking, normal optokinetic responses, and normal visual-vestibular interaction. Their mean age (±1 SD) was 46.1 ± 11.2 years (range, 31-63 years). Both patient groups complained of imbalance when walking. The patients with bilateral vestibular loss (5 women and 5 men) all had mark-edly decreased vestibulo-ocular reflex gain to sinusoidal
rotation over a broad frequency range (.3 SDs below the
normal mean at frequencies from 0.05 to 0.8 Hz).14They
had normal visual tracking, normal optokinetic
re-sponses, and normal visual-vestibular interaction.15The
mean age (±1 SD) was 45.6 ± 10.3 years (range, 25-59 years). In all cases, the vestibular loss had occurred in adulthood. The cause of the bilateral peripheral vestibular loss was oto-toxicity in 3 patients, bilateral autoimmune inner ear dis-ease in 1, and idiopathic in the remaining 6. Two of these latter patients had a family history of similar bilateral pe-ripheral vestibular loss. The patients with cerebellar atro-phy (7 women and 3 men) all exhibited normal vestibulo-ocular reflex gain but impaired visual tracking, optokinetic responses, and visual-vestibular interaction. The mean age (±1 SD) was 49.1 ± 12.1 years (range, 21-65 years). All were ambulatory but each had obvious gait and extremity ataxia on clinical examination. Clinical diagnoses in these 10 pa-tients were olivopontocerebellar atrophy in 6 and isolated cerebellar atrophy in the remaining 4.15One of the former and 2 of the latter patients had a family history of similar syndromes.
POSTUROGRAPHY TEST PROCEDURES
The Chattecx balance system (Chattecx Corp, Chatta-nooga, Tenn) uses vertical force transducers to determine instantaneous fluctuations in the center of pressure (COP).16 Grabiner et al17have shown that COP calculated in this fash-ion with the balance system is a good estimate of COP mea-sured with traditional biomechanical force plates. There are
2 pairs of independent force transducers, 1 pair for the fore-foot and heel of each fore-foot. The distance between the 2 fore-foot plates was maintained at 4 cm for all individuals tested. The foot plates sat on a motor-driven platform that tilted up and down about a central axis at a frequency of 0.1 Hz and a peak amplitude of 4°. Flat-soled shoes were worn for test-ing. Subjects stood on the platform with their feet cen-tered on the foot plates (in parallel) while wearing a secu-rity harness to prevent them from falling. They were instructed to look straight ahead at the surrounding room with arms at the sides and were allowed to stand on the platform until they felt secure. The standard test battery included measurements of sway for 10 seconds with eyes open and eyes closed under each of 4 conditions: (1) plat-form still (static); (2) foam rubber (thickness, 7.6 cm;
den-sity, 30.3 kg/m3; Specialty Composites Corp,
Indianapo-lis, Ind) on a still platform; (3) platform tilting in the AP direction; and (4) platform tilting in the ML direction.
Complete details of the analysis have been reported else-where.16In brief, the balance system measures the relative vertical loading or distribution of weight (vertical force) be-neath the heel and forefoot of each leg. The COP was cal-culated from these vertical forces. To obtain a measure-ment of average amplitude (A) of sway in each direction (AAP and AML), we calculated the root-mean-square about the mean COP for each 10-second test. We then differentiated the in-stantaneous COP units using a 2-point difference formula (25 Hz low-pass filter). To obtain a measure of the average velocity (V) of sway, we calculated the root-mean-square of VAPand VMLfor each 10-second test. Finally, we performed a frequency analysis (fast Fourier transform) of AAPand VAP and generated histograms of the power in 0.5-Hz bins from 0 to 5 Hz. We only assessed the frequency content of sway in the AP direction because prior reports found this mea-surement to be most useful for differentiating patients with
cerebellar lesions from controls.11To summarize the
fre-quency data in a single value, we calculated a frefre-quency quo-tient, defined as the power of frequencies between 2 and 5 Hz divided by the power of frequencies between 0 and 2 Hz. The cutoff between low- and high-frequency sway of 2 Hz was empirically chosen based on previously reported pilot data.16Because several patients with cerebellar atrophy were unable to stand on foam, testing on foam was only studied in the controls and patients with bilateral vestibular loss.
plitude and velocity measurements) (compare top and bottom ofTable 1). Sway amplitude and velocity in-creased when subjects stood on foam and when the plat-form moved, with the greatest increase in sway occur-ring in the direction of platform movement. The percentage increases in amplitude and velocity of sway during platform movement were about the same in the AP and ML directions. The Romberg ratio (sway with eyes closed/sway with eyes open) was on average about 1.5 in the static condition, increasing to near 2.0 in the dy-namic tests, and reaching a high of 3.0 for VAP
measure-ments on foam (Table 2). There was large variability in these measurements, however, with the SDs being about equal to the mean values, showing that some subjects had much greater increase in sway with eye closure than did others. One control subject had a Romberg ratio less than 1.0 for measurements on the static test (ie, amplitude and velocity of sway were greater with eyes open than with eyes closed). All subjects had greater amplitude and ve-locity of sway with eyes closed compared with eyes open on the other tests, with the highest ratios occurring on the foam test.
Table 1. Amplitude and Velocity of Sway in the Medial-Lateral and Anteroposterior Directions for Different Posturography Conditions in Controls and Patients*
Subject Group Controls
(n = 10)
Bilateral Vestibular Loss (n = 10) Cerebellar Atrophy (n = 10) Medial-Lateral Static EO AML 2.1 ± 0.69 3.0 ± 1.9‡ (40) 5.3 ± 2.3‡ (60) VML 6.0 ± 2.1 10.9 ± 5.1‡ (60) 13.3 ± 8.5 (50) EC AML 2.7 ± 1.4 9.0 ± 6.5 (40) 9.6 ± 5.9‡ (80) VML 8.5 ± 3.5 28.1 ± 26.5 (60) 28.1 ± 17.2‡ (80) Foam EO AML 2.7 ± 1.1 4.6 ± 3.3 (50) . . .\ VML 9.5 ± 3.1 20.7 ± 14.4 (50) . . . EC AML 5.6 ± 1.5 15.5 ± 6.0§ (100) . . . VML 21.2 ± 7.6 70.1 ± 38.4§ (90) . . . AP tilt EO AML 3.7 ± 1.5 6.6 ± 2.7‡ (40) 8.6 ± 6.7 (40) VML 10.6 ± 2.3 23.0 ± 11.8‡ (50) 35.8 ± 43.2 (90) EC AML 5.8 ± 1.4 14.7 ± 5.7§ (100) 10.8 ± 2.8§ (60) VML 19.6 ± 6.5 76.9 ± 30.2§ (100) 40.8 ± 11.8§ (60) ML tilt EO AML 14.7 ± 4.1 23.0 ± 4.2§ (60) 20.2 ± 5.7 (60) VML 27.9 ± 6.9 53.0 ± 17.2‡ (80) 53.5 ± 16.7§ (90) EC AML 18.7 ± 5.6 38.4 ± 5.7§ (100) 34.6 ± 8.0§ (90) VML 54.5 ± 16.0 109.7 ± 16.8§ (100) 98.1 ± 44.7‡ (60) Anteroposterior Static EO AAP 2.8 ± 0.87 6.0 ± 3.0‡ (70) 6.9 ± 4.6 (60) VAP 7.5 ± 2.4 16.4 ± 10.2‡ (60) 22.0 ± 10.5‡ (70) EC AAP 4.8 ± 1.3 14.9 ± 11.5‡ (70) 14.5 ± 7.2‡ (90) VAP 11.4 ± 2.8 60.2 ± 59.9‡ (70) 76.0 ± 52.5‡ (90) Foam EO AAP 4.3 ± 1.8 6.5 ± 2.5 (40) . . . VAP 9.2 ± 2.6 29.1 ± 19.9 (100) . . . EC AAP 5.6 ± 1.5 15.5 ± 6.0§ (100) . . . VAP 21.2 ± 7.6 70.1 ± 38.4§ (90) . . . AP tilt EO AAP 22.3 ± 8.6 32.4 ± 10.6 (40) 32.1 ± 6.6‡ (20) VAP 40.4 ± 5.6 99.0 ± 51.3§ (80) 89.6 ± 21.8‡ (100) EC AAP 26.5 ± 7.8 51.3 ± 9.2§ (90) 46.7 ± 8.7§ (90) VAP 99.0 ± 18.6 185.9 ± 47.8§ (100) 145.0 ± 52.3§ (80) ML tilt EO AAP 5.5 ± 2.0 9.0 ± 3.3‡ (40) 9.0 ± 1.8§ (60) VAP 17.4 ± 5.7 35.2 ± 14.4‡ (50) 43.7 ± 14.3§ (80) EC AAP 8.7 ± 2.2 22.3 ± 5.8§ (90) 21.4 ± 6.6§ (90) VAP 29.1 ± 8.9 122.8 ± 32.6§ (100) 103.4 ± 39.2§ (90)
*Data are given as mean ±1 SD, with number in parentheses representing percentage abnormal (.2 SDs from control mean). EO indicates eyes open;
EC, eyes closed; AP, anteroposterior; ML, medial-lateral; A, amplitude of sway; and V, velocity of sway. †Amplitude (A) values are in millimeters; velocity (V) values are in millimeters per second.
As expected, the frequency content of sway in the AP direction was greater for velocity than amplitude mea-surements (Table 3). None of the measurements had much energy in frequencies above 2 Hz for any of the tests in the controls. Unlike the amplitude and velocity measurements, there was relatively little change in the frequency of sway with eye closure (ie, the Romberg ra-tio was about 1.0 for all tests).
Overall, the static test condition was least sensitive for dis-tinguishing patients from controls. Sway amplitude and velocity in both the AP and ML directions were increased about the same amount on average, but several patients had values within the normal range (Table 1). The best separation between patients and controls occurred on the foam and dynamic tests with eyes closed. The differences between patients and controls on these tests were highly significant (P,.001) and nearly all patients were identi-fied as having abnormal measurements for both ampli-tude and velocity (Table 1). The Romberg ratio was less sensitive than absolute measurements with eyes closed in differentiating patients and controls (Table 2).
Measurements of the amplitude and velocity of sway in both the ML and AP directions overall increased about the same amount in the patients with cerebellar atrophy and in the patients with bilateral vestibular loss. There were no differential features identified on any of these measurements. On the other hand, measurements of the frequency of sway in the AP direction did discriminate between the 2 patient groups and between the patients with cerebellar atrophy and the controls (Table 3). The best discrimination occurred during the static testing. Seven of 10 patients with cerebellar atrophy had a sig-nificantly increased frequency of sway in the AP direc-tion when standing on a static platform with eyes open. None of the patients with bilateral vestibular loss had a significant increase in frequency of sway under similar conditions. This increase in the frequency of sway was even more pronounced with eye closure in the static dition and during the dynamic tests, but under these con-ditions, 3 of the patients with bilateral vestibular loss also had a significant increase in the frequency of sway com-pared with controls. The explanation for this finding is Table 2. Romberg Ratios for Amplitude and Velocity
of Sway in the Medial-Lateral and Anteroposterior Directions in Controls and Patients*
Condition Parameter Subject Group Controls (n = 10) Bilateral Vestibular Loss (n = 10) Cerebellar Atrophy (n = 10) Static AML 1.3 ± 2.0 2.0 ± 4.2 (30) 1.8 ± 2.6 (40) VML 1.4 ± 1.7 2.6 ± 5.6 (40) 2.1 ± 2.0 (60) AAP 1.7 ± 1.5 2.5 ± 3.4 (40) 2.1 ± 1.6 (50) VAP 1.5 ± 1.2 3.7 ± 5.9 (70) 3.5 ± 5.0 (50) Foam AML 2.1 ± 1.4 3.4 ± 2.1 (40) . . .† VML 2.2 ± 2.4 3.4 ± 2.7 (80) . . . AAP 1.8 ± 1.8 3.0 ± 2.8 (50) . . . VAP 3.0 ± 2.2 3.8 ± 2.5 (70) . . . AP tilt AML 1.5 ± 0.9 2.2 ± 2.1 (10) 1.2 ± 0.4 (0) VML 1.9 ± 2.8 3.3 ± 2.6 (20) 1.1 ± 0.3 (0) AAP 1.2 ± 0.9 1.6 ± 0.9 (10) 1.5 ± 1.3 (0) VAP 2.0 ± 3.3 1.9 ± 0.9 (0) 1.6 ± 2.4 (0) ML tilt AML 1.3 ± 1.4 1.7 ± 1.4 (0) 1.7 ± 1.4 (0) VML 2.0 ± 2.5 2.1 ± 1.0 (0) 1.8 ± 2.7 (0) AAP 1.6 ± 1.1 2.5 ± 1.8 (0) 2.4 ± 3.5 (0) VAP 1.7 ± 1.6 3.5 ± 2.7 (20) 2.4 ± 2.7 (10)
*Data are given as mean ±1 SD ratio (sway with eyes closed/sway with eyes
open), with numbers in parentheses representing percentage abnormal. For an explanation of the abbreviations, see the first footnote to Table 1.
†Patients with cerebellar atrophy were unable to stand on foam.
Table 3. Frequency Quotient (FQ) for Amplitude (A) and Velocity (V) of Sway in the Anteroposterior (AP) Direction in Controls and Patients*
Subject Group Controls
(n = 10)
Bilateral Vestibular Loss (n = 10) Cerebellar Atrophy (n = 10) Static EO FQ (AAP) 0.01 ± 0.01 0.01 ± 0.01 (0) 0.02 ± 0.10 (40) FQ (VAP) 0.19 ± 0.06 0.16 ± 0.08 (0) 0.50 ± 0.48† (70) EC FQ (AAP) 0.01 ± 0.00 0.02 ± 0.01 (30) 0.70 ± 0.06† (90) FQ (VAP) 0.19 ± 0.10 0.28 ± 0.28 (20) 1.44 ± 1.07 (80) AP tilt EO FQ (AAP) 0.00 ± 0.00 0.01 ± 0.01 (20) 0.04 ± 0.03‡ (40) FQ (VAP) 0.10 ± 0.04 0.17 ± 0.19 (20) 0.60 ± 0.48‡ (70) EC FQ (AAP) 0.01 ± 0.00 0.03 ± 0.04 (40) 0.12 ± 0.15† (40) FQ (VAP) 0.15 ± 0.11 0.66 ± 0.50† (60) 1.06 ± 0.67‡ (90) ML tilt EO FQ (AAP) 0.01 ± 0.01 0.02 ± 0.02 (20) 0.03 ± 0.03 (50) FQ (VAP) 0.26 ± 0.14 0.32 ± 0.30 (20) 0.51 ± 0.43 (40) EC FQ (AAP) 0.01 ± 0.01 0.05 ± 0.03† (60) 0.04 ± 0.02† (70) FQ (VAP) 0.24 ± 0.11 0.65 ± 0.35† (70) 0.65 ± 0.24‡ (90)
*Data are given as mean ±1 SD frequency quotient, with numbers in parentheses representing percentage abnormal (.2 SDs from control mean). For an
explanation of the abbreviations, see the first footnote to Table 1.
apparent when one looks at the frequency content of sway in the static and a dynamic condition for the 2 patient groups (Figure). In the static test condition, patients with bilateral vestibular loss have relatively little frequency con-tent above 2 Hz, whereas patients with cerebellar atro-phy have a second peak in frequency content between 2 and 3 Hz. During the dynamic tests, patients with bilat-eral vestibular loss continue to have the main peak in the frequency content around 1 Hz but the curve is shifted upward overall so that there is much more frequency con-tent above 2 Hz and the difference in curves between the 2 patient groups becomes less distinct.
Overall, we found that patients with bilateral vestibular loss and patients with cerebellar atrophy had increased sway compared with controls, particularly when stand-ing on foam or on a movstand-ing platform with eyes closed. Traditionally, it has been thought that increased sway with eye closure is characteristic of vestibular lesions and not cerebellar lesions.18This is the basis of the clinical Rom-berg test. However, we found that sway increased with eye closure to about the same degree in patients with cer-ebellar lesions and with bilateral vestibular loss. Others have also found that changes in sway with eye closure does not discriminate between these 2 patient groups.11 The Romberg ratio (sway with eyes closed/sway with eyes open) was less effective than absolute measurements of sway with eye closure in differentiating patients from con-trols mainly because of the wide range of normal Rom-berg ratios. For example, using the amplitude of sway in the AP direction on the static test, the Romberg ratios in control subjects ranged from 0.95 to 4.0. Others have found a similar range for Romberg ratios in control sub-jects.19Because standing on foam distorts propriocep-tive input from the feet, we expected that standing on foam with eyes closed would be the best subtest for
dis-criminating between patients with bilateral vestibular loss and controls. However, the percentage increase in sway with eye closure was about the same when patients stood on a tilting platform as when they stood on foam. An-gular tilt of the platform and the associated stretch re-flexes apparently destabilized the body as much as when standing on foam.
Sway amplitude and sway velocity were consis-tently greater in the AP direction than in the ML direc-tion in controls and patients, presumably owing to the increased mechanical stability of the ankle in the ML di-rection. Although sway (both amplitude and velocity) tended to increase slightly more in the AP direction in both patient groups, measurements of sway in either plane separated normal from abnormal results. Although we suspected that measurements of the velocity of sway might be a better indicator of the effort required to maintain balance during platform perturbations than the ampli-tude of sway,20amplitude and velocity measurements in-creased about the same amount in both patient groups on the dynamic tests.
The only response measurement that did show dif-ferential effects in the 2 patient groups was measure-ment of the frequency of sway in the AP direction. The frequency quotient (power above 2 Hz/power below 2 Hz) was significantly higher in the patients with cerebel-lar atrophy compared with the controls and patients with bilateral vestibular loss. The best distinction was achieved with measurement of the frequency of velocity of sway in the AP direction with either eyes open or eyes closed on a static platform. The frequency of sway increased fur-ther during platform tilting in the cerebellar group but it also increased in the bilateral vestibular group so that the separation between the 2 groups became less clear. Mauritz et al11suggested that this increase in the fre-quency of postural sway was specific for lesions of the anterior lobe of the cerebellum, particularly of the ver-mal and paraverver-mal parts of the anterior lobe. They reached this conclusion because the increased fre-quency of sway was typically seen in patients with cer-ebellar atrophy secondary to chronic alcoholism, a dis-order with remarkably localized abnormality in the anterior lobe of the cerebellum. Our patients had gen-eralized cerebellar atrophy so that our material was not suitable for localizing the source of the increased fre-quency of sway within the cerebellum.
The mechanism for the increase in postural sway seen in patients with vestibular and cerebellar lesions is poorly understood. Maintenance of balance when standing is a complex process that involves multiple peripheral sen-sory inputs, central integrating pathways, and efferent out-puts.21,22Postural sway presumably reflects noise and regu-latory activity within these afferent−efferent control loops. The amplitude and velocity of sway seems to increase in a nonspecific fashion with altered sensory input (ves-tibular, somatosensory, or visual) or with brainstem and cerebellar lesions. Vestibular signals may be critical for scaling the magnitude of the postural responses.23,24The approximate 3-Hz postural tremor in the AP direction recorded in patients with cerebellar lesions probably re-sults from delays within the long loop cerebellar pos-tural reflexes.25 32 24 16 8 0 1 2 3 4 5 0 1 2 3 4 5 0 1 2 3 4 5 0 1 2 3 4 5 Sway V elocity , mm/s 320 240 160 80 800 600 400 200 1800 1200 600 Frequency, Hz
Static Anteroposterior Tilt
Cerebellar Atrophy Bilateral Vestibular Loss
Frequency content of sway in the static condition and a dynamic condition for the 2 patient groups with eyes open (top) and eyes closed (bottom).
Does posturography have a role in the clinical di-agnosis of patients with balance disorders? As currently conducted, the answer is probably no, although more studies in well-documented patient groups are needed. There is a large intraindividual and interindividual vari-ance in normal sway measurements, on both static and
dynamic posturography.16Normal and abnormal
re-sults often overlap even when assessing patients with ob-vious deficits such as those studied in this report. The characteristic AP postural tremor recorded in patients with cerebellar lesions is an exception, but the tremor in our patients could be seen at the bedside without the need for recording equipment. We do not know if posturog-raphy can identify subclinical AP tremor in patients with more subtle cerebellar deficits. Distorting somatosen-sory and visual signals with sway referencing seems a logi-cal method for separating the different sensory inputs but does not reliably separate peripheral from central le-sions. Although certain patterns are common in pa-tients with vestibular lesions, papa-tients with well-documented vestibular lesions often have normal posturography results.26Sensitivity and specificity prob-ably could be improved by combining posturography with other tests such as electromyography from postural muscles2and by development of more informative analy-sis techniques.27
Accepted for publication August 25, 1997.
This work was supported by grants AG9063 and PO1 DC02952 from the National Institutes of Health, Bethesda, Md.
Reprints: Robert W. Baloh, MD, Department of Neu-rology, University of California–Los Angeles, Box 951769, Los Angeles, CA 90095-1769 (e-mail: firstname.lastname@example.org).
1. Mirka A, Black FO. Clinical application of dynamic posturography for evaluating sensory integration and vestibular dysfunction.Neurol Clin. 1990;8:351-359. 2. Nashner LM, Peters JF. Dynamic posturography in the diagnosis and
manage-ment of dizziness and balance disorders.Neurol Clin. 1990;8:331-349. 3. Diener HC, Dichgans J, Bacher M, Gompf B. Quantification of postural sway in
normals and patients.Electroencephalogr Clin Neurophysiol. 1984;57:134-142. 4. Yoneda S, Tokumatsu K. Frequency analysis of body sway in the upright pos-ture: statistical study in cases of peripheral vestibular disease.Acta Otolaryngol (Stockh). 1986;102:87-92.
5. Pyykko¨ I, Aalto H, Starck J, Ishizaki H. Postural stability on moving platform
oscillating at high frequencies: effect of vestibular lesion.Acta Otolaryngol (Stockh). 1991;481(suppl):572-575.
6. Voorhees RL. Dynamic posturography findings in central nervous system dis-orders.Otolaryngol Head Neck Surg. 1990;103:96-101.
7. Nelson SR, DiFabio RP, Anderson JH. Vestibular and sensory interaction defi-cits assessed by dynamic platform posturography in patients with multiple scle-rosis.Ann Otol Rhinol Laryngol. 1995;104:62-68.
8. Baloh RW, Spain S, Socotch TM, Jacobson KM, Bell T. Posturography and bal-ance problems in older people.J Am Geriatr Soc. 1995;43:638-644. 9. Nashner LM, Black FO, Wall C III. Adaptation to altered support and visual
conditions during stance: patients with vestibular deficits.J Neurosci. 1982;2: 536-544.
10. Maki BE, Holliday PJ, Topper AK. A prospective study of postural balance and risk of falling in an ambulatory and independent elderly population.J Gerontol Med Sci. 1994;49:M72-M84.
11. Mauritz KH, Dichgans J, Hufschmidt A. Quantitative analysis of stance in late cor-tical cerebellar atrophy of the anterior lobe and other forms of cerebellar ataxia. Brain. 1979;102:461-482.
12. Furman JM, Baloh RW, Kamran B, et al. Assessment: posturography—Report of the Therapeutics and Technology Assessment Subcommittee of the Ameri-can Academy of Neurology.Neurology. 1993;43:1261-1264.
13. Baloh RW, Langhofer L, Honrubia V, Yee RD. On-line analysis of eye move-ments using a digital computer.Aviat Space Environ Med. 1980;51:563-567. 14. Baloh RW, Honrubia V, Yee RD, Hess K. Changes in the human vestibulo-ocular
reflex after loss of peripheral sensitivity.Ann Neurol. 1984;16:222-228. 15. Moschner C, Perlman S, Baloh RW. Comparison of oculomotor findings in the
progressive ataxia syndromes.Brain. 1994;117:15-25.
16. Baloh RW, Fife TD, Zwerling L, et al. Comparison of static and dynamic pos-turography in young and older normal people.J Am Geriatr Soc. 1994;42:405-412.
17. Grabiner MD, Lundin TM, Feuerbach JW. Converting Chattecx balance system vertical reaction forces to center of pressure excursion.Phys Ther. 1993;73: 316-319.
18. Dow RS, Moruzzi G.The Physiology and Pathology of the Cerebellum. Minne-apolis: The University of Minnesota Press; 1958.
19. Black FO, Wall C III, Rockette HE, Kitch R. Normal subject postural sway during the Romberg test.Am J Otolaryngol. 1982;3:309-318.
20. Hufschmidt A, Dichgans J, Mauritz KH, Hufschmidt M. Some methods and pa-rameters of body sway quantification and their neurological applications.Arch Psychiatr Nervenkr. 1980;228:135-150.
21. Murphy JT, Wong YC, Kwan HC. Afferent-efferent linkages in motor cortex for single forelimb muscles.J Neurophysiol. 1975;38:990-1014.
22. Nashner LM. Adapting reflexes controlling the human posture.Exp Brain Res. 1976;26:59-72.
23. Allum JHJ, Honegger F, Pfaltz CR. The role of stretch and vestibulo-spinal re-flexes in the generation of human equilibrating reactions. In: Allum JHJ, Hulliger M, eds.Progress in Brain Research. Amsterdam, the Netherlands: Elsevier Sci-ence Publishers; 1989:80.
24. Inglis JT, Macpherson JM. Bilateral labyrinthectomy in the cat: effects on the postural response to translation.J Neurophysiol. 1995;73:1181-1191. 25. Mauritz KH, Schmitt C, Dichgans J. Delayed and enhanced long latency reflexes
as the possible cause of postural tremor in late cerebellar atrophy.Brain. 1981; 104:97-116.
26. Fetter M, Diener HC, Dichgans J. Recovery of postural control after an acute uni-lateral vestibular lesion in humans.J Vestib Res. 1991;1:373-383.
27. Collins JJ, DeLuca CJ. Open-loop and closed-loop control of posture.Exp Brain Res. 1993;95:308-318.