Benign Paroxysmal Positioning Vertigo and Sleep: A Polysomnographic Study of Three Patients
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Sleep Research Online 5(2): 53-58, 2003 1096-214X
http://www.sro.org/2003/Monstad/53/ © 2003 WebSciences
Printed in the USA. All rights reserved.
Benign Paroxysmal Positioning Vertigo and Sleep:
A Polysomnographic Study of Three Patients
Per Monstad
Department of Neurology, Vest Agder Sentralsykehus, N-4604 Kristiansand, Norway
In three elderly patients with a clinical diagnosis of Benign Paroxysmal Positioning Vertigo (BPPV), two with posterior canal
BPPV and one with horizontal canal BPPV, polysomnography was performed with a position detector attached to the
forehead. A total of 14 head movements were recorded during sleep. None of these were followed by nystagmus, while head
movements during awake induced the expected nystagmus. However, a low sleep efficiency was seen in all cases, and 13 of
the head movements were followed by at least one epoch of awake. BPPV might be a cause of sleep problems, but the
polysomnographic 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 evoke
no nystagmus but are associated with awakenings and might be a cause of sleep disturbance.
Benign paroxysmal positioning vertigo (BPPV) is the most these patients do not experience vertigo and nystagmus when
common cause of vertigo in the elderly, with a reported subjected to vestibular stimulation during sleep. Some data has
prevalence of unrecognized BPPV of 9% in a recent been published indicating that oculovestibular reflexes are
population study by Oghalai et al. (2000), and is also very diminished or absent during sleep (Reding and Fernandez,
common in younger age groups. The pathophysiology of the 1968; Kasper et al., 1992; Cabungcal et al., 2001). The present
disorder has been elucidated in recent years (Brandt, 1999). report of polysomnographic studies of three patients suffering
The etiology of this form of vestibular vertigo is the from BPPV is intended to shed some light on this theory.
appearance of particles in the endolymph of the semicircular
canals in the inner ear, probably caused by dislodged otoconia METHODS
or spontaneously occurring calcium crystals, thus producing
particles that are heavier than the endolymph. When the Three patients with a clinical diagnosis of Benign
position of the subject’s head is changed, the particle will Paroxysmal Positioning Vertigo, based on characteristic
slowly descend through the semicircular canal, deflecting the vertigo and nystagmus during positional testing (Hallpikes
cupula and thus producing vertigo and nystagmus of some Test), were studied by conventional polysomnography,
seconds duration. including standard sleep EEG channels, electrooculogram
In the most common form of BPPV, the posterior canal type (EOG), submental EMG, ECG, respiratory movement sensors,
(pBPPV), the vertigo is most pronounced when lying down in thermistor, pulse oxymetry and position sensors. The only non-
bed, and especially so if the subject rotates his or her head to standard feature of the recording was that the position sensor
the affected side. Getting up from bed induces similar was taped to the forehead instead of the chest, as
responses, while rotating the head from side to side in the conventionally done.
supine position will produce inconsistent symptoms. In the Nystagmus, defined as repetitive eye movements with no
less common, horizontal canal variety (hBPPV), the symptoms pauses between movements and with an easily-discernible
and signs are most readily induced by rotating the head in the slow and fast phase, was identified in the EOG records using
supine position to either side. the standard gain and time constant (0.6 seconds).
Most patients with BPPV experience vertigo in the morning, All patients presented some degree of sleep complaints:
either on awakening or when rising from bed, a pattern named excessive diurnal sleepiness (Patients 1 and 3) and difficulties
“matutinal vertigo” by Fisher (1967). Although many BPPV falling asleep (Patient 2). Repeated tests of rolling from side to
patients complain of insufficient sleep, abnormal nocturnal side and from supine to prone position were done in all patients
awakenings from sleep accompanied by vertigo are not prior to falling asleep. Treatment with particle reposition
common complaints in these patients, in our experience. maneuvers (Semont maneuver) was successful in Patients 1 and
Possible explanations for this might be that patients suffering 3. In Patient 2, suffering from horizontal canal BPPV, a modified
from BPPV move less during sleep compared to healthy Epley maneuver (“barbeque rotation”) did not succeed, while
persons, that awakenings caused by BPPV attacks might be too prolonged positioning with the right ear lowermost, as described
short to be remembered in the morning, or, alternatively, that by Vannucchi et al. (1997), cured the vertigo.
Correspondence: Per Monstad, M.D., Department of Neurology, Vest Agder Sentralsykehus, N-4604 Kristiansand, Norway, E-mail:
per.monstad@enitel.no.54 MONSTAD
Patient 1: Female, 79 yrs. old sleep and the other three from Stages 1 and 2, two from supine
Right posterior canal BPPV of six-months duration. to the right, and two from the right side to supine position. All
Provoking factors: lying down, rising from bed, rolling from changes of head position were followed by at least one epoch
side to side. of the awake state.
Patient 2: Female, 77 yrs. old In Patient 2, who suffered from left horizontal canal BPPV,
Left horizontal canal BPPV of three-days duration. every rotational movement from supine to the left or right
Provoking factors: rolling from side to side in supine position. position evoked nystagmus during the awake state. A degree of
Patient 3: Female, 65 yrs. old habituation was seen as the nystagmus became shorter in
Right posterior canal BPPV of one-year duration. duration on repeated tests. The most intense and long-lasting
Provoking factors: lying down, rising from bed, neck nystagmus was seen after positional changes to the left,
extension, rarely rolling from side to side. especially when rotating the head from the right to the left
position. During sleep, seven head movements were seen: one
RESULTS from Stage 4 and the other six from Stages 1 and 2. Three of the
head movements were from the right side to a supine position,
In Patients 1 and 3, both suffering from the more common one from supine to the right, and three from the left side to
posterior canal BPPV, rotational movements while awake only supine. All head movements were followed by at least one
occasionally evoked any nystagmus; nystagmus was identified epoch of the awake state. No nystagmus was seen immediately
in 6 of 11 and 6 of 8 head movements to the right side (in two following any of the head movements. A few nystagmoid jerks
subjects) and 5 of 10 vs. 7 of 12 movements to the left side. were seen in one instance, ten seconds after the movement
This nystagmus was generally of short duration, despite the (Figure 3). Four head movements were recorded during the first
patients’ subjective feelings of vertigo in the seconds after 30 seconds after awakenings; no nystagmus was associated
most positional changes (Figure 1). During sleep, no positional with any of these movements (Figures 3, 4 and 5).
changes evoked any nystagmus (Figure 2). Sleep fragmentation and low sleep efficiency were seen in
In Patient 1, three head movements during sleep, all from the all three subjects (Table 1). An apnea index of 5.5 was seen in
supine to the right position were seen: one in Stage 1, one in Patient 1; no respiratory disturbances were seen during sleep in
Stage 2, and one in REM sleep. Awakenings from sleep were the other two patients. No other etiology for their sleep
seen in association with two of the movements. In Patient 3, complaints was found. However, only two patients were
four changes in head position were seen: one from Stage 3 screened 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.BENIGN PAROXYSMAL POSITIONING VERTIGO AND SLEEP 55 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 jerks are seen 10 seconds later.
56 MONSTAD Figure 4. Continuation of Figure 3: no nystagmus is seen during a new positional change (from right side to supine and back) less than 30 seconds after awakening; a new position change is seen in the last two seconds of the page, evoking nystagmus in Figure 5. Figure 5. Continuation of Figure 4: intense nystagmus is evoked after a new positional change more than 50 seconds after awakening; the change from right side to supine occurred at the end of Figure 4.
BENIGN PAROXYSMAL POSITIONING VERTIGO AND SLEEP 57
Table 1 stimulation disturbs sleep. In BPPV, the spontaneous head
Sleep Inter-sleep movements during sleep will move the otoconial debris and
Patient TST Efficiency Wake Stage Shifts
stimulate the utriculus, producing a sensory stimulus that is
1 447 min 78% 14% 345
unpleasant in the awake state. The present study gives some
2 256 min 43% 54% 210 indications (but no proof) that BPPV might be a cause of
3 175 min 32% 60% 146 disturbed sleep.
Table 1. Total Sleep Time (TST), Sleep Efficiency (from lights out), A low sleep efficiency was seen, and 13 of the 14 head
Inter-sleep Wake Time and Sleep Stage Shifts in the Three Patients. movements during sleep were associated with at least one
epoch of awake after the “movement time” epoch where the
DISCUSSION head movement was recorded. However, there is a lack of
normative data regarding head movements during sleep.
Head movements that would be expected to evoke vertigo Whether the head movements recorded in the study caused the
and nystagmus during the awake state did not produce awakenings, or rather are a result of the awakenings, is not
nystagmus during sleep in these BPPV patients; neither did clear. A larger study with healthy controls will be necessary to
head movements shortly after awakening (within 30 seconds) finally decide on this issue.
evoke any nystagmus in these patients. Although it seems premature to include BPPV among the known
The nystagmus during unilateral vestibular stimulation is medical causes of disturbed sleep in the elderly, it seems prudent to
generally thought to consist of two components: a three-neuron inquire for symptoms of the disorder when interviewing patients
arc serving the primary compensatory movement of the eyes with sleep problems. Simply inquiring about vertigo when
intended to keep the eyes fixated on target, and a secondary, awakening in the morning is not sufficient. “Matutinal vertigo” is
multisynaptic pathway that generates fast repositioning of the an unspecific phenomenon, occurring in other diseases of the
eyes, i.e., the fast phase or saccadic part of the nystagmus. peripheral vestibular system as well as the central nervous system,
It should be noted that the standard electrooculography, as as found by Maton et al. (1980) and Berkowitz (1985); in the
performed during polysomnography, is not well suited to pick author’s experience, it is not an obligatory symptom in BPPV
up an unidirectional compensatory eye movement during a patients. The polysomnogram will not disclose any specific
head movement, owing to technical (movement) artifacts and findings as the clinical sign of the disorder, nystagmus after
the rather short time-constant used for EOG recordings. With positional change, disappears during sleep.
this caution in mind, the findings described above indicate that
the oculovestibular reflex, or at least the saccadic part of it, is ACKNOWLEDGMENTS
abolished during sleep. This is in accordance with other data.
Reding et al. (1968) and Jones and Sugie (1972) found The author does not wish to include any acknowledgments.
decreased and eventually disappearing oculovestibular reflexes
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