scholarly journals 022 Patient-initiated event monitoring for acute vertigo

2019 ◽  
Vol 90 (e7) ◽  
pp. A8.2-A8
Author(s):  
Allison S Young ◽  
Corinna Lechner ◽  
Andrew P Bradshaw ◽  
Hamish G MacDougall ◽  
Deborah A Black ◽  
...  

IntroductionThe diagnosis of vestibular disorders may be facilitated by analysing patient-initiated capture of ictal nystagmus.MethodsAdults with a history of recurrent vertigo were taught to self-record spontaneous and positional-nystagmus at home while symptomatic, using video-goggles. Patients with final diagnoses of disorders presenting with recurrent vertigo were analysed: 121 patients with Ménière’s Disease (MD), Vestibular Migraine (VM), Benign Positional Vertigo (BPV), Episodic Ataxia Type II (EAII), Vestibular Paroxysmia (VP) or Superior Semicircular Canal Dehiscence (SSCD) were included.ResultsOf 43 MD patients, 40 showed high-velocity spontaneous horizontal-nystagmus (median slow-phase velocity (SPV) 39.7 degrees/second (°/s); Twenty-one showed horizontal-nystagmus reversing direction within 12-hours (24 on separate days). In 44 of 67 patients with VM, low velocity spontaneous horizontal (n=28, 4.9°/s), up-beating (n=6, 15.5°/s) or down-beating-nystagmus (n=10, 5.1°/s) was observed; Sixteen showed positional-nystagmus only, and seven had no nystagmus. Spontaneous horizontal-nystagmus with SPV >12.05°/s had a sensitivity and specificity of 95.3% and 82.1% for MD. Nystagmus direction-change within 12-hours was highly specific (95.7%) for MD. Spontaneous vertical-nystagmus was highly specific (93.0%) for VM. In the seven BPV patients, spontaneous-nystagmus was absent or <3°/s, and characteristic paroxysmal positional nystagmus was observed in all cases. Patients with central and MD-related positional vertigo demonstrated persistent nystagmus. Two patients with EAII showed spontaneous vertical nystagmus, one patient with VP showed short bursts of horizontal-torsional nystagmus lasting 5–10s, and one patient with SSCD demonstrated paroxysmal torsional down-beating nystagmus when supine.ConclusionsPatient-initiated vestibular event-monitoring is feasible and could facilitate rapid and accurate diagnosis of episodic vestibular disorders.

Neurology ◽  
2019 ◽  
Vol 92 (24) ◽  
pp. e2743-e2753 ◽  
Author(s):  
Allison S. Young ◽  
Corinna Lechner ◽  
Andrew P. Bradshaw ◽  
Hamish G. MacDougall ◽  
Deborah A. Black ◽  
...  

ObjectiveTo facilitate the diagnosis of vestibular disorders by patient-initiated capture of ictal nystagmus.MethodsAdults from an Australian neurology outpatient clinic reporting recurrent vertigo were recruited prospectively and taught to self-record spontaneous and positional nystagmus at home while symptomatic, using miniature video-oculography goggles. Consenting patients with ictal videorecordings and a final unblinded clinical diagnosis of Ménière disease (MD), vestibular migraine (VM), or benign paroxysmal positional vertigo (BPPV) were included.ResultsIctal eye videos of 117 patients were analyzed. Of 43 patients with MD, 40 showed high-velocity spontaneous horizontal nystagmus (median slow-phase velocity [SPV] 39.7°/s; 21 showed horizontal nystagmus reversing direction within 12 hours [24 on separate days]). In 44 of 67 patients with VM, spontaneous horizontal (n = 28, 4.9°/s), upbeating (n = 6, 15.5°/s), or downbeating nystagmus (n = 10, 5.1°/s) was observed; 16 showed positional nystagmus only, and 7 had no nystagmus. Spontaneous horizontal nystagmus with SPV >12.05°/s had a sensitivity and specificity of 95.3% and 82.1% for MD (95% confidence interval [CI] 0.84–0.99, 0.71–0.90). Nystagmus direction change within 12 hours was highly specific (95.7%) for MD (95% CI 0.85–0.99). Spontaneous vertical nystagmus was highly specific (93.0%) for VM (95% CI 0.81–0.99). In the 7 patients with BPPV, spontaneous nystagmus was absent or <3°/s. Lying affected-ear down, patients with BPPV demonstrated paroxysmal positional nystagmus. Median time for peak SPV to halve (T50) was 19.0 seconds. Patients with VM and patients with MD demonstrated persistent positional nystagmus (median T50; 93.1 seconds, 213.2 seconds). T50s <47.3 seconds had a sensitivity and specificity of 100% and 77.8% for BPPV (95% CI 0.54–1.00, 0.64–0.88).ConclusionPatient-initiated vestibular event monitoring is feasible and could facilitate rapid and accurate diagnosis of episodic vestibular disorders.


2020 ◽  
Vol 30 (6) ◽  
pp. 345-352
Author(s):  
Allison S. Young ◽  
Sally M. Rosengren ◽  
Mario D’Souza ◽  
Andrew P. Bradshaw ◽  
Miriam S. Welgampola

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.


2019 ◽  
Vol 30 (10) ◽  
pp. 883-895
Author(s):  
M. Dawn Nelson ◽  
Larissa Mann ◽  
Christine Nicholson ◽  
Mark Lehman

AbstractA repeat of the seminal 1973 study on static positional nystagmus (PN) using more accurate recording techniques.The purpose was to further characterize PN and, using current data, introduce new clinical criteria for its identification.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).One hundred healthy patients who were asymptomatic with no known neurological disorders were tested.No intervention was used.Analysis of variance, descriptive statistics, and confidence intervals were used to describe 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.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.


2019 ◽  
Vol 90 (e7) ◽  
pp. A2.1-A2
Author(s):  
Benjamin Nham ◽  
Nicole Reid ◽  
Emma Argaet ◽  
Allison Young ◽  
Kendall Bein ◽  
...  

IntroductionAcute vertigo is often accompanied by ictal-nystagmus which may assist with diagnosis. We examine the merits of a structured assessment combined with vestibular event-monitoring in the Emergency Department (ED).MethodsWe undertook a structured clinical assessment and video-nystagmography in 220 non-consecutive patients presenting to a public-hospital ED with acute vertigo, during a 10-month period. The records of 115 consecutive vertiginous patients who underwent standard-assessment were compared.ResultsFor the structured assessment group: 54% presented with acute vestibular syndrome (AVS), 24% with episodic spontaneous vertigo (EVS), and 20% with recurrent positional-vertigo (RPV).For AVS (n=119), most common diagnoses were vestibular neuritis (34%), stroke (34%) and vestibular migraine (13%). Nystagmus slow-phase velocity (SPV) for VN, stroke and VM were 11±5.5o/s, 5.6±2.5o/s, 5.4±5.9o/s; Mean ipsilesional video-head impulse gains were 0.51±0.29, 0.89±0.20 and 0.96±0.13. For EVS(n=53), diagnoses included vestibular migraine (63%), Meniere’s Disease (11%) and others (26%). Nystagmus SPV was 5.4±3.6o/s, 7.6±6.3o/s, 4.1±1.5o/s. In RPV (n=43), common diagnoses were posterior-canal BPPV (66%), horizontal-canal BPPV (23%), migraine (7%). Positional nystagmus SPV profile showed Peak SPV of 42.5o/s, 77.6o/s, 20.64o/s and Time-constants of 6.52s, 22.51s, 34.56s for Posterior-canal BPPV, Horizontal-canal BPPV and Atypical Positional-Vertigo. A final diagnosis was reached in 96% of patients.In the ED control group, only 77% were separated into spontaneous or positional-vertigo. A diagnosis was provided in 57% and was concordant with the history and examination in 34%.ConclusionVestibular event-monitoring and structured clinical assessment secured a diagnosis in 96% of cases compared with 34% for the control group, reinforcing its merit.


2019 ◽  
Vol 90 (e7) ◽  
pp. A8.1-A8
Author(s):  
Emma C Argaet ◽  
Corinna Lechner ◽  
Andrew P Bradshaw ◽  
G Michael Halmagyi ◽  
Miriam S Welgampola

IntroductionBenign positional vertigo (BPV) has a characteristic pattern of nystagmus specific to the affected semicircular canal and the underlying mechanism of canalithiasis (where otoconia float freely) or cupulolithiasis (where otoconia are adherent to the cupula).MethodsWe analysed the nystagmus slow-phase velocity (SPV) profiles of 100 subjects with posterior-canalithiasis, 30 with lateral-canalithiasis, 10 with lateral-cupulolithiasis and 3 with anterior-canalithiasis. Subjects were examined on the Epley Omniax Rotator, a mechanical chair with real-time video-oculography. Video data was analysed using custom-made LabVIEW software. Nystagmus onset, duration, peak-velocity, peak-latency and time taken for the peak-velocity to halve (t50), were measured.ResultsIn posterior-canalithiasis, nystagmus occurred within 14.2 seconds of positioning and lasted 2.5–34.5 seconds. The median vertical peak-SPV was 37.3°/s. The median peak-latency was 2.9 seconds and the median t50 was 3.4 seconds. In lateral-canalithiasis, nystagmus onset was mostly immediate. With the affected ear down, the median peak-SPV was 52.2°/s and the median peak-latency was 3.6 seconds; the t50 was 7 seconds (median) and the paroxysms lasted 9.9–48.5 seconds. In lateral-cupulolithiasis, nystagmus onset was instantaneous. With the unaffected ear down, the median peak-SPV was 69.6°/s. The peak-latency (median 18.6 s) and t50 (median 34.5 s) were significantly prolonged compared to canalithiasis. For anterior-canalithiasis, the onset was 0–2.9 seconds, the peak-latency was 3–5.4 seconds, the t50 was 6.4–10.5 seconds and the duration was 13.4–23.1 seconds.ConclusionsCanalithiasis and cupulolithiasis produce distinct SPV profiles, which enable their identification and the separation of BPV from other causes of positional nystagmus.


1985 ◽  
Vol 53 (2) ◽  
pp. 481-496 ◽  
Author(s):  
N. H. Barmack ◽  
V. E. Pettorossi

The horizontal optokinetic reflex (HOKR) and the horizontal vestibuloocular reflex (HVOR) were tested in 21 rabbits before and after unilateral lesions were made in the left cerebellar flocculus. The immediate effect, observed within 15 min following placement of a floccular lesion, was a conjugate nystagmus with the slow phase toward the side opposite to the lesion when the animal was placed in total darkness. This spontaneous nystagmus lasted from several hours to two days depending on the extent of damage to the flocculus. It was reversed in sign if the subjacent vestibular nuclei or vestibular nerve were damaged by the operation, and it was totally absent if the unilateral floccular lesions were made in rabbits that had been bilaterally labyrinthectomized. The spontaneous drift of the eyes observed immediately postoperatively caused a bias in measurement of the HVOR that was dependent on the frequency of vestibular stimulation. When measured 50 days postoperatively the HVOR had a normal gain and normal bias. When measured 50 days postoperatively the monocular HOKR (posteroanterior stimulation of the left eye) was significantly reduced in gain at stimulus velocities below 5 degrees/s. A quantitative anatomical analysis of the degeneration of inferior olivary neurons caused by lesions of the flocculus demonstrated contralateral cell loss of as much as 65% of the dorsal cap neuronal population. These data reveal a permanent deficit in the HOKR, but not the HVOR, following unilateral floccular lesions and are consistent with the idea that the flocculus contributes to the regulation of the low-velocity eye movements through the inhibitory modulation of the activity of the subjacent vestibular nuclei.


2019 ◽  
Vol 134 (1) ◽  
pp. 86-89
Author(s):  
F Comacchio ◽  
N Cutrì ◽  
M Mion

AbstractBackgroundPeriodic alternating nystagmus is a rare condition characterised by spontaneous horizontal nystagmus that periodically reverses direction, indicating an alteration of the velocity storage mechanism. Windmill nystagmus is a peculiar and rare variant of periodic alternating horizontal nystagmus with a superimposed periodic alternating vertical nystagmus. It is generally observed in blind patients.Case reportThis paper presents the unique case of a normally sighted patient with a windmill nystagmus triggered by an episode of benign paroxysmal positional vertigo due to bilateral posterior canalolithiasis. Videonystagmography revealed an anticlockwise up-beating nystagmus followed by a clockwise down-beating nystagmus with a cycle lasting 2 minutes, followed by a brief burst of horizontal left-beating nystagmus.ConclusionThis case report represents the first observation of a new type of windmill nystagmus, probably provoked by a malfunction of the velocity storage mechanism, gaze-stabilisation and short-adaptation networks, with a loss of cerebellar inhibition.


1988 ◽  
Vol 60 (3) ◽  
pp. 1022-1035 ◽  
Author(s):  
M. Ariel ◽  
F. R. Robinson ◽  
A. G. Knapp

1. Eye movements were observed following an injection of picrotoxin, a GABA antagonist, into the vitreous of one eye. A spontaneous nystagmus was observed in cats, rabbits, and turtles, even in total darkness, with slow-phase eye movements in the temporal-to-nasal direction for the injected eye. 2. During visual stimulation by a horizontal drifting pattern, injected eyes moved in the temporal-to-nasal direction, irrespective of stimulus direction. In cats, however, the nystagmus was usually slower when the injected eye viewed nasal-to-temporal motion (opposite to the direction of the spontaneous nystagmus). The spontaneous nystagmus could be halted or even reversed by allowing cats to view motion opposite to the direction of the nystagmus with the uninjected eye alone. The nystagmus could not be overridden in this fashion in rabbits or turtles. 3. The nystagmus induced by picrotoxin could also be modified by vestibular stimulation. When cats were placed on their sides, the spontaneous horizontal nystagmus often decreased and spontaneous vertical nystagmus with upward slow phase movements occurred. During sinusoidal horizontal vestibular stimulation, the horizontal nystagmus due to picrotoxin added to the vestibuloocular reflex as a velocity offset in the temporal-to-nasal direction. 4. Following bilateral ablation of the cat visual cortex, picrotoxin's effect became even more pronounced than before the ablation. Therefore, at least some picrotoxin-sensitive cells can use subcortical pathways, perhaps to the accessory optic nuclei. The visual cortex, which also processes directional information, may be able to compensate for changes in retinal processing induced by picrotoxin in intact animals. 5. This study demonstrates the importance of retinal GABA in the control of eye stability. As GABA is known to be responsible for null direction inhibition of directionally sensitive retinal ganglion cells, these results suggest that the output of these cells may be critical for the normal functioning of central optokinetic pathways, even in the absence of visual cortex.


2000 ◽  
Vol 114 (11) ◽  
pp. 844-847 ◽  
Author(s):  
Najam-Ul-Hasnain Khan F.C.P.S. ◽  
Mohammad Mujeeb

Benign paroxysmal positional vertigo (BPPV) is one of the commonest causes of peripheral vestibular disorders. In this prospective study 21 patients with BPPV were treated by Epley’s manoeuvre. All patients had an immediate improvement in their symptoms. Recurrence was noted in three patients who required further treatment sessions with resultant improvement in all. However, one patient who originally had suffered from Me´nie`re’s disease involving the same ear for more than 14 years developed another recurrence which was treated successfully by further application of Epley’s manoeuvre. This study supports the usefulness of Epley’s manoeuvre for the treatment of BPPV.


1991 ◽  
Vol 1 (3) ◽  
pp. 279-289
Author(s):  
Krister Brantberg ◽  
Måns Magnusson

The symmetry of primary and secondary optokinetic afternystagmus (OKAN I and OKAN II, respectively) was studied in 14 patients with vestibular neuritis, as well as in 50 normals. The patients were examined at onset of symptoms and at follow-up 3 and 12 months later. At onset, OKAN was found mainly to reflect the spontaneous nystagmus. Although the spontaneous nystagmus disappeared in all patients within 3 months, both OKAN I and OKAN II was asymmetric at the 3- and 12-month check-ups. OKAN beating toward the lesioned ear was weaker than the OKAN beating toward the healthy ear. Thus, the asymmetric vestibular function was reflected not only in the OKAN I, but also by an asymmetry in OKAN II. Between the 3- and 12-month check-ups, asymmetry in OKAN declined, even among those patients who showed no improvement in caloric response during that time. The decreasing asymmetry in OKAN with time after lesion was, however, related to the disappearance of a positional nystagmus. Hence, the results may be interpreted as suggesting OKAN not only to be affected by vestibular side-difference, but also to be modified by the process responsible for vestibular compensation following a peripheral vestibular lesion.


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