Positional nystagmus is observed in the vast majority of healthy individuals.

INTRODUCTION: Benign paroxysmal positional vertigo (BPPV) is a vestibular disease characterized by brief  positional vertigo. When examined, characteristic patterns of positional nystagmus (PN) are found with specific head position changes. Previous studies have shown a high prevalence of PN among vestibular healthy subjects. Considering the current diagnostic criteria of BPPV and the potentially high prevalence of PN in healthy individuals, this raises the question of potential over diagnosing BPPV, if diagnostics are based exclusively upon objective findings. This study aims to determine the prevalence of PN within a healthy, adult population and furthermore include a characterization of the PN observed. METHODS: This is a prospective cross-sectional study. 78 subjects were included. The subjects underwent four standardized positional tests for BPPV in a mechanical rotational chair while using a VNG-goggle to monitor and record eye movements. RESULTS: Positional nystagmus was recorded in 70.5% (55/78) of the subjects. Of the 55 subjects, who presented with PN, 81.8% (45/55) had upbeating PN. The 95th percentile of the maximum a-SPV was found to be 10.4 degrees per second, with a median of 4. Five subjects (6.4%) in total presented with PN mimicking BPPV. CONCLUSION: This study found PN to be a common finding within a healthy, adult population based on the high prevalence of PN in the study population. Upbeating PN mimicking posterior canalolithiasis was found in numerous subjects. The authors recommend a cautious approach when diagnosing BPPV, especially in cases of purely vertical PN (without a torsional component) and if no vertiginous symptoms are present during Dix-Hallpike and Supine Roll Test examinations.

Vestibular, locomotor, and vestibulo-autonomic research: 50 years of collaboration with Bernard Cohen.

My collaboration on the vestibulo-ocular reflex with Bernard Cohen began in 1972. Until 2017, this collaboration included studies of saccades, quick phases of nystagmus, the introduction of the concept of velocity storage, the relationship of velocity storage to motion sickness, primate and human locomotion, and studies of vasovagal syncope. These studies have elucidated the functioning of the vestibuloocular reflex, the locomotor system, the functioning of the vestibulo-sympathetic reflex, and how blood pressure and heart rate are controlled by the vestibular system. Although it is virtually impossible to review all the contributions in detail in a single paper, this article traces a thread of modeling that I brought to the collaboration, which, coupled with Bernie Cohen's expertise in vestibular and sensory-motor physiology and clinical insights, has broadened our understanding of the role of the vestibular system in a wide range of sensory-motor systems. Specifically, the paper traces how the concept of a relaxation oscillator was used to model the slow and rapid phases of ocular nystagmus. Velocity information that drives the slow compensatory eye movements was used to activate the saccadic system that resets the eyes, giving rise to the relaxation oscillator properties and simulated nystagmus as well as predicting the types of unit activity that generated saccades and nystagmic beats. The slow compensatory component of ocular nystagmus was studied in depth and gave rise to the idea that there was a velocity storage mechanism or integrator that not only is a focus for visual-vestibular interaction but also codes spatial orientation relative to gravity as referenced by the otoliths. Velocity storage also contributes to motion sickness when there are visual-vestibular as well as orientation mismatches in velocity storage. The relaxation oscillator concept was subsequently used to model the stance and swing phases of locomotion, how this impacted head and eye movements to maintain gaze in the direction of body motion, and how these were affected by Parkinson's disease. Finally, the relaxation oscillator was used to elucidate the functional form of the systolic and diastolic beats during blood pressure and how vasovagal syncope might be initiated by cerebellar-vestibular malfunction.

Suppressive control of optokinetic and vestibular nystagmus by the primate frontal eye field.

When the eyes are fixated on a spot, fixation neurons in the frontal eye field (FEF) show an increase in activity. Our previous study suggested that fixation neurons in the FEF contribute to the suppression of saccades and smooth pursuit eye movements to maintain active fixation. The present study examined the role of the FEF in the suppressive control of reflexive eye movements, optokinetic and vestibular nystagmus, in trained monkeys. Electrical stimulation in the FEF suppressed the quick and slow phases of optokinetic and vestibular nystagmus at an intensity lower than the threshold for eliciting electrically evoked saccades. Relatively weak suppression influenced the slow phase of vestibular nystagmus. During optokinetic or vestibular nystagmus, presentation of a stationary small spot to the eyes followed by fixation is known to suppress both the quick and slow phases of eye movements. We recorded the activity of fixation neurons in the FEF and found that fixation neurons usually showed a decrease in activity during optokinetic and vestibular nystagmus and an increase in activity during the suppression of nystagmus by visual fixation. The present results show that the activity of fixation neurons in the FEF is related to the suppressive control of optokinetic and vestibular nystagmus for maintaining active fixation. We discuss the role of a generalized visual fixation system that can maintain visual attention on an interesting object.NEW & NOTEWORTHY In this study, electrical stimulation in the frontal eye field (FEF) suppressed the quick and slow phases of optokinetic and vestibular nystagmus at an intensity subthreshold for eliciting saccades. Furthermore, the activity of fixation neurons in the FEF was related to the suppression of optokinetic and vestibular nystagmus by visual fixation. This suggests that a common neuronal assembly in the FEF may contribute to the suppressive control of different functional classes of eye movements.

Central mimics of benign paroxysmal positional vertigo: an illustrative case series.

Benign paroxysmal positional vertigo (BPPV) is the most common peripheral vestibular disorder that is diagnosed based solely on clinical findings. Rarely, central lesions can present with positional vertigo and nystagmus, mimicking BPPV. Recognised red flags that may help distinguish central mimics from BPPV include the presence of additional neurological symptoms and signs, atypical nystagmus patterns, and the absence of a sustained response to repositioning manoeuvres. We present seven cases that illustrate how heuristic bias may affect the detection of these features in practice. Furthermore, our cases suggest that isolated downbeat positional nystagmus (simulating anterior canal BPPV) and apogeotropic horizontal nystagmus on the supine roll test (simulating horizontal canal BPPV) should be considered additional red flags.

Mental tasking and rotary Chair-Induced vestibular nystagmus utilizing Video-Oculography.

Objective: To investigate whether the use of mental tasking, when compared to no mental task, affects measurement of nystagmus response with regard to gain, phase & symmetry, and artefact when utilising video-oculography (VOG) as the measurement technique in rotary chair testing (RCT).Design: A within-subject repeated-measures design was utilised.Study samples: Seventeen (17) healthy adults were evaluated (age 22-25 years). Each participant underwent slow harmonic acceleration (SHA) testing for 0.01, 0.02, 0.04, 0.08, and 0.16 Hz using RCT at two separate counterbalanced visits. At one visit mental tasking was utilised while the other visit did not utilise mental tasking. The following outcomes were measured for each visit: gain, phase, symmetry, and artefact.Results: No significant difference between the tasking conditions with regard to gain, phase, symmetry, or artefact. Significant frequency affects were noted, as expected, for gain, phase, and artefact. Analysis of individual subject data did, however, describe significant effects of tasking with regard to gain, phase, symmetry, and artefact.Conclusion: These results suggest that the use of mental tasking during RCT using VOG had no significant group effect on SHA gain, phase, symmetry, and artefact. However, individual subject effects were observed indicating variability in the effects of mental tasking during RCT.

A decade of magnetic vestibular stimulation: from serendipity to physics to the clinic.

For many years, people working near strong static magnetic fields of magnetic resonance imaging (MRI) machines have reported dizziness and sensations of vertigo. The discovery a decade ago that a sustained nystagmus can be observed in all humans with an intact labyrinth inside MRI machines led to a possible mechanism: a Lorentz force occurring in the labyrinth from the interactions of normal inner ear ionic currents and the strong static magnetic fields of the MRI machine. Inside an MRI, the Lorentz force acts to induce a constant deflection of the semicircular canal cupula of the superior and lateral semicircular canals. This inner ear stimulation creates a sensation of rotation, and a constant horizontal/torsional nystagmus that can only be observed when visual fixation is removed. Over time, the brain adapts to both the perception of rotation and the nystagmus, with the perception usually diminishing over a few minutes, and the nystagmus persisting at a reduced level for hours. This observation has led to discoveries about how the central vestibular mechanisms adapt to a constant vestibular asymmetry and is a useful model of set-point adaptation or how homeostasis is maintained in response to changes in the internal milieu or the external environment. We review what is known about the effects of stimulation of the vestibular system with high-strength magnetic fields and how the understanding of the mechanism has been refined since it was first proposed. We suggest future ways that magnetic vestibular stimulation might be used to understand vestibular disease and how it might be treated.

Characteristics and mechanism of apogeotropic central positional nystagmus.

Here we characterize persistent apogeotropic type of central positional nystagmus, and compare it with the apogeotropic nystagmus of benign paroxysmal positional vertigo involving the lateral canal. Nystagmus was recorded in 27 patients with apogeotropic type of central positional nystagmus (22 with unilateral and five with diffuse cerebellar lesions) and 20 patients with apogeotropic nystagmus of benign paroxysmal positional vertigo. They were tested while sitting, while supine with the head straight back, and in the right and left ear-down positions. The intensity of spontaneous nystagmus was similar while sitting and supine in apogeotropic type of central positional nystagmus, but greater when supine in apogeotropic nystagmus of benign paroxysmal positional vertigo. In central positional nystagmus, when due to a focal pathology, the lesions mostly overlapped in the vestibulocerebellum (nodulus, uvula, and tonsil). We suggest a mechanism for apogeotropic type of central positional nystagmus based on the location of lesions and a model that uses the velocity-storage mechanism. During both tilt and translation, the otolith organs can relay the same gravito-inertial acceleration signal. This inherent ambiguity can be resolved by a 'tilt-estimator circuit' in which information from the semicircular canals about head rotation is combined with otolith information about linear acceleration through the velocity-storage mechanism. An example of how this mechanism works in normal subjects is the sustained horizontal nystagmus that is produced when a normal subject is rotated at a constant speed around an axis that is tilted away from the true vertical (off-vertical axis rotation). We propose that when the tilt-estimator circuit malfunctions, for example, with lesions in the vestibulocerebellum, the estimate of the direction of gravity is erroneously biased away from true vertical. If the bias is toward the nose, when the head is turned to the side while supine, there will be sustained, unwanted, horizontal positional nystagmus (apogeotropic type of central positional nystagmus) because of an inappropriate feedback signal indicating that the head is rotating when it is not.

Vestibulo-cortical hemispheric dominance: The link between anxiety and the vestibular system?

Vestibular processing and anxiety networks are functionally intertwined, as demonstrated by reports of reciprocal influences upon each other. Yet whether there is an underlying link between these two systems remains unknown. Previous findings have highlighted the involvement of hemispheric lateralisation in processing of both anxiety and vestibular signals. Accordingly, we explored the interaction between vestibular cortical processing and anxiety by assessing the relationship between anxiety levels and the degree of hemispheric lateralisation of vestibulo-cortical processing in 64 right-handed, healthy individuals. Vestibulo-cortical hemispheric lateralisation was determined by gaging the degree of caloric-induced nystagmus suppression following modulation of cortical excitability using trans-cranial direct current stimulation targeted over the posterior parietal cortex, an area implicated in the processing of vestibular signals. The degree of nystagmus suppression yields an objective biomarker, allowing the quantification of the degree of right vestibulo-cortical hemisphere dominance. Anxiety levels were quantified using the Trait component of the Spielberger State-Trait Anxiety Questionnaire. Our findings demonstrate that the degree of an individual's vestibulo-cortical hemispheric dominance correlates with their anxiety levels. That is, those individuals with greater right hemispheric vestibulo-cortical dominance exhibited lower levels of anxiety. By extension, our results support the notion that hemispheric lateralisation determines an individual's emotional processing, thereby linking cortical circuits involved in processing anxiety and vestibular signals, respectively.

Recovery of positional nystagmus after benign paroxysmal positional vertigo fatigue.

PURPOSE: In benign paroxysmal positional vertigo (BPPV), positional nystagmus is generally weaker when the Dix-Hallpike test is repeated. This phenomenon is known as BPPV fatigue. The positional nystagmus induced by the Dix-Hallpike test can be observed again when time has passed. There has been no study regarding the length of time required to recover the positional nystagmus. The purpose of this study was to examine whether positional nystagmus recovers within 30 min after the disappearance of the nystagmus by BPPV fatigue. METHODS: This was a prospective observational study. Twenty patients with posterior canal type of BPPV (canalolithiasis of the posterior canal) were included. Dix-Hallpike tests were performed three times for each patient. A second Dix-Hallpike test was performed immediately after the first Dix-Hallpike test. A third Dix-Hallpike test was performed 30 min after the second Dix-Hallpike test. We recorded positional nystagmus induced by the Dix-Hallpike tests and analyzed maximum slow-phase eye velocity (SPEV) of the positional nystagmus. RESULTS: The average maximum SPEV of positional nystagmus induced by the second Dix-Hallpike test (4.8°/s) was statistically lower than that induced by the first Dix-Hallpike test (48.0°/s); this decrease was caused by BPPV fatigue. There was no statistical difference between average maximum SPEV of positional nystagmus induced by the first Dix-Hallpike test and that induced by the third Dix-Hallpike test (41.6°/s); this indicates that the effect of BPPV fatigue disappeared. The effect of BPPV fatigue disappears within 30 min. CONCLUSIONS: A second Dix-Hallpike test should be performed at least 30 min after the first.

Effects of Sustained Otolith-Only Stimulation on Post-Rotational Nystagmus.

Constant velocity rotations in darkness evoke vestibulo-ocular reflex in form of pre- and post-rotational nystagmus under cerebellar supervision. Reorientation of the head with respect to gravity, stimulating otolith and semicircular canal, during post-rotational phase rapidly suppresses the post-rotational nystagmus. We asked if pure otolith stimulation without semicircular canal signal is sufficient for the suppression of post-rotational nystagmus. The experimental paradigm comprised of on-axis rotations in the horizontal plane when the subject was sitting upright, followed by a novel stimulus that combined off-axis centrifugation in the horizontal plane with amplitude matched, yet out-of-phase, on-axis horizontal rotation-double centrifugation. The resultant effect of double centrifugation was pure otolith stimulation that constantly changed direction, yet completely canceled out angular velocity (no horizontal semicircular canal stimulation). Double centrifugation without pre-existing on-axis rotations evoked mixture of horizontal and vertical eye movements, latter reflected the known uncertainty of the vestibular system to differentiate whether the sensory signal is related to low-frequency translations in horizontal plane or head tilts relative to the gravity. Double centrifugation during post-rotational phase suppressed the peak slow phase eye velocity of the post-rotational nystagmus, hence affecting the vestibular ocular reflex gain (eye velocity/head velocity) matrix. The decay time constant, however, was unchanged. Amount of suppression of the peak slow phase eye velocity of the post-rotational nystagmus during double centrifugation correlated with the peak vertical eye velocity evoked by the pure otolith stimuli in the absence of pre-existing on axis rotations. In post-rotational phase, the pure otolith signal affects vestibular ocular reflex gain matrix but does not affect the time constant.

Impaired Tilt Suppression of Post-Rotatory Nystagmus and Cross-Coupled Head-Shaking Nystagmus in Cerebellar Lesions: Image Mapping Study.

We sought to determine the cerebellar structures responsible for tilt suppression of post-rotatory nystagmus. We investigated ocular motor findings and MRI lesions in 73 patients with isolated cerebellar lesions who underwent recording of the vestibulo-ocular reflex (VOR) using rotatory chair tests. Tilt suppression of post-rotatory nystagmus was diminished in 27 patients (27/73, 37.0 %). The gains of the VOR and the TCs of per- and post-rotatory nystagmus did not differ between the patients with diminished and with normal tilt suppression. The patients with impaired tilt suppression showed perverted ("cross-coupled") head-shaking nystagmus (pHSN) and central positional nystagmus (CPN) more frequently than those with normal responses. Tilt suppression was impaired in five (71.4 %) of the seven patients with isolated nodulus and uvular infarction. Probabilistic lesion-mapping analysis showed that the nodulus and uvula are responsible for tilt suppression. Impaired tilt suppression may be ascribed to disruption of cerebellar contribution to the vestibular velocity-storage mechanism, which integrates information from the semicircular canals and otolith organs to help derive the brain's estimate of the head orientation relative to the pull of gravity.

Cold Thermal Irrigation Decreases the Ipsilateral Gain of the Vestibulo-Ocular Reflex.

OBJECTIVES: During head rotations, neuronal firing rates increase in ipsilateral and decrease in contralateral vestibular afferents. At low accelerations, this "push-pull mechanism" is linear. At high accelerations, however, the change of firing rates is nonlinear in that the ipsilateral increase of firing rate is larger than the contralateral decrease. This mechanism of stronger ipsilateral excitation than contralateral inhibition during high-acceleration head rotation, known as Ewald's second law, is implemented within the nonlinear pathways. The authors asked whether caloric stimulation could provide an acceleration signal high enough to influence the contribution of the nonlinear pathway to the rotational vestibulo-ocular reflex gain (rVOR gain) during head impulses. DESIGN: Caloric warm (44°C) and cold (24, 27, and 30°C) water irrigations of the left ear were performed in 7 healthy human subjects with the lateral semicircular canals oriented approximately earth-vertical (head inclined 30° from supine) and earth-horizontal (head inclined 30° from upright). RESULTS: With the lateral semicircular canal oriented earth-vertical, the strongest cold caloric stimulus (24°C) significantly decreased the rVOR gain during ipsilateral head impulses, while all other irrigations, irrespective of head position, had no significant effect on rVOR gains during head impulses to either side. CONCLUSIONS: Strong caloric irrigation, which can only be achieved with cold water, reduces the rVOR gain during ipsilateral head impulses and thus demonstrates Ewald's second law in healthy subjects. This unilateral gain reduction suggests that cold-water caloric irritation shifts the set point of the nonlinear relation between head acceleration and the vestibular firing rate toward a less acceleration-sensitive zone.

Factors Associated with Benign Paroxysmal Positional Vertigo: A Chinese Case-Control Study.

BACKGROUND Benign paroxysmal positional vertigo (BPPV) is one of the most common and most successfully treated vestibular disorders. However, there is a lack of predictive factors for BPPV in clinical practice. We aimed to explore several possible predictive factors for BPPV in the Chinese population. MATERIAL AND METHODS We enrolled 240 patients with BPPV from Beijing Chaoyang Hospital between July 2013 and July 2016. Biochemical and hematological markers were obtained along with the history of cardiovascular and cerebrovascular diseases. RESULTS Serum uric acid (SUA) [279.0±84.7 vs. 331.0±82.7], hemoglobin A1C (HbA1c) [5.75±1.17 vs. 6.61±1.00], albumin [38.1±3.71 vs. 40.9±4.1], and creatinine [68.4±19.3 vs. 81.5±24.1] were significantly lower in patients with BPPV compared with controls (P<0.05). Multiple logistic regression analysis showed that lower levels of HbA1c and albumin were independently associated with BPPV (P<0.05), with odds ratio (OR) 0.680 (95% CI 0.551-0.839) and 0.338 (95% CI 0.190-0.603), respectively. However, the level of SUA was not independently related with BPPV [OR=0.999 (95% CI 0.991-1.006), P=0.713]. There were no significant differences between the parameters of systolic blood pressure, diastolic blood pressure, blood routine examination, lipid profiles, homocysteine, pre-albumin, and blood urea nitrogen in patients with BPPV vs. controls (P>0.05). CONCLUSIONS Lower levels of HbA1c and albumin were independently associated with BPPV. Although the level of SUA was lower in BPPV patients, SUA was not an independent risk factor for BPPV.

The video head impulse test during post-rotatory nystagmus: physiology and clinical implications.

The aim of this study was to test the effects of a sustained nystagmus on the head impulse response of the vestibulo-ocular reflex (VOR) in healthy subjects. VOR gain (slow-phase eye velocity/head velocity) was measured using video head impulse test goggles. Acting as a surrogate for a spontaneous nystagmus (SN), a post-rotatory nystagmus (PRN) was elicited after a sustained, constant-velocity rotation, and then head impulses were applied. 'Raw' VOR gain, uncorrected for PRN, in healthy subjects in response to head impulses with peak velocities in the range of 150°/s-250°/s was significantly increased (as reflected in an increase in the slope of the gain versus head velocity relationship) after inducing PRN with slow phases of nystagmus of high intensity (>30°/s) in the same but not in the opposite direction as the slow-phase response induced by the head impulses. The values of VOR gain themselves, however, remained in the normal range with slow-phase velocities of PRN < 30°/s. Finally, quick phases of PRN were suppressed during the first 20-160 ms of a head impulse; the time frame of suppression depended on the direction of PRN but not on the duration of the head impulse. Our results in normal subjects suggest that VOR gains measured using head impulses may have to be corrected for any superimposed SN when the slow-phase velocity of nystagmus is relatively high and the peak velocity of the head movements is relatively low. The suppression of quick phases during head impulses may help to improve steady fixation during rapid head movements.

Neutral position of persistent direction-changing positional nystagmus.

The aim of this study was to measure the neutral position of direction-changing apogeotropic positional nystagmus (heavy cupula of the horizontal semicircular canal) and persistent direction-changing geotropic positional nystagmus (light cupula of the horizontal semicircular canal). We conducted a prospective case series study on 31 patients with heavy cupula (12 males, 19 females; mean age, 64.3 years) and 33 patients with light cupula (10 males, 23 females; mean age, 60.9 years). We measured the angle of the neutral position in patients with heavy cupula (θ 1) and that in patients with light cupula (θ 2) using a large protractor. The mean value and standard deviation of θ 1 was 31.6 ± 22.4°, minimum value was 5°, and maximum value was 89°. The mean value and standard deviation of θ 2 was 44.4 ± 20.5°, minimum value was 5°, and maximum value was 85°. θ 2 was significantly greater than θ 1 (p < 0.05). The neutral position varies widely. Some patients exhibit a great angle (more than 40°); therefore, examiners should make patients adopt a completely lateral position in the supine head roll test and should confirm the direction of nystagmus in order to avoid mistaking positional nystagmus for spontaneous nystagmus.

[The vestibular craniovertebral joints]. / Die vestibulären Kopfgelenke.

INTRODUCTION: The significance of cervical proprioception for human balance has thus far not been sufficiently elucidated. The aim of this study was to provoke selective cervico-vestibular stimulation using the trunk excursion test (TET) we ourselves constructed. This chair is designed to enable evaluation of cervico-ocular reactions during isolated trunk excursion and possible effects of aging. METHODS: The previously used head excursion test (HET) was statistically compared to the TET. In both methods, 100 healthy subjects of two age groups (group(26): median age = 26 years, n = 50; group(50): median age = 50 years, n = 50) were randomized for comparison of similar neck-to-trunk-positions. RESULTS: HET enabled detection of significant nystagmus modulation in horizontal and vertical dimensions; whereas in pure cervical stimulation using the new TET, this was only evident in the horizontal dimension and only during trunk torsion. Comparison of the two methods confirmed significantly stronger nystagmus modulation through head excursion. In terms of the HET, group(50) showed significantly more vertical nystagmus activity than group(26). However, no significant difference was found between the groups in terms of their reactions to trunk excursion in the TET. In a group-specific comparison of the methods, group(26) showed a significant increase in horizontal nystagmus in head compared to trunk excursion, whereas group(50) generally displayed a significantly greater response to provocation by head excursion in HET. Analysis of the significant vertical nystagmus modulation produced with the TET method showed predominance of upbeat- (UBN) over downbeat-nystagmus (DBN). Through head excursion with the HET, DBN was more frequently evoked in group(50) than in group(26). No significant age-dependent difference could be derived in UBN. CONCLUSION: The results of the pilot study indicate that head-to-trunk provocation is a suitable means of evaluating cervicotonic provocation nystagmus. Only by evaluation of adequate excursion limits and consistent analysis of patients with cervical deficiency can the effects of the method be further assessed.

[A Patient with Early-Stage Multiple System Atrophy Showing Augmented Nystagmus in Light].

The ability to fix the eyes on a target, visual fixation, is important for the maintenance of equilibrium. The visual suppression (VS) test is one method of measuring the function of visual fixation. The test records caloric nystagmus by electrooculography, and the maximum slow phase velocity of caloric nystagmus in darkness is compared with the slow phase velocity in light with eyes fixed. Lesions of the cerebellum, brain stem, and cerebrum cause abnormalities of VS. We report a patient whose VS became a clue in the diagnosis of a disorder of the central nervous system. A 54-year-old man complained of dizziness, which gradually increased in frequency over 5 months. He visited several clinics, where vestibular neutritis and cervical spondylosis were suspected and treated without improvement. Although a pure-tone auditory test revealed bilateral normal hearing, a caloric test showed a weak response and VS was lost with augmentation of caloric nystagmus in light on both sides. Both eye tracking and optokinetic nystagmus tests were abnormal. Although magnetic resonance imaging showed no abnormalities, single photon emission computed tomography revealed decreased blood flow in the parietal area. VS of caloric nystagmus towards the side of a lesion is reduced or abolished after unilateral flocculus damage, and is abolished bilaterally after bilateral flocculus damage. In the case of a parietal lobe or pontine lesion, VS is strongly abolished, and even augmentation of caloric nystagmus may be observed. In the present case, the patient was diagnosed with multiple-system atrophy after onset of dizziness.

Lying-down nystagmus and head-bending nystagmus in horizontal semicircular canal benign paroxysmal positional vertigo: are they useful for lateralization?

BACKGROUND: Lateralization of horizontal semicircular canal benign paroxysmal positional vertigo (HSC-BPPV) is very important for successful repositioning. The directions of lying-down nystagmus (LDN) and head-bending nystagmus (HBN) have been used as ancillary findings to identify the affected sites. This retrospective study was performed to evaluate the lateralizing values of LDN and HBN using clinical and laboratory findings for lateralizing probabilities in patients with HSC-BPPV. METHODS: For 50 HSC-BPPV patients with asymmetric direction-changing horizontal nystagmus (DCHN) during the head-rolling test (HRT) using Frenzel goggles, the directions of LDN and HBN were evaluated and compared to those determined by video-oculography. Directional LDN was defined as the contralesional direction of nystagmus in geotropic types and the ipsilesional direction in apogeotropic types. Directional HBN was defined as the opposite direction relative to directional LDN. We also analyzed LDN and HBN in 14 patients with a history of ipsilesional peripheral vestibulopathy, caloric abnormality or conversion from other types of BPPV (such as probable localized HSC-BPPV, pro-BPPV). RESULTS: LDN and HBN were seen in 68% (34/50) and 76% (38/50) of patients, respectively. Of these, 19 (55.9%), and 28 (73.7%) patients showed directional LDN and HBN, respectively. The proportion of patients with directional LDN and HBN was much smaller among the pro-BPPV patients (4/12 for LDN, 3/10 for HBN). CONCLUSIONS: LDN and HBN did not seem to predict lateralization in patients with HSC-BPPV. To improve the prediction of lateralization of HSC-BPPV, it is necessary to modify the maneuvers used to elicit LDN or HBN, especially in cases of symmetric DCHN during HRT.

Geotropic central paroxysmal positional nystagmus in a patient with human immunodeficiency virus encephalopathy.

Central vestibular lesions may cause paroxysmal positional nystagmus (PPN) or paroxysmal positional vertigo as a result of lesions involving the brainstem dorsolateral to the fourth ventricle or the cerebellar nodulus/uvular region. PPN usually presents as persistent downbeating nystagmus during head hanging or as apogeotropic horizontal nystagmus during head turning in the supine position. Geotropic PPN during head turning in the supine position has not been previously reported. We report such a case in a patient with HIV encephalopathy.

The headshake enhances oculomotor response to galvanic vestibular stimulation in healthy subjects.

OBJECTIVE: To investigate whether a headshake applied during galvanic vestibular stimulation (GVS) can enhance GVS-induced nystagmus in healthy subjects. METHODS: In nineteen healthy participants, we evaluated an average slow-phase velocity (aSPV) of nystagmus in a head-still and after the headshake conditions, with/out the bitemporal 2 mA GVS. The GVS was applied also with polarity congruent (supporting) or incongruent (suppressing) to any preexisting spontaneous nystagmus. RESULTS: The orientation of GVS-induced nystagmus depended on GVS polarity. In the head-still condition, the GVS-induced nystagmus in 14 subjects (74%) for congruent and in 12 subjects (63%) for incongruent GVS. During headshake, we recorded nystagmus in 16 subjects (84%) for congruent and 15 subjects (79%) for incongruent GVS. The aSPV of congruent GVS-induced nystagmus was higher (p = 0.0003) by 1.33 (SE 0.26) deg/s for headshake compared to head-still condition. The aSPV of incongruent GVS also induced higher nystagmus (p = 0.0014) by 1.24 (SE 0.28) deg/s for the headshake condition. CONCLUSION: Our study adds a new principle to the knowledge of the central processing of a GVS response in healthy subjects. The GVS-safety profile of current up to 2 mA was sufficient to elicit a significant GVS nystagmus response in a head-still position in 63% and after a headshake in 79%. Compared to the GVS head-still condition, a headshake enhanced the GVS-induced nystagmus more than twice. SIGNIFICANCE: The headshake helps to identify GVS-induced nystagmus, which can be weak or absent during the head-still condition.