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.

Evaluation of the reliability and validity of the upright head roll test for lateral semicircular canal benign paroxysmal positional vertigo.

BACKGROUND: The upright head roll test (UHRT) is a recently introduced diagnostic maneuver for lateral semicircular canal benign paroxysmal positional vertigo (LSC-BPPV). OBJECTIVE: This study aimed to evaluate the reliability and validity of the UHRT. METHODS: Two separate studies were conducted. Study 1 analyzed 827 results of videonystagmography (VNG) to assess UHRT reliability, and Study 2 analyzed 130 LSC-BPPV cases to evaluate UHRT validity. RESULTS: The inter-test reliability between UHRT and the supine head roll test (SHRT) showed substantial agreement (Cohen's kappa = 0.753) in direction-changing positional nystagmus (DCPN) and almost perfect agreement (Cohen's kappa = 0.836) in distinguishing the direction of DCPN. The validity assessment of UHRT showed high accuracy in diagnosing LSC-BPPV (80.0%) and in differentiating the variant types (74.6%). UHRT was highly accurate in diagnosing the canalolithiasis type in LSC-BPPV patients (Cohen's kappa = 0.835); however, it showed only moderate accuracy in diagnosing the cupulolithiasis type (Cohen's kappa = 0.415). The intensity of nystagmus in UHRT was relatively weaker than that in SHRT (P < 0.05). CONCLUSION: UHRT is a reliable test for diagnosing LSC-BPPV and distinguishing subtypes. However, UHRT has a limitation in discriminating the affected side owing to a weaker intensity of nystagmus than SHRT.

Five subtypes of benign paroxysmal positional vertigo.

BACKGROUND: Benign paroxysmal positional vertigo is classified into five subtypes according to the features of positional nystagmus: lateral canalolithiasis, lateral light cupula, lateral heavy cupula, posterior canalolithiasis and posterior heavy cupula. OBJECTIVES: The first aim of the study was to clarify whether the lateral canal type or posterior canal type was more common. The second aim of the study was to assess the aetiology of benign paroxysmal positional vertigo by investigating the onset time of each subtype. METHODS: The subjects were 512 consecutive patients with benign paroxysmal positional vertigo. The patients were prospectively aggregated, and interviews were used to evaluate onset time. RESULTS: The lateral canal type (55.5 per cent) was more common than the posterior canal type (44.5 per cent). Time of awakening was the most common onset time in every subtype. CONCLUSION: The incidence of lateral canal type is higher than that of posterior canal type. The aetiology of benign paroxysmal positional vertigo is closely related to sleep.

Nystagmus characteristics of healthy controls.

BACKGROUND: Healthy controls exhibit spontaneous and positional nystagmus which needs to be distinguished from pathological nystagmus. OBJECTIVE: Define nystagmus characteristics of healthy controls using portable video-oculography. METHODS: One-hundred and one asymptomatic community-dwelling adults were prospectively recruited. Participants answered questions regarding their audio-vestibular and headache history and were sub-categorized into migraine/non-migraine groups. Portable video-oculography was conducted in the upright, supine, left- and right-lateral positions, using miniature take-home video glasses. RESULTS: Upright position spontaneous nystagmus was found in 30.7% of subjects (slow-phase velocity (SPV)), mean 1.1±2.2 degrees per second (°/s) (range 0.0 - 9.3). Upright position spontaneous nystagmus was horizontal, up-beating or down-beating in 16.7, 7.9 and 5.9% of subjects. Nystagmus in at least one lying position was found in 70.3% of subjects with 56.4% showing nystagmus while supine, and 63.4% in at least one lateral position. While supine, 20.8% of subjects showed up-beating nystagmus, 8.9% showed down-beating, and 26.7% had horizontal nystagmus. In the lateral positions combined, 37.1% displayed horizontal nystagmus on at least one side, while 6.4% showed up-beating, 6.4% showed down-beating. Mean nystagmus SPVs in the supine, right and left lateral positions were 2.2±2.8, 2.7±3.4, and 2.1±3.2°/s. No significant difference was found between migraine and non-migraine groups for nystagmus SPVs, prevalence, vertical vs horizontal fast-phase, or low- vs high-velocity nystagmus (<5 vs > 5°/s). CONCLUSIONS: Healthy controls without a history of spontaneous vertigo show low velocity spontaneous and positional nystagmus, highlighting the importance of interictal nystagmus measures when assessing the acutely symptomatic patient.

Light Cupula: To Be Or Not to Be?

Benign paroxysmal positional vertigo (BPPV) represents the most common form of positional vertigo. It is caused by dislodged otoconia that freely float in the semicircular canals (canalolithiasis) or attach to the cupula (cupulolithiasis). A cupulolithiasis-type (or a heavy cupula-type) of BPPV implicating the lateral semicircular canal (LSCC) exhibits persistent ageotropic direction-changing positional nystagmus (DCPN) in a head-roll test. However, in some cases, unlike any type of BPPV, persistent geotropic DCPN cannot be explained by any mechanisms of BPPV, and don't fit the current classifications. Recently, the notion of light cupula has been introduced to refer to the persistent geotropic DCPN. In this study, we looked at the clinical features of light cuplula and discussed the possible mechanisms and therapeutic strategies of the condition. The notion of light cupula is a helpful addition to the theory of peripheral positional vertigo and nystagmus.

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.

Upright positioning-related reverse nystagmus in posterior canal benign paroxysmal positional vertigo and its effect on prognosis.

BACKGROUND: Positional nystagmus elicited by the Dix-Hallpike maneuver often reverses its direction as the patient is re-seated from the provoking head hanging position. The incidence of reverse nystagmus and its association with prognosis in posterior canal benign paroxysmal positional vertigo (pcBPPV) is not clear. OBJECTIVE: To determine the incidence of upright positioning-related reverse nystagmus and its association with the success of canalith repositioning (Epley) maneuver (CRM) treatment in pcBPPV. METHODS: The records of patients that had been tested with video-nystagmography in a tertiary care center, between October 2016 and March 2019, were reviewed. Data were obtained from detailed analysis of video recordings of 321 patients with typical pcBPPV. RESULTS: Reverse nystagmus was determined in 85% of the patients with pcBPPV. The number of CRMs required for treatment was lower in patients with reverse nystagmus (1.32±0.68) compared to patients without reverse nystagmus (1.81±0.98) (p < 0.001). There was not a statistically significant relationship between reverse nystagmus and recurrence (p = 0.623). CONCLUSIONS: The absence of reverse nystagmus on upright positioning during the Dix-Hallpike test predicts poor success for the CRM, as repetitive repositioning maneuvers might be required to achieve successful treatment in pcBPPV.

The role of vertical semicircular canal function in the vertical component of skull vibration-induced nystagmus.

Background: Generally, vertical component of the skull vibratory nystagmus (VCN) is ignored in the clinical practise. Thus, the relative contribution of the vestibular organs in the presence of VCN remains unknown.Objectives: To determine the association between vertical semicircular canal (vSCC) function and the presence of VCN.Material and methods: Comparisons were made between Video Head Impulse Test and SVINT (100 Hz) results at the time of the acute peripheral vestibular lesion (PVL) and at the post-acute phase in patients diagnosed PVL. Later on, a paired analysis was performed restricting the assessments to patients with vestibular explorations in both the acute and post-acute phases.Results: In an univariable analysis, larger mean total gain differences (TGD) between vSCC VOR gains, significantly related with the appearance of VCN in nystagmography in the acute phase (p = .001), unlike the post-acute phase (p = .46). After a multivariate analysis, mean TGD was the only predictive factor of the VCN (p = .013). In the paired analysis, we found an increase in the post-acute phase mean TGD, approaching zero value.Conclusions and significance: Global relation between all vertical canals has at least a contributory role in the presence of the vertical component of nystagmus in SVINT.

Subjective benign paroxysmal positional vertigo in patients with osteoporosis or migraine / Vertigem posicional paroxística benigna subjetiva em pacientes com osteoporose ou migrânea

Abstract Introduction Subjective benign paroxysmal positional vertigo is a form of benign paroxysmal positional vertigo in which during the diagnostic positional maneuvers patients only present vertigo symptoms with no nystagmus. Objective To study the characteristics of subjects with subjective benign paroxysmal positional vertigo. Methods Prospective multicenter case-control study. All patients presenting with vertigo in the Dix-Hallpike test that presented to the participating hospitals were included. The patients were separated into two groups depending on whether nystagmus was present or not. An Epley Maneuver of the affected side was performed. In the follow-up visit, patients were checked to see if nystagmus and vertigo were present. Both groups of patients were compared to assess the success rate of the Epley maneuver and also to compare the presence of 19 variables. Results 259 patients were recruited, of which 64 belonged to the subjective group. Nystagmus was eliminated in 67.2% of the patients with benign paroxysmal positional vertigo. 89.1% of the patients with subjective benign paroxysmal positional vertigo remained unaffected by nystagmus, thus showing a significant difference (p = 0.001). Osteoporosis and migraine were the variables which reached the closest to the significance level. In those patients who were taking vestibular suppressors, the percentage of subjective benign paroxysmal positional vertigo was not significantly higher. Conclusions Subjective benign paroxysmal positional vertigo should be treated using the Epley maneuver. More studies are needed to establish a relationship between osteoporosis, migraine and subjective benign paroxysmal positional vertigo. The use of vestibular suppressants does not affect the detection of nystagmus.

Resumo Introdução A vertigem posicional paroxística benigna subjetiva é um tipo de vertigem posicional paroxística benigna na qual, durante as manobras posicionais diagnósticas, os pacientes apresentam apenas sintomas vertiginosos sem nistagmo. Objetivo Estudar as características de indivíduos com vertigem posicional paroxística benigna subjetiva. Método Estudo prospectivo multicêntrico de caso-controle. Foram incluídos todos os pacientes com vertigem no teste de Dix-Hallpike, que se apresentaram nos hospitais participantes. Os pacientes foram separados em dois grupos, dependeu da presença ou não do nistagmo. Uma manobra de Epley foi realizada no lado afetado. Na consulta de seguimento, os pacientes foram avaliados para verificar a presença ou não do nistagmo e da vertigem. Ambos os grupos de pacientes foram comparados para avaliar a taxa de sucesso da manobra de Epley e também para comparar a presença de 19 variáveis. Resultados Foram recrutados 259 pacientes, dos quais 64 pertenciam ao grupo subjetivo. O nistagmo foi eliminado em 67,2% dos pacientes com vertigem posicional paroxística benigna. Em 89,1% dos casos, os pacientes com vertigem posicional paroxística benigna subjetiva mantiveram-se não afetados pelo nistagmo, mostraram uma diferença significativa (p = 0,001). Osteoporose e enxaqueca foram as variáveis que atingiram o nível mais próximo ao de significância. Nos pacientes que tomavam supressores vestibulares, a porcentagem de vertigem posicional paroxística benigna subjetiva não foi significativamente maior. Conclusões A vertigem posicional paroxística benigna subjetiva deve ser tratada com a manobra de Epley. Mais estudos são necessários para estabelecer uma relação entre osteoporose, enxaqueca e vertigem posicional paroxística benigna subjetiva. O uso de supressores vestibulares não afeta a detecção do nistagmo.

Subjective benign paroxysmal positional vertigo in patients with osteoporosis or migraine.

INTRODUCTION: Subjective benign paroxysmal positional vertigo is a form of benign paroxysmal positional vertigo in which during the diagnostic positional maneuvers patients only present vertigo symptoms with no nystagmus. OBJECTIVE: To study the characteristics of subjects with subjective benign paroxysmal positional vertigo. METHODS: Prospective multicenter case-control study. All patients presenting with vertigo in the Dix-Hallpike test that presented to the participating hospitals were included. The patients were separated into two groups depending on whether nystagmus was present or not. An Epley Maneuver of the affected side was performed. In the follow-up visit, patients were checked to see if nystagmus and vertigo were present. Both groups of patients were compared to assess the success rate of the Epley maneuver and also to compare the presence of 19 variables. RESULTS: 259 patients were recruited, of which 64 belonged to the subjective group. Nystagmus was eliminated in 67.2% of the patients with benign paroxysmal positional vertigo. 89.1% of the patients with subjective benign paroxysmal positional vertigo remained unaffected by nystagmus, thus showing a significant difference (p=0.001). Osteoporosis and migraine were the variables which reached the closest to the significance level. In those patients who were taking vestibular suppressors, the percentage of subjective benign paroxysmal positional vertigo was not significantly higher. CONCLUSIONS: Subjective benign paroxysmal positional vertigo should be treated using the Epley maneuver. More studies are needed to establish a relationship between osteoporosis, migraine and subjective benign paroxysmal positional vertigo. The use of vestibular suppressants does not affect the detection of nystagmus.

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.

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.

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.

Reversal of paradoxical stimulation (false inversion) in perforated tympanic membranes by increasing the time of warm stimulation, evidenced by a physical model.

OBJECTIVE: To measure the time required in patients with tympanic perforation to reverse paradoxical stimulation (reverse pseudo-nystagmus) and to create a physical model of the process. METHOD: An analytical, observational, cross-sectional study with vestibular evaluation (electronystagmography) of 52 individuals with tympanic membrane perforation without otorrhea or concomitant disease. Increased duration of caloric stimulation in the presence of paradoxical stimulation (reverse pseudo-nystagmus) reverses nystagmic responses. RESULTS: Reversal of nystagmus was observed in 90.9% of patients. The average reversal time was 105.5 seconds. The physical model we prepared provided supporting evidenced for the effects seen in these individuals: warm stimulation in a moist environment initially caused a decrease in temperature (nystagmus to the unexpected side, which characterizes paradoxical stimulation in the warm caloric test); but, as time passed by, the moisture evaporated, and the temperature gradually increased (reversal of nystagmus). CONCLUSIONS: Increasing the stimulation time can be used as a strategy to differentiate reverse nystagmus from paradoxical stimulation. Confusion is thus avoided in diagnostic findings, allowing peripheral alterations to be distinguished from central ones.

Central positional nystagmus: Characteristics and model-based explanations.

The central vestibular system operates to precisely estimate the rotational velocity and gravity orientation using the inherently ambiguous information from peripheral vestibular system. Therefore, any lesions disrupting this function can generate positional nystagmus. Central positional nystagmus (CPN) can be classified into the paroxysmal (transient) and persistent forms. The paroxysmal CPN has the features suggesting a semicircular canal origin regarding the latency, duration, and direction of nystagmus. Patients with paroxysmal CPN commonly show several different types of nystagmus classified according to the provoking positioning. The persistent form of CPN mostly appears as downbeat nystagmus while prone or supine, or apogeotropic or geotropic horizontal nystagmus when the head is turned to either side while supine. CPN may be ascribed to erroneous neural processing within the velocity-storage circuit that functions in estimating angular head velocity, gravity direction, and inertia. Paroxysmal CPN appears to be post-rotatory rebound nystagmus due to lesions involving the cerebellar nodulus and uvula. In contrast, persistent CPN may arise from erroneous gravity estimation. The overlap of lesion location responsible for both paroxysmal and persistent CPN may account for the frequent coexistence of both forms of nystagmus in a single patient.

Central positional vertigo: A clinical-imaging study.

The diagnosis of central positional vertigo (CPV) is challenging, mainly because symptoms overlap with the common variants of benign paroxysmal positional vertigo (BPPV). Recent correlations of imaging with neurotologic exams have improved our understanding of CPV and ability differentiate it from BPPV. Yet, there is still a need to develop better diagnostic algorithms to improve timely diagnosis and early intervention. Here we present a retrospective review of the clinical characteristics, neurotologic evaluation and imaging of CPV in a cohort of 27 patients and propose a diagnostic algorithm to be tested in future prospective fashion. Most patients had positional nystagmus (downbeat and apogeotropic horizontal), cerebellar ocular motor abnormalities and truncal ataxia indicative of a central lesion. 61.5% of our cohort had paroxysmal CPV, 30.5% had a non-paroxysmal CPV and 8% paroxysmal-evolving-to-non-paroxysmal CPV. The most common pattern of positional nystagmus evoked with maneuvers was positional downbeat nystagmus (pDBN, 69.2%), apogeotropic horizontal nystagmus (42.3%), geotropic (7.69%) and multiplanar (23.0%). Notably, 13 (50%) of patients had cerebral imaging prior to CPV being on the differential diagnosis, whereas another 50% of patients had CPV diagnosis preceding their work-up. Unilateral lesions on imaging were 4× less likely to exhibit nausea and vomiting, nearly 2× less likely to exhibit paroxysmal nystagmus, and 2× less likely to exhibit nystagmus with habituality. Findings of pDBN or apogeotropic nystagmus alone were enough to diagnose CPV in 50% of our patient cohort, underscoring the importance of clinical evaluation in a time when an "imaging-first" philosophy is gaining popularity in Neurology.

Static Positional Nystagmus in the Healthy Vestibular System.

BACKGROUND: A repeat of the seminal 1973 study on static positional nystagmus (PN) using more accurate recording techniques. PURPOSE: The purpose was to further characterize PN and, using current data, introduce new clinical criteria for its identification. RESEARCH DESIGN: Static PN was recorded in ten positions with vision denied. Each position was analyzed using age, gender, presence, direction, and persistence of nystagmus while taking into account the number of beats and mean slow-phase velocity (SPV). STUDY SAMPLE: One hundred healthy patients who were asymptomatic with no known neurological disorders were tested. INTERVENTION: No intervention was used. DATA COLLECTION: Analysis of variance, descriptive statistics, and confidence intervals were used to describe results. RESULTS: Results showed 74% of normal participants had horizontal nystagmus in at least one position. Only 7% of the observed nystagmus was persistent. The average SPV was 2°/sec. The mean number of positions in which nystagmus was observed was three. Neither age nor gender influenced the occurrence of nystagmus. Forty-three percent of the participants had vertical nystagmus in at least one position; however, the SPV was 2°/sec or less. CONCLUSIONS: The present study demonstrated that intermittent or persistent PN in four or fewer positions should not be considered pathological when the SPV is 4°/sec or less (n = 100). Observance of vertical nystagmus in one position should not be considered pathological if the SPV is 2°/sec or less. Suggested positions for positional testing should include seated-upright, supine, head right, head left, head-hanging, and the precaloric (30° supine) positions. Fixation when PN is observed is indicated.

Characteristics of positional nystagmus in patients with horizontal canal canalolithiasis or cupulopathy.

OBJECTIVES: Positional nystagmus can be related to various kinds of disorders. The current study aims to compare the direction-changing horizontal positional nystagmus (DCPN) characteristics in horizontal canal canalolithiasis (HC-canalolithiasis), heavy cupula of the horizontal canal (HC-Hcu), and light cupula of the horizontal canal (HC-Lcu), especially the temporal patterns of positional nystagmus in three disorders. METHODS: 52 patients (22 males, 30 females; mean age, 49.6 years) presenting with geotropic or apogeotropic DCPN were enrolled, and they were divided into HC-canalolithiasis, HC-Hcu, or HC-Lcu groups according their nystagmus characteristics. We compared their latency, time constant, peak slow-phase velocity (SPV), time to reach peak SPV intensity (Tpeak), and time to decay to half-peak intensity (T1/2peak). RESULTS: The time to reach peak SPV did not differ significantly between the HC-Hcu (23.1 ± 8.6 s) and HC-Lcu (24.4 ± 9.9 s) groups (p = 0.733), but was significantly longer than that of the HC-canalolithiasis group (5.4 ± 3.5 s; p ≤ 0.001). The peak intensity did not differ among the canalolithiasis (36.4 ± 20.6º/s), HC-Hcu (30.1 ± 23.6º/s), and HC-Lcu (21.4 ± 12.7º/s) groups (p = 0.133). The onset latency also had no statistical difference among three groups (p = 0.200). The nystagmus patterns of HC-Lcu and HC-Hcu groups were similar, including latency, peak SPV intensity, Tpeak, T1/2peak, and SPV in 20 s, 40 s, 60 s, 80 s. CONCLUSIONS: The nystagmus characteristics of HC-Hcu and HC-Lcu are similar, except for the fact that movement was in opposite directions, suggesting that HC-Hcu and HC-Lcu may result from a similar pathophysiological mechanism (cupulopathy) differing from that underlying canalolithiasis.

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.