Keywords
benign paroxysmal positional vertigo - vestibular - nystagmus - dix-hallpike
Benign paroxysmal positional vertigo (BPPV) is a common cause of peripheral vestibular
dysfunction. Individuals with BPPV typically experience brief episodes of dizziness
provoked by changes in head position. Episodes typically last seconds and tend to
occur with mobility in bed and performance of overhead activities. In most instances,
the suspected mechanism for BPPV is “canalithiasis,” which involves a cluster of free-floating
fragmented utricular membranes with attached and detached otoconia disturbing normal
semicircular canal mechanics.[1]
[2] Position changes induce a migration of otoconia to the most dependent location within
the endolymph-filled semicircular canal. This creates a pressure differential within
the canal which displaces the cupula and its associated hair cells. This displacement
results in the illusion of head movement. BPPV commonly involves the posterior semicircular
canal accounting for 85 to 95% of BPPV cases.[3]
BPPV is commonly idiopathic but may also be secondary to genetic predisposition,[4]
[5] Meniere's disease,[6] vestibular neuritis,[7] recent ear surgery,[8] and head trauma or serum vitamin D level.[9] The incidence of BPPV increases with age with a cumulative incidence of nearly 10%
at the age of 80 years.[10] The condition is more common in females than in males at a ratio of approximately
2:1.[11]
BPPV can have a significant impact on productivity and quality of life; therefore,
an accurate and timely diagnosis is critical. One study[10] reported that 86% of subjects with BPPV required a medical consultation, experienced
an interruption in daily activities, or required time off from work. Additionally,
treatment of BPPV may lessen the risk of falls.[12]
The gold standard for diagnosis of posterior canal BPPV is the Dix-Hallpike maneuver.
A positive test induces an excitatory-driven upbeat torsional nystagmus toward the
involved ear due to utriculofugal displacement of the cupula within the posterior
canal. The Dix-Hallpike maneuver is reported to have a sensitivity of 79%.[13]
[14] Variables that may impact the sensitivity of the Dix-Hallpike maneuver include the
particle–canal wall interactions and the degree of dispersal of the particulate matter
within the canal.[15] The sensitivity of Dix-Hallpike testing improves with repeat testing.[14]
[16]
The presence of nystagmus with return to a seated position following the dependent
position of Dix-Hallpike testing may also be a useful indication of posterior canal
BPPV. With return to sitting, it can be postulated that migrating debris induces utriculopetal
displacement of the posterior canal cupula. This results in an inhibitory-driven downbeating
nystagmus with a torsional component away from the involved ear ([Supplementary Video 1], online only). Henceforth, the term “reversal nystagmus” will be utilized in this
article to describe this type of nystagmus regardless of the presence or absence of
nystagmus with the dependent position of Dix-Hallpike testing. Postural instability
is commonly associated with reversal nystagmus ([Supplementary Video 2], online only). While reversal nystagmus has been previously reported as a feature
of posterior canal BPPV,[3]
[17] its prevalence and relationship to the dependent position of the Dix-Hallpike have
not been formally investigated to our knowledge.
Supplementary Video 1
Reversal nystagmus in subject with right posterior canal BPPV.
Supplementary Video 2
Postural instability associated with reversal nystagmus in subject with left posterior
canal BPPV.
The aim of this study is to report the prevalence of reversal nystagmus and its relationship
to the dependent position of Dix-Hallpike testing in subjects with known posterior
canal BPPV. Information on this diagnostic finding with Dix-Hallpike testing may enhance
recognition of posterior canal BPPV and expedite treatment.
Methods
The study protocol was approved by the Institutional Review Board Committee at Geisinger
Medical Center. All individuals presenting to the Geisinger Otolaryngology Vestibular
and Balance Center between March 2017 and August 2017 with symptoms consistent with
BPPV were screened for inclusion. Informed consent was obtained from all participants.
A total of 28 subjects met the inclusion criteria. A single clinician, J.W., interviewed
and examined each subject. Exclusion criteria: the use of vestibular sedatives within
24 hours of the appointment, history of associated emesis, inability to tolerate or
refusal to participate in the study protocol, limited spinal mobility, presence of
spontaneous, gaze-evoked, or static positional nystagmus, individuals with variant
forms of BPPV (multicanal BPPV, horizontal canal, bilateral BPPV, or cupulolithiasis),
and failure to demonstrate nystagmus with the Dix-Hallpike testing protocol outlined
in this study.
The study involved six testing trials per subject. Dix-Hallpike testing was considered
negative if no nystagmus was evoked within 30 seconds. If nystagmus was evoked, the
dependent position was maintained for an additional 30 seconds after the nystagmus
abated. Subjects were transitioned from the dependent position of Dix-Hallpike testing
to sitting within 2 seconds. Immediately in the upright position, the participants
were observed for reversal nystagmus. Eye movements were video-recorded with the use
of Micromedical monocular “Real Eyes” infrared goggles. To minimize saccadic eye movements,
subjects were instructed to maintain primary gaze and fixation was consistently permitted.
The examiner determined if reversal nystagmus was present, which included video review
if needed. One minute of recovery time was provided between each of the six testing
trials.
Results
The study population was made up of 28 subjects, which included 16 females and 12
males with a mean age of 59.6 years (standard deviation: 12.73). All study participants
included in this report demonstrated nystagmus consistent with single-sided posterior
canal BPPV, canalithiasis type with Dix-Hallpike testing.
There were a total of 167 Dix-Hallpike maneuvers performed (note: one participant
could only tolerate five testing trials due to nausea and emesis); reversal nystagmus
was observed with 134 trials (80.2%; [Table 1]). A total of 19 trials did not elicit any nystagmus with the dependent position
of Dix-Hallpike testing; however, 13 (68.4%) of these trials demonstrated reversal
nystagmus. Most study participants (27/28, 96.4%) exhibited reversal nystagmus on
at least one of the six trials of Dix-Hallpike testing. With initial Dix-Hallpike
testing, 21 of 28 subjects demonstrated reversal nystagmus (75%). With combining trial
one and two, 25 of 28 subjects demonstrated reversal nystagmus with at least one of
the trials (89.2%). The absence of reversal nystagmus was noted in 11 instances with
trials one and two and 11 instances with trials five and six of Dix-Hallpike testing;
therefore, the likelihood of evoking reversal nystagmus did not appear to change with
repeated testing.
Table 1
Results of the six testing trials for the 28 study participants
|
Subject #
|
Trial 1
|
Trial 2
|
Trial 3
|
Trial 4
|
Trial 5
|
Trial 6
|
|
1
|
+/+
|
−/+
|
−/+
|
−/−
|
+/+
|
+/+
|
|
2
|
+/−
|
+/−
|
+/+
|
+/−
|
+/−
|
+/−
|
|
3
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/[a]
|
|
4
|
−/−
|
+/+
|
+/+
|
+/−
|
+/+
|
+/+
|
|
5
|
+/+
|
+/+
|
+/+
|
−/−
|
+/+
|
+/+
|
|
6
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
7
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
8
|
+/−
|
+/+
|
+/+
|
+/−
|
+/−
|
+/+
|
|
9
|
−/−
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
10
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
11
|
+/+
|
+/+
|
+/−
|
+/+
|
+/+
|
+/+
|
|
12
|
−/+
|
+/+
|
+/+
|
−/−
|
+/−
|
+/−
|
|
13
|
+/+
|
+/+
|
−/+
|
+/+
|
+/+
|
+/+
|
|
14
|
+/−
|
+/−
|
+/+
|
−/+
|
+/−
|
−/−
|
|
15
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
16
|
+/+
|
+/−
|
+/+
|
+/+
|
+/+
|
+/+
|
|
17
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
18
|
+/+
|
+/+
|
+/+
|
−/+
|
−/+
|
−/+
|
|
19
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
20
|
+/+
|
+/+
|
+/+
|
−/+
|
+/+
|
−/+
|
|
21
|
+/+
|
+/+
|
+/−
|
+/+
|
+/−
|
+/−
|
|
22
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
23
|
+/−
|
+/+
|
+/−
|
+/−
|
+/+
|
+/+
|
|
24
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
25
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
26
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
+/+
|
|
27
|
+/−
|
+/−
|
+/−
|
+/−
|
+/−
|
+/−
|
|
28
|
+/+
|
+/+
|
+/+
|
−/+
|
−/+
|
−/+
|
|
Summary
|
25/21
|
27/24
|
26/24
|
21/20
|
26/22
|
24/23
|
Note. Result of each trial refers to the frequency that nystagmus was present with Dix-Hallpike
testing/frequency of reversal nystagmus.
+/+ : Nystagmus was evoked with the dependent position of Dix-Hallpike testing and
reversal nystagmus was present.
+/− : Nystagmus was evoked with the dependent position of Dix-Hallpike testing and
reversal nystagmus was absent.
−/+ : Nystagmus was absent with the dependent position of Dix-Hallpike testing and
reversal nystagmus was present.
−/− : Nystagmus was absent with the dependent position of Dix-Hallpike testing and
reversal nystagmus was absent.
a Reversal nystagmus was not assessed in the sixth trial for subject 3 due to nausea/emesis.
Discussion
Dix-Hallpike testing is well established for the diagnosis of BPPV. However, prior
studies have not formally investigated the prevalence of reversal nystagmus. This
study suggests that reversal nystagmus is quite common in individuals with posterior
canal BPPV and can be present when no nystagmus is evoked with the head-dependent
position of Dix-Hallpike testing.
Current BPPV clinical practice guidelines state that “clinicians should diagnose posterior
semicircular canal BPPV when vertigo associated with torsional, up-beating nystagmus
is provoked by the Dix-Hallpike maneuver.”[17] According to research in the primary care setting by Hanley et al, a positive Dix-Hallpike
test is associated with an 83% positive predictive value, and a negative test is associated
with a 52% negative predictive value.[18] Thus, a negative Dix-Hallpike test does not exclude BPPV. Subjects with BPPV, but
an absence of nystagmus with the dependent position of Dix-Hallpike testing, may still
exhibit reversal nystagmus as demonstrated in this study. Observation of reversal
nystagmus may improve the negative predictive value of Dix-Hallpike testing. In instances
where repeated canalith repositioning maneuvers have failed, it may be helpful to
confirm the presence of reversal nystagmus. This would further assure that the etiology
is canalithiasis and not an alternative cause.
There are several limitations of this study. Subjects were closely observed by an
experienced clinician with video infrared goggles. It is possible that an inexperienced
clinician without goggles may have more difficulty identifying reversal nystagmus.
Another limitation of our study is that some potential subjects refused participation
in the study protocol due to anxiety or nausea. This may have biased our study population
toward mild-to-moderate BPPV. Additionally, this study was not designed to formally
investigate sensitivity or specificity. Further study would be needed to address these
values. The findings from this study are likely not applicable to other less common
variants of BPPV (cupulolithiasis, horizontal canal BPPV). Lastly, this study did
not measure nystagmus velocity. Current videonystagmography technology measures horizontal
and vertical eye movements only, not torsional nystagmus. Torsion is prominent with
reversal nystagmus. Measurement of torsional nystagmus currently relies on the use
of scleral coils which is not practical in a large-scale clinical study.
Conclusion
Reversal nystagmus is commonly demonstrated in individuals with posterior canal BPPV,
canalithiasis type. It is frequently evoked even when there is no nystagmus with the
dependent position of Dix-Hallpike testing. Observation of reversal nystagmus should
be considered as an option with standard Dix-Hallpike testing especially in cases
where no nystagmus is evoked with the dependent position of Dix-Hallpike testing.
