Positional vertigo

Positional DizzinessTerry D. Fife, MD, FAAN, FANS

ABSTRACTPurpose: This article reviews themost common conditions that are caused by changesin head or body positions. Practical clinical methods to help distinguish vestibular fromnonvestibular and central from peripheral vestibular positional dizziness are discussed.This article also reviews the treatment methods of selected canal variants of benignparoxysmal positional vertigo (BPPV).Recent Findings: Two recent evidence-based guidelines have established canalithrepositioning maneuvers (Epley and Semont maneuvers) as safe and highly effectivein the treatment of posterior canal BPPV. Recent studies suggest the Gufoni and theLempert roll (barbecue) maneuvers are effective in treating lateral canal forms ofBPPV.Summary: Most cases of positional vertigo are of peripheral vestibular origin and canbe effectively treated by simple positioning maneuvers. This article reviews the variantsof BPPV encountered in clinical practice, including mechanistic cause, differential diag-nosis, prognosis, and treatment. Generous use of figures is intended to aid in under-standing the most effective treatment maneuver techniques for the more commonforms of BPPV. Clinicians who can recognize the types of nystagmus associated withthe various canal types of BPPV can usually recognize CNS causes as distinct.

Continuum Lifelong Learning Neurol 2012;18(5):1060–1085.

EVALUATIONWhen a patient reports positionaldizziness, further clarification of thehistory is needed to determine what ismeant by the term dizziness and whatis meant by positional. Positional diz-ziness refers to dizziness caused bychanges in head or body position. Po-sitional vertigo is a subset of positionaldizziness in which a sensation of spin-ning results from a change in headposition. Vertigo from any cause is aggra-vated by head movement. Positionalvertigo, however, implies that spinningoccurs with certain specific types of headposition changes. For example, a patientwith dizziness that occurs upon standingbut is absent when lying flat most likelydoes not have positional vertigo butrather has postural dizziness causedby orthostatic hypotension (Case 4-1).Box 4-1 provides a glossary of terms en-countered in this article.

NONVESTIBULAR POSITIONALDIZZINESSA number of conditions may cause pa-tients to report dizziness related to posi-tion changes. Among the most commoncauses of positional dizziness is ortho-static hypotension, which patients maynotice when they arise from bed or froma chair to stand. A momentary decre-ment in cerebral perfusion pressuremaycause a near-faint sensation. Most peo-ple instinctively try to sit, but when thesensation occurs suddenly, it may culmi-nate in a wilting fall or overt syncope. Toconfuse matters further, some patients,as in Case 4-1, have two separate kindsof positional dizziness. Some patientsmay also experience near faintness dueto delayed orthostatic hypotension onlysporadically.1 Because they do not feeldizzy every time they stand, they havenot discerned a connection betweenbeing upright and experiencing dizziness.

Address correspondence toDr Terry D. Fife, BarrowNeurological Institute, 240West Thomas Road, Suite 301.Phoenix, Arizona 85013,[email protected].

Relationship Disclosure:Dr Fife reports no disclosure.

Unlabeled Use ofProducts/InvestigationalUse Disclosure:Dr Fife reports no disclosure.

* 2012, American Academy ofNeurology.

Supplemental digital content:Videos accompanying this ar-ticle are cited in the text asSupplemental Digital Content.Videos may be accessed byclicking on links provided inthe HTML, PDF, and iPadversions of this article; theURLs are provided in the printversion. Video legends beginon page 1081.

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Tilt table testing can be helpful in iden-tifying these patients when routinepostural vital signs are unrevealing.2

Other causes of nonvestibular posi-tional dizziness may include cerebralhypoperfusion due to cardiac valvularstenosis, arrhythmia, and severe heartfailure. Cerebrovascular insufficiencymay infrequently produce such symp-toms but more often causes TIAs withfocal neurologic features. Rarely CSFhemodynamic problems, such assevere intracranial hypotension aswith CSF overshunting, may producepostural dizziness and headaches.Rarer yet, CSF flow blockage from acolloid cyst can periodically block the

foramen of Monro, leading to positionaland transient equilibrium problems onthe basis of obstructive hydrocephalus.Cervical dizziness is commonly men-tioned as a possible concern. At present,little scientific clarity is available regard-ing a putativemechanism and diagnosticcriteria for this entity.3

POSITIONAL VERTIGOPositional vertigo is a vestibular disordercaused by an inappropriate asymmetryoriginating either from the labyrinths(eg, benign paroxysmal positional ver-tigo [BPPV]) or from dysfunctional in-tegration of CNS vestibular inputs (eg,acute lateral medullary infarct).

KEY POINT

h Positional vertigo is asubset of positionaldizziness in which asensation of spinningresults from a change inhead position.

Case 4-1A 71-year-old man presented with several months of episodic spinning,lightheadedness, and imbalance. The most recent episode occurred forabout 10 seconds when he got out of bed. He sat down and within20 seconds felt normal again. In another episode, he was awakenedfrom sleep with a rotational feeling. At other times, he had a spinningsensation for approximately 20 seconds while reaching into an uppercabinet. His most recent spell was of lightheadedness while standing inline at a grocery store. A cardiac workup discovered no cardiacabnormalities. A brain MRI was normal. Laboratory studies, includingcomplete blood count, electrolytes, and liver enzymes, were normal.

Examination was normal except for paroxysmal positional upbeat andclockwise cyclotorsional nystagmus with Dix-Hallpike positioning to theleft side. Canalith repositioning was performed. With repeat positioning,all symptoms and nystagmus were gone. At follow-up 3 weeks later, hereported continuing episodic dizziness occurring when standing orwalking. The Dix-Hallpike maneuver was normal with no vertigo ornystagmus. A tilt table study demonstrated gradually declining bloodpressure with nadir of 75 mm Hg systolic at 20 minutes of head-up tilt thatwas associated with lightheadedness. Heart rate and rhythm remainednormal throughout the period of declining blood pressure. He was treatedwith an adjustment in his antihypertensive medications and low-dosefludrocortisone with resolution of the lightheadedness.

Comment. This case illustrates how some patients do not recognizethat they are experiencing two distinct types of dizziness. This patientreported both spinning and lightheadedness, but each occurred in adifferent circumstance. Following treatment of the patient’s left-sidedbenign paroxysmal positional vertigo (BPPV), he still had dizziness becauseof delayed orthostatic hypotension that eluded detection by routineorthostatic blood pressure measurements but was confirmed by a tilttable study.

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BOX 4-1 Glossary of Terms

Benign paroxysmal positional vertigo (BPPV): An inner ear vertigo syndrome caused by calcium carbonatematerial in a semicircular canal, presumably dislodged from the utricle, that inappropriately stimulates theampulla of one of the semicircular ducts by the effect of gravity during certain changes in head position.Benign positional vertigo (BPV) is used synonymously with BPPV.

Benign paroxysmal vertigo of childhood: A condition unrelated to BPPV consisting of spontaneous attacksof vertigo in children typically aged 4 to 10 years and generally considered to be an acephalgicmanifestation of migraine. Similar to benign recurrent vertigo.

Benign recurrent vertigo: A condition unrelated to BPPV that causes recurrent spontaneous episodes of vertigothat are not positional. Most cases are attributable to migraine-associated vertigo.

Canalith (or canalolith) repositioning maneuver: Maneuver described by Epley that consists of a seriesof positioning maneuvers intended to move dense calcium debris from within the long arm of the affectedsemicircular canal back into the main vestibule; it particularly applies to the treatment of posterior canalBPPV. The terms canalith repositioning treatment or procedure are often used interchangeably withcanalith repositioning maneuver.

Canalithiasis (or canalolithiasis): Calcium carbonatematerial free floating or loose in the semicircular duct (canal).

Cupula: The vestibular sense organ of the semicircular canals consisting of a gelatinous structure overlyingspecialized hair cells. The nerve impulses generated relate to the degree of deflection of the cupula thatis affected by fluid (endolymph) movement in the semicircular canal. Each canal has its own cupula, andthe bulge in which the cupula resides is referred to as the ampulla.

Cupulolithiasis: Calcium carbonate material adherent to the cupula.

Dix-Hallpike maneuver: A specific maneuver that elicits paroxysmal positional nystagmus and vertigo inBPPV of the posterior semicircular canal.

Epley maneuver(s): A series of positioning maneuvers originally called canalith repositioning by Epley thatlater became known as the Epley maneuver or modified Epley maneuver (if a vibration device on the mastoidwas not used). This term is often used interchangeably with canalith repositioning maneuver or procedure.

Liberatory maneuver: Maneuver described by Semont in 1988 that entails position changes that treatposterior canal BPPV by moving calcium particles from the posterior canal to the main vestibule.

Mastoid oscillation: Direct application of vibration stimulus to the mastoid process done with the intentionto ‘‘loosen up’’ and enhance movement of canalith material during canalith repositioning maneuvers.

Modified Epley maneuver: Any of the various alterations on the original maneuver described by Epley in 1992.

Nylen-Barany maneuver: Often used to refer to the Dix-Hallpike maneuver, although the originaldescription entailed moving the head in differing positions to elicit nystagmus.

Otoconia: Calcium carbonate (calcite crystals) ranging from 5 2m to 25 2m in diameter that is part of theotolithic membrane of the maculae.

Particle repositioning maneuver: Another name for the canalith repositioning maneuver.

Roll test: Supine head turning to elicit horizontal canal BPPV nystagmus; sometimes referred to as thesupine head-turn test or Lempert head-turn test.

Semicircular canal: One of three (anterior or superior, posterior or inferior, and lateral or horizontal) bonychannels within the labyrinth of the temporal bone. The membranous labyrinth inside this canal is thesemicircular duct. The term canal is often used instead of duct.

Semont maneuver: The maneuver originally called the liberatory maneuver by Semont in his originalpublication but that later became called the Semont maneuver.

Utricle: Along with the saccule, a portion of the membranous labyrinth that generates and utilizes otoconiain their respective maculae to detect linear acceleration. The utricle and saccule are often referred to asthe ‘‘otolith organs’’ of the inner ear.


Positional Dizziness


The history and examination are of-ten sufficient to distinguish CNS causesfrom peripheral vestibular causes of po-sitional vertigo (Figure 4-1, Table 4-1).Central causes of positional vertigo thatbegin suddenly, such as stroke or hem-orrhage, may be associated with sig-nificant nausea and vomiting. Slowlyprogressive or chronic central causesare often associated with very littlenausea. Nausea is common with mostperipheral forms of positional vertigo,depending on the severity and dura-tion of the attack and the patient’s in-nate susceptibility to motion sickness.Head movement in a specific planetriggers peripheral forms of positionalvertigo such as BPPV, whereas centralcauses are often affected by less specifichead movements.

The nystagmus of BPPV is charac-terized by specific directional features(Table 4-2). If positional nystagmus isuncharacteristic of BPPV, a central causeshould be strongly considered (Case 4-2).Spontaneous downbeat or upbeat nys-

tagmus is a central abnormality andmayintensify with positioning or while su-pine. Downbeat positional nystagmuscan occur with some central lesions butmay occasionally indicate recovery nys-tagmus after very strong posterior canalBPPV nystagmus or with the less com-monly encountered anterior canal var-iant of BPPV.4

BENIGN PAROXYSMALPOSITIONAL VERTIGOEpidemiologyBPPV is the most common cause of epi-sodic vertigo in adults, with a lifetimeprevalence of 2.4%.5 BPPV may occursecondary to other inner ear conditions,such as head trauma, Meniere disease,vestibular neuritis, and idiopathic sen-sorineural hearing loss.6

Head trauma causes BPPV whensudden acceleration or deceleration cre-ates ruptures in segments of the macula.About 13% of patients with traumaticbrain injury report positional vertigo, andhalf have BPPV responsive to treatment.7

KEY POINT

h The history andexamination are oftensufficient to distinguishCNS causes fromperipheral vestibularcauses of positionalvertigo.

FIGURE 4-1 Algorithm for evaluating positional vertigo.

CRM = canalith repositioningmaneuver; BPPV = benign paroxysmal positional vertigo.



BPPV resulting from trauma is usually ap-parent within 1 week of trauma providedthe patient has been moving and activeenough to elicit symptoms. BPPV is themost common vestibular problem fol-lowing head trauma.

Labyrinthitis may cause BPPV by in-flammatory effects within or near thema-cula or by compromise of the vascularsupply that leads to dislodgement ofotoliths that may fall from the utricularspace to that of one of the semicircular

TABLE 4-1 Features Distinguishing Central From Peripheral Causesof Positional Vertigo

Feature Central Peripheral

Severe nausea + +++

Worse with nonspecific head movement ++ -

Evoked only by specific head movements(eg, Dix-Hallpike positioning, supine head roll)

+ +++

Paroxysmal upbeat and torsional nystagmus withDix-Hallpike maneuver

- +++

Paroxysmal downbeat nystagmus with Dix-Hallpikemaneuver

++ +

Paroxysmal horizontal directionYchanging nystagmus(geotropic or apogeotropic) evoked by supinehead turning

+ ++

Persistent downbeat nystagmus in any position +++ -

Nystagmus diminishes (fatigues) with repeatpositioning

- +++

Nystagmus resolves following positionaltreatment maneuver

- +++

TABLE 4-2 Comparison of Benign Paroxysmal Positional Vertigo byCanal Type

CanalType

EstimatedFrequency

ProvocativeManeuver Nystagmus

Posterior 81%Y89% Dix-Hallpikea Upbeat, torsional withtop pole beatingtoward the down ear

Horizontal 8%Y17% Supine roll test(Pagnini-McClure)

Horizontal directionchanging

Anterior 1%Y3% Dix-Hallpikea Downbeat,b torsional(torsional elementnot always visible)

a In posterior canal benign paroxysmal positional vertigo (BPPV), nystagmus is provoked followingDix-Hallpike positioning with the affected ear down. In anterior canal BPPV, nystagmus is provokedfollowing Dix-Hallpike positioning with the affected ear up.

b The observation of downbeat positional nystagmus requires careful assessment to rule out brainstemor cerebellar lesions.




canals.8 Labyrinthine infarction can alsolead to BPPV. The anterior vestibularartery supplies the anterior and hori-zontal semicircular canals and utricle,making it possible to have BPPV evenwhen no caloric responses occur onthat side, because the posterior semi-circular canal receives its blood supply

from a different vessel, the posteriorvestibular artery (Case 4-3).

PathophysiologyBackground anatomy. The vestibularsystem consists of three semicircularcanals, the saccule, and the utricle. Thecanals respond to angular acceleration

Case 4-2A 63-year-old man with a 1-year history of unsteadiness and dizzinessassociated with quick head movements underwent Dix-Hallpikepositioning and was found to have nystagmus. He had been seeing aphysical therapist for canalith repositioning treatments. After 10 visits withthe therapist, he had not improved. He had no hearing loss or sensationof spinning, but low-velocity downbeat spontaneous nystagmuswas present.With Dix-Hallpike positioning to both the right and left sides and in thestraight supine position, the downbeat nystagmus was more prominent.The rapid movement during positioning produced momentary dizziness.The remainder of the examination was normal, except for inability to walkin tandem and mild horizontal gaze-evoked nystagmus.

Comment. This patient had central nystagmus that localizes to themidline cerebellum or cervicomedullary junction. Further evaluationconfirmed sporadic cerebellar degeneration. The downbeat nystagmuswas accentuated by rapid movement backward. The nystagmus wasuncharacteristic of any form of BPPV because low-amplitude spontaneousdownbeat nystagmus, more prominent when supine, was present. Thiscase illustrates that the type and direction of nystagmus is important indetermining the cause of positional vertigo.

Case 4-3A 52-year-old woman had the onset of vertigo with left-sided hearing lossthat persisted for several weeks but gradually abated. Two months latershe felt much better with only slight unsteadiness when turning her headquickly. The hearing loss remained unchanged, however. Two monthsafter the onset of her vertigo, she awoke in the morning with a sensationof severe spinning when she rolled over in bed to turn off her alarm clock.This episode was brief, lasting only 30 seconds, but seemed to recurperiodically with bending or tilting her head backward. A brain MRI wasperformed with normal results, and formal vestibular testing confirmedabsence of caloric vestibular responses from the left ear. Positional testing,nevertheless, revealed prominent paroxysmal nystagmus followingDix-Hallpike positioning to the left side.

Comment. Caloric and rotational chair vestibular tests assess only thefunction of the horizontal semicircular canal. Since the posterior canal wasaffected in this case, it is an example of selectively damaged vestibularfunction. Not all parts of the vestibular apparatus are equally affected byviral or ischemic events.9



or turning movements of the head. Thecupula, the motion sensor for the semi-

circular canal, is composed of special-ized hair cells that have a kinociliumand stereocilia that are imbedded intoand covered by a gelatinous material(Figure 4-2). When the head moves inthe plane of the canal, endolymphmoves, thereby deflecting the cupulaand producing nerve excitation.

The saccule and utricle each con-tain a macula composed of hair cellsensory epithelium that is covered byan extracellular mass of calcium car-bonate crystals (otoconia) (Figure 4-3).The otoconial mass consists of thou-sands of otoconia about 10 Hm long,held together by beaded filaments andattached to a gelatinous matrix or so-called globular substance that actuallygenerates the calcium carbonate crys-tals (calcite). Themacules of the sacculeand utricle respond to linear acceler-ation and sustained head tilt relative togravity. Linear acceleration (includingtilt of the head) causes the otoconialmass to move and thereby bend thekinocilium and stereocilia of the haircells, evoking a change in the firing ratethrough the vestibular nerve.

KEY POINT

h Benign paroxysmalpositional vertigo occurswhen some of thedense calciumcarbonate crystals fromthe utricle dislodge andfall into one of thesemicircular canals.

FIGURE 4-2 Crista ampullaris. Thecrista ampullaris is thesensory epithelium

structure present in each semicircularcanal. Turning the head causes theendolymph fluid within the semicircularduct to move, which bends the cupula andthe kinocilia and stereocilia of the haircells. Bending in one direction is excitatoryand in the other direction is inhibitory.

FIGURE 4-3 Macula. The macula is the motion transducerfor the utricle and saccule and consists of haircells. Each hair cell has a kinocilium and

stereocilia imbedded in the gelatinous matrix of the otolithicmembrane. The gelatinous material or ‘‘globular substance’’actually generates the calcium carbonate crystals, referred toas otoconia.




The principal matrix protein in theotoconial membrane is otoconin 90.The otoconial membrane is also com-posed of type II collagen, glycopro-teins, and proteoglycans that maintainthe calcium crystal content and holdit to the sensory epithelium.10,11 As aresult of the aging process, trauma, in-flammation, and perhaps other factors,calcite crystals may dislodge from theotolithic membrane and sink into theendolymph fluid.

Mechanism. BPPVoccurs when someof the dense calcium carbonate crystalsfrom the utricle dislodge and fall intoone of the semicircular canals. The pos-terior semicircular canal is affected inmost cases of BPPV, most likely becausethe opening and positioning of the pos-terior canal are in a gravity-dependentposition. BPPVmay also affect the othersemicircular canals but with lower prev-alence. The movement of the calciumcarbonate material stimulates the semi-circular canals, resulting in brief epi-sodes of positional vertigo.

The calcium sediment has beenobserved intraoperatively in patientswith a history of BPPV.12 BPPV may beassociated with a number of condi-tions, but most cases are idiopathic.The likelihood of developing BPPV mayrelate in part to the metabolic consid-erations and the elastic and adhesiveproperties of the gelatinous matrix thatgenerate and maintain otoconia withinthe maculae.10

Canalithiasis refers to mobile calciumcarbonate debris that moves within thecanal during certain head movements,resulting in stimulation of the cupulathat in turn causes vertigo and nystag-mus related to the affected canal. Thismechanism is the most common and re-ferred to as canalithiasis (Figure 4-4).

Cupulolithiasis occurs when thecalcium carbonate material becomesattached to the cupula itself, render-ing it sensitive to gravity. Whether the

mechanism is the more common canal-ithiasis or the less common cupulolithia-sis, the resulting excitatory ampullarynerve response is reflected in the eyemovements producing the nystagmus.

Abnormalities of the lumen of semi-circular ducts may also be a factor insome refractory cases of BPPV. High-resolution MRI of the membranous laby-rinth suggests that narrowing, stenosis,or other luminal irregularities may occurin some patients with intractable BPPV.13

Diagnosis and TreatmentBPPV usually presents with brief attacksof spinning vertigo lasting 10 to 30 sec-onds, often after turning in bed, gettingup from the supine position, or bend-ing or tilting the head. While vertigo isthe typical sensation, minimally provo-cative head movements can produce asensation of floating or disequilibrium,often more prominent in the morningsafter getting up from sleep. Some pa-tients are able to determine that turningto one side seems to induce the symp-tom, and that is often the offending side.

Relatively few clues from the historycan ascertain which canal is affected.Side-to-side rolling in bed that causes

KEY POINTS

h The movement of thecalcium carbonatematerial stimulates thesemicircular canals,resulting in briefepisodes of positionalvertigo.

h The likelihood ofdeveloping benignparoxysmal positionalvertigo may relate inpart to the metabolicconsiderations andthe elastic and adhesiveproperties of thegelatinous matrix thatgenerate and maintainotoconia within themaculae.

h Canalithiasis refersto mobile calciumcarbonate debris thatmoves within the canalduring certain headmovements, resulting instimulation of cupulathat in turn causesvertigo and nystagmus.

FIGURE 4-4 Theoretical mechanism of cupulardisplacement in canalithiasis andcupulolithiasis.



vertigo in both directions suggestshorizontal canal BPPV but can alsooccur in patients with bilateral posteriorcanal BPPV. Hence, the examination isthe best way to determine which canalor canals are affected.

The examination, clinical observa-tions, and treatment differ for BPPVrelated to each of the canals and willbe described separately.

Posterior canal. Two techniqueshave been found to be effective to evokethe symptoms and nystagmus in BPPVrelated to the posterior canal: (1) theDix-Hallpike maneuver (Figure 4-5;Supplemental Digital Content 4-1,links.lww.com/CONT/A7) and (2) theside-lyingmaneuver (Figure 4-6). Bothmaneuvers cause movement of otoco-nia through the posterior canal as thepatient is moved from the sitting tothe recumbent position. Each maneu-ver is also the initial step in treat-ment: the Dix-Hallpike maneuver forcanalith repositioning treatment (CRT)and the side-lying test for the Semontmaneuver.

The nystagmus for the posterior canalis characterized as a 3- to 10-secondlatency, and a fast phase of nystagmus ispredominantly upbeat and torsionalwith the top pole rotating toward thedownward ear (Table 4-2). This type ofnystagmus often fatigues with repeatedpositioning maneuvers. Although asmall horizontal component frequentlybeats away from the downward ear, thiselement of the nystagmus is oftenbarely visible but may be seen on eyemovement recordings. Such recordings,however, are rarely necessary.

KEY POINTS

h Cupulolithiasis occurswhen the calciumcarbonate materialbecomes attached tothe cupula itself,rendering it sensitiveto gravity.

h Benign paroxysmalpositional vertigousually presents withbrief attacks of spinningvertigo lasting 10 to30 seconds, often afterturning in bed, gettingup from the supineposition, or bending ortilting the head.

h The nystagmus for theposterior canal ischaracterized as a3- to 10 second-latency,and a fast phase ofnystagmus ispredominantly upbeatand torsional with thetop pole rotatingtoward thedownwardear.

FIGURE 4-5 Dix-Hallpike maneuver to the right (A) andleft (B) sides to evoke nystagmus in posteriorcanal benign paroxysmal positional vertigo.

FIGURE 4-6 Side-lying test to the right (A) and left (B) sides to evoke nystagmus in posteriorcanal benign paroxysmal positional vertigo.




links.lww.com/CONT/A7

Two bedside treatments for posteriorcanal BPPV are very effective and estab-lished with high-quality evidence.14Y16

One is the CRT17 (also called particlerepositioning procedure or maneuver,Epley maneuver or procedure, or modi-fied Epley maneuver) (Figure 4-7,Table 4-3; Supplemental Digital Con-tent 4-2, links.lww.com/CONT/A8).The other is the Semont liberatorymaneuver18 (also called the liberatory

maneuver or treatment, or Semontmaneuver or treatment) (Figure 4-8,Table 4-4; Supplemental Digital Con-tent 4-3, links.lww.com/CONT/A9).

The CRT is the most commonly usedmethod for treatment of posterior canalBPPV in the United States, whereas theSemont maneuver is somewhat morecommonly used in Western Europe.Each has minor advantages and disad-vantages, but both are highly effective

FIGURE 4-7 Canalith repositioning maneuver for the right side.





when done properly. Perhaps the most-common reason that these techniquesdo not work in patients with an accuratediagnosis is insufficient extension of thehead. Particularly for CRT, if the head is

not tilted back at least somewhat, theotoconia may not move through thecanal as intended. Severe kyphosis canmake the positioning of the head diffi-cult. In such cases, the maneuver can beperformed on a table in the Trendelen-burg position or one can try the Semontmaneuver. There appears to be nocompelling indication for mastoid vibra-tion to enhance effectiveness despitesome early reports that it was helpful oreven necessary.

The Semont maneuver may be diffi-cult to perform in some older or obesepatients because of the quick sweepingmovement from one side to the other.For some patients with back pain, how-ever, the Semont maneuver may beeasier to tolerate. It may be used forBPPV of the posterior canal causedby canalithiasis or for refractory cases

KEY POINT

h Perhaps themost common reasonthat the canalithrepositioning treatmentand Semont maneuverdo not work in patientswith an accuratediagnosis is insufficientextension of the head.

TABLE 4-3 A Stepwise Method of Performing the CanalithRepositioning Treatment (Epley Maneuver) of thePosterior Semicircular Canal

b Step 1 Seat the patient on a table positioned so he or shemay be takenback tothe head-hanging position with the neck in slight extension. Stabilize the headwith your hands and move the head 45- toward the side you will test. Move thehead, neck, and shoulders en bloc to avoid neck strain or forced hyperextension.

b Step 2 Observe the eyes; hold them open if necessary. Wait for all thenystagmus to stop and then continue to observe the eyes about half as longas the nystagmus lasted (usually about 10 seconds after it stops).

b Step 3 Keeping the head back with the neck slightly hyperextended, turnthe head about 90- toward the opposite side and wait 20 to 30 seconds.Then roll the patient all the way onto his or her side and wait 10 to 15seconds (step not shown in Figure 4-7).

b Step 4 From this side-lying position, turn the head to face the ground andhold it there 10 to 15 seconds. No nystagmus should occur. If the patientreports a little dizziness, it is usually a favorable sign that the particles aremoving and the treatment will be successful.

b Step 5 Keeping the head somewhat in the same position, have the patient situp and then straighten the head. Hold onto the patient for a moment becausesome patients feel a sudden but very brief tilt when sitting up. This may becaused by particles affecting the macula as they fall back in the vestibule.

b Repeat After waiting 30 seconds or so, repeat the maneuver. If noparoxysmal nystagmus or symptom is present during Dix-Hallpikepositioning (steps 1 and 2), then complete the canalith repositioningtreatment. The rate of success is approximately 95%.

FIGURE 4-8 Semont liberatory maneuver for treatment ofright benign paroxysmal positional vertigo.




presumed to be caused by cupuloli-thiasis. Treatment of posterior canalBPPV using either the CRT or theSemont maneuver is established careand effective in eliminating vertigo andnystagmus in more than 90% ofpatients.14Y16,19,20

Some cases of BPPV are refractory,but these cases are uncommon. For pa-tients who are disabled and deemedsurgical candidates, canal plugging canbe considered. This procedure re-quires certainty about the side andthe canal affected since plugging of thecanal will render that canal nonfunc-tional and leave the patient with somedizziness for several weeks. Most pa-tients adapt well to this procedure, butperforming a destructive procedure fora benign condition requires that thepatient be made fully aware of possiblecomplications.

Following head trauma, BPPV is ty-pically evident from the first time thepatient is mobilized in a manner likelyto evoke the vertigo. Weeks to a fewmonths may elapse before immobilized,sedated, or unresponsive patients are ac-tive enough to be aware of the positionalvertigo, as Case 4-4 illustrates. Recurrentsymptoms within 1 day of treatment areprobably due to the same otoconia. Re-currences of BPPV after weeks of being

symptom free are most likely due to dif-ferent otoconia (Case 4-4).

Posttreatment instructions. Rela-tively little firmdata support any specificinstruction, although many clinicians rec-ommend keeping the head elevated atleast 30- on the night of the treatment.The recommendation is based on thetheoretical possibility of recurrence sincethe calcium particles are still presumablyloose in the utricle for a few days aftertreatment. Use of a cervical collar or re-quiring patients to sleep in a chair isunnecessary.21Y24 Pretreatment with ves-tibular suppressant medications is gener-ally not required but may be consideredin patients prone to motion sickness ornausea. Sedation does not detract fromthe success rateof themaneuver providedthe patient is alert enough to cooperate.

Occasionally, patients report subjec-tive positional dizziness but no nystag-mus is visible. Although generally noharm results from treatment, the diag-nosis should be considered suspect un-less nystagmus is seen. The nystagmus ofBPPV is usually visible if the patient hasany degree of vertigo. If repeated treat-ments produce no symptom resolution,the diagnosis should be reconsidered.

BPPV may be an isolated conditionor may be recurrent for many years.Recurrence rates range from 30% to

KEY POINTS

h Treatment of posteriorcanal benign paroxysmalpositional vertigo usingeither the canalithrepositioning treatmentor the Semont maneuveris established care and iseffective in eliminatingvertigo and nystagmusin more than 90% ofpatients.

h The nystagmus ofbenign paroxysmalpositional vertigo isusually visible if thepatient has any degreeof vertigo. If repeatedtreatments do notproduce symptomresolution, the diagnosisshould be reconsidered.

TABLE 4-4 Steps in Performing the Semont Liberatory Maneuver

b Step 1 Start with the patient sitting on a table or flat surface with headturned away from the affected side.

b Step 2 Quickly put the patient into the side-lying position, toward theaffected side with the head turned up. Nystagmus will occur shortly afterarriving at the side-lying position. Keep the patient in this position until atleast 20 seconds after all nystagmus has ceased.

b Step 3 Quickly move the patient back up and through the sitting positionso that he or she is in the opposite side-lying position with head facing down(head did not turn during the position change). Keep the patient in thisposition for about 30 seconds (some experts recommend up to 10 minutes).

b Step 4 Atanormal or slow rate, bring thepatient backup to the sittingposition.



50%.25 A small subpopulation may beparticularly susceptible to multiplerecurrences, perhaps based on as yetundefined characteristics of the oto-conial membrane. The recurrence rateincreases with age and possibly followinghead trauma, although there is dis-agreement on the latter point.6

Some patients with BPPV developanxiety and a sense of loss of controland confidence that may account forprolonged symptoms of dizziness evenafter successful resolution of all signs ofBPPV.26 Symptoms may be relieved byeducating, reassuring, and instructingthe patient about what to do if vertigorecurs following successful treatment.27

Education should be a part of the careof patients with BPPV, particularly ifan accompanying element of anxietyis present.

Home self-treatment. Some patientscan successfully perform treatment ma-neuvers at home as a complementaryapproach to in-office care.28,29 Radtkeand colleagues30 followed 70 patientswho performed self-administered treat-ments for BPPV using the Semont orEpley maneuvers. Success was definedas complete resolution of vertigo and

nystagmus after 1 week. Self-treatmentwith the Semont maneuver (n = 33)was successful in 58% of patients; self-treatment using a modified Epley ma-neuver (n = 37) was successful in 95%.Clinicians should be prepared for thelikelihood that some patients are un-able to perform these self-treatment ap-proaches on their own.

Another guide to aid patients in self-treatment is a proprietary plastic devicemounted on the bill of a ball cap thatshows the movements of a small col-ored ball moving through fluid thatsimulates the intended movement ofcalcium particles. Several studies have in-dicated this treatment to be effective.31

Many clinicians provide photocopiesof Brandt-Daroff exercises to patientsto use for self-treatment of BPPV. Thisexercise is quite similar to the Semontmaneuver except that the head isturned during the change from oneside-lying position to the other. Giventhe improved effectiveness of the ma-neuvers described by Semont andEpley, there is little need to use theseexercises any longer.

Horizontal canal. Horizontal canalBPPV represents about 10% to 17% of

KEY POINTS

h Some patients withbenign paroxysmalpositional vertigo (BPPV)develop anxiety and asense of loss of controland confidence thatmay account forprolonged symptomsof dizziness even aftersuccessful resolution ofall signs of BPPV.

h Patient educationshould be a part of thecare of patients withbenign paroxysmalpositional vertigo,particularly if anaccompanying elementof anxiety is present.

h Some patients cansuccessfully performtreatment maneuversat home as acomplementaryapproach to in-officecare.

Case 4-4A 58-year-old truck driver fell from the truck, which resulted in closed headtrauma with loss of consciousness, rib fractures, and a vertebral bodyfracture. He was hospitalized and relatively immobile for 1 week. Whenhe was transferred from the intensive care unit and began trying to sit up,he noted a spinning sensation. Examination confirmed bilateral benignparoxysmal positional vertigo (BPPV) that was successfully treated withresolution of the vertigo. After 1 month of being completely free ofvertigo, he awoke with intense spinning that was brief and positional.Examination confirmed right BPPV, which was successfully treated.

Comment. This case illustrates how immobilized patients may haveBPPV and not experience symptoms until they recover enough to moveabout. BPPV occurs spontaneously but is common with traumatic BPPV.Multiple recurrences of BPPV may also occur, presumably from mechanicalinjury or degradation of the otoconial mass, for months to 1 year ormore following trauma.




cases of BPPV.32Y35 Horizontal canalBPPV is often but not always evokedby the Dix-Hallpike maneuver. Thenystagmus of horizontal canal BPPV,unlike that of posterior canal BPPV, isdistinctly horizontal and changesdirection with changing head position.The best way to diagnose horizontalBPPV is by a supine head-turn maneu-ver (head yaw test or Pagnini-McCluretest) in which the patient is in the supineface-up position. Turning his or her headquickly to the right, look for horizontalnystagmus, then turn the head to theleft looking for a change in the di-rection of nystagmus (Figure 4-9;Supplemental Digital Content 4-4,links.lww.com/CONT/A10).35,36 Thedirection-changing nystagmus may beeither geotropic or apogeotropic.36 Thelatency is often brief, and the durationmay be 15 to 60 seconds. This nystag-mus appears less apt to fatigue with re-peat positioning; consequently, patientsare more likely to become ill withattempts to fatigue this form of BPPV.

Geotropic direction-changing posi-tional nystagmus is the most commonform of nystagmus in patients withhorizontal canal BPPV. The nystagmusis right beating upon turning the headto the right while supine and then leftbeating when turning the head backto the left side. By contrast, apogeo-tropic positional nystagmus is seenless often and refers to nystagmus thatis right beating with head turns to theleft while supine and left beating withhead turns to the right. One theory toexplain this is that, in the geotropicform, calcium particles are in the longarm of the semicircular duct and turn-ing to the affected side causes endo-lymph flow toward the ampulla, whichis excitatory, and thus the nystagmusbeats toward the affected ear. Turningthe head in the opposite directioncauses endolymph to flow away fromthe ampulla, which inhibits the ampulla

of the affected ear, causing the nystag-mus to change to the opposite direc-tion. Apogeotropic forms of horizontalcanal BPPV occur because the calciumparticles are located on the other side ofthe cupula in the short arm of the canaland thus, the same movements havethe opposite effects on the cupula.34

A number of treatments have beenadvocated for horizontal canal BPPV,including the 360- roll maneuver (alsocalled barbecue roll or Lempert ma-neuver), forced prolonged position(Vannucchi technique), and Gufoni ma-neuver. It is worth noting that nearly90% of cases of apogeotropic horizontalcanal BPPV resolved in one study within7 days and all had resolved by 28days.37,38 All forms seem to self-resolveeven more often than cases of poste-rior canal BPPV.

Determining the affected side. If thehorizontal canal BPPV occurred aftertreatment for posterior canal BPPV,the affected ear is likely to be the sameear affected by the posterior canalBPPV. In cases where the horizon-tal canal BPPV occurs de novo, other

KEY POINT

h The nystagmus ofhorizontal canal benignparoxysmal positionalvertigo (BPPV), unlikethat of posterior canalBPPV, is distinctlyhorizontal and changesdirection with changinghead position. Thebest way to diagnosehorizontal BPPV is by asupine head-turnmaneuver (head yawtest or Pagnini-McCluretest) in which thepatient is in the supineface-up position.Turning his or her headquickly to the right, lookfor horizontalnystagmus, then turnthe head to the leftlooking for a changein the direction ofnystagmus.

FIGURE 4-9 Supine roll test. The patient’s head is movedrapidly from the straight supine position (1) to theright side (2). At this point, the eyes are observed

for horizontal nystagmus and the direction and intensity arenoted. Then the patient is returned to position 1 until nystagmussubsides, then taken to the left (3) and again the eyes areobserved for the intensity and direction of horizontal nystagmus.The side resulting in the strongest nystagmus is the affected side.




methods are used to determine theside to treat.

The supine head-turn maneuver(Figure 4-9) is the most commonlyused method for determining whichhorizontal canal is affected. The sideassociated with the most severe nys-tagmus is presumed to be the affectedside for the geotropic form and theopposite side for the apogeotropicform of horizontal canal BPPV.39

Another method advocated by someis the seated supine positioning test,which is done by rapidly moving thepatient from the seated to the straightsupine position. This technique evokesnystagmus beating toward the healthyside in the geotropic forms and towardthe affected side in the apogeotropicforms.34,39 Occasionally, the sideinvolved remains equivocal; thus, onemay simply begin on one side and latertreat the other side.

The use of an Epley or Semont ma-neuver, intended to treat posterior canalBPPV, is unlikely to be successful intreating horizontal canal BPPV. 40,41 Con-sequently, the approach must be alteredif the nystagmus observed is paroxysmalhorizontal and changes direction withchanging the head position (ie, direction-changing positional nystagmus).

Roll maneuver. The 360- (barbecue)roll maneuver (Lempert roll maneu-ver) (Figure 4-10; Supplemental Dig-ital Content 4-5, links.lww.com/CONT/A11) is a commonly used treat-ment method for horizontal canalBPPV. With the 360- roll treatmentthe patient’s head is positioned withthe affected ear down, and the head isthen turned quickly 90- toward theunaffected side (face up). A series of90- turns toward the unaffected side isthen undertaken sequentially until thepatient has turned 360- and is back tothe affected earYdown position. Fromthere, the patient is turned to the face-up position and then brought up to the

sitting position. The successive headturns can be done with intervals of 15to 20 seconds even when the nystagmuscontinues. Waiting longer does no harmbut may lead to nausea, and the shorterinterval does not appear to detract fromthe effectiveness of the treatment. Thegoal of this maneuver is to utilize theeffect of gravity to move the otoconiafrom the long arm of the lateral canal tothe vestibule.41Y43

Gufoni maneuver. In 1998, Gufoniand colleagues44 described a differenttreatment in which the patient is quicklylain from a sitting position to the healthyearYdown (for geotropic forms) or to theaffected earYdown position (for apogeo-tropic forms) (Figure 4-11; SupplementalDigital Content 4-6, links.lww.com/CONT/A12; Supplemental Digital Content 4-7,links.lww.com/CONT/A14).

Then the head is turned 45- towardthe floor andmaintained in that positionfor 30 to 60 seconds. Then the patientreturns to the sitting position. This pro-cedure may be repeated. Using thismethod, 22 of 24 patients achieved reso-lution of symptoms.44 In a comparisonwith forced prolonged positioning,both the Gufoni maneuver and forcedprolonged positioning achieved suc-cess in more than 80% of patients, butno statistically significant difference wasfound between the two methods.45 Re-cently, a class II prospective random-ized sham-controlled study of 157patients with the apogeotropic form ofhorizontal canal BPPV found that theGufoni maneuver (PG.001) and headshaking (P=.026) were more effectivethan a sham maneuver for both imme-diate improvement and improvementat 1 month following treatment.46

A recent class I randomized controlledtrial comparing the Lempert (barbecueroll) to the Gufoni maneuver for thegeotropic form of lateral canal BPPVfound both maneuvers significantlymore effective than a sham maneuver

KEY POINT

h The use of an Epley orSemont maneuver,intended to treatposterior canal benignparoxysmal positionalvertigo (BPPV), isunlikely to be successfulin treating horizontalcanal BPPV.









on the day of treatment and also at1-month follow-up.47

A class III prospective study of 60patients with geotropic horizontal canalBPPV found that forced prolongedpositioning and the Gufoni maneuverwere both more effective in eliminationof nystagmus than a single iteration of aroll maneuver.48

Another class II randomized pro-spective clinical trial of 147 patientsaffected by horizontal canal BPPV (103geotropic, 44 apogeotropic) found thatamong those with geotropic horizontalcanal BPPV, 44 of 54 patients (81%)treated with the barbecue roll maneu-ver plus forced prolonged positioningwere symptom free compared to 54 of58 (93%) treated with the Gufonimaneuver.49 The authors concludedthat the slightly greater response ratecombined with the greater ease ofperforming the Gufoni maneuver make

it the maneuver of choice for horizontalcanal BPPV, whether geotropic or apo-geotropic. A growing body of literatureseems to support this conclusion.

Forced prolonged positioning. Thistreatment technique was first describedby Vannucchi and colleagues in 1997.50

Forced prolonged positioning is per-formed by having the patient seatedon a bed or table. He or she is thenquickly lain down on the affected side;then a passive 45- downward rotationof the head is performed. The positionis maintained for 12 hours before thepatient is returned to the starting position.Some clinicians maintain the positiononly 3 to 5 minutes, but no comparativestudies are available to determine theminimum time needed to achieve suc-cess. In studies using this method, mostpatients reported resolution of symp-toms, including those with refractoryhorizontal canal BPPV.43Y45 It is ideal

FIGURE 4-10 Lempert 360- roll maneuver for the treatment of right horizontal canal benignparoxysmal positional vertigo with geotropic-type nystagmus.



to eliminate all nystagmus or to convertthe more difficult-to-clear apogeotropicnystagmus to the more treatment-responsive geotropic nystagmus formof horizontal canal BPPV.43,51 With thisstrategy, remission rates of 75% to 90%can be achieved.

Anterior canal. This form of BPPVis usually transitory and most commonlyseen in the course of treating othermore common forms of BPPV. Chronicor persistent anterior canal BPPV is rare.Hence, a careful neurologic examinationand brain MRI are suggested unless thenystagmus can be made to completelyresolve with positioning treatments.

The nystagmus is downbeat with aminor torsional component.42,49,52,53

Of all the types of BPPV, anterior canal

BPPV seems to resolve spontaneouslymost often, although horizontal canalBPPV also resolves within 2 to 4 weeksif not sooner.38 Paroxysmal downbeatnystagmus as may occur with anteriorcanal BPPVmay bemimicked by centrallesions of the brainstem or cerebellum(Case 4-5). Bertholon and colleagues54

reviewed 50 patients with downbeatpositional nystagmus and found thatthree-fourths had CNS disease; at leastsome of the remaining one-fourth ofcases were thought to have a form ofanterior canal BPPV. If the nystagmusdoes not completely resolve with theinitial positioning treatment, brainimaging should be performed.

The Dix-Hallpike and side-lying testsused for the posterior canal BPPV can

KEY POINTS

h It is ideal to eliminateall nystagmus or toconvert the moredifficult-to-clearapogeotropicnystagmus to the moretreatment-responsivegeotropic nystagmusform of horizontal canalbenign paroxysmalpositional vertigo.

h Of all the types ofbenign paroxysmalpositional vertigo(BPPV), anterior canalBPPV seems to resolvespontaneously mostoften, althoughhorizontal canal BPPValso resolves within 2 to4 weeks if not sooner.

h Paroxysmal downbeatnystagmus as may occurwith anterior canalbenign paroxysmalpositional vertigo maybe mimicked by centrallesions of the brainstemor cerebellum.

FIGURE 4-11 The Gufoni maneuver is a method of treatment for right-sided horizontal canalbenign paroxysmal positional vertigo (BPPV) that is geotropic (A) orapogeotropic (B). A, For the geotropic nystagmus type of lateral canal BPPV, the

patient is taken from the sitting position to the straight side-lying position on the unaffectedside (left in this case) and maintained there for 1 minute. The patient’s head is quickly turnedtoward the ground 45- to 60- and held in the position for 2 minutes. The patient then sitsup again with the head held toward the left shoulder until sitting upright again. B, For righthorizontal canal BPPV with apogeotropic-type nystagmus, the patient is taken from the sittingposition to the straight side-lying position on the unaffected side (right in this case) for 1 minute.Then the patient’s head is quickly turned toward the ground and held in the position for2 minutes. The patient then sits up again with the head held toward the right shoulderuntil upright.




also be used to provoke and diagnoseanterior canal BPPV, and the samemaneuvers used to treat posterior canalBPPV can be used to treat anterior canalBPPV.55 A recent retrospective study of13 patients is described in one report,56

but comparison to a control group maybe particularly important in assessingeffectiveness for this BPPV variant sinceit seems to have a high rate of sponta-neous resolution.

The affected side is not always en-tirely obvious. If the paroxysmal down-beat positional nystagmus from anteriorcanal BPPV developed in the context ofa ‘‘canal switch’’ during treatment of theposterior canal BPPV treatment, thenthe side of the original BPPV is likely the

same side.57 Because the torsional ele-ment of nystagmus may not be obvious,49

the direction of torsional nystagmuscannot be used to reliably ascertain theaffected ear.

For rare cases that are refractory totreatments used for posterior canalBPPV, a prolonged forced positionprocedure with the affected anteriorcanal in the uppermost position forseveral hours should be tried beforeany invasive procedure such as canalplugging is considered.58

Canal SwitchOccasionally, freely mobile otoconiamoving within the lumen of one semi-circular canal can be moved during

KEY POINT

h The same maneuversused to treat posteriorbenign paroxysmalpositional vertigo (BPPV)can be used to treatanterior canal BPPV.

Case 4-5A 35-year-old software writer presented with several months of positional vertigo that seemed tobegin after a rear-end motor vehicle collision in which he sustained soft tissue neck pain. The spellswere brief but occurred when he wrestledwith his children and with bending or tiltinghis head. On examination he experiencedbrief paroxysmal downbeat nystagmuslasting about 5 seconds with positioningfrom sitting to supine whether his head wasturned to the right or left side. Attemptsto treat with canalith repositioningtreatment resulted in no change in thenystagmus or symptoms. Brain MRI wasobtained (Figure 4-12) and showed a lipoidtumor of supracerebellar region. An attemptto surgically resect this lesion was abortedbecause of its extensive vascular elements.The pathologic diagnosis was lipoangioma.

Comment. This patient’s nystagmus wasmost suspicious for a central form ofpositional vertigo, but after the brain MRIconfirmed a chronic lesion, the questionbecame whether this lesion was the cause.Over time and considering its inferiorextension to the nodulus and anterior vermis,it was concluded to be likely related to thelesion. Any contribution from the motorvehicle accident remained a matter ofspeculation.

FIGURE 4-12 Brain MRI showing an extensivesupracerebellar lipoangioma responsible forparoxysmal downbeat positional nystagmus

in Case 4-5. A, Magnetic resonance T1-weighted images.B, Axial images of brain MRI.



the course of treatment, not back tothe utricle as intended, but to one ofthe adjacent canals. This is possible be-cause the canals directly communicatewith one another. This canal switchchanges the appearance of nystagmusfrom that of the original affected canalto that of the newly affected canal.59,60

The most common canal switch is fromthe posterior to the horizontal and pos-terior to anterior canals (Case 4-6).

Multicanalar. In some situationsmore than one canal is affected at thesame time.53,61,62 The most commoncircumstance is probably bilateral pos-terior canal BPPV. This can be diagnosedby the presence of typical nystagmuswith the Dix-Hallpike or side-lyingmaneuvers on both sides. In unilateralBPPV, the nystagmus is only present onDix-Hallpike positioning to the affectedside, and no nystagmus is evident onthe other side. Other multicanalar formsmay also occur, the most common be-ing combinations of posterior and hor-

izontal canal, and posterior and anteriorcanal.34 They can be recognized basedon the maneuver used to evoke thenystagmus and the direction of the nys-tagmus. Treatments are the same asthose used for individual canal types ofBPPV and can be done on the samevisit in some cases or spread over sev-eral visits with more than 90% responserates.63

CENTRAL POSITIONAL VERTIGOTable 4-5 outlines some of the con-ditions associated with central positionalvertigo, and Figure 4-1 outlines someways of segregating central from pe-ripheral causes. Slowly progressive le-sions affecting the cerebellum, pontinetegmentum, and dorsal medulla canlead to surprisingly mild positionaldisequilibrium. Such conditions maybe associated with paroxysmal posi-tional nystagmus and gaze-evoked nys-tagmus or other focal neurologic signs.The degree of nausea and severity of

Case 4-6A 68-year-old woman with 6 weeks of positional vertigo of brief durationwas found to have robust upbeat and counterclockwise torsionalnystagmus with Dix-Hallpike positioning to the right. She was takenthrough canalith repositioning and returned to the sitting position. Theexaminer repeated Dix-Hallpike positioning to the right to be sure allthe nystagmus had cleared and upon positioning noted prominenthorizontal right-beating nystagmus that persisted for 40 seconds. Theexaminer concluded that canal switch from the right posterior to the righthorizontal canal had taken place during the previous maneuver. Whilethe patient was still supine with the head to the right, her head was thenturned 180- to the left whereupon the left-beat nystagmus occurred.The patient was then moved in 90- steps to the left (unaffected) side. Thepatient went from supine head left to face down, to right ear down,and then back to straight supine (face up). The patient then sat up.Repeat Dix-Hallpike maneuver showed no further upbeat or horizontalnystagmus on either side.

Comment. Canal switch occurs when otoconial debris moves from onecanal to another during the course of canalith repositioning. It isrecognized by a change in the direction of the nystagmus. Upon seeingthis kind of change in nystagmus, the examiner should adapt theprocedure to treat the newly affected canal.




vertigo are generally less prominentwith slowly progressive central lesions,at least up to a point.

Acute or more rapidly progressivelesions of the CNS are often associatedwith more intense vertigo or nausea(Case 4-7). Neurologic signs that lo-calize to the brainstem or cerebellumare often, but not always, present.

The conditions most likely to exhibitfew other clinical signs besides positionalvertigowith or occasionally withoutmuchnystagmus include cerebellar cavernousmalformation, arteriovenous malforma-tion, hemangioblastoma, and small mid-line or paramedian cerebellar lesions.Carcinomatous or lymphomatous menin-gitis can result in positional vertigo butmore commonly results in head motionYrelated dizziness. Multiple sclerosis can

be associated with central forms of nys-tagmus and positional vertigo. Migraine-related vertigo can be associated with thedevelopment of nausea, occasionallywith static positional nystagmus thatmay build over a period of minutesupon assuming certain head positions.64

Chiari malformation is usually associ-ated with occipital headaches and maybe associated with downbeat nystag-mus in the straight head-hanging posi-tion. Direction-changing positionalnystagmus that does not entirely disap-pear after treatment for horizontalcanal BPPV should raise suspicion fora central lesion, such as a stroke of thecerebellar nodulus.65

Brain MRI is very helpful in excludingstructural causes of positional vertigo.Peripheral forms of positional vertigo

KEY POINTS

h The degree of nauseaand severity of vertigoare generally lessprominent with slowlyprogressive centrallesions, at least up toa point.

h Acute or more rapidlyprogressive lesions ofthe CNS are oftenassociated with moreintense vertigo ornausea.

TABLE 4-5 Differential Diagnosis of Positional Vertigo

b Central positional vertigo with nystagmus

b Cerebellar lesions (eg, tumors, strokes, masses, bleeding)

b Pontomedullary lesions (eg, lateral medullary infarction)

b Multiple sclerosis

b Chiari malformationVoften neck pain; obtain MRI

b Cerebellar degenerationVspontaneous downbeat nystagmus, impairedpursuit, gaze-evoked nystagmus

b Vertebrobasilar vascular insufficiency

b Subclavian steal syndrome

b Atlantoaxial subluxation

b Drug effects (eg, phenytoin toxicity)

b Peripheral vestibular forms of positional vertigo

b Benign paroxysmal positional vertigo and related variants

b Uncompensated unilateral vestibular loss

b Static positional nystagmus and associated dizziness

b Saccular or utricular positional vertigo

b Alcohol positional vertigo

b Migraine-associated vertigo with a positional component

b Motion sickness



are nearly always associated with a nor-mal brain MRI.

Central forms of positional vertigomay occasionally elude detection by astandard brain MRI; these include somecerebellar degeneration syndromes,atlantoaxial subluxation, vertebrobasilarinsufficiency, chronic basilar menin-gitides, and drug toxicities. Additionalstudies that are sometimes necessaryinclude CSF studies, vascular imagingby CT angiography or MR angiography,cervical spine radiography or CT, anddrug-level testing.

Treatment ApproachTreatment of central positional vertigodepends on the underlying cause. Con-

ditions with fixed static injury, such asoccurs with stroke, trauma, and hem-orrhage, may be amenable to habitu-ation physical therapy exercises. Thistherapy is discussed elsewhere in this

issue but in essenceinvolves exposure to the kinds of headmovements that aggravate the vertigowhile also working on general balanceand ocular motor control.

Progressive disorders such as meta-static tumors, astrogliomas, and carci-nomatous meningitis require treatmentof the underlying condition. Symp-toms can be managed with vestibularsuppressants.

Sometimes central positional vertigois related to an unstable condition.

KEY POINTS

h Central forms ofpositional vertigo mayoccasionally eludedetection by a standardbrain MRI; these includesome cerebellardegenerationsyndromes, atlantoaxialsubluxation,vertebrobasilarinsufficiency, chronicbasilar meningitides,and drug toxicities.

h Conditions with fixedstatic injury, such asoccurs with stroke,trauma, andhemorrhage, maybe amenable tohabituation physicaltherapy exercises.

Case 4-7A 62-year-old man had experienced several weeks of episodic isolatedvertigo lasting minutes. He then developed severe ataxia, an inability towalk, dysarthria, and vertigo that persisted, prompting him to go to theemergency department. He was found to have pronounced vertigo andattempts to sit up inbed or stand elicitedvomiting. BrainMRI (Figure 4-13)revealed a largeposterior inferiorcerebellar arterydistribution strokeon the right side.

Comment. Thiscase illustrates howan acute infarct canlead to severevertigo, nausea, andvomiting. This is lesscommonwith slowlyenlarging lesions,suggesting thatplastic properties ofthe CNSmay be ableto compensate tosome extent incentral vestibularlesions. Acute central positional vertigo can in some cases produce significantvertigo and vomiting.

FIGURE 4-13 Brain MRI showing an acute stroke ondiffusion-weighted images (A) and on axialfluid-attenuated inversion recovery fast spin

echo (B) in the right inferior cerebellum and right lateralmedulla in the distribution of the right posterior inferiorcerebellar artery (PICA). The red arrow shows cytotoxicedema affecting midline cerebellar structures. Green arrowsshow infarction of the right lateral medulla. Blue arrowsshow infarction of the right cerebellum in the PICAdistribution.




Chiari malformation, defined as morethan 5 mm of cerebellar tonsillar her-niation below the foramen magnum,may be associated with positionalvertigo. Symptoms of Chiari malforma-tion may progress as a result of aging,trauma, and degenerative effects on thecraniocervical junction even though low-lying cerebellar tonsils are congenital.Chiari malformation is treated by sub-occipital surgical decompression, re-moving some of the occipital bone toallow more space for the inferior cere-bellum and ensure normal CSF flow.

Another unstable condition is vas-cular narrowing of the vertebrobasilarsystem. Vertebral artery narrowing asthe vessel crosses the arch of C1 canresult in vertigo associated with headturning in one direction. Head turningcauses some narrowing of the vesseland may lead to symptoms of transientischemia. Antiplatelet agents, vertebralartery angioplasty, or surgical place-ment of a stent are treatment options.Atlantoaxial subluxation is instability ofC1 (atlas) onC2 (axis) ofmore than 3mmfrom the C1 arch and odontoid process.This condition often arises due to weak-ness of the transverse ligament and isespecially associated with rheumatoidarthritis and Down syndrome. Treat-ment is surgical fusion of C1 and C2.

TRENDS AND FUTUREDIRECTIONSTreatment of positional vertigo haschanged significantly during the past20 years, and more patients are receiv-ing treatment for BPPV. The physicaltherapy and positioning treatments forthe more common posterior canalvariant of BPPV are nowwell establishedand can be successfully used in generalmedical practice.66 Treatments are beingrefined for all other variants of BPPV,but due to their infrequency, treatmentfor the less common versions of BPPVwill likely be limited to those with a spe-

cial interest in the field. Our understand-ing of the mechanisms and metabolicpredispositions for developing BPPV orfor havingmultiple recurrences will alsolikely expand over time.

We will likely see more researchemerge on selective dysfunction of theutricle and saccule and the role of thesestructures in causing some forms of po-sitional vertigo.

VIDEO LEGENDSThe maneuvers depicted in the follow-ing videos may need to be modified forsome patients with reduced neck flexi-bility by turning of the head and should-ers together (en bloc).

Supplemental Digital Content 4-1

Video demonstrates the Dix-Hallpikemaneuver to the right. This maneuvershould evoke paroxysmal positional nys-tagmus for right-sided benign parox-ysmal positional vertigo related to theposterior semicircular canal. The mir-ror image of this maneuver constitutesa left-sided Dix-Hallpike maneuver.links.lww.com/CONT/A7Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2008, American Academy of Neurology.


Video demonstrates canalith reposition-ing treatment for right posterior canalbenign paroxysmal positional vertigo(BPPV). Themirror imagemaneuver canbe done for left posterior canal BPPV.links.lww.com/CONT/A8Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2008, American Academy of Neurology.






Video demonstrates the Semont liber-atory maneuver for right posterior canalbenign paroxysmal positional vertigo(BPPV). The mirror image maneuver canbe done for left posterior canal BPPV.links.lww.com/CONT/A9Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2012, American Academy of Neurology.


Video demonstrates the supine roll(Pagnini-McClure) test to determine theaffected side in horizontal canal benignparoxysmal positional vertigo. The sidethat induces the most intense horizon-tal positional nystagmus is presumedto be the affected side.links.lww.com/CONT/A10Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2012, American Academy of Neurology.


Video demonstrates the Lempert (bar-becue) roll maneuver for right geotropichorizontal canal benign paroxysmalpositional vertigo (BPPV). The mirrorimage maneuver can be done for leftgeotropic horizontal canal BPPV.links.lww.com/CONT/A11Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2012, American Academy of Neurology.


Video demonstrates the Gufoni ma-neuver for geotropic variant of right

horizontal canal benign paroxysmal po-sitional vertigo (BPPV). Themirror imagemaneuver can be done for the geotropicvariant of left horizontal canal BPPV.links.lww.com/CONT/A12Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2012, American Academy of Neurology.


Video demonstrates the Gufoni maneu-ver for apogeotropic variant of righthorizontal canal benign paroxysmal po-sitional vertigo (BPPV). Themirror imagemaneuver can be done for apogeotropicvariant of left horizontal canal BPPV.links.lww.com/CONT/A14Reproduced with permission from Fife TD,Iverson DJ, Lempert T, et al. Practice parameter:therapies for benign paroxysmal positionalvertigo (an evidence-based review): report ofthe Quality Standards Subcommittee of theAmerican Academy of Neurology. Neurology2008;70(22):2067Y2074.B 2012, American Academy of Neurology.

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