Accepted Manuscript Video-Clinical Corners Polysomnography reveals nystagmus from benign paroxysmal positional vertigo Yulia Valko, Esther Werth, Christopher J. Bockisch, Philipp O. Valko, Konrad P. Weber PII: DOI: Reference:

S1389-9457(14)00080-X http://dx.doi.org/10.1016/j.sleep.2013.12.018 SLEEP 2393

To appear in:

Sleep Medicine

Received Date: Revised Date: Accepted Date:

3 October 2013 12 December 2013 16 December 2013

Please cite this article as: Valko, Y., Werth, E., Bockisch, C.J., Valko, P.O., Weber, K.P., Polysomnography reveals nystagmus from benign paroxysmal positional vertigo, Sleep Medicine (2014), doi: http://dx.doi.org/10.1016/ j.sleep.2013.12.018

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Y. Valko et al. Video-Clinical Corners Polysomnography reveals nystagmus from benign paroxysmal positional vertigo Yulia Valkoa,b,*, Esther Wertha, Christopher J. Bockischa,b,c, Philipp O. Valkoa, Konrad P. Webera,b a

Department of Neurology, University Hospital Zurich, Switzerland

b c

Department of Ophthalmology University Hospital Zurich, Switzerland

Department of Otorhinolaryngology, University Hospital Zurich, Switzerland

*Corresponding author. Address: Department of Neurology, University Hospital Zurich, Frauenklinikstrasse 26, 8091 Zurich, Switzerland. Tel.: +41 44 255 55 11; fax: +41 44 255 43 80. E-mail address: [email protected] (Y. Valko). 1. Introduction Benign paroxysmal positional vertigo (BPPV) is the most common cause of dizziness with a lifetime prevalence of 2.4% [1]. Calcium carbonate crystals of the vestibular organ (otoconia), become dislodged from the otolithic membrane and freely float within the endolymphatic fluid of the semicircular canals. Since otoconia and the endolymph possess different densities, head movements may cause the otoconia to overstimulate the vestibular mechanoreceptors, thereby causing disabling episodes of vertigo accompanied by nystagmus. The diagnosis can easily be confirmed by inducing nystagmus using specific positional testing, such as the Dix–Hallpike maneuver for the posterior canals and the supine head-rolling procedure for the horizontal canals [2,3]. Despite the availability of highly effective canalolith-repositioning procedures, the condition remains underdiagnosed, which too often means unnecessary long-lasting suffering and dangerous falls [4–6]. Whereas it is well known that changes of head position in bed often elicit BPPV, videopolysomnography (PSG) has not yet been considered as a tool to detect unrecognized BPPV. 2. Case description A 59-year-old woman was admitted to our emergency department due to repeated violent attacks of rotational vertigo, triggered by head movements while supine. Vomiting and unsteadiness followed the vertigo for several hours. She had been suffering from similar symptoms for three years, often with several episodes over 24 h, which were however much shorter and milder before. Her medical history was otherwise unremarkable, particularly without previous head trauma. Brain magnetic resonance imaging did not reveal any structural

abnormality. When quickly rotating her head to ear-down position while supine, we observed a persisting horizontal nystagmus (Video) beating in apogeotropic direction (towards the upper ear) with a delay of 2–3 s, and the patient reported the typical rotational vertigo. Head rotation to the right caused an even stronger nystagmus, establishing the diagnosis of a left lateral canal cupulolithiasis. Since the attacks were often precipitated by changes of body position at night and thus interfering with the quality of her sleep, we decided to perform a whole-night video-PSG. We used a conventional 16-channel recording system (Somnologica software; Embla N7000, Embla, Broomfield, CO, USA) containing a built-in, three-dimensional sensor for measurement of body position and movements. The patient slept worse than usually, achieving a sleep efficiency of only 60%. Apnea–hypopnea index was 1.0/h, no periodic leg movements were observed. During the entire registration period, the patient changed body position 15 times, and six times we were able to observe an apogeotropic positional nystagmus. In addition, we noted several episodes with changes of head position but unaltered body position, also triggering a positional nystagmus (Fig. 1, Video). 3. Brief discussion This case provides evidence that video-PSG can detect positional nystagmus from BPPV. Since BPPV is a frequent and underdiagnosed condition, it appears plausible that careful analysis of electro-oculography (EOG) may point to a previously unrecognized BPPV. EOG exhibits the ocular oscillations of a nystagmus, consisting of a slow eye movement in one direction and a fast or saccadic eye movement in the other direction, which denominates the direction of the nystagmus. The EOG pattern of positional nystagmus is highly distinctive – it occurs during wakefulness, shows a delay of several seconds after change of head position, nystagmus direction shows a characteristic reversal after change of head position, and the time course of the eye movements demonstrates a characteristic crescendo–decrescendo. As highlighted in Fig. 2, positional nystagmus can be easily differentiated from other characteristic EOG features, and the direction-depending EOG morphology of the nystagmus can be deduced by the biphasic eye movement and the placement of the EOG and reference electrodes. The interaction between vestibular disease and sleep has been almost completely neglected. Although our patient does not suffer from any daytime vigilance disturbance (the score of the Epworth Sleepiness Scale was 2, and that of the Fatigue Severity Scale was 1.4), it seems conceivable that repeated attacks of positional vertigo with associated discomfort may exert a negative influence on night-time sleep quality. Vertigo attacks at night may cause prolonged

awakenings and prevent rapid re-entrance into sleep. One may speculate that positional vertigo also occurs during sleep and consecutively induces awakening. In our patient, however, all body and head movements were preceded by awakenings. On the other hand, previous work suggested that certain brainstem reflexes including those underlying vestibular or saccadic eye movements are suppressed during decreased consciousness and sleep [7]. While the impact of BPPV on sleep quality has to be elucidated by future work, a few groups have regarded sleep position as a potential predisposing factor for BPPV. The preferred lateral sleep position was found to be associated with the side of the affected canal in BPPV [8], especially in patients with recurrent BPPV [9]. In addition, right-sided BPPV has been reported to be more common than left-sided BPPV, which might be explained by the fact that humans seem to prefer to sleep on the right body side [10,11]. Immobility is a well-known risk factor for BPPV, and the reported correlation between laterality of sleep position and affected ear suggests that gravitational force may favor aggregation of otoconia. In conclusion, sleep specialists should be aware of BPPV and the EOG appearance of positional nystagmus, because this cumbersome condition is highly prevalent yet often overlooked, whereas diagnosis is easy and treatment is safe, inexpensive and highly effective. Acknowledgments This study was supported by a research grant from the Forschungskredit Universität Zürich and the Betty and David Koetser Foundation for Brain Research. The authors thank Elena Buffone and Judith Meier for technical support. References 1. Neuhauser HK, von Brevern M, Radtke A, et al. Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology 2005;65:898–904. 2. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med 1952;45:341–54. 3. McClure JA. Horizontal canal BPV. J Otolaryngol 1985;14:30–5. 4. Wang H, Yu D, Song N, Su K, Yin K. Delayed diagnosis and treatment of benign paroxysmal positional vertigo associated with current practice. Eur Arch Otorhinolaryngol 2014;271:261– 4. 5. Kerrigan MA, Costigan MF, Blatt KJ, Mathiason MA, Domroese ME. Prevalence of benign paroxysmal positional vertigo in the young adult population. PM R 2013;5:778–85.

6. Oghalai JS, Manolidis S, Barth JL, Stewart MG, Jenkins HA. Unrecognized benign paroxysmal positional vertigo in elderly patients. Otolaryngol Head Neck Surg 2000;122:630–4. 7. Buettner UW, Zee DS. Vestibular testing in comatose patients. Arch Neurol 1989;46:561–3. 8. Sato G, Sekine K, Matsuda K, Takeda N. Effects of sleep position on time course in remission of positional vertigo in patients with benign paroxysmal positional vertigo. Acta Oto-Laryngologica 2012;132:614–17. 9. Shigeno K, Ogita H, Funabiki K. Benign paroxysmal positional vertigo and head position during sleep. J Vestib Res 2012;22:197–203. 10. Korres SG, Papadakis CE, Riga MG, Balatsouras DG, Dikeos DG, Soldatos CR. Sleep position and laterality of benign paroxysmal positional vertigo. J Laryngol Otol 2008;122:1295–8. 11. De Koninck J, Lorrain D, Gagnon P. Sleep positions and position shifts in five age groups: an ontogenetic picture. Sleep 1992;15:143–9. Fig. 1. This 30 s epoch of the patient’s video-polysomnographic recording shows the characteristic direction-changing positional nystagmus (arrowheads) for benign paroxysmal positional vertigo. In the first half of the epoch the patient’s head is turned to the right and the nystagmus beats in apogeotropic direction towards her left ear. Note that the direction of the nystagmus reverses shortly after the patient turns her head to the left, now beating towards the right ear (apogeotropic). The left EOG (E1–M2) was placed at the left outer canthus and slightly above the horizontal plane, and the right EOG (E2–M2) was placed at the right outer canthus and slightly below the horizontal plane. The right mastoid was used as reference electrode. The nystagmus is named after the direction of the quick eye movement, indicating whether the nystagmus beats towards the ground (geotropic) or towards the sky (apogeotropic). EMG, electromyography; EOG, electro-oculography; EEG, electroencephalography. Fig. 2. Thirty-second electro-oculogram traces of different types of eye movements during wakefulness and sleep states. EOG, electro-oculography; BPPV, benign paroxysmal positional vertigo; EEG, electroencephalography; NREM, non-rapid eye movement. [Figs 1 and 2. Colour halftones.] Supplementary video. The first part shows the polysomnographic sequence that is described in Fig. 1. In the second part, the video shows a positional horizontal nystagmus, beating in

apogeotropic direction (towards the upper ear) in the supine roll test on the turntable, where the patient underwent the therapeutic repositioning maneuver.

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Chin EMG EOG

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right eye E2-M2

EEG EEG

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frontal F4-M1

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occipital O2-M1

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EOG

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left eye

Nystagmus from BPPV beating in apogeotropic direction towards the left ear in right ear down position

right eye

B Nystagmus from BPPV beating in apogeotropic direction towards the right ear in left ear down position

left eye right eye

C left eye

Rapid eye movements and eye blinks during wakefulness, eyes open

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Rapid eye movements during wakefulness, eyes closed

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Slow eye movements during NREM1 sleep right eye

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Rapid eye movements during REM sleep

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G EEG artifacts in EOG traces during slow wave sleep

Polysomnography reveals nystagmus from benign paroxysmal positional vertigo.

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