Dizziness is a common symptom reported by patients with sleep apnea (1). Sleep apnea is complete or partial cessation of breathing while sleeping, reported as apneas or hypopneas that result in night-time hypoxemia. The obstructive form (OSA) is characterized by snoring; it results from partial or complete airway collapse, often followed by arousals and gasping. The central form occurs when central initiation of breathing is impaired resulting in pauses in breathing while asleep.
Sleep disordered breathing is a risk factor for vascular morbidity and mortality. It has been associated with transient ischemic attacks, stroke, heart failure, and myocardial infarction (2). Night-time hypoxemia from sleep apnea can result in sympathetic over-activity during waking hours, endothelial damage, platelet aggregation, and chronic systemic and pulmonary hypertension (3). Morning headaches are common. In OSA patients with migraine, headaches are more severe and frequent when OSA is untreated (4). Hypertension and migraine are themselves risk factors for cerebrovascular and cardiovascular disease, so sleep apnea is both a primary vascular risk factor and a secondary risk factor through these allied conditions.
Dizziness has been associated with cerebrovascular disorders (5). The inner ear receives all of its arterial inflow via intracerebral arteries without extracerebral collaterals, so processes that result in vasospasm or occlusion of vessels in the head could result in impaired flow to the inner ears. Dizziness can also be reported due to presyncope, microsleep episodes, or central ischemia and each of these is likely to occur in OSA (6–8).
The goal of the present study is to examine the vestibular symptoms encountered in dizzy patients with sleep-disordered breathing and to define symptoms and diagnoses that may be unique or at increased frequency in them. We also sought to determine the response of vestibular symptoms to treatment with continuous positive airway pressure treatment (CPAP).
We retrospectively reviewed charts on all patients with a diagnosis of sleep apnea seen from 2008 to 2015 in the dizziness clinic at the University of Colorado who had received 1) a new diagnosis of sleep apnea, 2) had a confirmatory pulse oximetry or polysomnogram, and 3) received sleep apnea treatment through our center. Fifty-two patients met these criteria. Sixty-five percent of the sample was male and 35% female. The mean age was 55 ± 14 years, and the mean BMI was 31 ± 7. All charts contained a narrative history, examination, and vestibular diagnoses by an experienced neurotologist. Neurotologic testing included videonystagmography, vestibular-evoked myogenic potentials, video head impulse testing, audiometry, and MRI as indicated.
The procedures followed were in accordance with the ethical standards of the Colorado Multiple Institutional Review Board on human experimentation and with the Helsinki Declaration (COMIRB Protocol 15-0679).
Forty-eight of 52 patients were treated with CPAP and 4 of 52 underwent surgical treatment with uvulopalatopharyngoplasty.
MAIN OUTCOME MEASURE
We collected the self-reported symptoms of dizziness, and vestibular diagnoses. Menière's disease (MD) diagnosis was based on AAOHNS criteria (9) and vestibular migraine was based on International Headache Society (IHS) criteria (10).
To determine whether the dizziness could be caused by OSA, we identified 19 patients (“Definite” responder group) with an initial diagnosis of OSA, and complete resolution of dizziness with treatment of OSA on long-term follow-up of at least 2 years. Mean follow-up duration was 51 ± 21 months. Thirty-three patients were assigned to the “Indeterminate” responder group for the following reasons: 15 of 33 (45%) had no chart notation regarding dizziness after CPAP was initiated; 8 of 33 (24%) were unable to tolerate CPAP; and 10 of 33 (30%) failed to show complete resolution of dizziness on CPAP.
We then compared the dizziness symptoms of the Definite responder group (8 F, 11 M) to the remaining 33 patients to determine if the spectrum of symptoms were similar across the entire patient group.
The 19 Definite responders did not differ demographically from the 33 Indeterminate responders (Table 1). The Definite responder group had a nonsignificantly higher Apnea-Hypopnea Index (47 ± 34) than the Indeterminate responder group (31 ± 28). The mean Apnea-Hypopnea Index overall was 30, suggesting that dizziness may arise when OSA becomes moderate to severe. However, (14/52) 27% had mild OSA but also reported dizziness. Normal vestibular test results were found in over 60% of both groups (Table 2).
TABLE 1 -
||Age (Mean + SD)
||BMI (Mean + SD)
||AHI (Mean + SD)
||18 F (35%)34 M (65%)
||55 ± 14
||31 ± 7
||30 ± 27
||7 F (37%)12 M (63%)
||55 ± 13
||32 ± 9
||47 ± 34
||11 F (33%)22 M (67%)
||55 ± 15
||31 ± 8
||31 ± 28
|95% Confidence interval
||55 ± 3.8
||31 ± 1.9
||30 ± 7
AHI, Apnea-Hypopnea Index
TABLE 2 -
Vestibular test results
||Normal Caloric Test
||Mean and Range of Canal Paresis
||Mean 64%Range 44–100%
||Mean 42%Range 29–61%
VNG indicates videonystagmography.
Vestibular descriptions fell into four general types. A third of patients reported sudden, spontaneous internal vertigo with near falls (Table 3). The events occurred spontaneously or were head-motion triggered. Patients described “jolts,” “head rushes,” “flickers,” or “flashes” of sudden dizziness.
TABLE 3 -
||Sudden SNHL With Vertigo
|All patients (52)
|General population mean
PPPD indicates persistent postural perceptive dizziness; SNHL, sensorineural hearing loss.
Vestibular migraine was diagnosed in patients with nauseating headaches and dizziness meeting IHS criteria. Patients frequently reported visual motion-induced vertigo and motion sickness. Migraine was 10 times more common in both groups than in the general population (11).
Those meeting MD by AAOHNS criteria reported classic Menière's attacks, with hours-long vertigo spells associated with hearing loss in the affected ear(s). MD was found at 115 times the level in the normal population (12).
MD was found in 12 of 52 (23%) of all OSA patients in the study. In the Definite responder group, 3 of 19 (16%) had MD (2 unilateral, 1 bilateral) and all had complete resolution of their Menière's attacks with CPAP during 2 to 5 years of follow-up after failing traditional therapy with repeated attacks in the 3 months before initiation of CPAP. Patients usually continued on their pre-existing therapies.
In the Indeterminate responder group 9 of 33 (27%) had MD (1 bilateral, 8 unilateral). Two of 9 (22%) underwent ablation so the effect of CPAP on dizziness could not be assessed. Two of 9 (22%) had no further notations in the chart regarding dizziness. Three of 9 (33%) were unable to tolerate or refused CPAP. Two of 9 (22%) were adequately treated with CPAP but continued to have Menière's attacks. Of the 12 of 52 patients with MD in the entire patient group we had long-term outcome data on 5/12. Three of 5 (60%) showed complete resolution of dizziness on CPAP, and 2 of 5 (40%) showed no improvement with CPAP.
The least common form of vestibular presentation in OSA patients was acute vestibular syndrome with sensorineural hearing loss (SNHL), with symptoms of acute vertigo at or near the onset of sudden permanent and severe hearing loss, followed by gradual improvement in vertigo over weeks. Sudden SNHL was found at 200 times the general population frequency (13).
Persistent postural perceptive dizziness was reported as a low grade, poorly characterized dizziness waxing and waning throughout the day. This category overlapped with other categories of dizziness and was somewhat greater in frequency to that in the general population (42% in patients vs 30% in the general population) (14).
Sleep apnea is associated with four general categories of vestibular symptoms, three of which fall within current vestibular diagnoses: Vestibular migraine, MD, and acute vestibular syndrome with SNHL. One of these is unusual: momentary bouts of internal spinning dizziness lasting seconds that recur multiple times per day and are not positional. This type of dizziness was the most frequent type reported by those who showed a complete resolution of dizziness with OSA treatment. Phenotypically the presentation resembles vestibular paroxysmia. Our non-Menière's patients lacked other typical symptoms of vestibular paroxysmia, such as minutes-long spells, unilateral tinnitus, aural numbness, and hearing loss (15). Vestibular paroxysmia has been attributed to ephaptic discharges in the vestibular nerves responsive to antiepileptic medication (carbamazepine). In this series patients responded to OSA treatment, suggesting a different mechanism. Vascular cross compression, an underlying presumed cause of vestibular paroxysmia, was not found on imaging in our patients with unilateral findings on testing. We therefore advocate that OSA should be considered in the differential diagnosis of vestibular paroxysmia.
Migraine, Menière's, and sudden SNHL are more common in those with vascular risk factors (16–18), so the connection between OSA and these types is likely to be through OSA's detrimental effect on intracerebral blood flow. In the Definite responder group, those with vestibular migraine and MD all had complete resolution of their vestibular symptoms with CPAP as the only added treatment, suggesting that OSA was the underlying exacerbating factor for these conditions. The single responder with compensated sudden unilateral loss also had ongoing brief dizziness typical of OSA, and it was the brief dizziness that resolved after CPAP treatment. The success of CPAP in treating dizziness suggests that a history of snoring and other symptoms of OSA (hypertension, headaches, somnolence) should be sought in all dizzy patients, particularly those who have failed traditional treatments for their dizziness disorders.
Of our 5 of 12 MD patients who tolerated CPAP, and on which follow-up data were available, 60% had a complete resolution of attacks after having failed to control symptoms with standard therapies. This suggests that testing to rule out sleep apnea should be considered in MD patients, and that CPAP be considered in this patient group.
Our study's sample population was of dizziness patients at a single site who were found to have OSA, not unselected OSA patients. Prospective, randomized controlled studies are needed to further delineate the frequency of dizziness in OSA, the presence of OSA in MD, and the response of MD and other OSA-linked vestibular disorders to CPAP treatment.
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