Benign paroxysmal positioning vertigo (BPPV) is the mostcommon cause of vertigo in the elderly, with a reportedprevalence of unrecognized BPPV of 9% in a recentpopulation study by Oghalai et al. (2000), and is also verycommon in younger age groups. The pathophysiology of thedisorder has been elucidated in recent years (Brandt, 1999).The etiology of this form of vestibular vertigo is theappearance of particles in the endolymph of the semicircularcanals in the inner ear, probably caused by dislodged otoconiaor spontaneously occurring calcium crystals, thus producingparticles that are heavier than the endolymph. When theposition of the subject’s head is changed, the particle willslowly descend through the semicircular canal, deflecting thecupula and thus producing vertigo and nystagmus of someseconds duration.

In the most common form of BPPV, the posterior canal type(pBPPV), the vertigo is most pronounced when lying down inbed, and especially so if the subject rotates his or her head tothe affected side. Getting up from bed induces similarresponses, while rotating the head from side to side in thesupine position will produce inconsistent symptoms. In theless common, horizontal canal variety (hBPPV), the symptomsand signs are most readily induced by rotating the head in thesupine position to either side.

Most patients with BPPV experience vertigo in the morning,either on awakening or when rising from bed, a pattern named“matutinal vertigo” by Fisher (1967). Although many BPPVpatients complain of insufficient sleep, abnormal nocturnalawakenings from sleep accompanied by vertigo are notcommon complaints in these patients, in our experience.Possible explanations for this might be that patients sufferingfrom BPPV move less during sleep compared to healthypersons, that awakenings caused by BPPV attacks might be tooshort to be remembered in the morning, or, alternatively, that

these patients do not experience vertigo and nystagmus whensubjected to vestibular stimulation during sleep. Some data hasbeen published indicating that oculovestibular reflexes arediminished or absent during sleep (Reding and Fernandez,1968; Kasper et al., 1992; Cabungcal et al., 2001). The presentreport of polysomnographic studies of three patients sufferingfrom BPPV is intended to shed some light on this theory.

METHODS

Three patients with a clinical diagnosis of BenignParoxysmal Positioning Vertigo, based on characteristicvertigo and nystagmus during positional testing (HallpikesTest), were studied by conventional polysomnography,including standard sleep EEG channels, electrooculogram(EOG), submental EMG, ECG, respiratory movement sensors,thermistor, pulse oxymetry and position sensors. The only non-standard feature of the recording was that the position sensorwas taped to the forehead instead of the chest, asconventionally done.

Nystagmus, defined as repetitive eye movements with nopauses between movements and with an easily-discernibleslow and fast phase, was identified in the EOG records usingthe standard gain and time constant (0.6 seconds).

All patients presented some degree of sleep complaints:excessive diurnal sleepiness (Patients 1 and 3) and difficultiesfalling asleep (Patient 2). Repeated tests of rolling from side toside and from supine to prone position were done in all patientsprior to falling asleep. Treatment with particle repositionmaneuvers (Semont maneuver) was successful in Patients 1 and3. In Patient 2, suffering from horizontal canal BPPV, a modifiedEpley maneuver (“barbeque rotation”) did not succeed, whileprolonged positioning with the right ear lowermost, as describedby Vannucchi et al. (1997), cured the vertigo.

In three elderly patients with a clinical diagnosis of Benign Paroxysmal Positioning Vertigo (BPPV), two with posterior canalBPPV and one with horizontal canal BPPV, polysomnography was performed with a position detector attached to theforehead. A total of 14 head movements were recorded during sleep. None of these were followed by nystagmus, while headmovements during awake induced the expected nystagmus. However, a low sleep efficiency was seen in all cases, and 13 ofthe head movements were followed by at least one epoch of awake. BPPV might be a cause of sleep problems, but thepolysomnographic findings are unspecific, as the oculovestibular reflexes are abolished during sleep.

CURRENT CLAIM: Head movements during sleep in patients suffering from benign paroxysmal positioning vertigo evokeno nystagmus but are associated with awakenings and might be a cause of sleep disturbance.

Sleep Research Online 5(2): 53-58, 2003http://www.sro.org/2003/Monstad/53/ Printed in the USA. All rights reserved.

Correspondence: Per Monstad, M.D., Department of Neurology, Vest Agder Sentralsykehus, N-4604 Kristiansand, Norway, E-mail:per.monstad@enitel.no.

1096-214X© 2003 WebSciences

Benign Paroxysmal Positioning Vertigo and Sleep: A Polysomnographic Study of Three Patients

Per Monstad

Department of Neurology, Vest Agder Sentralsykehus, N-4604 Kristiansand, Norway

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Patient 1: Female, 79 yrs. oldRight posterior canal BPPV of six-months duration.Provoking factors: lying down, rising from bed, rolling fromside to side.

Patient 2: Female, 77 yrs. oldLeft horizontal canal BPPV of three-days duration.Provoking factors: rolling from side to side in supine position.

Patient 3: Female, 65 yrs. oldRight posterior canal BPPV of one-year duration. Provoking factors: lying down, rising from bed, neckextension, rarely rolling from side to side.

RESULTS

In Patients 1 and 3, both suffering from the more commonposterior canal BPPV, rotational movements while awake onlyoccasionally evoked any nystagmus; nystagmus was identifiedin 6 of 11 and 6 of 8 head movements to the right side (in twosubjects) and 5 of 10 vs. 7 of 12 movements to the left side.This nystagmus was generally of short duration, despite thepatients’ subjective feelings of vertigo in the seconds aftermost positional changes (Figure 1). During sleep, no positionalchanges evoked any nystagmus (Figure 2).

In Patient 1, three head movements during sleep, all from thesupine to the right position were seen: one in Stage 1, one inStage 2, and one in REM sleep. Awakenings from sleep wereseen in association with two of the movements. In Patient 3,four changes in head position were seen: one from Stage 3

sleep and the other three from Stages 1 and 2, two from supineto the right, and two from the right side to supine position. Allchanges of head position were followed by at least one epochof the awake state.

In Patient 2, who suffered from left horizontal canal BPPV,every rotational movement from supine to the left or rightposition evoked nystagmus during the awake state. A degree ofhabituation was seen as the nystagmus became shorter induration on repeated tests. The most intense and long-lastingnystagmus was seen after positional changes to the left,especially when rotating the head from the right to the leftposition. During sleep, seven head movements were seen: onefrom Stage 4 and the other six from Stages 1 and 2. Three of thehead movements were from the right side to a supine position,one from supine to the right, and three from the left side tosupine. All head movements were followed by at least oneepoch of the awake state. No nystagmus was seen immediatelyfollowing any of the head movements. A few nystagmoid jerkswere seen in one instance, ten seconds after the movement(Figure 3). Four head movements were recorded during the first30 seconds after awakenings; no nystagmus was associatedwith any of these movements (Figures 3, 4 and 5).

Sleep fragmentation and low sleep efficiency were seen inall three subjects (Table 1). An apnea index of 5.5 was seen inPatient 1; no respiratory disturbances were seen during sleep inthe other two patients. No other etiology for their sleepcomplaints was found. However, only two patients werescreened for PLMS.

Figure 1. Positional change from supine to the right side in the awake state evokes nystagmus–traces FP1A1 and FP2A1, last 10 seconds of page.Patient 1: head position in the “body” trace–RS for right side; SU for supine; lower trace “Lys”–light intensity; EEG channels–C3-A2 and C4-A1.

55BENIGN PAROXYSMAL POSITIONING VERTIGO AND SLEEP

Figure 2. Change from supine to right side during awakening from Stage 2 sleep evokes no nystagmus. Patient 1: traces as in Figure 1.

Figure 3. Change of head position from supine to the right side during Stage 3 sleep in Patient 2 evokes no nystagmus; a few nystagmoid jerksare seen 10 seconds later.

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Figure 5. Continuation of Figure 4: intense nystagmus is evoked after a new positional change more than 50 seconds after awakening; the changefrom right side to supine occurred at the end of Figure 4.

Figure 4. Continuation of Figure 3: no nystagmus is seen during a new positional change (from right side to supine and back) less than 30seconds after awakening; a new position change is seen in the last two seconds of the page, evoking nystagmus in Figure 5.

DISCUSSION

Head movements that would be expected to evoke vertigoand nystagmus during the awake state did not producenystagmus during sleep in these BPPV patients; neither didhead movements shortly after awakening (within 30 seconds)evoke any nystagmus in these patients.

The nystagmus during unilateral vestibular stimulation isgenerally thought to consist of two components: a three-neuronarc serving the primary compensatory movement of the eyesintended to keep the eyes fixated on target, and a secondary,multisynaptic pathway that generates fast repositioning of theeyes, i.e., the fast phase or saccadic part of the nystagmus.

It should be noted that the standard electrooculography, asperformed during polysomnography, is not well suited to pickup an unidirectional compensatory eye movement during ahead movement, owing to technical (movement) artifacts andthe rather short time-constant used for EOG recordings. Withthis caution in mind, the findings described above indicate thatthe oculovestibular reflex, or at least the saccadic part of it, isabolished during sleep. This is in accordance with other data.

Reding et al. (1968) and Jones and Sugie (1972) founddecreased and eventually disappearing oculovestibular reflexesduring drowsiness and sleep. The saccadic phase disappearsfirst, during transition from awake to sleep, followed by theslow phase (the “true” oculovestibular reflex) as shown byJones and Sugie (1972) and Kasper et al. (1992).

Eisenehr et al. (2001) demonstrated that even a complete andrecent unilateral loss of vestibular input produced no nystagmusor other signs of oculovestibular imbalance during REM sleep,as well as a loss of nystagmus during NREM sleep.

The neurophysiological basis for this disappearance ofoculovestibular reflexes is not known in detail, but Lenze et al.(1968) found that the monosynaptically-transmitted, evokedpotential in the medial longitudinal fasciculus was intactduring NREM sleep after electrical stimulation of thevestibular nerve in cats. This evoked potential was also intactduring REM sleep with one exception: during rapid eyemovements, the potential decreased.

This indicated that the sensory function of the vestibularsystem is intact during NREM and during most parts of REMsleep and thus, that the suppression of reflexive eyemovements might be located in the oculomotor nuclei.Vestibular stimulation might thus be an arousal stimulus duringsleep despite the absence of reflexive eye movements.

Weak, low frequency, vestibular (otolithic) stimulation doesnot disturb sleep (Woodward et al., 1990). There are no studiestesting whether stronger, more unpleasant vestibular

stimulation disturbs sleep. In BPPV, the spontaneous headmovements during sleep will move the otoconial debris andstimulate the utriculus, producing a sensory stimulus that isunpleasant in the awake state. The present study gives someindications (but no proof) that BPPV might be a cause ofdisturbed sleep.

A low sleep efficiency was seen, and 13 of the 14 headmovements during sleep were associated with at least oneepoch of awake after the “movement time” epoch where thehead movement was recorded. However, there is a lack ofnormative data regarding head movements during sleep.Whether the head movements recorded in the study caused theawakenings, or rather are a result of the awakenings, is notclear. A larger study with healthy controls will be necessary tofinally decide on this issue.

Although it seems premature to include BPPV among the knownmedical causes of disturbed sleep in the elderly, it seems prudent toinquire for symptoms of the disorder when interviewing patientswith sleep problems. Simply inquiring about vertigo whenawakening in the morning is not sufficient. “Matutinal vertigo” isan unspecific phenomenon, occurring in other diseases of theperipheral vestibular system as well as the central nervous system,as found by Maton et al. (1980) and Berkowitz (1985); in theauthor’s experience, it is not an obligatory symptom in BPPVpatients. The polysomnogram will not disclose any specificfindings as the clinical sign of the disorder, nystagmus afterpositional change, disappears during sleep.

ACKNOWLEDGMENTS

The author does not wish to include any acknowledgments.

REFERENCES

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Table 1. Total Sleep Time (TST), Sleep Efficiency (from lights out),Inter-sleep Wake Time and Sleep Stage Shifts in the Three Patients.

Table 1 Sleep Inter-sleep

Patient TST Efficiency Wake Stage Shifts

1 447 min 78% 14% 345

2 256 min 43% 54% 210

3 175 min 32% 60% 146

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12. Vannucchi P, Giannoni B, Pagnini P. Treatment ofhorizontal semicircular canal benign paroxysmalpositional vertigo. J Vestib Res 1997; 7(1): 1-6.

13. Woodward S, Tauber E, Spielman AJ, Thorpy MJ. Effectsof otolithic vestibular stimulation on sleep. Sleep 1990;13(6): 533-7.

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