Crevits, Luc

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SHORT REPORTTreatment of anterior canal benign paroxysmal positionalvertigo by a prolonged forced position procedureL Crevits. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .J Neurol Neurosurg Psychiatry 2004;75:779–781. doi: 10.1136/jnnp.2003.025478This report presents a therapeutic procedure for refractorybenign paroxysmal positional vertigo (antBPPV) of theanterior canal. Two patients with refractory antBPPV weretreated by a prolonged forced position procedure (PFPP). Thetechnique is based on the assumption that the pathophysio-logical mechanism of antBPPV is similar to that generatingposterior canal canalolithiasis. The patients recovered fromrefractory antBPPV after one or more PFPPs. The rationale forthis therapy is that when the patient lies in the proposedforced position, the affected anterior canal is uppermost in analmost gravitationally vertical position. If the patient remainsin this position for several hours, the floating particles lying inthe non-ampullary arm of the canal can gradually slip out ofthe canal towards the vestibule due to gravity. Werecommend trying PFPP when the side of lithiasis cannot bedetermined, in cases that are resistant to particle reposition-ing canal manoeuvres, and before considering canalplugging for refractory antBPPV.Benign paroxysmal positional vertigo (BPPV) usuallypresents as a distinct clinical syndrome characterisedby brief spells of violent rotational vertigo induced bychanges in head position. The diagnosis is confirmed bytypical findings of the Dix-Hallpike positioning tests.1 2 BPPVcan involve any of the semicircular canals (SC), although theposterior SC type is by far the most frequent. BPPVcommonly is attributed to either canalolithiasis or cupulo-lithiasis (debris free floating in the canal or attached to thecupula).1 Although remission is common and the condition isbenign, persisting episodic BPPV may be disruptive forpatients. Therapy is mechanical and aimed at moving thefree floating debris into the vestibule. However, the regimenmust be specific to type and location of the lithiasis.The anterior SC BPPV (antBPPV) is not frequent. Honrubiaet al described four patients (1.3%) with anterior SCcanalolithiasis out of 292 patients with BPPV.2 The initialevaluation of this group provides a clear indication of therelative involvement of the anterior SC. An incidence of lessthan 2% of BPPV cases was confirmed in a retrospectiveseries.3 Anterior SC canalolithiasis is assumed to be rare dueto its anatomically superior position during most activitiesand the posterior arm of the anterior SC descending directlyinto the common crus and vestibule. Thus, debris within theanterior canal should be self clearing. It is unclear why thisdoes not happen in antBPPV. The almost vertical orientationof the ampullary segment of the anterior SC could result inextensive contact between the debris and the cupula, thusfacilitating cupulolithiasis. In contrast to canalolithiasis,cupulolithiasis does not show adaptation and habituationof vertigo and nystagmus.2In anterior SC canalolithiasis, the nystagmus is mainlydown beating with a smaller torsional component. Thetorsional component may be weak because of the predomi-nantly sagittal orientation of the anterior canal, and may notbe readily seen clinically. Video-oculography may be neces-sary for its detection. Moreover, the direction of the torsionalcomponent does not seem to be uniform or is disputed.3–5 It isstriking that the Dix-Hallpike test could provoke a nystagmusfrom either side. This can be explained by the upward verticalorientation of the ampullary segment of the anterior SC inthe normal upright head position. This orientation requires afurther downward movement of the head, often achievedwith the straight head-hanging position, to provoke migra-tion of the canaliths.5Therapeutic information for antBPPV is extremely scarce.Honrubia et al mention a ‘‘reverse Epley’’ particle reposition-ing procedure (PRP) and obtained success in two of fourpatients.2 No further details of the manoeuvre were given.Rahko studied a remarkably large group (57 patients) thathad residual symptoms of antBPPV after treatment forposterior and horizontal BPPV.6 He applied a treatmentmanoeuvre whereby the patient lies on the healthy side, thehead is tilted downwards 45 ,˚ then horizontally, thenupwards 45˚for 30 seconds each, and finally the patient sitsup and stays there, well supported, for at least three minutes.‘‘Good results’’ were ascribed to the fact that the other canalshad been treated before. However, the diagnosis and resultswere not based on nystagmus characteristics and relied onmethods that have not been validated.We introduce a prolonged forced position procedure(PFPP) as treatment for refractory antBPPV.METHODSPatientsCase 1A 50 year old woman complained of episodic vertigo lastingseveral hours and occurring once a month since four years.The vertigo was accompanied by tinnitus on the left side. Shewas prescribed betahistine.She presented to the otoneurological unit because of a newcomplaint of short lasting paroxysmal positional vertigo sinceseveral weeks. The positional vertigo was brief (seconds),consisting of a sense of spinning and manifesting mainly onlying down. Prior history included hypertension andmigraine. There was no history of trauma.The right Dix-Hallpike manoeuvre triggered positionalvertigo and a down beating nystagmus (DN)—that is, fastphase beating to the chin. The DN had a latency of fourseconds, a duration of 15 seconds and habituated onrepeated testing. No torsional component could be detectedunder Frenzel’s glasses. In the left Dix-Hallpike and in thehead-hanging position, a similar DN pattern could be elicited,Abbreviations: AntBPPV, anterior SC BPPV; BPPV, benign paroxysmalpositional vertigo; DN, down beating nystagmus; MRI, magneticresonance imaging; PFPP, prolonged forced position procedure; PRP,particle repositioning procedure; SC, semicircular canal779www.jnnp.combut with a lesser intensity, and reversal of the nystagmus didnot occur. Horizontal SC manoeuvres were negative.Neurological examination was normal.Caloric and rotatory responses showed a directionalpreponderance of the induced nystagmus to the right. Puretone audiogram, electrocochleogram and brainstem auditoryevoked potentials were normal. A brain magnetic resonanceimaging (MRI) scan was unremarkable.The longer lasting episodic vertigo with tinnitus on the leftand the vestibular findings suggested left labyrinthine involve-ment. The positional tests were compatible with antBPPV.Because the side of the antBPPV could not be determined,we tried a PFPP (see below) instead of a reverse Epley PRP.Two days after the PFPP, the patient was re-examined and nonystagmus could be elicited on positional tests. She remainedfree of vertigo for three months. Then she again experiencedvery short bursts of positional vertigo. In the right Dix-Hallpike, a DN of duration three seconds was seen after alatency of 30 seconds. The complaints, however, were notconsidered severe enough to be treated. However, after fivemonths, the vertigo became more embarrassing. On exam-ination, the right Dix-Hallpike manoeuvre elicited a transientDN and a torsional component was observed. The direction,however, could not be specified under Frenzel’s glasses. Areverse Epley PRP remained unsuccessful after two trials. Asecond PFPP was successful. No positional vertigo or nys-tagmus could be elicited immediately after the PFPP andduring a follow up period of three months. Then the patienthad a new episode of antBPPV. Neurological examinationremained normal and a repeat MRI of the brain and inner eardid not reveal any anatomical anomalies, especially theanterior SC showed normal morphology on both sides. Thepatient was treated with a PFPP for the third time.Case 2This 57 year old woman was known to have Me´nie`re’sdisease since 13 years and was being treated with betahistine.The history included a skull fracture of the left occipital bonein a traffic accident 36 years ago, one tonic clonic seizure fouryears ago that had been treated with carbamazepine for somemonths, and several hyperventilation attacks. She presentedbecause of positional vertigo when turning over in bedespecially to the right side, since two months.The right and left Dix-Hallpike manoeuvres, as well aspositioning to head-hanging evoked positional vertigo and aDN (fast phase beating to the chin). The pattern of the DNwas essentially similar in the three positions. Latency was of3–5 seconds, duration 5–15 seconds and habituationoccurred on repeated testing. In the left Dix-Hallpikeposition, a discrete torsional (geotropic) component wassuspected and reversal of the nystagmus did not occur.Horizontal canal manoeuvres were negative. Neurologicalexamination was unremarkable.Vestibular tests revealed caloric hypofunction on the right.Pure tone audiometry showed a right neurosensorial hearingloss of 45 db, nearly flat for frequencies from 250 Hz to8000 Hz. Electrocochleography was disturbed on the right fortones and clicks. Electroencephalography, MRI of the poster-ior fossa and x rays of the craniocervical junction werenegative.The patient was admitted for a PFPP (see below). However,the procedure had to be terminated prematurely due to neckpain. Because of refractory positional vertigo for another fivemonths, the PFPP was tried again, but now with myorelaxa-tion using diazepam. The patient was re-examined immedi-ately after the PFPP and twice during a follow up period ofseven months. No positional nystagmus could be provokedand the patient remained free of vertigo, except for onetypical Me´nie`re attack.Prolonged forced position procedureFor the PFPP, the patients were admitted to hospital. In anorthopaedic bed, the positional test with hanging head wasfirst carried out to induce DN and to be sure of the provokingposition. Thus the patient was rapidly moved from sitting tolying supine with the head bent backwards as far aspossible—that is, with the vertex about 60˚ below thehorizontal. The head was supported in this hanging positionfor 30 minutes. During this period, the debris were thoughtto sediment into the superior part of the anterior canal (nowthe most dependent) and clot (fig 1). Then the head wasmoved quickly forwards, as far as possible—that is, with thevertex near the vertical. Due to inertia, the canaliths lagsomewhat behind and then move to the common crus of theanterior and the posterior canals (fig 1). In this forcedposition, the head was fastened with the help of a pulleysystem that allowed the head to hang slightly (fig 2). Thepatient was not allowed to stand up. After 24 hours, thepatient was asked to sit and stay in the sitting position withthe head straight for some minutes to allow the clot to movefurther in the utricle through the common crus. Followingthis no position or movement restrictions were applied. Afterthe PFPP, positional tests were repeated to verify the effectand to exclude conversion into another variant of BPPV.DISCUSSIONCentral positional nystagmus can be mistaken for BPPV. Thisis especially true for DN, being posture dependent and knownto have pluriform manifestation.7 8 DN can be caused eitherby cerebellar degeneration, Arnold-Chiari malformation andother dysfunctions of the cerebellar flocculus, or by lesions ofthe medial longitudinal fasciculus in the floor of the fourthventricle.9 Recently, Bertholon et al considered possibleanterior SC canalolithiasis in patients with positional DNwithout evidence of central nervous dysfunction.5 Oneproblem of antBPPV concerns the contradictory interpreta-tions as to whether an ipsilesional or a contralesionalHallpike manoeuvre provokes nystagmus. Due to thecoplanar orientation of the left posterior canal with the rightanterior canal, the left Hallpike manoeuvre should provoke aright antBPPV.10 However, a left–right lateralisation seemsless specific in antBPPV as in the other canal types.5 11 It hasbeen suggested that the anterior SC can be cleared ofcanaliths by using the same positioning sequence forcontralateral posterior canalolithiasis.12The present patients suffered from longstanding vestibulo-pathy of the Me´nie`re type.13 However, they presented withparoxysmal positional vertigo and manifested positional DNFigure 1 Schematic representation (lateral view) of the semicircularcanals with debris in the uppermost part of the anterior canal in thehead-hanging position. In the prolonged forced position for anteriorcanal benign paroxysmal positional vertigo, the debris moves into thecommon crus and the vestibule. ASC, PSC, HSC, anterior, posterior andhorizontal semicircular canal, respectively.780 Crevitswww.jnnp.comwith features of BPPV (latency, short duration and habitua-tion or fatigability of the nystagmus). There were no signs ofneurological disorders, especially multiple system atrophy,cerebellar degeneration, and Arnold-Chiari malformationcould be ruled out. As our patients had not been treatedbefore, their antBPPV could not be ascribed to a complicationof a PRP.4 Since the site of the lesion could not be determinedthe reverse Epley manoeuvre or the procedure of Rahko couldnot be performed although the reverse Epley PRP was triedwithout success in case 1.The reason why anterior SC canalolithiais continues for along time or relapses (case 1) could be due to theconglomerate of debris being too large, continuous produc-tion of debris, failure of disaggregating, or narrow commoncrus. It is to be noted that in our patients antBPPV mighthave been influenced by concomitant peripheral vestibulo-pathy. However, this could be coincidental. Cupulolithiasiscan be a cause of refractory BPPV; however, in the case ofcupulolithiasis less adaptation or habituation should occur.Canalith ‘‘jam’’ is another type of vestibular lithiasis. It refersto locking of the cupula in a fixed position by debris, as canoccur as a complication of a PRP.2 12 The ensuing vertigo andnystagmus, however, are not affected by head position.Hence the reason for refractory antBPPV in the presentpatients remained unclear.We applied a new therapeutic procedure for antBPPV. Ourtechnique is based on the assumption that antBPPV has apathophysiological mechanism similar to the one generatingposterior SC canalolithiasis—that is, there are some particlesheavier than endolymph that are free to move into the SCand that are capable of causing some abnormal endolym-phatic movement due to the force of gravity. Freeing thecanal of all its particles can prevent this process. This conceptled us to suggest that therapy for antBPPV would be effectivewhen the patient lies with the head fixed upward for a longtime. This forced prolonged position might allow the heavyparticles to gradually be drawn into the vestibule by the forceof gravity. Prior to the forced position, however, the debrishas to sediment in the superior part of the anterior SC withthe patient lying down in the head-hanging position asdescribed in the Methods section.Since spontaneous remission of BPPV is common,improvement cannot be clearly ascribed to therapy.However, our patients had, and ultimately recovered from,refractory antBPPV. The time course too, was very suggestiveof a relation between PFPP and remission of antBPPV. Thebest way to know whether the patients are symptom freebecause of the manoeuvre or as a result of spontaneousrecovery is to examine the patients the same day, after asufficient interval to avoid fatigability effects.14 Therefore,patients were examined immediately after the PFPP andrepeatedly during the ambulatory follow up to verify recoveryand exclude conversion into another variant of BPPV.The PFPP presented here has the advantage over PRP ofcircumventing the difficult problem of lateralisation ofantBPPV. The rather long and uncomfortable bed stay for24 hours is an inconvenience. The technique can havecomplications: if the head is brought too far forwards duringthe PFPP, the debris could move to the ampullar part of theanterior SC causing cupulolithiasis. Therefore, the pulleysystem should allow the head to hang slightly backwards.When the head bends too far backwards, the clot can descendinto the posterior SC. Fortunately, this complication caneasily be detected by a Dix-Hallpike positioning test and becured by an Epley PRP. Conversion into another variant ofBPPV can not always be avoided due to individual anatomicalvariation in orientation of the SC. Therefore, a carefulexamination after the PFPP is mandatory. A side effect ofkeeping the head in the forced position is a stiff neck andtherefore myorelaxation is indicated. We recommend tryingPFPP when the side of lithiasis cannot be determined, incases that are resistant to particle repositioning canalmanoeuvres, and before considering canal plugging inrefractory cases of antBPPV.Competing interests: none declaredCorrespondence to: Luc Crevits, MD, PhD, Department of Neurology,Oto-Neuro-Ophthalmology Unit, Ghent University Hospital, DePintelaan 185, B-9000 Ghent, Belgium, Tel: +32.9.240.45.39, Fax:+32.9.240.49.71; E-mail: luc.crevits@ugent.beReceived 7 August 2003In revised form 12 October 2003Accepted 22 October 2003REFERENCES1 Bronstein AM. Benign paroxysmal positional vertigo: some recent advances.Curr Opin Neurol 2003;16:1–3.2 Honrubia V, Baloh RW, Harris MR, et al. Paroxysmal positional vertigosyndrome. Am J Otol 1999;20:465–70.3 Korres S, Balatsouras DG, Kaberos A, et al. Occurrence of semicircular canalinvolvement in benign paroxysmal positional vertigo. Otol Neurotol2002;23:926–32.4 Herdman S, Tusa RJ. Complications of the canalith repositioning procedure.Arch Otolaryngol Head Surg 1996;122:281–6.5 Bertholon P, Bronstein AM, Davies RA, et al. Positional downbeatingnystagmus in 50 patients: cerebellar disorders and possible anteriorsemicircular canalithiasis. J Neurol Neurosurg Psychiatry 2002;72:366–72.6 Rahko T. The test and treatment methods of benign paroxysmal positionalvertigo and an addition of the management of vertigo due to the superiorvestibular canal (BPPV-SC). Clin Otolaryngol 2002;27:392–5.7 Crevits L. Downbeat nystagmus. Pluriform manifestation. Neuro-ophthalmology 1991;11:103–4.8 Crevits L, Reynaert C. Posture dependent direction reversal of spontaneousvertical nystagmus. Neuro-ophthalmology 1991;11:285–7.9 Baloh RW, Spooner JW. Downbeat nystagmus: a type of central vestibularnystagmus. Neurology 1981;31:304–10.10 Bronstein AM. Vestibular reflexes and positional manoeuvres. J NeurolNeurosurg Psychiatry 2003;74:289–93.11 Brantberg K, Bergenius J. Treatment of anterior benign paroxysmal positionalvertigo by canal plugging: a case report. Acta Otolaryngol 2002;122:28–30.12 Epley JM. Human experience with canalith repositioning maneuvers. N Y AcadSci 2001;942:179–91.13 American Academy of Otolaryngology, Committee on Hearing andEquilibrium. Guidelines for the diagnosis and evaluation of therapy inMenie`re’s disease. Otolaryngol Head Neck Surg 1995;113:181–5.14 Nuti D, Nati C, Passali D. Treatment of benign paroxysmal positional vertigo:no need for postmaneuver restrictions. Otolaryngol Head Neck Surg2000;122:440–4.Figure 2 A patient in the prolonged forced position for anterior canalbenign paroxysmal positional vertigo. The arms of the goniometerindicate the angle between the vertex and horizontal in the head-hanging position.From the head-hanging position the head has beenmoved forwards over about 120˚ to achieve the position shown.Prolonged forced position for antBPPV 781www.jnnp.com

Treatment of anterior canal benign paroxysmal positional vertigo by a prolonged forced position procedure

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Treatment of anterior canal benign paroxysmal positional vertigo by a prolonged forced position procedure

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