I read with interest the editorial by Furman
and Hain [1] concerning the home treatment of benign paroxysmal
positional vertigo (BPPV). This is also reported by Radtke et al. [2,3] The first two treatments were
designed when the understanding of the mechanism of the disease
was erroneous. The condition was known as
cupulolithiasis, believed to result from adventitious deposits in the
cupula of the posterior semicircular canal (PSC) changing the organ into a
gravity sensor.
Following the observations of Parnes [4], it was accepted
that the pathology of BPPV consisted of the presence in the fluid of the
PSC of aggregated otoconia detached from the vestibular maculae, changing
the hydrodynamics of the endolymphatic fluid inside the canal. The result
is an abnormal function of the crista sensory organ, albeit with different
characteristics than the predicted by cupulolithiasis, and more consistent
with clinical observations whereby vertigo is produced by quick head
rotations only in the plane of the affected PSC, a key in the diagnosis of
the condition.
Epley’s article [5] concerning the canalith repositioning
procedure as a treatment for BPPV provided strong evidence that particles
could be extracted from the canal by rotating the patient’s head in the
geometrical plane of the canal, facilitating the particle’s excursion
towards the vestibule as propelled by the force of the gravitational
vector upon the slug of heavier particles if executed within an
appropriate time course. The success of the standard Epley maneuver for
treatment of the PSC variety of BPPV has been reported as having an 88% success rate [6], and the new understanding of the pathophysiology has been shown
to be theoretically correct [7,8].
Using the modified Epley maneuver, as proposed in Radtke’s paper [3] does not result in the removal of the particles from
the canal. After one day of treatment, more than 80% of patients
were still vertiginous (e.g., Figs. 2 of Refs. 2 and 3), raising questions
about the effectiveness of the treatment as a repositioning maneuver.
What is it about the modified Epley maneuver that could account for the
disparity? In the standard Epley maneuver (during steps 1 and
2), the head is hanging 30-40 degrees from the horizontal plane below the
plane of a hard table surface where the patient rests during the test. This is to
facilitate the relocation of particles toward the distal limb of the canal
(e.g., see Figs. 9-2 and 9-3 of Ref. 9).
During step 3, the particles pass
the zenith of the canal curvature to enter the common crux and progress
away toward the vestibule where they enter during the 4th step. As
illustrated in the two papers by Radtke, the angle of head extension
appears to be smaller than necessary based on the well-known anatomy of the canals. More importantly, in the
unsupervised home exercises, the maneuver is subject to uncontrolled
errors due to either the patient’s incorrect execution (being vertiginous
at the time) or to differences in accessory equipment (e.g., table,
pillows.). The modified Epley maneuver obviously does not accomplish
the removal of the particles from the canal as well as the standard Epley.
Instead, the modified Epley represents no more than a variation of the
Semont Liberatory Maneuver, a type of “shake and loose” treatment.
Radtke et al should have attempted to cure the BPPV
with the standard Epley when they gave the patient
instructions on how to conduct the modified Epley procedure at home. It
would have not taken any additional “costly and time consuming medical
care.” Patients treated with maneuvers other than the standard Epley are
unknowingly subjected to unnecessary daily vertiginous distress that can
be avoided by correct treatment.
The current understanding of the condition is that patients with
BPPV of the posterior canal variety should be properly diagnosed, to avoid other coincidental vertigo provoking pathologies. They should be treated
immediately with the standard Epley repositioning maneuver because it is
noninvasive, quick and effective, and has minimal contraindications.
Furthermore, if treatment is not
successful, or there is a recurrence, the relapses do not necessarily
take place in the same canal or with the same pathology and require other
therapeutic procedures. [6] A follow-up visit one week after the
procedure reassures the patient or allows for additional treatment if needed.
There are many important questions yet to be answered about the cause
of the majority of cases of BPPV. Is it due to aging, degenerative,
metabolic or infectious causes? Almost half of the patients have been
found to have unsuspected vestibular paresis of the horizontal
semicircular canal or other inner ear maladies. [9] Is it possible
to diagnose the condition in the at-risk population before the attacks
occur? What therapeutic steps can be taken to avoid their recurrence?
There is very limited information about the etiology and treatment of
other varieties of BPPV involving the other semicircular canals. Research has to move
forward on the basis of clear understanding of the advances made so far.
Holding onto old concepts is not the enlightened course to follow.
Endorsement of the Brandt-Daroff,
Semont, or modified Epley maneuvers for unsupervised home treatment of
BPPV is a disservice to patients and places them unnecessarily at risk for
accidents.
References
1. Furman JM, Hain TC. “Do try this at home” Self-treatment of BPPV.
Neurology 2004;63:8-9.
2. Radtke A, Neuhauser H, von Brevern M, Lempert T. A modified Epley’s
procedure for self-treatment of benign paroxysmal positional vertigo. Neurology 1999;53:1358-1360.
3. Radtke A, von Brevern M, TielWilck K, Mainz-Perchalla A, Neuhauser H,
Lempert T. Self-treatment of benign paroxysmal positional vertigo; Semont
maneuver vs Epley procedure. Neurology 2004;63:150-152.
4. Parnes LS, McClure JA. Free-floating endolymph particles: A new
operative finding during posterior semicircular canal occlusion.
Laryngoscope 1992;102:988-992.
5. Epley JM. The canalith repositioning procedure: for treatment of
benign paroxysmal position vertigo. Otolarynogl Head Neck Surg
1992;107:399-404.
6. Honrubia V, Baloh RW, Harris MR, Jacobson KM. Paroxysmal Positional
Vertigo Syndrome. Am J Otology 1999;20:465-470.
7. Honrubia V, House M. Mechanism of posterior semicircular canal
stimulation in patients with benign paroxysmal positional vertigo. Acta
Oto-Laryngologica, 2001; 21:234-240.
8. House M, Honrubia V. Theoretical Models for the Mechanisms of Benign
Paroxysmal Positional Vertigo. Audiology & Neuro-Otology 2003;8:91-
99.
9. Baloh RW, Honrubia V. Clinical Neurophysiology of the Vestibular
System. FA Davis, Philadelphia. Third Ed., 2001.