Peripheral Vestibular Deficit Research Articles

Cognitive Rehabilitation in Bilateral Vestibular Patients: A Computational Perspective.

There is evidence that vestibular sensory processing affects, and is affected by, higher cognitive processes. This is highly relevant from a clinical perspective, where there is evidence for cognitive impairments in patients with peripheral vestibular deficits. The vestibular system performs complex probabilistic computations, and we claim that understanding these is important for investigating interactions between vestibular processing and cognition. Furthermore, this will aid our understanding of patients’ self-motion perception and will provide useful information for clinical interventions. We propose that cognitive training is a promising way to alleviate the debilitating symptoms of patients with complete bilateral vestibular loss (BVP), who often fail to show improvement when relying solely on conventional treatment methods. We present a probabilistic model capable of processing vestibular sensory data during both passive and active self-motion. Crucially, in our model, knowledge from multiple sources, including higher-level cognition, can be used to predict head motion. This is the entry point for cognitive interventions. Despite the loss of sensory input, the processing circuitry in BVP patients is still intact, and they can still perceive self-motion when the movement is self-generated. We provide computer simulations illustrating self-motion perception of BVP patients. Cognitive training may lead to more accurate and confident predictions, which result in decreased weighting of sensory input, and thus improved self-motion perception. Using our model, we show the possible impact of cognitive interventions to help vestibular rehabilitation in patients with BVP.

The Dizziness Handicap Inventory does not correlate with vestibular function tests: a prospective study

The Dizziness Handicap Inventory (DHI) is believed to quantitate the handicap related to the presence or severity of underlying vestibular dysfunction. However, patients with chronic vestibular diseases may manifest various degrees of behavioural and physiological adaptation resulting in variances of the DHI. Our primary study objective is to evaluate the correlation between the DHI and measurable vestibular parameters. Secondarily, we compared DHI among different vestibular disorders (central, peripheral and functional), and different types of anatomic deficits (semicircular canal vs otolithic). We also correlated the DHI and posturography. We prospectively evaluated 799 patients with precise vestibular diagnoses using video head impulse testing (vHIT), caloric irrigation, and cervical/ocular vestibular-evoked myogenic potentials (c/oVEMP). Posturography was done for 84 patients. All participants completed the DHI. No significant correlation was found between DHI and (1) vestibulo-ocular reflex parameters: unilateral weakness r = - 0.018, total calorics r = 0.055, vHIT right r = 0.007, vHIT left r = - 0.091, vHIT asymmetry r = 0.013; (2) otolith parameters: cVEMP amplitude right r = - 0.034, amplitude left r = - 0.004, asymmetry r = 0.016; oVEMP amplitude right r = 0.044, amplitude left r = - 0.007, asymmetry r = - 0.008. Patients with central vestibular disorders had higher DHI than those with peripheral (z = - 4.743, p = 0.001) or functional disorders (z = - 2.902, p = 0.004). DHI of patients with deficits of canal or otolith function did not differ significantly from those with no deficits (z = 2.153, p = 0.541). There was no significant correlation between DHI and postural sway on posturography. Therefore, the DHI does not correlate with vestibular tests, and neither reflects the presence nor severity of peripheral vestibular deficits.

The Effect of Peripheral Vestibular Recovery on Improvements in Vestibulo-ocular Reflexes and Balance Control After Acute Unilateral Peripheral Vestibular Loss.

Patients with an acute unilateral peripheral vestibular deficit (aUPVD), presumed to be caused by vestibular neuritis, show asymmetrical vestibular ocular reflexes (VORs) that improve over time. Questions arise regarding how much of the VOR improvement is due to peripheral recovery or central compensation, and whether differences in peripheral recovery influence balance control outcomes. Thirty patients were examined at aUPVD onset and 3, 6, and 13 weeks later with four different VOR tests: caloric tests; rotating (ROT) chair tests performed in yaw with angular accelerations of 5 and 20 degrees/s; and video head impulse tests (vHIT) in the yaw plane. ROT and vHIT responses and balance control of 11 patients who had a caloric canal paresis (CP) more than 90% at aUPVD onset and no CP recovery (no-CPR) at 13 weeks in caloric tests were compared with those of 19 patients with CP recovery (CPR) to less than 30%, on average. Balance control was measured with a gyroscope system (SwayStar) recording trunk sway during stance and gait tasks. ROT and vHIT asymmetries of no-CPR and CPR patients reduced over time. The reduction was less at 13 weeks (36.2% vs. 83.5% on average) for the no-CPR patients. The no-CPR group asymmetries at 13 weeks were greater than those of CPR patients who had normal asymmetries. The greater asymmetries were caused by weaker deficit side responses which remained deficient in no-CPR patients at 13 weeks. Contra-deficit side vHIT and ROT responses remained normal. For all balance tests, sway was slightly greater for no-CPR compared with CPR patients at aUPVD onset and 3 weeks later. At 13 weeks, only sway during walking eyes closed was greater for the no-CPR group. A combination of 5 degrees/s ROT and balance tests could predict at onset (90% accuracy) which patients would have no-CPR at 13 weeks. These results indicate that for ROT and vHIT tests, central compensation is observed in CPR and no-CPR patients. It acts primarily by increasing deficit side responses. Central compensation provides approximately 60% of the VOR improvement for CPR patients. The rest of the improvement is due to peripheral recovery which appears necessary to reduce VOR asymmetry to normal at 13 weeks on average. Balance control improvement is more rapid than that of the VOR and marginally affected by the lack of peripheral recovery. Both VOR and balance control measures at onset provide indicators of future peripheral recovery. For these reasons VOR and balance control needs to be tested at aUPVD onset and at 13 weeks.

Impaired math achievement in patients with acute vestibular neuritis

Broad cognitive difficulties have been reported in patients with peripheral vestibular deficit, especially in the domain of spatial cognition. Processing and manipulating numbers relies on the ability to use the inherent spatial features of numbers. It is thus conceivable that patients with acute peripheral vestibular deficit show impaired numerical cognition. Using the number Stroop task and a short math achievement test, we tested 20 patients with acute vestibular neuritis and 20 healthy, age-matched controls. On the one hand, patients showed normal congruency and distance effects in the number Stroop task, which is indicative of normal number magnitude processing. On the other hand, patients scored lower than healthy controls in the math achievement test. We provide evidence that the lower performance cannot be explained by either differences in prior math knowledge (i.e., education) or slower processing speed. Our results suggest that peripheral vestibular deficit negatively affects numerical cognition in terms of the efficient manipulation of numbers. We discuss the role of executive functions in math performance and argue that previously reported executive deficits in patients with peripheral vestibular deficit provide a plausible explanation for the lower math achievement scores. In light of the handicapping effects of impaired numerical cognition in daily living, it is crucial to further investigate the mechanisms that cause mathematical deficits in acute PVD and eventually develop adequate means for cognitive interventions.

Validation of the Italian Version of the Dizziness Handicap Inventory, the Situational Vertigo Questionnaire, and the Activity-Specific Balance Confidence Scale for Peripheral and Central Vestibular Symptoms.

Neurophysiological measurements of the vestibular function for diagnosis and follow-up evaluations provide an objective assessment, which, unfortunately, does not necessarily correlate with the patients’ self-feeling. The literature provides many questionnaires to assess the outcome of rehabilitation programs for disequilibrium, but only for the Dizziness Handicap Inventory (DHI) is an Italian translation available, validated on a small group of patients suffering from a peripheral acute vertigo. We translated and validated the reliability and validity of the DHI, the Situational Vertigo Questionnaire (SVQ), and the Activities-Specific Balance Confidence Scale (ABC) in 316 Italian patients complaining of dizziness due either to a peripheral or to a central vestibular deficit, or in whom vestibular signs were undetectable by means of instrumental testing or clinical evaluation. Cronbach’s coefficient alpha, the homogeneity index, and test–retest reproducibility, confirmed reliability of the Italian version of the three questionnaires. Validity was confirmed by correlation test between questionnaire scores. Correlations with clinical variables suggested that they can be used as a complementary tool for the assessment of vestibular symptoms. In conclusion, the Italian versions of DHI, SVQ, and ABC are reliable and valid questionnaires for assessing the impact of dizziness on the quality of life of Italian patients with peripheral or central vestibular deficit.

Central not peripheral vestibular processing impairs gait coordination.

Gait coordination is generated by neuronal inter-connections between central pattern generators in the spinal cord governed by cortical areas. Malfunction of central vestibular processing areas generates vestibular symptoms in the absence of an identifiable peripheral vestibular system lesion. Walking in the dark enforces a coordinated afference primarily from the vestibular and somatosensory systems. We hypothesized that patients with aberrant central vestibular processing would demonstrate unique gait characteristics, and have impaired gait coordination compared with those patients with abnormal peripheral vestibular function and healthy controls. One-hundred and eighteen subjects were recruited. Peripheral vestibular function was determined based on laboratory and clinical examinations. Patients with abnormal central vestibular processing had normal peripheral vestibular function. Subjects were instructed to walk at a comfortable pace during three visual conditions; eyes open, eyes open and closed intermittently, and eyes closed. Both patient groups showed a similar spatiotemporal gait pattern, significantly different from the pattern of the healthy controls. However, only the central vestibular patient group had an abnormal coordination of gait as measured by the phase coordination index (PCI). There were no significant interactions between the groups and walking conditions. Peripheral vestibular deficits impair gait though our data suggest that it is the central processing of such peripheral vestibular information that has a greater influence. This impairment may be related to a neural un-coupling between the brain and central pattern generator of the spinal cord based on the abnormal PCI, which seems to be a good indicator of the integrity of this linkage.

Differences in head impulse test results due to analysis techniques.

Different analysis techniques are used to define vestibulo-ocular reflex (VOR) gain between eye and head angular velocity during the video head impulse test (vHIT). Comparisons would aid selection of gain techniques best related to head impulse characteristics and promote standardisation. Compare and contrast known methods of calculating vHIT VOR gain. We examined lateral canal vHIT responses recorded from 20 patients twice within 13 weeks of acute unilateral peripheral vestibular deficit onset. Ten patients were tested with an ICS Impulse system (GN Otometrics) and 10 with an EyeSeeCam (ESC) system (Interacoustics). Mean gain and variance were computed with area, average sample gain, and regression techniques over specific head angular velocity (HV) and acceleration (HA) intervals. Results for the same gain technique were not different between measurement systems. Area and average sample gain yielded equally lower variances than regression techniques. Gains computed over the whole impulse duration were larger than those computed for increasing HV. Gain over decreasing HV was associated with larger variances. Gains computed around peak HV were smaller than those computed around peak HA. The median gain over 50-70 ms was not different from gain around peak HV. However, depending on technique used, the gain over increasing HV was different from gain around peak HA. Conversion equations between gains obtained with standard ICS and ESC methods were computed. For low gains, the conversion was dominated by a constant that needed to be added to ESC gains to equal ICS gains. We recommend manufacturers standardize vHIT gain calculations using 2 techniques: area gain around peak HA and peak HV.

Acute peripheral vestibular deficit increases redundancy in random number generation

Unilateral peripheral vestibular deficit leads to broad cognitive difficulties and biases in spatial orientation. More specifically, vestibular patients typically show a spatial bias toward their affected ear in the subjective visual vertical, head and trunk orientation, fall tendency, and walking trajectory. By means of a random number generation task, we set out to investigate how an acute peripheral vestibular deficit affects the mental representation of numbers in space. Furthermore, the random number generation task allowed us to test if patients with peripheral vestibular deficit show evidence of impaired executive functions while keeping the head straight and while performing active head turns. Previous research using galvanic vestibular stimulation in healthy people has shown no effects on number space, but revealed increased redundancy of the generated numbers. Other studies reported a spatial bias in number representation during active and passive head turns. In this experiment, we tested 43 patients with acute vestibular neuritis (18 patients with left-sided and 25 with right-sided vestibular deficit) and 28 age-matched healthy controls. We found no bias in number space in patients with peripheral vestibular deficit but showed increased redundancy in patients during active head turns. Patients showed worse performance in generating sequences of random numbers, which indicates a deficit in the updating component of executive functions. We argue that RNG is a promising candidate for a time- and cost-effective assessment of executive functions in patients suffering from a peripheral vestibular deficit.

Recovery of Vestibulo-Ocular Reflex Symmetry After an Acute Unilateral Peripheral Vestibular Deficit: Time Course and Correlation With Canal Paresis.

We investigated how response asymmetries and deficit side response amplitudes for head accelerations used clinically to test the vestibular ocular reflex (VOR) are correlated with caloric canal paresis (CP) values. 30 patients were examined at onset of an acute unilateral peripheral vestibular deficit (aUPVD) and 3, 6, and 13 weeks later with three different VOR tests: caloric, rotating chair (ROT), and video head impulse tests (vHIT). Response changes over time were fitted with an exponential decay model and compared with using linear regression analysis. Recovery times (to within 10% of steady state) were similar for vHIT-asymmetry and CP (>10 weeks) but shorter for ROT asymmetry (<4 weeks). Regressions with CP were similar (vHIT asymmetry, R = 0.68, ROT, R = 0.62). Responses to the deficit side were also equally well correlated with CP values (R = 0.71). Specificity for vHIT and 20 degrees/s ROT deficit side responses was 100% in comparison to CP values, sensitivity was 74% for vHIT, 75% for ROT. A decrease in normal side responses occurred for ROT but not for vHIT at 3 weeks. Normal side responses were weekly correlated with CP for ROT (R = 0.49) but not for vHIT (R = 0.17). These results indicate that vHIT deficit side VOR gains are slightly better correlated with CP values than ROT, probably because of similar recovery time courses of vHIT and caloric responses and the lack of normal side vHIT changes. However, specificity and sensitivity is the same for vHIT and ROT tests.

Recovery times of stance and gait balance control after an acute unilateral peripheral vestibular deficit.

Acute unilateral peripheral vestibular deficit (aUPVD) patients have balance deficits that can improve after several weeks. Determining differences in vestibulo-spinal reflex (VSR) influences on balance control and vestibular ocular reflex (VOR) responses with peripheral recovery and central compensation would provide insights into CNS plasticity mechanisms. Also, clinically, knowing when balance control is approximately normal again should contribute to decisions about working ability after aUPVD. Usually VORs are employed for this purpose, despite a lack of knowledge about correlations with balance control. Given this background, we examined whether balance and VOR measures improve similarly and are correlated. Further whether balance improvements are different for stance and gait. 26 patients were examined at onset of aUPVD, and 3, 6 and 13 weeks later. To measure balance control and thereby assess the contribution of VSR influences during stance and gait, body-worn gyroscopes mounted at lumbar 1-3 recorded the angular velocity of the lower trunk in the roll (lateral) and pitch (anterior-posterior) directions. These signals were integrated to yield angle deviations. To measure VOR function, rotating chair (ROT) tests were performed with triangular velocity profiles with accelerations of 20°/s(2) and 5°/s(2), and caloric tests with bithermal (44 and 30°C) water irrigation of the external auditory meatus. Changes in average balance and VOR measures at the 4 examination time points were modelled with exponential decays. Improvements were assumed to plateau when model values were to within 10% of steady state. Balance improvement rates were task and direction dependent, ranging from 3-9 weeks post aUPVD, similar to the range of ROT VOR improvement rates. Stance balance control improved similarly in the pitch and roll directions. Both reached steady state at 7.5 weeks. However, changes in visual and proprioceptive influences on stance sway velocities continued to decrease in favour of vestibular influences for over 10 weeks with the visual influence being correlated with ROT deficit side responses (R= 0.475). Spontaneous nystagmus and stance roll velocity were weakly correlated (R= 0.24). Pitch control during gait tests improved faster than roll. Gait speed was slower and only recovered normal velocity at 6-9 weeks. Pitch velocity when walking eyes closed was correlated (R= 0.38) with ROT asymmetry. Other balance and VOR measures were more weakly correlated (R< 0.2) even if these had similar improvement rates. These results indicate that balance control for stance improves equally fast in the pitch and roll directions. For gait, pitch control improves faster than roll. On average, stance and gait tests show normal balance control at 6-9 weeks post aUPVD onset. As few balance measures are correlated with those of VOR function and then with low (R< 0.5) coefficients, we suggest that VOR tests should not be used to assess improvements in balance control after aUPVD. The lack of strong correlations between balance and VOR measures included in this study during peripheral recovery and central compensation of aUPVD supports the hypothesis that recovery of balance function after an aUPVD involves different CNS pathways and neural plasticity mechanisms.

P35. Neglect and vestibular failure – Spatial or attentional deficit?

Objectives Acute peripheral vestibular failure (VF) and neglect show similarities in clinical presentation and neglect can be ameliorated by vestibular stimulation. Furthermore, cortical areas involved in neglect patients overlap in part with the multisensory cortical vestibular network ( Karnath and Dieterich, 2006 ). Thus, the question did arise whether acute VF can induce spatial neglect. The aim of the current study was to find out whether patients with an acute VF show spatial neglect and if test scores were related to the severity of the deficit. Methods 28 patients with acute VF were assessed for signs of vestibular deficits and spatial neglect clinically as well as with common standard paper pencil neglect testing (bells test ( Gauthier et al., 1989 ), Albert’s test ( Albert, 1973 ), line bisection task ( Schenkenberg et al., 1980 ), figure copying). The laterality in the cancellation tasks was further analyzed using the Center of Cancellation method (CoC) ( Rorden and Karnath, 2010 ). The deficit was correlated with deviation of subjective visual vertical (SVV) and the degree of canal paresis. Results All patients had clear peripheral vestibular deficit at the time of testing. Mean time from symptom onset to neglect testing was 1.8 days (SD 1.7 d), to SVV testing 1.9 days (SD 1.8 d, mean deviation ± 7.3°) and to caloric testing 2.3 days (SD 2.3, mean reduction of caloric excitability 51%). Three patients showed pathologic scores in neglect tests (10%), two contralesionally and one ipsilesionally. One of these patients had a score fulfilling the criteria for spatial neglect in the bells test ( Gauthier et al., 1989 ) but not in the CoC method ( Rorden and Karnath, 2010 ). In contrast, the patient with a pathological CoC score did not meet the criteria for spatial neglect using the original method. One patient omitted one line in the Albert’s test contralaterally. Only one patient had pathological test scores in two tests but deviations in line bisection were both ipsilateral and contralateral. No patient showed congruent bias to one side in two different tests or analysis methods. There was no significant correlation between the total number of omissions in the bells test and the magnitude of SVV deviation or canal paresis. A group wise comparison of patients with and without pathological scores was carried out but the effect size was not strong enough to produce reliable results due to the small number of three patients. Conclusions VF patients occasionally showed pathological scores on single and different neglect tests. No correlation was found between omissions and SVV deviation or canal paresis. The three patients with pathologic scores did not show neglect behavior and the pattern of omissions is far less pronounced in the patients with VF compared to neglect patients. Thus, we suggest that these findings represent an attentional deficit and that novel tools to assess this deficit are needed. These should take spatial exploration and attention in a three-dimensional space into account to differentiate an attentional from a true spatial deficit. Acknowledgements This study was supported by the German Federal Ministry of Education and Research (BMBF, grant code 01 EO 0901) and the German Foundation for Neurology to MD.

Gaze Stabilization Test Asymmetry Score as an Indicator of Previous Concussion in a Cohort of Collegiate Football Players.

Vestibular dysfunction may lead to decreased visual acuity with head movements, which may impede athletic performance and result in injury. The purpose of this study was to test the hypothesis that athletes with history of concussion would have differences in gaze stabilization test (GST) as compared with those without a history of concussion. Cross-sectional, descriptive. University Athletic Medicine Facility. Fifteen collegiate football players with a history of concussion, 25 collegiate football players without a history of concussion. Participants completed the dizziness handicap inventory (DHI), static visual acuity, perception time test, active yaw plane GST, stability evaluation test (SET), and a bedside oculomotor examination. Independent samples t test was used to compare GST, SET, and DHI scores per group, with Bonferroni-adjusted alpha at P < 0.01. Receiver operating characteristic curve analysis and area under the curve (AUC) were used to assess the clinical performance of the GST and SET. Athletes with previous concussion had a larger GST asymmetry score [mean (M) = 12.40, SD = 9.09] than those without concussion (M = 4.92, SD = 4.67; t (18.70) = -2.955, P = 0.008, 95% CI, -12.79 to -2.18, d = -1.37). Clinical performance of the GST (AUC = 0.77) was better than the SET (AUC = 0.61). Results suggest peripheral vestibular or vestibular-visual interaction deficits in collegiate athletes with a history of concussion. The results support further research on the use of GST for sport-related concussion evaluation and monitoring. Inclusion of objective vestibular tests in the concussion protocol may reveal the presence of peripheral vestibular or visual-vestibular deficits. Therefore, the GST may add an important perspective on the effects of concussion.

Standardization of rotatory chair velocity step and sinusoidal harmonic acceleration tests in an adult population

Objective To standardize the rotatory chair sinusoidal harmonic acceleration and velocity step tests in an adult population. Study design Prospective study. Setting Clinical tertiary care vestibular function test center. Patients One hundred normal participants (66 men and 34 women without suspected vestibular disorder) were evaluated using bithermal binaural caloric and sinusoidal and step-velocity rotary chair tests. Intervention Hearing, videonystagmography, and rotary chair tests. Materials and methods All participants were selected according to the following criteria: (a) no history of dizziness; (b) normal otological examination; (c) normal hearing evaluation; (d) normal videonystagmography testing; and (e) rotational chair testing. The patient was positioned and secured to the rotational chair with the patient's head restrained and adjusted so that both lateral semicircular canals were close to the plane of stimulus (30΀ forward tilt), the rotational chair testing paradigms used in this study were: (a): the rotational sinusoidal harmonic acceleration (SHA) test and (b): the rotational velocity step test. Results The demographic criteria for the study group were as follows: the age range was 18-56 years, mean age 36.47 years, and 66% of the participants were men and 34% were women. The mean, SD, range, and 95% confidence limits of the SHA and rotational velocity step test were calculated and compared with the manufacturer's normal values. No statistically significant differences were found between our lab test results and the manufacturer-measured values of the rotational SHA test and the rotational step velocity test (SVT); this could be attributed to the strict selection criteria of the study group. Conclusion In summary, the information obtained from rotational chair testing may provide valuable information in the diagnosis and subsequent management of patients with vestibular disorders. It completes the spectrum of tests necessary for the diagnosis of vestibular abnormalities and aids the identification of peripheral vestibular deficits not detectable with existing procedures. The major clinical advantage of computerized rotational testing is the ability to produce angular accelerations that can be precisely controlled and repeated. Multiple stimuli of varying intensities can be applied to the vestibular system within a relatively short time.

Relation Between Head Impulse Tests, Rotating Chair Tests, and Stance and Gait Posturography After an Acute Unilateral Peripheral Vestibular Deficit

Vestibulo-ocular reflex (VOR) deficits and balance instability during stance and gait are typical for an acute unilateral peripheral vestibular deficit (AUPVD). The relation between different VOR measures with recovery is unknown, as is the relation of VOR measures to balance control. To answer these questions, we examined changes over time in caloric canal paresis (CP), head impulse tests (HIT), whole body rotation (ROT) tests of the horizontal VOR, and changes in trunk sway during stance and gait tests, for cases of presumed vestibular neuritis. HIT was performed with short ca. 200 degrees per second head turns, ROT with triangular 24-second velocity profiles (peak 120 degrees per second, acceleration 20 degrees per second squared). To measure balance control, body-worn gyroscopes measured pitch (anterior-posterior) and roll (lateral) sway angles and angular velocities at lumbar 1 to 3. Changes during recover in ROT and HIT responses to the deficit side were equally well related (R = 0.8, p < 0.001) to changes in caloric CP values. ROT but not HIT responses to the normal side were also related to CP responses (R = 0.53, p = 0.02). Spontaneous nystagmus levels were related to changes instance balance control (R = 0.52, p = 0.001). Balance during gait improved over time but was not well correlated with changes in VOR measures (R = 0.26 max., p > 0.05). Both HIT and ROT track VOR recovery on the deficit side due to central compensation and peripheral recovery. However, only ROT track changes in the central compensation of normal side responses. The weak correlations between VOR and stance and gait tests suggest that the latter should also be tested to judge the effect of an AUPVD on balance control.

Vestibular compensation in acute unilateral medullary infarction

The aim of this fluorodeoxyglucose (FDG)-PET study was to determine whether the activation pattern in patients with an acute unilateral central vestibular lesion (e.g., lesion of the vestibular nucleus) differs from that known in patients with an acute peripheral vestibular deficit. Twelve patients with circumscribed unilateral medullary brainstem infarctions (6 right, 6 left) causing acute vestibular imbalance underwent resting-state (18)F-FDG-PET. Regional cerebral glucose metabolism was measured twice without any stimulation and with eyes closed: in the acute phase after infarct onset on mean day 8 (range 4-12), and again 6 months later in 7 patients after recovery. Group subtraction analyses and comparisons with a dataset of 12 age-matched controls were done with Statistic Parametric Mapping. In the acute stage, the pattern of signal increases differed from that in peripheral vestibular lesions: whereas signals in the infratentorial areas in the contralateral medulla and cerebellum (peduncle, vermis, hemispheres) were increased, areas at the cortical level were largely spared. Signal decreases were found in similar sites in the visual cortex bilaterally. The current data provide evidence that the lesion site significantly modifies the glucose metabolism pattern in an acute vestibular lesion. Different compensation strategies seem to be apparent: after vestibular nucleus lesions, compensation occurs preferably in brainstem-cerebellar loops; after peripheral lesions, it occurs at the cortical level.

Teaching Neuro Images : Compression of the eighth cranial nerve causes vestibular paroxysmia

A 55-year-old man reported having recurrent spontaneous attacks of rotatory vertigo lasting 1–5 seconds and occurring up to 10 times daily and often associated with attacks of right ear tinnitus for more than 3 years. Caloric testing showed a right peripheral vestibular deficit. Cervical vestibular myogenic potentials showed impaired function of the right saccule. An audiogram was normal. MRI (figure, A and B) showed that the eighth nerve was in contact with the anterior inferior cerebellar artery. Vestibular paroxysmia was diagnosed.1,2 Carbamazepine resolved the symptoms but the patient discontinued it due to side effects. The symptoms recurred, and surgery was performed. Intraoperatively, compression of the eighth nerve was found (figure, C and D). He has had no further symptoms and takes no medication. These findings support the view that vascular compression of the root entry zone of the eighth cranial nerve can cause vestibular paroxysmia. The authors thank Dr. Jennifer Linn for evaluation of the MRI scans.

末梢前庭機能評価の観点からみた振子様手動回転による前庭眼反射検査の有用性

This study included 209 patients with vertigo of various causes who underwent both manually rotated vestibulo-ocular reflex (VOR) testing and bithermal air caloric testing at our hospital from January 2009 to July 2012. The VOR directional predominance (VOR-DP%) values in the 79 patients with greater than 30% caloric canal paresis (CP) were significantly higher than those in the 43 normal subjects. On the other hand, the VOR-DP% values in 81% of patients with CP were within normal limits, as those in the 43 normal subjects varied widely (the normal range is considered to be wide). In all of the vertiginous cases, the VOR-DP% values showed only a slight correlation with the CP% values. However, the VOR-DP% was well-correlated with the CP% in patients with vestibular neuritis, Hunt syndrome and sudden deafness with vertigo, especially in the acute stage within 2 weeks of the onset. The VOR-DP% values in these latter patients with vestibular neuritis, Hunt syndrome and sudden deafness with vertigo decreased with time, regardless of the presence or absence of recovery from CP. Manually rotated VOR testing is thought to be one of the useful tools in daily clinical practice, that allows estimation of both peripheral vestibular function and the degree of recovery from imbalance in patients with acute unilateral peripheral vestibular deficit.

Selective Vestibular Neurolabyrinthitis of the Lateral and Superior Semicircular Canal Ampulla and Ampullary Nerves

The diagnosis of vestibular neurolabyrinthitis is based on the sudden appearance of vertigo that lasts for hours or days without associated cochlear or central nervous system signs or symptoms. The advent of the video head impulse test, cervical vestibular evoked myogenic potential testing, and ocular vestibular evoked myogenic potential testing has provided interesting clinical evidence for evaluating and monitoring the damage to specific compartments of the vestibular apparatus. These various methods of testing individual end-organ functions may have a clinical impact on the vestibular workup of neurolabyrinthitis. This report describes 3 patients with acute vestibular neurolabyrinthitis in whom caloric tests, cervical vestibular evoked myogenic potentials, ocular vestibular evoked myogenic potentials, and the video head impulse test led to a suspicion of peripheral vestibular deficits of the lateral or superior semicircular canal ampulla or ampullary nerves. In our patients, the examination results (normal hearing, absence of responses on caloric testing, and bilateral preservation of cervical and ocular vestibular evoked myogenic potentials) disclosed an acute partial superior vestibular neurolabyrinthitis. To our knowledge, these are the first reported cases in which selective damage to the lateral and superior semicircular canals and their nerves caused by neurolabyrinthitis was demonstrated clinically. Our clinical results indicate that the damage can be selective for specific vestibular end organs.

Determining the preferred modality for real-time biofeedback during balance training

Vestibular rehabilitation therapy has been shown to improve balance and gait stability in individuals with vestibular deficits. However, patient compliance with prescribed home exercise programs is variable. Real-time feedback of exercise performance can potentially improve exercise execution, exercise motivation, and rehabilitation outcomes. The goal of this study is to directly compare the effects of visual and vibrotactile feedback on postural performance to inform the selection of a feedback modality for inclusion in a home-based balance rehabilitation device. Eight subjects (46.6±10.6years) with peripheral vestibular deficits and eight age-matched control subjects (45.3±11.1years) participated in the study. Subjects performed eyes-open tandem Romberg stance trials with (vibrotactile, discrete visual, continuous visual, and multimodal) and without (baseline) feedback. Main outcome measures included medial–lateral (M/L) and anterior–posterior mean and standard deviation of body tilt, percent time spent within a no-feedback zone, and mean score on a comparative ranking survey. Both groups improved performance for each feedback modality compared to baseline, with no significant differences in performance observed among vibrotactile, discrete visual, or multimodal feedback for either group. Subjects with vestibular deficits performed best with continuous visual feedback and ranked it highest. Although the control subjects performed best with continuous visual feedback in terms of mean M/L tilt, they ranked it lowest. Despite the observed improvements, continuous visual feedback involves tracking a moving target, which was noted to induce dizziness in some subjects with vestibular deficits and cannot be used during exercises in which head position is actively changed or during eyes-closed conditions.

Postural Response to Unexpected Changes

Objective: 1) Determine the characteristics of postural responses to unexpected changes in the support-surface in patients with unilateral peripheral vestibular deficit and analyze differences between patients achieving a clinical compensated status and those without. 2) Find out which is the best clinical data to predict the vestibular compensation status. Method: Twenty-seven adults suffering unilateral peripheral vestibular deficits (vestibular neuritis, Ménière’s disease, neurinoma, trauma and benign recurrent vertigo) were included. Neurocom equipment was used to create pulses unexpectedly. Sway Star system was used to measure the angle and the angular velocity of the body during the stimulus. Results: The range of peak to peak excursion, the area of the displacement angle, the range of peak to peak velocity excursion in pitch and roll directions and the mean path velocity were studied. When using the caloric test results to classify the patients as compensated or not compensated significant differences (p minor to 0.001) of the body angle in the roll direction were found, although all the stimuli were made in the pitch direction. However, when using the caloric test, the cardiovascular risk or the patient’s clinical course to classify the groups, no differences were found. Conclusion: The rotatory test is the best diagnostic method to predict vestibular compensation status of patients with vestibular deficits. Patients suffering vestibular deficit with an uncompensated status, have more difficulties to give an appropriate postural response in the roll direction to unexpected support-surface movements.