Particle Repositioning Maneuver for Benign Paroxysmal Positional Vertigo

D. Bradley Welling, MD; Douglas E. Barnes, MD

The recent demonstration of free-floating particles in the endolymph of the posterior semicircular canal in patients with benign paroxysmal positional vertigo (BPPV)1 has renewed interest in the physiology and treatment of this entity. The particle repositioning maneuver (PRM) relocates the free-floating particles from the posterior semicircular canal back into the utricle, relieving the patient of bothersome, often long-standing vertigo.

This report represents a prospective study of 27 consecutive patients seen with a diagnosis of BPPV. Eighty-four percent of the patients treated with the particle repositioning maneuver who had no other associated pathology were cured or significantly improved with this new technique. Two patients who failed conservative management went on to surgical intervention with the posterior semicircular canal occlusion.

The authors find the particle repositioning maneuver effective for many patients with benign positional vertigo and recommend it as the first-line treatment modality for BPPV.

INTRODUCTION

Benign paroxysmal positional vertigo was first described by Barany² in 192l and was more fully defined by Dix and Hallpike3 in 1952. Dix and Hallpike described the maneuver, which places the posterior semicircular canal in the earth vertical position to allow stimulation of the posterior canal cupula by gravity when BPPV is present. They also identified correctly the undermost ear as the ear causing the rotatory nystagmus which is characteristic of BPPV. The nystagmus classically has a latent onset of several seconds and fatigues with repetition. The course of BPPV was traditionally thought to be self-limited and therefore termed “benign” however Baloh and Honrubia4 reported symptoms longer than 1 year in one third of their 240 patients with BPPV.

Schuknecht and Ruby5 described basophilic deposits of particulate matter attached to the cupula of the posterior semicircular canal in histologic sections from patients with BPPV. It was theorized that the particulate matter made the crista ampullaris sensitive to gravitational pull in various head positions. With the demonstration of free-floating particles in the semicircular canal by Parnes and McClure1 at the time of posterior semicircular canal occlusion, the mechanism of BPPV has become more evident. This finding helps explain the brief latent period for the onset of vertigo when the posterior canal is placed into the vertical position. Several seconds are necessary for the hydrodynamic drag of the particles to begin to pull on the affected cupula. This results in the classical rotatory nystagmus directed toward the floor (i.e., counterclockwise with the right ear down and clockwise with the left ear down). Resumption of the upright position then incites rotatory nystagmus in the opposite direction as the particles settle back into the inferior-most aspect of the posterior canal with the Hallpike maneuver.

The fatigability of the Hallpike maneuver with repetition is most likely explained by dispersion of the clumped particulate matter thereby reducing the hydrodynamic drag on the cupula. If the patient is in a stable position for 10 minutes, the particles reaccumulate and again become able to stimulate the neuroepithelium of the cupula as head position changes.

Placing the patient in the contralateral ear down position prior to assuming the offending position does not cause nystagmus as the particles are impeded by the cupula and do not cause the necessary hydrodynamic drag or cupular deflection to cause rotatory nystagmus.

Treatment of BPPV has ranged from expectant nonintervention to destructive surgical procedures. Cawthorne6 advocated “vestibular habituation therapy” wherein the patient would repetitively assume the position of maximal stimulation with the affected ear in the dependent or floor down position. This was thought to build tolerance to the stimulus. Selective ablation via the singular nerve neurectomy as reported by Gacek7 or the posterior canal occlusion as reported by Parnes and McClure8 have been advocated for intractable disease. Nonsurgical management has also included specific exercises designed by Brandt and Daroff9 and Semont, et $a l.^{10}$ to disperse heavy debris from the labyrinth with variable success. Epleyll summarized the historical development of treatment for BPPV and added the use of a bone vibrator to supplement the particle repositioning maneuver (PRM). He recently reported a $100\%$ success rate in 30 patients treated.

Fig..Topleft.AftertheHallikemanuverisperformed,thepatientisleft inthe sittingpositionforiminutes to allow theparticlestoaccumulateinthemostdependentpositionoftheposteriorcanal.Topright.Theheadisextendedoverthe edge ofthetable withtheaffctedeardownandthevertexoftheheadpointedtoward theflooratapproximatelya20- degree angle.Bottomleft.The patientis then rotated18odegrees fromthestartingposition now withtheoppositeear downandtheheadagainpointedtowardthefloorNotethe movementoftheparticlestowardthecommoncrus.Bottom right.nthis position,the particles should move intotheutricle bywayof thecommoncrus.Once the nystagmusand vertigo haveceased,the patientisagain brought into the sitting position andthe nystagmusagain isobserved at the completion of the procedure.

MATERLALSANDMETHODS

All patients with the classic findings of BPPV on the Hallpike maneuver to present at The Ohio State University from March 1992 to December 1992 were included in this prospective study. This resulted in a series of 27 patients ranging in age from 32 to 75 years with a mean of 53 years. The mean and median duration of symptoms were 25 months and 6 months, respectively, with a range of 2 weeks to 10 years. Each patient underwent a complete otologic and neurotologic evaluation. Vestibular testing was obtained when appropriate.

Procedure

The diagnosis of BPPV and identification of the offending ear is established by the Hallpike maneuver. Following the Hallpike maneuver, the patient is left in a sitting position for 10 minutes to allow the particles to accumulate in the most gravity-dependent portion of the posterior semicircular canal $\scriptstyle(c f.$ Fig. 1 for a complete description of the particle repositioning maneuver).

The patient is seated on an examination table close enough to the end so the neck may be extended over the edge of the table when the patient becomes supine. The patient is then placed into the supine position with the head rotated

45 degrees toward the affected ear with the neck slightly extended over the edge of the table. The vertex of the head is pointed toward the floor at approximately a 20-degree angle. The subjective report of vertigo is recorded along with the nystagmus latency, duration, and direction. When all vertigo has completely subsided, the patient is asked to roll slowly onto their side opposite the offending ear. As this is done, the examiner gently rotates the patient’s head 180 degrees from the starting position maintaining the vertex angulation toward the floor. The patient’s eyes are examined for the direction of the vertigo as the maneuver is performed by watching the scleral blood vessels. The examiner would, when necessary, gently retract the upper lid to allow maximal visualization of the nystagmus if present. Directing the patient’s gaze toward the floor accentuates the rotatory component of the nystagmus, thus making it somewhat easier to determine the direction. If the rotatory nystagmus continues in the direction it began when assuming the Hallpike position as the patient rolls over, the particles are moving in the correct direction up into the common crus. If, however, the direction of the rotatory nystagmus changes with this part of the maneuver, it is assumed that the particulate matter is attached to the cupula of the posterior canal thus allowing gravity to act in the opposite direction on the cupula. An attempt is then made to loosen the particles by gently shaking the head prior to repeating the repositioning. After the patient has been rolled into the lateral position and all vertigo stops, they are assisted in resuming the sitting position. Again the eyes are observed for nystagmus and the direction noted.

An attempt to reduce visual fixation has not been made as all patients tested have had sufficiently strong nystagmus to be readily observed in spite of fixation. No medication was given prior to performing the maneuver; however, the patients are reassured that they will not be allowed to fall during the repositioning as the vertigo is at times severe enough to warrant such a concern.

The patients are then asked to maintain an upright position for the next 48 hours to prevent the particulate matter from reentering the posterior canal. Sleeping with the head elevated at no less than a 45-degree angle from the floor is recommended. The patients are allowed to resume normal activities and head positions after 2 days and followup is obtained within 1 week. For the purpose of this study, a second contact was made by telephone for long-term followup. If the patients failed the first attempt at the particle repositioning,a second maneuver was performed on followup. If the repositioning_ maneuver was not successful a second time, conventional Cawthorne’s exercises were given and the patient was referred to our vestibular physical therapist for specific instruction in habituation exercises. Vascular studies and a magnetic resonance imaging (MRI) scan were considered at this point. Patients who failed conservative measures including the particle repositioning maneuver twice and habituation exercises were considered to be candidates for surgical intervention.

RESULTS

. Of the 27 patients to present with classic findings of BPPV on Hallpike maneuver, 2 patients were discovered to have concomitant pathology. One had a perilymphatic fistula associated with a previous stapedectomy; the fistula was repaired surgically. The second patient was found, after failing the particle repositioning technique twice, to have a cerebral glioma on MRI. These two patients were therefore excluded. Of the remaining 25 patients who underwent_the particle repositioning maneuver, 19 had complete resolution of all symptoms and 2 had complete resolution of the positional vertigo but some degree of unsteadiness persisted. This accounts for an $84\%$ success rate with 21 of 25 patients cured or markedly improved.

Four patients did not have resolution with the particle repositioning technique. Two are currently using habituation exercises with reported improvement and the remaining two patients who failed both the PRM and Cawthorne’s exercises went on to operative intervention with a posterior canal occlusion.

DISCUSSION

The degree of difficulty of diagnosis and treatment of many balance disorders has made the addition of the particle repositioning technique to our armamentarium for BPPV patients particularly pleasing. Some of the most grateful patients are those who have successfully had their BPPV alleviated by this useful technique. This attests to the severity of symptoms in some of the patients with this “benign” disease which, as noted earlier by Baloh and Honrubia,4 is not necessarily self-limited or benign. The term “intractable” is appropriately substituted for “benign” in cases of paroxysmal positional vertigo when the symptoms do not spontaneously resolve within 3 months. Ten of our patients had symptoms longer than 1 year but became immediately symptom free following the particle repositioning maneuver.

The mechanism of vestibular habituation therapy or Cawthorne’s exercises for BPPV has been assumed to be via central nervous system compensation, but it is also likely that the mechanical force of the habituation exercise helps disperse and eventually disrupt or dissolve the particles, thus hastening recovery.

Interestingly, several of our patients reported an increased instability following the particle reposition maneuver when walking or stopping suddenly. This is probably due to the new position of the particulate matter in the vestibule resting against the utricle in an unfamiliar position. An attempt was made to document a change in postural stability pre– and postparticle repositioning using dynamic posturography; however no objective change was observed in the patients tested. The new sensation has spontaneously resolved in all patients within 24 to 48 hours.

Two of our patients were found to have concomitant pathology. One patient presented with classical BPPV symptoms but was found to have a glioma after progressive neurological deterioration ensued. A second patient had a history of previous stapedectomy and had fluctuating hearing in her only hearing ear along with classic findings of BPPV on a Hallpike maneuver. A perilymphatic fistula was found at tympanotomy with a slipped prosthesis. These two patients serve as a reminder that concomitant pathology may occur with BPPV, thus emphasizing the need for a thorough evaluation and follow-up of each patient with apparent BPPV. Failure to respond to the maneuver promptly or the emergence of new symptoms warrant continued investigation such as an MRI. This report addresses only patients with classical symptoms of BPPV; however atypical symptoms of positional vertigo may be due to vascular compromise, central nervous system dysfunction, or dysautonomia and warrant further work-up.

The direction of the nystagmus with the PRM was suggestive of being useful in predicting success with the procedure but was at times difficult to observe. Rotatory nystagmus which continued in the same direction as the initiating Hallpike position when the head was rolled 18o degrees was generally considered a positive indicator for success of the procedure. All patients who clearly had the same direction of rotation with the maneuver went on to have a successful result. When the direction of the rotatory nystagmus changed with the maneuver, it was believed that the particles were attached to the cupula of the posterior canal and therefore could not be easily displaced. The latter condition may represent true cupulolithiasis. One patient clearly demonstrated a reversal of the rotatory nystagmus direction and went on to fail conservative treatment but was cured of positional vertigo with a posterior canal occlusion. These findings support the possibility of two different clinical entities, one caused by free-floating particles and one caused by particles attached firmly to the cupula preventing dislodgement with the maneuver

as described.

The long-term likelihood of recurrence following this maneuver is as yet unknown, but the maneuver can be easily repeated if necessary. Thus far we have had only two patients with recurrent symptoms following a successful repositioning maneuver.

In Eply’s11 report of $100\%$ success using a similar procedure, he incorporated the use of a bone vibrator (either a conventional audiometric bone vibrator at ${700}\mathrm{{Hz}}$ or an Oster handheld vibrator at $80\mathbb{H}\mathbf{z}.$ . This additional vibration may dislodge particulate matter adherent to the cupula and thereby improve the overall results when used concomitantly with the particle repositioning maneuver.

The two patients from this study who had posterior semicircular canal occlusions performed for intractable positional vertigo after failure of conservative measures had resolution of their positional vertigo. We have performed a total of five canal occlusions. All patients had a temporary mild mixed hearing loss in the operated ear which resolved over a 2-month period. There has been no permanent hearing loss, which supports the safety of this procedure as reported by Parnes and McClure.8

CONCLUSIONS

The particle repositioning technique is useful for the management of BPPV. It has been effective in $84\%$ of our patients thus far and is therefore recommended as the first line of therapy for patients with BPPV. Patients who do not respond promptly to the particle repositioning technique should undergo further investigation.

BIBLIOGRAPHY

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2. Barany, R., cited by Dix, R. and Hallpike, C.S.: Diagnose von Krankheitserscheinungen im Bereiche des Otolithenapparates. Acta Otolaryngol (Stockh), 2:434-437,1921.
   
3. Dix, R. and Hallpike, C.S.: The Pathology, Symptomatology, and Diagnosis of Certain Common Disorders of the Vestibular System. Proc R Soc Med, 54:341-354, 1952.
   4.Baloh, R.W. and Honrubia, V: Benign Positional Vetigo. In: Clinical Neurophysiology of the Vestibular System (2nd ed.). F.A. Davis $\mathbf{Co}_{\bullet}$ Philadelphia, pp. 209-213,1990.
   
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6. Gacek, R.: Singular Neurectomy Update. II. Review of 102 Cases. LARYNGOSCOPE,101:855-862,1991.
   
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8. Brandt, T. and Daroff R.B.: Physical Therapy for Benign Paroxysmal Positional Vertigo. Arch Otolaryngol, 106:484- 485,1980.
   
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