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184 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
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Technique
Patients are asked to stand with their arms at their sides in the following four test conditions: (1) firm surface with eyes open, (2) firm surface with eyes closed, (3) compli­ant surface (foam) with eyes open, and (4) compliant surface (foam) with eyes closed. The foam should be of sufficient density and thickness to support the indi­vidual’s bodyweight. Each position is timed for 30 s. If patients are unable to maintain the position for 30 s, they are provided two additional attempts, and the times for the three trials are averaged. The position of the feet (feet together versus feet apart) and footwear do not influence the scores (Whitney & Wrisley, 2004; Wrisley & Whitney, 2004). A total score is calculated by add­ing the times (or average times if more than one trial is required) for the four test positions together.
Results
Normal Results
Normative data for the CTSIB has been published in 69 healthy adults aged 20 to 70 years (El-Kashlan, Shepard, Asher, Smith-Wheelock, & Telian, 1998). Cohen et al. (1993) also presented data for a group of neurologically asymptomatic adults for the CTSIB. While a maximum score on the CTSIB is 180 (30 s for each of six test conditions), only four of the test condi­tions are performed for the mCTSIB. Normal subjects should be able to maintain the four test positions for approximately 30 seconds, with a score close to 120.
Abnormal Results
An inability to maintain the four test positions for approximately 30 seconds is considered to be abnormal.
Mechanism
The medial and lateral vestibulospinal and reticulospi­nal tracts are important components of the vestibular contribution to postural control. The medial vestibulo­spinal tract originates in the medial vestibular nucleus and contributes fibers to the medial longitudinal fas­ciculus. The lateral vestibulospinal tract originates in the lateral vestibular nucleus and carries vestibular and cerebellar information to the lower motor neurons. The lateral vestibular nucleus receives afferent information from the eighth nerve, as well as efferent information from the vermis and fastigial nuclei in the cerebel­lum. Descending projections from the fastigial nuclei
to the vestibular nuclei and reticular formation influ­ence axial and proximal motor control (Zhang, Wang, & Zhu, 2016). The reticulospinal tract originates from the reticular formation and influences muscle tone. It also facilitates or inhibits volitional movement (pyra­midal system) and myotatic reflexes. Myotatic reflexes contribute to postural control by maintaining joint stiffness. Volitional movement contributes to postural control through the execution of learned, purposeful movements. These purposeful movements can prevent or counteract a loss of balance.
Test Performance
The mCTSIB is correlated with condition 2 (firm sur­face with eyes closed; r = 0.48), condition 4 (sway­referenced surface with eyes open; r = 0.30), and condition 5 (sway-referenced surface with eyes closed; r = 0.51) on the Sensory Organization Test (SOT) (Wris­ley & Whitney, 2004). Weber and Cass (1993) found that the mCTSIB condition 4 (standing on a compliant sur­face [foam] with eyes closed) had a sensitivity of 95% and a specificity of 90% in comparison to the SOT in patients with complaints of dizziness and imbalance. Individuals with posterior canal BPPV demonstrated greater sway velocity when standing on foam with eyes open or eyes closed during the instrumented mCTSIB (Zhou et al., 2015). No postural deficits were observed in individuals with horizontal canal BPPV compared with healthy controls (Zhou et al., 2015). In patients with unilateral vestibulopathy, correlations between the conditions on the CTSIB and the SOT composite score ranged from −0.23 to −0.65 (Park et al., 2013). Park et al. (2013) found the resulting sensitivity was 42% and the specificity was 68% for the mCTSIB to cor­rectly identify individuals with unilateral vestibulopa­thy from healthy controls.
The VEDGE task force determined that the mCTSIB was Reasonable to Recommend at this time for patients with acute (zero to six weeks) and chronic (greater than six weeks) vestibular disorders. The mCTSIB was Reasonable to Recommend at this time for patients with peripheral or central dysfunction and in individuals with BPPV.
SUMMARY
The results of bedside tests of vestibular function such as those described in this chapter are commonly con­sidered to be well-established criteria for the appropri-
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ate referral of patients for diagnostic testing. However, a review of published literature regarding the tests in question do have conflicting results. Rather, the tests may be most appropriately used as a screening to alert the examiner that additional testing is warranted or to inform the examiner of specific functional impair­ments experienced by the patient. Although the tests reviewed in this chapter tend to exhibit high specific­ity, their attendant low sensitivity renders them rela­tively unsuitable for diagnostic purposes in clinical use. As such, these informal assessment tools should not be considered to be substitutes for electrophysi­ologic testing, imaging studies, or other diagnostic testing. If bedside tests are included in the screening and referral process, new or improved versions and combinations of the tests must be developed, investi­gated, and proven by clinician scientists. Without such developments, it is likely that reliance on bedside tests of vestibular function may lead to missed diagnoses or inappropriate referrals for testing and follow-up care.
referenCes
Alexander, G. (1912). Die Ohrenkrankheiten im Kindesalter.
In M. Pfaundler & A. Schossmann (Eds.), Handbuch der Kinderheilkunde (pp. 84–96). Leipzig, Germany: Vogel.
Angelaki, D. E., & Perachio, A. A. (1993). Contribution of
irregular semicircular canal afferents to the horizontal vestibule-ocular response during constant velocity rota­tion. Journal of Neurophysiology, 69, 996–999.
Bance, M. L., O’Driscoll, M., Patel, N., & Ramsden, R. T.
(1998). Vestibular disease unmasked by hyperventilation. Laryngoscope, 108(4), 610–614.
Bárány, R. (1907). Untersuchungen uber Verhalten des Ves-
tibularapparates bei Kopftraumen und ihre practische Bedeuntung. Verhandugen der Deutxchen Otol Gessellschaft, pp. 252–266.
Barber, H. O. (1984). Vestibular neurophysiology. Otolaryngol-
ogy–Head and Neck Surgery, 92, 151–157.
Beynon, G. J., Jani, P., & Baguley, D. M. (1998). A clinical
evaluation of head impulse testing. Clinical Otolaryngol- ogy, 106, 6–9.
Borries, G. V. (1923). Klinische Untersuchungen uber die-
durch Kopfbewegungen und Kopfstellungen ausgelosten Nystagmussantalle. Monatschr Ohrenheilk, 57, 644–683.
Brandt, T., & Strupp, M. (2005). General vestibular testing.
Clinical Neurophysiology, 116, 406–426.
Brantberg, K., Bagger-Sjoback, D., Mathiesen, T., Witt, H., &
Pansell, T. (2006). Posterior canal dehiscence syndrome caused by an apex cholesteatoma. Otology and Neuro- Otology, 27(4), 531–534.
Brantberg, K., Bergenius, J., Mendel, L., Witt, H., Tribukait,
A., & Ygge, J. (2001). Symptoms, findings and treatment
in patients with dehiscence of the superior semicircular canal. Acta Otolaryngolica, 121(1), 68–75.
Brantberg, K., Greitz, D., & Pansell, T. (2004). Subarcuate
venous malformation causing audio-vestibular symptoms similar to those in superior canal dehiscence syndrome. Otology and Neuro-Otology, 25(6), 993–997.
Brickner, R. M. (1936). Oscillopsia: A new symptom com-
monly occurring in multiple sclerosis. Archives of Neuro- logical Psychiatry, 36, 586–589.
Burgio, D. L., Blakely, B. W., & Myers, S. F. (1991). An evaluation
of the head-shaking nystagmus test. Acta Oto-Laryngologica Supplement, 540, 27–33.
Burgio, D. L., Blakely, B. W., & Myers, S. F. (1992). The high-
frequency oscillopsia test. Journal of Vestibular Rehabilita- tion, 2, 221–226.
Califano, L., Iorio, G., Salafia, F., Mazzone, S., & Califano, M.
(2015). Hyperventilation-induced nystagmus in patients with vestibular schwannoma. Otology & Neurotology, 36(2), 303–306.
Cass, S. P., Kartush, J. M., & Graham, M. D. (1992). Patterns
of vestibular function following vestibular nerve section. Laryngoscope, 102, 388–394.
Chee, N. W., & Tong, H. M. (2002). Acoustic neuroma present-
ing as exercise-induced vertigo. Journal of Laryngology and Otology, 116(8), 630–632.
Choi, K. D., Cho, H. J., Koo, J. W., Park, S. H., & Kim, J. S.
(2005). Hyperventilation-induced nystagmus in vestibular schwannoma. Neurology, 64(12), 2062.
Cohen, B., Henn, V., Raphan, T., & Dennett, D. (1981). Velocity
storage, nystagmus, and visual vestibular interactions in humans. Annals of the New York Academy of Sciences, 374, 421–433.
Cohen, B., Matsuo, V., & Raphan, T. (1977). Quantitative anal-
ysis of the velocity characteristics of optokinetic nystag­mus and optokinetic afternystagmus. Journal of Physiology, 270, 321–344.
Cohen, H., Blatchly, C. A., & Gombash, L. L. (1993). A study of
the clinical test of sensory interaction and balance. Physical Therapy, 73(6), 351-354.
Cremer, P. D., Halmagyi, G. M., Aw, S. T., Curthoys, I. S.,
McGarvie, L. A., Todd, M. J., . . . Hannigan, I. P. (1998). Semicircular canal plane head impulses detect absent func­tion of individual semicircular canals. Brain, 121, 699–716.
Cremer, P. D., Minor, L. B., Carey, J. P., & Della Santina, C.
C. (2000). Eye movements in patients with superior canal dehiscence syndrome align with the abnormal canal. Neu- rology, 55(12), 1833–1841.
Davies, R. (2004). Bedside neuro-otological examination and
interpretation of commonly used investigations. Journal of Neurology, Neurosurgery, and Psychiatry, 75(Suppl. 4), 32–44.
Dayal, V. S., Tarantino, L. Farkashidy, J., & Paradisgarten, A.
(1974). Spontaneous and positional nystagmus: A reas­sessment of clinical significance. Laryngoscope, 84(11), 2033–2044.
Demer, J. L., Honrubia, V., & Baloh, R. W. (1994). Dynamic
visual acuity: A test of oscillopsia and vestibulo-ocular reflex function. American Journal of Otology, 16, 97–103.
186 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
Drachman, D. A., & Hart, C. W. (1972). An approach to the
dizzy patient. Neurology, 22(4), 323–334.
El-Kashlan, H. K., Shepard, N. T., Asher, A. M., Smith-Whee-
lock, M., & Telian, S. A. (1998). Evaluation of clinical mea­sures of equilibrium. Laryngoscope, 108(3), 311–319.
Fetter, M., & Dichgans, J. (1990). Adaptive mechanisms of
VOR compensation after unilateral peripheral vestibular lesions in humans. Journal of Vestibular Research, 1, 9–22.
Fisher, C. M. (1969). The neurological examination of the
comatose patient. Acta Neurologica Scandinavica, 45(Suppl.
36), 1–56.
Foster, C. A., Foster, B. D., Spindler, J., & Harris, J. P. (1994).
Functional loss of the horizontal doll’s eye reflex following unilateral vestibular lesions. Laryngoscope, 104(4), 473–478.
Fujimoto, M., Rutka, J., & Mai, M. (1993). A study into the
phenomenon of head-shaking nystagmus: Its presence in a dizzy population. Journal of Otolaryngology, 22(5), 376–379.
Furman, J. M., Balaban, C. D., & Pollack, I. F. (1997). Vestibu-
lar compensation in a patient with a cerebellar infarction. Neurology, 48, 916–920.
Giardina, B., Mosca, D., & De Rosa, M. C., (2004). The Bohr
effect of haemoglobin in vertebrates: An example of molecular adaptation to different physiological require­ments. Acta Physiologica Scandia, 182(3), 229–244.
Goebel, J. A. (2001). The ten-minute examination of the dizzy
patient. Seminars in Neurology, 21(4), 391–398.
Goebel, J. A., & Garcia, P. (1992) Prevalence of post-head
shake nystagmus in patients with caloric deficits and ver­tigo. Otolaryngology–Head and Neck Surgery, 106, 121–127.
Goldberg, J. M., & Fernandez, C. (1971). Physiology of
peripheral neurons innervating semicircular canals of the squirrel monkey. I. Resting discharge and response to con­stant angular acceleration. Journal of Neurophysiology, 34, 634–660.
Guidetti, G., Monzani, D., & Civiero, N. (2002) Head shak-
ing nystagmus in the follow-up of patients with vestibular diseases. Clinical Otolaryngology, 27, 124–128.
Guidetti, G., Monzani, D., & Rovatti, V. (2006). Clinical exami-
nation of labyrinthine-defective patients out of the vertigo attack: Sensitivity and specificity of three low-cost meth­ods. Acta Otorhinolaryngologica Italia, 26, 96–101.
Hain, T. C. (2006). Hyperventilation in dizzy persons. Retrieved
from http://www.dizziness-and-balance.com/practice/ hyperventilation.htm
Hain, T. C., Fetter, M., & Zee, D. S. (1987). Head-shaking nys-
tagmus in patients with unilateral peripheral vestibular lesions. American Journal of Otolaryngology, 8, 36–47.
Hain, T. C., & Spindler, J. S. (1993). Head-shaking nystagmus.
The vestibulo-ocular reflex and vertigo. New York, NY: Raven Press.
Hall, S. F., & Laird, M. E. (1992). Is head-shaking nystagmus
a sign of vestibular dysfunction? Journal of Otolaryngology, 21, 209–212.
Halmagyi, G. M., Aw, S. T., McGarvie, L. A., Todd, M. J., Brad-
shaw, A., Yavor, R., & Fagan, P. A. (2003). Superior semi­circular canal dehiscence simulating otosclerosis. Journal of Laryngology and Otology, 117, 553–557.
Halmagyi, G. M., Black, R. A., Thurtell, M. J., & Curthoys, I.
S. (2003). The human horizontal vestibulo-ocular reflex in response to active and passive head impulses after uni­lateral vestibular deafferentation. Annals of the New York Academy of Sciences, 1004, 325–336.
Halmagyi, G. M., & Curthoys, I. S. (1988). A clinical sign of
canal paresis. Archives of Neurology, 45, 737–739.
Halmaygi, G. M., Curthoys, I. S., & Cremer, P. D., (1990). The
human horizontal vestibule-ocular reflex in response to high-acceleration stimulation before and after unilateral vestibular neurectomy. Experimental Brain Research, 81, 479–490.
Harvey, S. A., & Wood, D. J. (1996). The oculocephalic
response in the evaluation of the dizzy patient. Laryngo- scope, 104, 473–478.
Harvey, S. A., Wood, D. J., & Feroah, T. R. (1997). Relation-
ship of the head impulse tests and head-shake nystagmus in reference to caloric testing. American Journal of Otology, 18, 207–213.
Herdman, S. J., Schubert, M. C., Das, V. E., & Tusa, R. J. (2003).
Recovery of dynamic visual acuity in unilateral vestibular hypofunction. Archives of Otolaryngology–Head and Neck Surgery, 129, 819–824.
Herdman, S. J., Tusa, R. J., Blatt, P., Suzuki, A., Venuto, P. J.,
& Roberts, D. (1998). Computerized dynamic visual acu­ity test in the assessment of vestibular deficits. American Journal of Otology, 19, 790–796.
Hillman, T. A., Kertesz, T. R., Hadley, K., & Shelton, C. (2006).
Reversible peripheral vestibulopathy: The treatment of superior canal dehiscence. Otolaryngology–Head and Neck Surgery, 134(3), 431–436.
Igarashi, M., & Ishikawa, K. (1985). Post-labyrinthectomy bal-
ance compensation with preplacement of cerebellar ver­mis lesion. Acta Otolaryngolica, 99(3–4), 452–458.
Iwasaki, S., Ito, K., Abbey, K., & Murofushi, T. (2004). Predic-
tion of canal paresis using head shaking nystagmus test. Acta Oto-Laryngologica, 124, 803–806.
Jacobson, G. P., Newman, C. W., & Safadi, I. (1990) Sensitiv-
ity and specificity of the head-shaking test for detecting vestibular system abnormalities. Annals of Oto-Rhino- Laryngology, 99, 539–542.
Jacobson, G. P., Pearlstein, R., Henderson, J., Calder, J. H., &
Rock, J. (1998). Recovery nystagmus revisited. Journal of the American Academy of Audiology, 9, 263–271.
Kamei, T., & Kornhuber, H. H. (1964). Spontaneous and head-
shaking nystagmus in normals and in patients with cen­tral lesions. Canadian Journal of Otolaryngology, 3, 372–380.
Kaufman, G. D., Anderson, J. H., & Beitz, A. J. (1992). Brain-
stem Fos expression following acute unilateral labyrin­thectomy in the rat. NeuroReport, 3(10), 829–832.
Kelly, D. H. (1985). Visual processing of moving stimuli. Jour-
nal of the Optometry Society of America, 2(2), 216–225.
Kroenke, K., Lukas, C. A., Rosenberg, M. L., Scherokman,
B., Herbers, J. E. Jr., Wehrle, P. A., & Boggi, J. O. (1992). Causes of persistent dizziness. A prospective study of 100 patients in ambulatory care. Annals of Internal Medicine, 117(11), 898–904.
9. BEdsidE AssEssmEnt oF tHE vEstiBulAr systEm 187
https://t.me/medicina_free
Lee, M. H., Durnford, S. J., & Crowley, J. S. (1997). Visual ves-
tibular interaction in the dynamic visual acuity test dur­ing voluntary head rotation. Aviation Space Environmental Medicine, 68, 111–117.
Lee, M. Y., Son, H. R., Rah, Y. C., Jung, J. Y., & Suh, M. W.
(2019). Recovery phase spontaneous nystagmus, its exis­tence and clinical implication. Journal of Audiology and Otology, 23(1), 33–38.
Lehnen, N., Aw, S. T., Todd, M. J., & Halmagyi, G. M. (1994).
Head impulse test reveals residual semicircular canal function after vestibular neurectomy. Neurology, 62, 2294–
2296.
Leigh, R. J., & Zee, D. S. (1999). The neurology of eye move-
ments (3rd ed.). New York, NY: Oxford University Press. Longridge, N. S., & Mallinson, A. I. (1984). A discussion of the dynamic illegible E test: A new method of screening for aminogylcoside vestibulotoxicity. OtolaryngologyHead and Neck Surgery, 92, 671–676.
Longridge, N. S., & Mallinson, A. I. (1987a). The dynamic
illegible E (DIE) tests. A simple technique for assessing the ability of the vestibulo-ocular reflex to overcome vestibu­lar pathology. Journal of Otolaryngology, 16, 97–103.
Longridge, N. S., & Mallinson, A. I. (1987b). The dynamic illeg-
ible E-test. Acta Otolaryngologica (Stockholm), 103, 273–279.
Lustig, L. R., & Jackler, R. K. (1999). The history of otology
through eponyms II: The clinical examination. American Journal of Otology, 20(4), 535–550
McClure, J. A., & Lycett, P. (1978). Recovery nystagmus. Jour-
nal of Otolaryngology, 7(2), 141–148.
Miller, J. W., & Ludvigh, E. J. (1962). The effect of relative
motion on visual acuity. Surveys in Ophthalmology, 7, 83–116.
Minor, L. B. (2000). Superior canal dehiscence syndrome.
American Journal of Otology, 21(1), 9–19.
Minor, L. B., Cremer, P. D., Carey, J. P., Della Santina, C. C.,
Streubel, S. O., & Weg, N. (2001). Symptoms and signs in superior canal dehiscence syndrome. Annals of the New York Academy of Sciences, 942, 259–273.
Minor, L. B., Haslwanter, T., Straumann, D., & Zee, D. S.
(1999). Hyperventilation-induced nystagmus in patients with vestibular schwannoma. Neurology, 53(9), 2158–2168.
Monday, L. A., & Tetreault, L. (1980). Hyperventilation and
vertigo. Laryngoscope, 90, 1003–1010.
Moritz, W. Z. (1951). An analysis of nystagmus due to move-
ment of the head. Laryngology, Rhinology, and Otology, 30(6), 269–275.
Park, M. K., Kim, K. M., Jung, J., Lee, N., Hwang, S. J., &
Chae, S. W. (2013). Evaluation of uncompensated unilat­eral vestibulopathy using the modified clinical test for sensory interaction and balance. Otology & Neurotology, 34(2), 292–296.
Peitersen, E. (1967). Vestibulospinal reflexes X: Theoretical
and clinical aspects of the stepping test. Archives of Otolar- yngology, 85, 192–198.
Perez, N., & Rama-Lopez, J. (2003). Head impulse and caloric
tests in patients with dizziness. Otology and Neuro-Otology, 24, 913–917.
Rambold, H., Heide, W., Sprenger, A., Haendler, G., & Helm-
chen, C. (2001). Perilymph fistula associate with pulse­synchronous eye oscillations. Neurology, 56(12), 1769–1771.
Raphan, T., Matsuo, V., & Cohen, B. (1979). Velocity storage
in the vestibule-ocular reflex arc (VOR). Experimental Brain Research, 35, 229–248.
Rine, R. M., Roberts, D. Corbin, B. A., McKean-Cowdin, R.,
Varma, R., Beaumont, J., et al. (2012). New portable tool to screen vestibular and visual function tutes of Health Toolbox initiative. Journal of Rehabilitation Research and Development, 49, 209–20.
Rine, R. M., Schubert, M. C., Whitney, S. L., Roberts, D., Red-
fern, M. S., Musolino, M. C., et al. (2013). Vestibular function assessment using the NIH Toolbox. Neurology, 80, S25–S31.
Robichaud, J., DesRoches, H., & Bance, M. (2002). Is hyper-
ventilation-induced nystagmus more common in retro­cochlear vestibular disease than in end-organ vestibular disease? Journal of Otolaryngology, 31(3), 140–143.
Sakellari, V., Bronstein, A. M., Corna, S., Hammon, C. A.,
Jones, S., & Wolsley, C. J. (1997). The effects of hyperven­tilation on postural control mechanisms. Brain, 120(9), 1659–1673.
Sama, A., Meikle, J. C., & Jones, N. S. (1995). Hyperventila-
tion and dizziness: Case reports and management. British Journal of Clinical Practice, 49(2), 79–82.
Scherer, M. R., Horn, L. B., Dannenbaum, E., Fay, J. L., Lam-
bert, K. H., Rice, T. A., . . . Wrisley, D. M. (2014). Vestibu- lar EDGE (VEDGE). Academy of Neurologic Physical Therapy. Retrieved from http://www.neuropt.org/pro fessional-resources/neurology-section-outcome-mea sures-recommendations/vestibular-disorders
Schubert, M. C., Tusa, R. J., Grine, L. E., & Herdman, S. J.
(2004). Optimizing the sensitivity of the head thrust test for identifying vestibular hypofunction. Physical Therapy, 84, 151–158.
Serra, A., & Leigh, R. J. (2002). Diagnostic value of nystag-
mus: Spontaneous and induced ocular oscillations. Journal of Neurology, Neurosurgery, and Psychiatry, 73, 615–618.
Shepard, N. T. (1998). Caloric weakness needed to achieve a posi-
tive head thrust test. XXth Regular Meeting of the Bárány Society, Equilibrium in research and equilibriometry in modern treatment. Wurzberg, Germany: Elsevier.
Singer, E. P. (1958). The vestibulospinal test in unilateral
neurolabrinthitis. New York State Journal of Medicine, 58(9), 1494–1500.
Takahashi, S., Fetter, M., Koenig, E., & Dichgans, J. (1990).
The clinical significance of head-shaking nystagmus in the dizzy patient. Acta Otolaryngologica (Stockholm), 109, 8–14.
Tilikete, C., Krolak-Salmon, P., Truy, E., & Vighetto, A. (2004).
Pulse-synchronous eye oscillations revealing bone supe­rior canal dehiscence. Annals of Neurology, 56(4), 556–560.
Tseng, H. Z., & Chao, W. Y. (1997). Head-shaking nystagmus:
A sensitive indicator of vestibular dysfunction. Clinical Otolaryngology and Allied Sciences, 22(6), 549–552.
Vicini, C., Casani, A., & Ghilardi, P. (1989). Assessment of
head shaking in neuro-otological practice. Journal of Oto- rhinolaryngol and Related Specialties, 51, 8–13.
— National Insti-
188 BAlAnCE FunCtion AssEssmEnt And mAnAgEmEnt
https://t.me/medicina_free
Vogel, K. (1929) Differential diagnostische Anhaltspunkte fur
die Erkennung von Schadigungen des Gleichgewichsap­parates nach Schadelverletzungen. Deutsche Medizinische Wochenschrift, 7, 268–270.
Walker, M. F., & Zee, D. S. (1999). The effect of hyperven-
tilation on downbeat nystagmus in cerebellar disorders. Neurology, 53(7), 1576–1579.
Walker, M. F., & Zee, D. S. (2000). Bedside vestibular examina-
tion. Otolaryngology Clinics of North America, 33(3), 495–506.
Weber, P. C. & Cass, S. P. (1993). Clinical assessment of pos-
tural stability. American Journal of Otolaryngology, 14(6), 566–569.
Wei, D., Hain, T. C., & Proctor, L. R. (1989). Head-shaking
nystagmus: Associations with canal paresis and hearing loss. Acta Oto-Laryngologica (Stockholm), 108, 362–367.
Westheimer, G., & McKee, S. P. (1975). Visual acuity in the
presence of retinal image motion. Journal of Optometry Soci- ety of America, 65, 847–850.
Whitney, S. L. & Wrisley, D. M. (2004). The influence of foot-
wear on timed balance scores of the modified clinical test of sensory interaction and balance. Archives of Physical Medicine and Rehabilitation, 85(3): 439–443.
Wilson, W. R., & Kim, J. W. (1981). Study of ventilation testing
with electronystagmography. Annals of Otology Rhinology and Laryngology, 90(1 Pt. 1), 56–59.
Wrisley, D., & Whitney, S. (2004). The effect of foot position on
the modified clinical test of sensory interaction and balance. Archives of Physical Medicine and Rehabilitation, 85(2), 335–338.
Zee, D. S., & Fletcher, W. A. (1996). Bedside examination. In R.
W. Baloh & C. M. Halmagyi (Eds.), Disorders of the vestibu- lar system (pp. 178–190). New York, NY: Oxford University Press.
Zhang, X.-Y., Wang, J.-J., & Zhu, J.-N. (2016). Cerebellar fasti-
gial nucleus: From anatomic construction to physiological functions. Cerebellum & Ataxias, 3(1), 1–10.
Zhou, R., Liu, B., Zhang, S., Liu, D., Liu, J., Leng, Y., & Kong,
W. (2015). The balance function of the patients with benign paroxysmal positional vertigo during standing. Journal of Clinical Otorhinolaryngology, Head, and Neck Surgery, 29(22), 1966–1969.
Zuma e Maia, F. C., Cal, R., D’Albora, R., Carmona, S., &
Schubert, M. C. (2017). Head-shaking tilt suppression:
clinical test to discern central from peripheral causes of
A vertigo. Journal of Neurology, 264(6), 1264–1270.
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https://t.me/medicina_free
Eye Movement Recording and
Ocular Motility Testing
Neil T. Shepard, Michael C. Schubert, and Scott D. Z. Eggers
INTRODUCTION
Provided is a discussion of the technical aspects of eye movement recording techniques, the routine clini­cal evaluation of the ocular motor systems involved with gaze stability, saccade production, smooth pur­suit tracking, and the optokinetic system. In addition are the interpretations for each of these tests and how they can be used in routine clinical investigations of the dizzy patient, principally for the purpose of site-of­lesion determination.
To better understand the interpretation of these tests and how they can be used to localize lesions to the central nervous system (CNS), the reader is referred to Chapter 3 and other sources (Leigh & Zee, 2006) for a review of the neurologic pathways involved in each of the ocular motor tasks listed above. In a review of that nature, you find overlaps in the neural pathways espe­cially between gaze stability to an eccentric target and saccade production, gaze stability to a primary target and smooth pursuit, smooth pursuit and optokinetic activity. Therefore, although the tests for ocular motor functioning can be used to indicate CNS involvement and, in some cases, suggest differential lesions within the CNS, specific site-of-lesion determination clearly is not always possible. In many cases, both brainstem and cerebellar structures may be implicated, and fur­ther differentiation with physiologic testing alone is not possible with routine clinical techniques. There are, however, other combinations of results that are highly suggestive of specific regions of the brainstem or cer­ebellum involved in abnormal ocular motor control.
Using specific patient examples of abnormal eye move­ments, the following discussion attempts to delineate the global CNS indicators from those with more spe­cific site-of-lesion implications. But first we need to dis­cuss briefly the task of recording eye movement.
EYE MOVEMENT RECORDING TECHNIQUES
The measurement of the vestibulo-ocular reflex (VOR) and ocular motility requires the use of sophisticated methods to transform the movements of the eyes into signals that can be digitized, processed, and analyzed. There are at least three methods for accomplishing this. The methods include electro-oculography (EOG) (electronystagmography [ENG]), infrared videonys­tagmography (VNG) (i.e., video-oculography [VOG]) techniques and scleral search coil techniques. In this chapter we will constrain the discussion of eye move­ment recording techniques to those used in contem­porary vestibular system assessment clinics. Those techniques include ENG and VNG.
Electro-Oculography/ Electronystagmography
Origin of the Corneoretinal Potential and Electrode Use
The electrical transducer of the visual system is the ret­ina, which also serves as the source of the corneoretinal
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potential (CRP). The CRP is a bioelectrical signal that is measured during EOG, which is the recording tech­nique used in ENG. The eyeball has a dipolar orienta­tion like a “battery,” with the cornea being positively polarized and the retina negatively polarized. This standing potential is propagated through the eye by volume conduction, where it is capable of being recorded with conventional surface electrodes.
As the cornea is positively charged and the ret­ina is negatively charged, two electrodes placed at the outer canthus of each eye and routed into a differ­ential amplifier should “see” neither a positive nor a negative charge with the eyes in primary position (Fig­ure 10–1A). If the eyes move conjugately to the right, the electrode at the right outer canthus should record a positive charge (i.e., as the positive pole of the right eye is pointed toward it) and the electrode at the left outer canthus should record a less positive charge (i.e., as less of that cornea is pointing toward that electrode) (Figure 10–1B). A leftward conjugate eye movement of similar magnitude results in the left electrode record­ing positive charge and the right electrode with a less positive charge (Figure 10–1C). The convention in EOG recordings is for upward trace deflections to represent rightward and upward eye deviations, and for down­ward trace deflections to represent leftward or down­ward eye deviations.
Assuming the examiner observes a full, conjugate range of movement of the eyes during informal test­ing, most clinicians record EOG using a “bitemporal” electrode array (Figure 10–2). It must be stated that for bitemporal recordings, electrical activity for the two eyes is “averaged.” This means that disconjugate move­ments of the eyes will be missed and underscores the importance for the clinician to examine informally the movements of the eyes to detect gross or subtle ocular motility disorders such as disconjugate eye movements before electrodes are placed on the face or goggles are placed over the eyes. An alternative to the bitemporal electrode placement is the monocular technique (Fig­ure 10–3). The monocular recording technique permits the recording of eye position for each eye separately.
The electrode pairs are routed to a differential amplifier that literally subtracts the electrical signal recorded by the inverting electrode input from the elec­trical signal recorded by the non-inverting electrode input (see Figures 10–2A through 10–2E). In doing this, electrical activity that is unrelated to the CRP (i.e., unwanted electrical interference) that is common to both the inverting and non-inverting electrodes (e.g., stray 60-Hz electrical signals, EKG interference) will be subtracted out (and eliminated), a technique referred to as common mode rejection (CMR). This should result in a reduction in the noisiness of the EOG recordings.
A B C
figure 10–1. The corneoretinal potential (CRP). The cornea is positively charged and the retinal is negatively charged. A. When the eye is in midline position a pair of electrodes placed on either side of the eye will see neither a positive nor a negative voltage. B. When the eye turns to the right, a positive electrical potential is generated. C.When the eye turns to the left, a negative electrical potential is generated.
A
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B
C
figure 10–2. Bitemporal electrode montage and the connections to a two-channel dif­ferential amplifier (i.e., two channels permit the recording of horizontal and vertical eye deviations). A. The horizontal and vertical amplifier outputs to a printer when the eyes are at primary (central) gaze (i.e., there is no pen deflection). B. The horizontal and vertical amplifier outputs to a printer for a rightward eye deviation. Notice that a rightward eye movement results in an upward pen deflection in the horizontal channel (a leftward eye deviation would result in a downward pen deflection). C . The horizontal and vertical ampli­fier outputs to a printer for an upward eye deviation. Notice that an upward eye deviation results in an upward pen deflection in the vertical channel (a downward eye movement would result in a downward pen deflection). continues
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D
E
Figure 10–2. continued D. The horizontal and vertical amplifier outputs to a printer for an oblique eye deviation (i.e., an up/right eye movement). represented by deflections in both the horizontal and vertical channels. E . and vertical amplifier outputs to a printer for a torsional eye movement. eye is rotating about its anterior/posterior axis there is neither a deviation in the horizontal nor in the vertical channels. This figure was adapted from An Introduction to ENG, by C . W. Stockwell, 2004. Schaumburg, IL: GN Otometrics.
The electrical signals resulting from conjugate horizontal eye deviations are approximately 20 µV per 1 degree of eye deviation in normal subjects with normal retinal function. These eye signals must be amplified by a factor of approximately 10,000 for the eye signals to be within an amplitude range that can be digitized and processed by most computerized data acquisition and processing systems. It should be noted as shown in Figure 10–2E, torsional movements of the eye without distinct horizontal or vertical movements result in tracings without any deviation, since there is no movement of the dipole laterally or vertically. Fig­ures 10–1 through 10–3 are shown with a strip chart recorder and pins for illustration. Currently, most sys­tems on the market illustrate the traces on to a com­puter monitor screen.
Notice that the eye movement is
The horizontal
Notice that as the
Infrared Video Recording Techniques
Although scleral search coils are still considered the gold standard for eye movement recordings, infrared video tracking systems have rapidly become the state­of-the-art technique for recording eye movements. A method for creating a vision-denied condition is the final component of the hardware. Video tracking sys­tems make use of pupil localization technology and the reflective properties of the corneal surface to calculate pupil position and angle of gaze. Implementation of the system varies between manufacturers, but most make use of a goggle-type headpiece to illuminate the eyes that contains infrared diodes, dichroic glass “mirrors” that reflect the image of the eyes into a single camera or a pair of cameras that record the image of the eye.
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Figure 10–3. Electrode locations and four-channel amplifier connections for a monocu­lar montage.
A headband holds the assembly over the eyes (Figures 10–4 and 10–5). This setup fixes the camera in place relative to the head, ensuring that changes in observed pupil position are caused solely by eye movements rather than a combination of head and eye movements.
The use of the dichroic glass allows the patient to follow the visual targets during ocular motility testing) but will reflect the eye image(s) into the left and right eye cameras. Last, there are controls on the goggles that permit the image of the eye to be raised, lowered, con­verged, diverged, or focused.
TECHNIQUE AND INTERPRETATIONS
OF OCULAR MOTILITY TESTING
In the evaluation of the dizzy patient, the eyes provide the most direct access to the evaluation of the periph­eral vestibular system. However, the pathways from the labyrinthine structures involve significant neuro­logic substrate in the brainstem and cerebellum with controlling influence from higher centers in the mid­brain and cerebral cortex. Therefore, correct interpreta­tion of eye movements relative to the periphery rely on normal function of the central pathways. Also, symp­toms of dizziness can result from lesions in the central
Figure 10–4. Model wearing a monocular, video eye movement recording system. The lens reflects the left eye image into a head-mounted video camera.
neural pathways or at the central nuclei. Secondary to these issues, it becomes important to use the eyes as our window into the CNS-controlling structures for eye