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| Journal of the New Zealand Medical Association,
19-September-2008, Vol 121 No 1282
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Superior canal benign positional vertigo
Jeremy Hornibrook
The most common cause of vertigo is benign positional
vertigo (BPV). Positionally-induced vertigo was recognised early in the
20th Century, but the clinical features of
“classical” BPV were not described until 1952 by Dix and
Hallpike,1 based on their provocative
positional test. The patient is seated near the end of the examination couch,
preferably wearing Fenzel glasses to magnify the eyes for the examiner.
The head is turned 45 degrees to one side and the patient
tipped back with the head down. After a few seconds the patient experiences
vertigo and has torsional geotropic (fast phase towards the ground) nystagmus
seen when the eyes are directed towards the symptomatic side. The nystagmus and
vertigo usually last less than 30 seconds. When the patient is sat up, the
nystagmus direction reverses.
Dix and Hallpike suspected the disorder was caused by an
abnormality of the otolith organs. With the advantage of high quality temporal
bone histology Schuknecht2 thought that the
nystagmus was explained by a posterior canal receptor made heavy, most likely by
an otoconial particle which had become attached to it.
Early attempts at treatment were based on that assumption.
Others, including Epley, made models and concluded that the
“classical” signs were better explained by a particle loose in the
posterior canal. A photograph of otoconia in a surgically opened posterior canal
and the eventual acceptance that repositioning treatments work have confirmed
the mechanism.3
In the early days of vestibular research (before video
cameras) torsional nystagmus was difficult to record. Electronystagmographic
recordings favoured nystagmus in the horizontal plane. However, it was by this
technique that the first recordings of horizontal canal BPV were
made.4 These confirmed Epley’s prediction
that BPV could be caused by otoconia in any semicircular
canal.5 Epley presented a chart showing the
likely pattern of nystagmus for each type.
In the 1960s, experiments in cats had defined the unique
three-neuron connection between canal receptors and the extraocular
muscles.6 Each receptor is connected to one
ipsilateral and one contralateral muscle. The second-order neurons are either
excitatory (to the agonist muscles) or inhibitory (to the antagonist muscles).
The connections for a posterior canal receptor and a superior canal receptor in
a left ear are shown in Figure 1 and Figure 2.
In “classical” posterior canal BPV, a
provocative positional test will cause an ampullo-fugal (excitatory) deflection
of the posterior canal receptor resulting in a torsional apogeotropic
(anatomically downward) deflection of the eyes, followed by their fast-phase
return (geotropic or anatomically upward). If there were a particle in a
superior canal, a similar ampullofugal receptor deflection could occur during a
provocative positional test when the symptomatic ear is upper-most (Figure
2).
Figure 1. Left posterior canal benign
positional vertigo. Left ear down
(IR=inferior rectus, SO=superior oblique, SR=superior
rectus, IO=inferior oblique)
 Figure 2. Left superior canal benign positional
vertigo. Left ear up
(IO=inferior oblique, SR=superior rectus, SO=superior
oblique, IR=inferior rectus)
 Case reportA 51-year-old female had an approximately 10-year history of
episodic positional vertigo lasting days which would occur twice a year. In 2000
it was confirmed as being “classical” left posterior canal BPV. In
2004 she presented after having awoken with postional vertigo. When sitting she
had no nystagmus.
A Hallpike provocative positional test was performed (Figure
3). With the left ear down there was no response. With the right ear down, after
5 seconds, she experienced vertigo and there was a nystagmus whose fast phase
was apogeotropic (anatomically downward), which ceased when she sat up. This
implied BPV generated by a superior canal receptor, most likely in the opposite
(left, upper) ear.
On that presumption two reverse (beginning with
left ear up) Epley canalith repositioning procedure
sequences7 were performed, after which no
positional nystagmus could be elicited. She remained free of symptoms until
approximately 6 months later when she presented with horizontal canal BPV in the
same ear. This patient has now had all three types of BPV in one ear.
Figure 3. Video-clip. Hallpike positional test
with right ear down and left ear up. Downbeat nystagmus with a latency of 5
seconds and a small torsional component
video.mpeg (8MB)
DiscussionVertical nystagmus, particularly downbeat, should alert the
clinician to the possibility of central pathology. Caudal brainstem compression
(e.g. Chiari malformation, hereditary spinocerebellar ataxia, and long-term
lithium therapy) is in approximately half of the main causes. In the other half
no cause is found.8
Until relatively recently it was assumed that
positionally-induced nystagmus that was not "classical" BPV must have a central
cause. The discovery of horizontal canal BPV explained most of the variations.
In 1995, Epley’s elegant description of superior canal BPV was
theoretical.
In 1994, Brandt9 had
alluded to “...the rare anterior [superior] canal BPPV, the spontaneous
symptoms occur when the affected ear is uppermost”. However, the first
detailed cases are attributed to Susan
Herdman10 who described two patients whose
positionally-induced vertigo was accompanied by downbeat and torsional nystagmus
likely to be caused by a superior canal receptor, and which ceased after
repositioning treatment appropriate for BPV. Subsequently superior canal BPV has
been recognised and reported by
others10–15 in whose series it represents
approximately 1% of all BPV diagnoses.
Bertholon et al13 reviewed
50 consecutive patients who had positionally-induced Nystagmus. In 75% there was
a central cause (multiple system atrophy, cerebellar degeneration and other
miscellaneous causes). In nearly all the downbeat nystagmus was triggered by the
Hallpike test, and its onset was immediate.
In 25% (“idiopathic”) who presented with
positional vertigo, the Hallpike test or a head-hanging test elicited vertigo
and downbeat nystagmus with a short latency. In half the subjects a torsional
component could be seen through Frenzel glasses, but in one it was only
discernible by video-imaging. Aw et al15
studied forty-four consecutive patients who had not responded to conventional
office repositioning treatments with 3-dimensional search coils in a 2-axis
whole-body rotator. Seven had downbeat nystagmus with a torsional component
assumed to indicate the symptomatic superior canal. All responded to a
“head-over-heels” forward rotation in the plane of the identified
canal.
Superior canal BPV is assumed to be rare because the
posterior arm of the canal descends directly to the common crus, and debris
within it should clear easily. For that reason, like horizontal canal BPV, it
often resolves quickly with changes in head orientation likely to occur in
everyday activities, or turning over in bed.
Differences in the orientation of the ampullary segments of
the posterior and superior canals explain why (1) superior canal BPV can be
elicited by a Hallpike test to either side, or to a head-hanging test, and (2)
the smaller torsional component for superior canal BPV, which is predominantly
downbeat.13,15
In summary, superior canal BPV is now recognised as rare
form of BPV, observed in approximately 1% of large series. The presenting
symptom is positional vertigo. As with all forms of BPV the patient
must experience vertigo on a Hallpike positional test, which may be
positive to either side, or on a head-hanging test.
The nystagmus has a short latency and is downbeat, with a
torsional component which may be indiscernible to clinical observation. A past
history of posterior or horizontal canal BPV supports the likelihood of superior
canal BPV. Otherwise, in a patient with positionally-induced downbeat nystagmus,
the absence of these features and non-response to respositioning treatment makes
a central cause likely.
Author information: Jeremy Hornibrook,
Otolaryngologist–Head & Neck Surgeon, Christchurch Hospital (and
Adjunct Professor in the Department of Communication Disorders, University of
Canterbury), Christchurch
Acknowledgment: I thank Professor GM
Halmagyii (at the Royal Prince Alfred Hospital, Sydney) for verification of the
observations and conclusions and for helpful comments.
Correspondence: Jeremy Hornibrook,
Department of Otolaryngology-HNS, Christchurch Hospital, Private Bag 4710
Christchurch, New Zealand. Fax: +64 (0)3 364 0273; email jhornibrook@paradise.net.nz
References:
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