pseudo-spontaneous and head-shaking nystagmus in ... · pdf filein horizontal canal benign...

Pseudo-Spontaneous and Head-Shaking Nystagmusin Horizontal Canal Benign Paroxysmal

Positional Vertigo

*Sun-Uk Lee, †Hyo-Jung Kim, and ‡Ji-Soo Kim

*Department of Neurology, Ajou University College of Medicine, Ajou University Hospital, Suwon; ÞKangwonNational University College of Medicine, Medical Research Institute, Seoul National University Bundang

Hospital, Seongnam; and þDepartment of Neurology, Seoul National University College of Medicine, SeoulNational University Bundang Hospital, Seongnam, Republic of Korea

Objectives: To determine the characteristics and diagnosticvalue of pseudo-spontaneous and head-shaking nystagmus(HSN) in benign paroxysmal positional vertigo involving thehorizontal semicircular canal (HC-BPPV).Study Design: Retrospective case series review.Methods: After excluding 19 patients with canal paresis, ab-normal head impulse test, recent history of peripheral or centralvestibular disorders, or poor cooperation, we retrospectivelyrecruited 127 patients with HC-BPPV from January 2009 toJuly 2012. The patients included 69 geotropic and 58 apogeo-tropic types. We analyzed the pattern of pseudo-spontaneousnystagmus and HSN according to the lesion side.Results: Pseudo-spontaneous nystagmus was observed in 87(87/127, 68.5%) patients, both in geotropic (46/69, 66.7%) andapogeotropic (41/58, 70.7%) types without difference in theprevalence between the types (p = 0.627). Pseudo-spontaneousnystagmus beat more to the lesion side in apogeotropic type

(28/41, 68.3%, p = 0.028) but in either direction without di-rectional preponderance in geotropic type (p = 0.659). Of the90 patients who underwent horizontal head-shaking, 27 (30.0%)showed HSN that was more common in apogeotropic than ingeotropic type (22/44 [50.0%] versus 5/46 [10.9%], p G 0.001).Patients with apogeotropic HC-BPPV showed predominantlycontralesional HSN (19/22 [86.4%], p = 0.001), whereaspatients with geotropic type did not show any directional pre-ponderance of HSN (contralesional in 2 and ipsilesional in 3).Conclusion:HSN is more common and mostly contralesional inapogeotropic HC-BPPV. HSN may be a lateralizing sign in apo-geotropic HC-BPPV. Different prevalence and patterns of HSNin apogeotropic and geotropic HC-BPPV suggest dissimilar cupulardynamics in those disorders. Key Words: Benign paroxysmalpositional vertigoVHead-shaking nystagmusVNystagmusVVertigo.

Otol Neurotol 35:495Y500, 2014.

Head shaking may reveal central as well as peripheralvestibular dysfunction by generating nystagmus (1). Hori-zontal head shaking usually induces nystagmus beatingto the intact or healthier side in patients with unilateralor asymmetrical peripheral vestibular disorders. This head-shaking nystagmus (HSN) of the peripheral type is explainedby the following: 1) asymmetrical vestibular inputs due toEwald’s second law, which states that the excitatory stimuliare more effective than the inhibitory ones in inducing ves-tibular responses (1Y3); and 2) central velocity storagemechanisms (1,4).

Benign paroxysmal positional vertigo (BPPV) is char-acterized by short-lasting vertigo that develops when thedependent position of the head is changed (5,6). BPPV isexplained by free floating otolithic debris in the endolymphof the semicircular canal (canalolithiasis) or debris nearor attached to the cupula (cupulolithiasis) (7,8). In BPPVinvolving the horizontal semicircular canal (HC-BPPV),

Address correspondence and reprint requests to Ji-Soo Kim, M.D.,Ph.D., Department of Neurology, Seoul National University College ofMedicine, Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, Republic ofKorea; E-mail: [email protected] study was supported by a grant of Korea Medical Device In-

dustrial Cooperative Association.Author contributionsDr. Lee wrote the manuscript and analyzed and interpreted the data.Ms. H. J. Kim analyzed and interpreted the data and revised the

manuscript.Dr. Kim conducted the design and conceptualization of the study,

interpretation of the data, and drafting and revision of the manuscript.DisclosureDr. Lee and H. J. Kim report no disclosures.Dr. J. S. Kim serves as anAssociate Editor ofFrontiers in Neuro-otology

and on the Editorial Boards of the Journal of Korean Society of ClinicalNeurophysiology, Research in Vestibular Science, Journal of ClinicalNeurology, Frontiers in Neuro-ophthalmology, Journal of Neuro-ophthalmology, Case Reports in Ophthalmological Medicine, and WorldJournal of Neurology; and received research support from SK Chemicals,Co. Ltd.

Otology & Neurotology35:495Y500 � 2014, Otology & Neurotology, Inc.

495

Copyright © 2014 Otology & Neurotology, Inc. Unauthorized reproduction of this article is prohibited.

2 different types have been recognized according to thepatterns of nystagmus induced when the head is turnedto either side while supine. In geotropic HC-BPPV, theevoked nystagmus beat to the ground and is explained byotolithic debris in the canal (9). In contrast, the evokednystagmus beating toward the ceiling in apogeotropicHC-BPPV has been ascribed to otolithic debris attachedor near to the cupula within the ampulla (3,10).

Patients with either type of HC-BPPV may show spon-taneous nystagmus in the sitting position, which is also re-ferred to pseudo-spontaneous because it showed positionalmodulations and disappearance with resolution of HC-BPPV (10Y13). The direction of pseudo-spontaneous nys-tagmus also has been known to have a lateralizing value inHC-BPPV (10Y12).

In HC-BPPV, the otolithic debris in the endolymph orattached to the cupula may alter the dynamics of the endo-lymph or the cupula during horizontal head shaking andgenerate HSN. Accordingly, analyzing the patterns of HSNmay provide a clue to the altered dynamics of the endo-lymph or cupula in HC-BPPV. However, no study hasattempted systematic analysis of HSN in patients withHC-BPPV. In this study, we analyzed the patterns ofpseudo-spontaneous nystagmus and HSN in a large num-ber of patients with either geotropic or apogeotropic typeof HC-BPPV.

MATERIALS AND METHODS

PatientsWe reviewed the medical records of 146 patients (47 men and

99 women; age range, 34Y92 yr; mean age T SD, 65.0 T 12.4)with HC-BPPV. The age did not differ between men and women(66.1 T 12.8 versus 65.0 T 12.4, p = 0.586). The recruitment wasperformed using our data base that represents all vestibularpatients seen at the Dizziness Clinic of Seoul National Univer-sity Bundang Hospital from January 2009 to July 2012. Thepatients included 76 geotropic and 70 apogeotropic types. Theright ear was involved in 80 patients (55.2%).The diagnosis of HC-BPPV was based on the following: 1) a

history of brief episodes of positional vertigo, 2) direction-changing horizontal nystagmus beating toward the ground(geotropic nystagmus) or to the ceiling (apogeotropic nystagmus)in head turned to either side in the supine position, and 3) absenceof identifiable central nervous system disorders that could other-wise explain the positional vertigo and nystagmus.To exclude patients with underlying peripheral vestibular

disorders or central positional nystagmus, all patients also re-ceived detailed neurotologic examinations including spontane-ous and gaze-evoked nystagmus, horizontal head impulse,horizontal and vertical smooth pursuit and saccades, limb ataxia,and balance function in addition to routine neurologic exami-nations. Even in patients with isolated vertigo, those with centralocular motor signs, limb ataxia, severe imbalance, or no re-sponse to repeated canalith repositioning maneuvers were ar-ranged for MRIs. We also excluded patients who showedpositive horizontal head impulse test (HIT) as determined atthe bedside, documented caloric paresis on bithermal calorictests, other neurologic deficits indicating central pathologies,and history of continuous vertigo that suggested peripheral orcentral vestibulopathy within one year. This was to avoid bias

from including the patients with asymmetric canal responsesbecause of peripheral or central vestibulopathies other thanBPPV. Although canal paresis or a positive HIT may result fromHC-BPPV itself (14,15), we excluded those cases with canalparesis or positive HIT to avoid bias from including patientswith underlying vestibulopathy.After excluding 19 patients with canal paresis (n = 12),

abnormal head impulse test (n = 2), previous history of othervestibulopathies (n = 2, one with Meniere’s disease and theother with lateral medullary infarction) and poor cooperationduring video-oculography (n = 3), we retrospectively analyzedthe patterns of pseudo-spontaneous nystagmus and HSN in127 patients.

Neurotologic EvaluationAfter measuring the pseudo-spontaneous nystagmus in sitting

position, patients lay supine from sitting (lying-down nystagmus)and turned their heads to either side while supine (head-turningnystagmus) to induce positional nystagmus. Then, the patientswere moved from a supine to sitting position, and the head wasbent down (head-bending nystagmus) (16). We excluded the pa-tients with BPPV involving the posterior or anterior canals.Nystagmus was first observed without fixation using a video-

Frenzel goggle system (SLMED, Seoul, Republic of Korea). Theaffected ear was determined by comparing the intensity of thenystagmus, with an assumption that the induced nystagmus ismore intense when the head is rotated to the affected side in thegeotropic type and to the intact side in the apogeotropic type.When the decision was inconclusive because of near symmetricalnystagmus, the direction of lying-down or head-bending nystag-mus was also considered. In recent studies, the lying-down nys-tagmus mostly beat to the intact ear (10,12,17,18), whereas thehead-bending nystagmus beat to the lesion side in geotropic HC-BPPV (10,16). In apogeotropic type, the directions of lying-downand head-bending nystagmus were mostly opposite to those in-duced in the geotropic type.Eye movements were also recorded using 3-dimensional video-

oculography (SMI, Teltow, Germany). Spontaneous nystagmuswas recorded both with and without fixation while sitting. Afterspontaneous nystagmus was subsided, HSN was induced using apassive head-shaking maneuver. The head was shaken in a sinu-soidal pattern at the frequency of 2.8 Hz paced to the sound of ametronome.Wemeasured the mean slow-phase velocity (SPV) ofthe first 3 beats of HSN. HSN was observed until it disappeared.The presence of HSN was defined only when the SPV of the in-duced nystagmus exceeded the values observed in normal controlsafter subtracting the SPV of pseudo-spontaneous nystagmus(horizontal HSN Q3 degrees per second; vertical HSN Q2 degreesper second; torsional HSN Q2 degrees per second), and when thenystagmus lasted more than 5 seconds (19).The head impulse test was performed manually with a rapid

rotation of the head at an approximate amplitude of 20 degreesin the yaw plane with a high acceleration. Bedside head impulsetest was considered abnormal if a corrective saccade was present(20). Two patients with abnormal HIT were excluded.Bithermal caloric tests were performed by irrigating the ears for

25 seconds with 50 ml of cold and hot water (30-C and 44-C,respectively). Asymmetry of vestibular function was calculatedusing Jongkees’ formula. Canal paresis was defined as a responsedifference of 25% or more between the ears (19), and 12 patientswith canal paresis were also excluded.No patients took any medications that could affect the ves-

tibular function during the evaluation.

496 S. YU. LEE ET AL.

Otology & Neurotology, Vol. 35, No. 3, 2014


Statistical AnalysisStatistical analyses were performed with SPSS (version 18.0,

Chicago, IL, USA). The clinical variables were compared usingthe W2 test (2 tailed), independent sample t test, and binomial test.

RESULTS

Pseudo-Spontaneous NystagmusPseudo-spontaneous nystagmus was observed in 87

(87/127, 68.5%) patients with HC-BPPV, both in geo-tropic (46/69, 66.7%) and apogeotropic (41/58, 70.7%)types without difference in the prevalence between thetypes (p = 0.627, W2 test; Fig. 1). Pseudo-spontaneousnystagmus was mostly mild with the mean SPV rangingfrom 0.2 to 4.6 degrees per second (mean T SD = 1.3 T 0.9degrees per second). Only 46 (52.9%) of the 87 patientsshowed mean SPV of pseudo-spontaneous nystagmusmore than 1.0 degrees per second. The pseudo-spontaneous nystagmus more commonly beat to thelesion side (28/41, 68.3%, p = 0.028, binomial test) inapogeotropic type but either to the intact (25/46, 54.3%)or lesioned (21/46, 45.7%) side without directional pre-ponderance (p = 0.659, binomial test) in the geotropicgroup (Fig. 1).

Head-Shaking NystagmusOf the 90 patients who underwent horizontal head shak-

ing, 27 (30.0%) showed horizontal HSN. Maximum SPV ofhorizontal HSN ranged from 3.1 to 9.9 degrees per second(mean T SD = 4.8 T 1.9 degrees per second), and its durationvaried from 5 to more than 15 seconds. HSN was morecommonly observed in the apogeotropic than in the geo-tropic type (22/44 [50.0%] versus 5/46 [10.9%], p G 0.001,W2 test, Fig. 2). Patients with apogeotropic BPPV showed

predominantly contralesional HSN (19/22, 86.4%, p =0.001, binomial test, Fig. 2) with a mean SPV at 4.4 T 1.4degrees per second, whereas the patients with geotropic typedid not show any directional preponderance of HSN (meanSPV T SD = 6.8 T 2.8 degrees per second, contralesional in2 and ipsilesional in 3, Fig. 2). HSN was induced in only 3(6.5%) of the 46 patients with pseudo-spontaneous nystag-mus from geotropic HC-BPPV and in 17 (41.5%) of the41 patients with pseudo-spontaneous nystagmus fromapogeotropic type (p G 0.001, W2 test). Of interest, 8 of28 patients with ipsilesional pseudo-spontaneous nystag-mus from the apogeotropic type had HSN in the opposite(contralesional) direction of the pseudo-spontaneous nys-tagmus (Fig. 3, Video, Supplemental Digital Content 1,http://links.lww.com/MAO/A192, which demonstrates re-versed HSN).

No differences were found in the clinical features be-tween the groups with and without HSN except the typesof HC-BPPV (independent sample t test, W2 test; Table 1).

DISCUSSION

Pseudo-spontaneous nystagmus is explained by the30-degree inclination of the horizontal semicircular canalfrom the horizontal plane (12). In our patients, pseudo-spontaneous nystagmus more frequently beats to the af-fected side in the apogeotropic type, which is consistentwith the previous explanation of the pseudo-spontaneousnystagmus in apogeotropic HC-BPPV (10Y12). However,the direction of pseudo-spontaneous nystagmus waseither ipsilesional or contralesional in geotropic HC-BPPV.The occurrence and direction of pseudo-spontaneous nys-tagmus in geotropic HC-BPPV would depend on the po-sition of the otolithic debris in the horizontal canal before

FIG. 1. Pseudo-spontaneous nystagmus. Pseudo-spontaneousnystagmus was observed both in geotropic and apogeotropictypes without difference in the prevalence between the types. Thepseudo-spontaneous nystagmus more commonly beat to the le-sion side in apogeotropic type but without directional preponder-ance in geotropic type.

FIG. 2. Head-shaking nystagmus (HSN). HSN was more com-mon in apogeotropic than in geotropic type. HSN mostly beat tothe intact side in apogeotropic type, whereas HSN showed nodirectional preponderance in geotropic one.

497PSEUDO-SPONTANEOUS AND HSN IN HC-BPPV



http://links.lww.com/MAO/A192

assuming the head upright position and should be inter-preted with caution.

Our patients with HC-BPPV frequently showed HSN,which was more common and mostly directed to the in-tact side in the apogeotropic type. The frequent occur-rence of HSN in our HC-BPPV patients without anyidentified underlying vestibulopathy indicates asymmet-ric vestibular inputs during horizontal head-shakingin HC-BPPV, probably because of otolithic debris inthe horizontal semicircular canal. In unilateral or asym-metric peripheral vestibular dysfunction, the HSN beatingaway from the lesion side is explained by accumulatedvestibular asymmetry favoring the intact side in the centralvelocity storage mechanism (21). In the horizontal semi-circular canal, deflection of the cupula toward the utricle(utriculopetal) activates it, whereas the utriculofugaldeflection results in inhibition. Because the inhibitoryvestibular nerve firing rate cannot decrease below zerowhile the firing rate may increase up to 350 to 400 Hzwith stimulation, the excitatory stimuli are more effectivethan the inhibitory ones in inducing vestibular responses(Ewald’s second law) (3). In persons with symmetricalperipheral vestibular function, the oppositely directed in-puts from both ears would be cancelled out during hori-zontal head shaking because of the push-and-pull actionsof the cupulae on both sides. However, in patients withunilateral or asymmetrical peripheral vestibular dysfunc-tion, the net vestibular input (excitatoryYinhibitory input)would be less in the (more severely) damaged ear duringeach cycle of head shaking, and this asymmetry wouldbe amplified during head shaking because of accumulationin the central velocity storage mechanism (1,4). Then, the

accumulated vestibular asymmetry finally discharges asnystagmus beating away from the lesion side after headshaking (HSN).

In our patients with HC-BPPV, HSN was more fre-quent and mostly contralesional in the apogeotropic type,whereas HSN was less common and either ipsilesional orcontralesional in the geotropic type. These findings indicatedecreased vestibular inputs from the involved ear during thehorizontal head shaking in patients with apogeotropic HC-BPPV. Because the apogeotropic HC-BPPV is explainedby otolithic debris attached or near to the cupula in theanterior arm of the horizontal canal, these otolithic debrismay have influenced the cupular dynamics during hori-zontal head shaking. In view of the decreased vestibularinputs from the affected side, we may presume interruptionor decreased transfer of the endolymph flow to the cupulabecause of mechanical blockage by the otolithic debris.That is, the otolithic debris near the inlet of the ampullamayhave played a role as a check valve, and thus allowed theendolymph to enter the ampulla and caused cupular devi-ation during initial rotation in one direction. In contrast,subsequent rotation in the opposite direction would movethemass into the ball-valve position, cutting off endolymphflow from the ampulla and preventing any cupular move-ment. After the first few head rotations, once the pressurehas risen in the ampulla, the pressure accumulation withinthe ampulla would equal the force exerted by endolymphmoving toward the ampulla, preventing any further inflowand tightly sealing the ball-valve into the ampullary neck.The presence of a ball-valve essentially acts as a semicir-cular canal plugging, leaving only one functioning ear. Thiswould result in asymmetric velocity storage and a typicalHSN beating away from the canal-plugged ear (Fig. 4)(1,4). In contrast, the rare occurrence and no directionalpreponderance of HSN in the geotropic type indicate thatotolithic debris in the canal generally do not exert a sig-nificant impact on the fluid dynamics of the endolymphduring head-shaking.

In previous reports, HSN usually indicates underlyingvestibular asymmetry because of peripheral or centralvestibular dysfunction. Indeed, HSN is one of the mostsensitive signs of vestibular neuritis and may also be

TABLE 1. Comparison of clinical features according to thepresence of HSN

HSN (+)(n = 27)

HSN (-)(n = 63) p

Age, yr (SD) 64.4 (11.4) 65.8 (11.8) 0.589Sex (%, women) 19/27 (65.1) 41/63 (70.4) 0.626Lesion side (%, Right) 16/27 (59.3) 32/63(50.8) 0.461Presence of SN (%) 20/27 (74.1) 45/63 (71.4) 0.797Direction of SN

(%, ipsilesional)12/20 (60.0) 23/45 (51.1) 0.507

Mean SPV of SN (O/s, SD) 0.87 (0.78) 0.86 (0.93) 0.944Subtype of HC-BPPV

(%, apogeotropic)22/27 (81.5%) 22/63 (34.9%) G0.001

HC-BPPV indicates horizontal canal benign paroxysmal positionalvertigo; HSN, head-shaking nystagmus; SN, pseudo-spontaneous nys-tagmus; SPV, slow-phase velocity.

FIG. 3. Recording of pseudo-spontaneous, head-shaking (HSN),and head-turning nystagmus in a patient with apogeotropic benignparoxysmal positional vertigo involving the left horizontal semicir-cular canal. A, The pseudo-spontaneous nystagmus beat to theinvolved left side while HSN beat to the healthy right side. B, Thepatient shows apogeotropic nystagmus in the head turned positionwhile supine, which was more intense when the head was turned tothe unaffected right side.




observed in lesions involving the brainstem and cere-bellum (1,4,19,21Y23). Our study shows that HSN maybe induced by deranged cupular dynamics because ofmechanical restriction and is not necessarily indicative ofunderlying vestibular dysfunction in HC-BPPV. HSNwas also described in HC-BPPV in a previous study (10).

In our patients with apogeotropic HC-BPPV, the HSNpredominantly beats to the intact side. In HC-BPPV, theinvolved side is usually determined by comparing theintensity of nystagmus observed in the head-turnedposition to either side. In the apogeotropic type, the in-duced nystagmus is usually more intense when the head isturned to the intact side (2,24). However, the intensity ofnystagmus is often inconclusive or misleading. In thosecases, the direction of pseudo-spontaneous, head-bendingand lying-down nystagmus aid in lateralization. Ourstudy adds the direction of HSN to the list of lateralizingsigns in apogeotropic HC-BPPV.

Of interest, 8 of 28 patients with ipsilesional pseudo-spontaneous nystagmus had HSN in the opposite direc-tion of the pseudo-spontaneous nystagmus. HSN in theopposite direction of spontaneous nystagmus is usuallyregarded a central sign and has been described in lateralmedullary or cerebellar infarctions (19,23). Our studyshows that this phenomenon may occur in apogeotropicHC-BPPV.

Our study has some limitations. First of all, it is a retro-spective single-center study. Second, although we excludedpatients with underlying unilateral or asymmetrical vestib-ular dysfunction, as was determined with horizontal headimpulse and caloric tests, these tests may be negative incompensated unilateral or asymmetrical vestibulopathies.

Accordingly, HSN may have resulted from underlyingcompensated vestibulopathy (25,26). Third, we did notreevaluate HSN after resolution of BPPV. However, thechance of false negative head impulse and bithermal calorictests seems reasonably low in patients with HSN.

CONCLUSION

Pseudo-spontaneous nystagmus beats more to the lesionside in apogeotropic HC-BPPV but in either direction inthe geotropic type. HSN was more common and mostlycontralesional in apogeotropic HC-BPPV. The differentprevalence and patterns of HSN in apogeotropic and geo-tropic HC-BPPV suggest dissimilar cupular dynamics inthose disorders. The direction of HSN seems to be moreuseful than the direction of pseudo-spontaneous nystag-mus for determining the affected side of apogeotropicHC-BPPV.

REFERENCES

1. Takahashi S, Fetter M, Koenig E, Dichgans J. The clinical significanceof head-shaking nystagmus in the dizzy patient. Acta Otolaryngol1990;109:8Y14.

2. Leigh RJ, Zee DS. The Neurology of Eye Movements. 4th ed. NewYork, NY: Oxford University Press, 2006.

3. Baloh RW, Honrubia V, Konrad HR. Ewald’s second law re-evaluated. Acta Otolaryngol 1977;83:475Y9.

4. ChoiKD, Kim JS. Head-shaking nystagmus in central vestibulopathies.Ann NY Acad Sci 2009;1164:338Y43.

5. Dix MR, Hallpike CS. The pathology, symptomatology and diag-nosis of certain common disorders of the vestibular system. Proc RSoc Med 1952;45:341Y54.

FIG. 4. A proposed mechanism for head-shaking nystagmus (HSN) in apogeotropic benign paroxysmal positional vertigo involving the lefthorizontal semicircular canal. After head-shaking, the otoconial debris near the inlet of the ampulla block the endolymph flow. By sealing offthe inlet of the ampulla, the otolithic debris may exert a canal plugging effect, which would leave only the right ear to function, and lead toright beating HSN.

499PSEUDO-SPONTANEOUS AND HSN IN HC-BPPV



6. Lee SH, Kim JS. Benign paroxysmal positional vertigo. J ClinNeurol 2010;6:51Y63.

7. Schuknecht HF. Cupulolithiasis. Arch Otolaryngol 1969;90:765Y78.8. Hall SF, Ruby RR, McClure JA. The mechanics of benign parox-

ysmal positional vertigo. J Otolaryngol 1979;8:151Y8.9. Baloh RW, Jacobson K, Honrubia V. Horizontal semicircular canal

variant of benign positional vertigo. Neurology 1993;43:2542Y9.10. Nuti D, Mandala M, Salerni L. Lateral canal paroxysmal positional

vertigo revisited. Ann N Y Acad Sci 2009;1164:316Y23.11. Asprella-Libonati G. Pseudo-spontaenous nystagmus: a new sign to

diagnose the affected side in lateral semicircular canal benign par-oxysmal positional vertigo. Acta Otorhinolaryngol Ital 2008;28:73Y8.

12. Asprella Libonati G. Diagnostic and treatment strategy of the lateralsemicircular canal canalolithiasis. Acta Otorhinolaryngol Ital 2005;25:277Y83.

13. Bisdorff AR, Debatisse D. Localizing signs in positional vertigo dueto lateral canal cupulolithiasis. Neurology 2001;57:1085Y8.

14. Strupp M, Brandt T, Steddin S. Horizontal canal benign paroxysmalpositioning vertigo: reversible ipsilateral caloric hypoexcitabilitycaused by canalolithiasis? Neurology 1995;45:2072Y6.

15. Heidenreich KD, Beaudoin K, White JA. Can active lateral canalbenign paroxysmal positional vertigo mimic a false-positive headthrust test? Am J Otolaryngol 2009;30:353Y5.

16. Lee SH, Choi KD, Jeong SH, Oh YM, Koo JW, Kim JS. Nystagmusduring neck flexion in the pitch plane in benign paroxysmal positionalvertigo involving the horizontal canal. J Neurol Sci 2007;256:75Y80.

17. Koo JW, Moon IS, Shim WS, Moon SY, Kim JS. Value of lying-down nystagmus in the lateralization of horizontal semicircular

canal benign paroxysmal positional vertigo. Otol Neurotol 2006;27:367Y71.

18. Han BI, Oh HJ, Kim JS. Nystagmus while recumbent in horizontalcanal benign paroxysmal positional vertigo. Neurology 2006;66:706Y10.

19. Choi KD, Oh SY, Park SH, Kim JH, Koo JW, Kim JS. Head-shakingnystagmus in lateral medullary infarction: patterns and possiblemechanisms. Neurology 2007;68:1337Y44.

20. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. ArchNeurol 1988;45:737Y9.

21. Hain TC, Fetter M, Zee DS. Head-shaking nystagmus in patientswith unilateral peripheral vestibular lesions. Am J Otolaryngol1987;8:36Y47.

22. Katsarkas A, Smith H, Galiana H. Head-shaking nystagmus (HSN):the theoretical explanation and the experimental proof. ActaOtolaryngol 2000;120:177Y81.

23. Huh YE, Kim JS. Patterns of spontaneous and head-shaking nys-tagmus in cerebellar infarction: imaging correlations. Brain 2011;134:3662Y71.

24. Brandt T. Vertigo: Its multisensory syndromes. 2nd ed. London,UK: Springer, 1999.

25. Choi KD, Oh SY, Kim HJ, Koo JW, Cho BM, Kim JS. Recovery ofvestibular imbalances after vestibular neuritis. Laryngoscope 2007;117:1307Y12.

26. MacDougall HG, Weber KP, McGarvie LA, Halmagyi GM,Curthoys IS. The video head impulse test: diagnostic accuracy inperipheral vestibulopathy. Neurology 2009;73:1134Y41.




pseudo-spontaneous and head-shaking nystagmus in ... · pdf filein horizontal canal benign...

Documents