Eggert 32 The main features of the eye movement recording devices mentioned in this chapter are summarized in table 1. Since the EOG is still the only method that allows measurement of eye movements while the eyes are closed, it remains important for specialized applications that require this possibility. Modern VOG systems can measure 2-D gaze direction at spatial resolutions comparable to those of search coil systems. The accuracy of VOG devices is also comparable to that of the search coil, but it depends on the ability of the subjects to fixate accu- rately. System noise and accuracy of ocular torsion is slightly better in search coil systems than in VOG. The main disadvantage of the search coil is that it is inva- sive compared with the EOG, IRD, or VOG. Therefore, search coil measurements are advisable only for relatively short recordings requiring high temporal resolu- tion, high accuracy, and an objective calibration. For most other applications, VOG seems to provide a good alternative to the search coil technique. Until recently, the IRD was still a reasonable noninvasive alternative to the search coil, at least for measuring horizontal (1-D) eye movements. In the meantime, the tem- poral resolution of VOG improved and is now sufficient to cover the temporal bandwidth of physiological eye movements. The robustness of the system linear- ity with respect to displacements between the device and the eye is much better in VOG than in the IRD. Therefore, the IRD appears to have been outdated by VOG. References 1 Wade NJ, Tatler BW, Heller D: Dodge-ing the issue: Dodge, Javal, Hering, and the measurement of saccades in eye-movement research. Perception 2003;32:793–804. 2 Wade NJ, Tatler BW: The Moving Tablet of the Eye: The Origins of Modern Eye Movement Research. Oxford, Oxford University Press, 2005. 3 Porterfield W: An essay concerning the motions of our eyes. I. Of their external motions. Edinburgh Med Essays Obs 1737;3:160–263. 4 Wells WC: An Essay Upon Single Vision with Two Eyes: Together with Experiments and Observations on Several Other Subjects in Optics. London, Cadell, 1792. 5 Javal LE: Essai sur la physiologie de la lecture. Ann Ocul 1879;82:242–253. 6 Lamare M: Des mouvements des yeux dans la lecture. Bull Mem Soc Fr Ophtalmol 1892;10:354–364. 7 Hering E: Über Muskelgeräusche des Auges. Sitzungsberichte der kaiserlichen Akademie der Wissenschaften in Wien. Math Naturwiss Kl Abt III 1879;79:137–154. 8 Ahrens A: Die Bewegungen der Augen beim Schreiben. Rostock, University of Rostock, 1891. 9 Delabarre EB: A method of recording eye movements. Am J Psychol 1898;9:572–574. 10 Huey EB: Preliminary experiments in the physiology and psychology of reading. Am J Psychol 1898;9:575–586. 11 Huey EB: On the psychology and physiology of reading. Am J Psychol 1900;11:283–302. 12 Javal LE: Essai sur la physiologie de la lecture. Ann Ocul 1878;80:240–274. 13 von Romberg G, Ohm J: Ergebnisse der Spiegelnystagmographie. Gräfes Arch Ophtalmol 1944; 146:388–402. 14 Dodge R, Cline TS: The angle velocity of eye movements. Psychol Rev 1901;8:145–157. 15 Crane HD, Steele CM: Generation-V dual-Purkinjeimage eyetracker. Appl Optics 1985;24:527–537. 16 Deubel H, Bridgeman B: Fourth Purkinje image signals reveal eye-lens deviations and retinal image distortions during saccades. Vision Res 1995;35:529–538. Eye Movement Recordings: Methods 33 17 Brandt T, Büchele W: Augenbewegungsstörungen: Klinik und Elektronystagmographie. Stuttgart, Gustav Fischer, 1983. 18 Schott E: Über die Registrierung des Nystagmus und anderen Augenbewegungen vermittels des Seitengalvanometers. Dtsch Arch Klin Med 1922:140:79–90. 19 Meyers IL: Electronystagmographie. A graphic study of the action currents in nystagmus. Arch Neurol 1929;21:901–908. 20 Mowrer OR, Ruch RC, Miller NE: The corneoretinal potential difference as the basis of the galvanometric method of recording eye movements. Am J Physiol 1936;114:423. 21 Jung R: Eine Elektrische Methode zur Mehrfachen Registrierung von Augenbewegungen und Nystagmus. J Mol Med 1939;18:21–24. 22 Torok N, Guillemin V, Barnothy JM: Photoelectric nystagmography. Ann Otol Rhinol Laryngol 1951;60:917–926. 23 Kimmig H, Greenlee MW, Huethe F, Mergner T: MR-eyetracker: a new method for eye movement recording in functional magnetic resonance imaging. Exp Brain Res 1999;126:443–449. 24 Howard IP, Evans JA: The measurement of eye torsion. Vision Res 1963;61:447–455. 25 Ruete CGT: Ocular physiology. Chapter 4. The muscles of the eye. Strabismus 1999;7:43–60; translated from Lehrbuch der Ophthalmologie, ed 2. Braunschweig, Vieweg, vol 1, 1846, pp 36–37. 26 Simonsz HJ: Christian Theodor Georg Ruete: the first strabismologist, coauthor of listing’s law, maker of the first ophthalmotrope and inventor of indirect fundoscopy. Strabismus 2004;12: 53–57. 27 von Helmholtz H: Handbuch der Physiologischen Optik. Hamburg, Voss, 1867. 28 Robinson DA: A method of measuring eye movement using a scleral search coil in a magnetic field. IEEE Trans Biomed Eng 1963;10:137–145. 29 Collewijn H, van der Mark F, Jansen TC: Precise recording of human eye movements. Vision Res 1975;15:447–450. 30 Collewijn H, Steen J, Ferman L, Jansen TC: Human ocular counterroll: assessment of static and dynamic properties from electromagnetic scleral coil recordings. Exp Brain Res 1985;59:185–196. 31 Kasper H, Hess BJ: Magnetic search coil system for linear detection of three-dimensional angular movements. IEEE Trans Biomed Eng 1991;38:466–475. 32 Straumann D, Zee DS, Solomon D, Kramer PD: Validity of Listing’s law during fixations, saccades, smooth pursuit eye movements, and blinks. Exp Brain Res 1996;112:135–146. 33 Brecher GA: Die optokinetische Auslösung von Augenrollung und rotatorischen Nystagmus. Pflügers Arch Ges Physiol 1934;234:13–28. 34 Miller EF: Counterrolling of the human eye produced by head tilt with respect to gravity. Acta Otolaryng (Stockh) 1962;59:479–501. 35 Young LR, Lichtenberg BK, Arrott AP, Crites TA, Oman CM, Edelman ER: Ocular torsion on earth and in weightlessness. Ann N Y Acad Sci 1981;374:80–92. 36 Clarke AH, Steineke C, Emanuel H: High image rate eye movement measurement. A novel approach using CMOS sensors and dedicated FPGA devices; in Lehmann T (ed): Bildverarbeitung in der Medizin. Berlin, Springer, 2000. 37 Haslwanter T, Moore ST: A theoretical analysis of three-dimensional eye position measurement using polar cross-correlation. IEEE Trans Biomed Eng 1995;42:1053–1061. 38 Nakayama K: Photographic determination of the rotational state of the eye using matrices. Am J Optom Physiol Opt 1974;51:736–741. 39 Dieterich M, Brandt T: Elektronystagmographie: Methodik und klinische Bedeutung. EEG Labor 1989;11:13–30. 40 Schmid-Priscoveanu A, Allum JHJ: Die Infrarot- und die Videookulographie – Alternativen zur Elektrookulographie? HNO 1999;47:472–478. 41 Marmor MF, Zrenner E: Standard for clinical electroretinography (1999 update). Doc Ophthalmol 1999;97:143–156. 42 Collewijn H, Erkelens CJ, Steinman RM: Binocular co-ordination of human horizontal saccadic eye movements. J Physiol 1988;404:157–182. 43 Ditterich J, Eggert T: Improving the homogeneity of the magnetic field in the magnetic search coil technique. IEEE Trans Biomed Eng 2001;48:1178–1185. Eggert 34 44 Tweed D, Cadera W, Vilis T: Computing three-dimensional eye position quaternions and eye velocity from search coil signals. Vision Res 1990;30:97–110. 45 Bartl K, Siebold C, Glasauer S, Helmchen C, Büttner U: A simplified calibration method for three-dimensional eye movement recordings using search-coils. Vision Res 1996;36:997–1006. 46 Imai T, Sekine K, Hattori K, Takeda N, Koizuka I, Nakamae K, Miura K, Fujioka H, Kubo T: Comparing the accuracy of video-oculography and the scleral search coil system in human eye movement analysis. Auris Nasus Larynx 2005;32:3–9. 47 Frens MA, van der Geest JN: Scleral search coils influence saccade dynamics. J Neurophysiol 2002;88:692–698. 48 Bergamin O, Ramat S, Straumann D, Zee DS: Influence of orientation of exiting wire of search coil annulus on torsion after saccades. Invest Ophthalmol Vis Sci 2004;45:131–137. 49 Irving EL, Zacher JE, Allison RS, Callender MG: Effects of scleral search coil wear on visual function. Invest Ophthalmol Vis Sci 2003;44:1933–1938. 50 Murphy PJ, Duncan AL, Glennie AJ, Knox PC: The effect of scleral search coil lens wear on the eye. Br J Ophthalmol 2001;85:332–335. 51 Karmali F, Shelhamer M: Automatic detection of camera translation in eye video recordings using multiple methods. Ann N Y Acad Sci 2005;1039:470–476. 52 Enright JT: Ocular translation and cyclotorsion due to changes in fixation distance. Vision Res 1980;20:595–601. 53 Wang JG, Sung E: Gaze determination via images of irises. Image Vis Comput 2001;19:891–911. 54 van der Geest JN, Frens MA: Recording eye movements with video-oculography and scleral search coils: a direct comparison of two methods. J Neurosci Methods 2002;114:185–195. 55 Clarke AH, Ditterich J, Druen K, Schönfeld U, Steineke C: Using high frame rate CMOS sensors for three-dimensional eye tracking. Behav Res Methods Instrum Comput 2002;34:549–560. 56 Houben MM, Goumans J, van der Steen J: Recording three-dimensional eye movements: scleral search coils versus video oculography. Invest Ophthalmol Vis Sci 2006;47:179–187. 57 Schneider E, Glasauer S, Dieterich M: Comparison of human ocular torsion patterns during nat- ural and galvanic vestibular stimulation. J Neurophysiol 2002;87:2064–2073. Web Links Hain TC (2005): Eye movement recording devices; http://www.dizziness-and-balance.com/practice/eyemove.html Marmor MF, Zrenner E (1999): Standard for clinical electroretinography; http://www.iscev.org/standards/eog.html Paulson EJ, Goodman KS (1999): Influential studies in eye movement research; http://www.readingonline.org/research/eyemove.html Schneider G, Kurt J (2000): Zur Rolle der Blicksteuerung bei Lesestörungen. Kapitel 7: Technische Prinzipien zur Messung der Augenbewegungen; http://www2.hu-berlin.de/reha/eye/Studie2000/tech.pdf Wooding D (2002): Eye movement equipment database; http://ibs.derby.ac.uk/cgi-bin/emed/emedsrch.cgi?opr1 ϭ OR&fld1 ϭ name&key1a ϭ *. Dr. T. Eggert Department of Neurology, Klinikum Grosshadern Marchioninistrasse 23 DE–81377 Munich (Germany) Tel. ϩ49 89 7095 4834, Fax ϩ49 89 7095 4801 E-Mail eggert@brain.nefo.med.uni-muenchen.de Straube A, Büttner U (eds): Neuro-Ophthalmology. Dev Ophthalmol. Basel, Karger, 2007, vol 40, pp 35–51 Vestibulo-Ocular Reflex Michael Fetter Department of Neurology, SRH Clinic Karlsbad-Langensteinbach, Karlsbad, Germany Abstract The vestibulo-ocular reflex (VOR) ensures best vision during head motion by moving the eyes contrary to the head to stabilize the line of sight in space. The VOR has three main components: the peripheral sensory apparatus (a set of motion sensors: the semicircular canals, SCCs, and the otolith organs), a central processing mechanism, and the motor output (the eye muscles). The SCCs sense angular acceleration to detect head rotation; the otolith organs sense linear acceleration to detect both head translation and the position of the head relative to gravity. The SCCs are arranged in a push-pull configuration with two coplanar canals on each side (like the left and right horizontal canals) working together. During angu- lar head movements, if one part is excited the other is inhibited and vice versa. While the head is at rest, the primary vestibular afferents have a tonic discharge which is exactly bal- anced between corresponding canals. During rotation, the head velocity corresponds to the difference in the firing rate between SCC pairs. Knowledge of the geometrical arrangement of the SCCs within the head and of the functional properties of the otolith organs allows to localize and interpret certain patterns of nystagmus and ocular misalignment. This is based on the experimental observation that stimulation of a single SCC leads via the VOR to slow- phase eye movements that rotate the globe in a plane parallel to that of the stimulated canal. Furthermore, knowledge of the mechanisms that underlie compensation for vestibular dis- orders is essential for correctly diagnosing and effectively managing patients with vestibular disturbances. Copyright © 2007 S. Karger AG, Basel The vestibulo-ocular reflex (VOR) helps to stabilize the retinal image by rotating the eyes to compensate for movements of the head. An ideal VOR, that tries to compensate for any arbitrary movement of the head in 3-D space, would generate eye rotations at the same speed as, but in the opposite direction to, head rotation independent of the momentary rotation axis of the head. The desired result is that the eye remains still in space during head motion, enabling clear vision. The VOR has two different physical properties. The angular VOR, mediated Fetter 36 by the semicircular canals (SCCs), compensates for rotation. The linear VOR, mediated by the otolith organs (saccule and utricle), compensates for translation. The angular VOR is primarily responsible for gaze stabilization. The linear VOR is most important in situations where near targets are being viewed [1, 2]. The VOR has three main components: the peripheral sensory apparatus (the labyrinth), a central processing mechanism, and the motor output (the eye muscles) [3]. The sensory input for the generation of the VOR is provided by a set of motion sensors, which send the information about head angular velocity, linear acceleration, and orientation of the head with respect to gravity to the central nervous system (specifically the vestibular nucleus complex and the cerebellum). In the central nervous system, these signals are combined with other sensory information (e.g. from the somatosensors) at as early stages as the vestibular nucleus complex to estimate head orientation. The output of the cen- tral vestibular system is sent to the ocular muscles and the spinal cord to serve the VOR and the vestibulospinal reflex (VSR), the latter generating compen- satory body movement in order to maintain head and postural stability, thereby preventing falls. The information goes also to cortical structures (e.g. posterior insular vestibular cortex, PIVC) where it is further integrated with visual, pro- prioceptive, auditory and tactile input to generate a best possible perception of motion and space orientation [4]. The performance of the VOR and VSR is monitored by the central nervous system, and readjusted as necessary by adap- tive processes with immense capability of repair and adaptation mainly involv- ing cerebellar function (fig. 1) [5]. The Peripheral Sensory Apparatus The peripheral vestibular system includes the membranous and bony labyrinths, and the motion sensors of the vestibular system, the hair cells. Each Sensory input Central processing Motor output Visual Vestibular Proprioceptive Adaptive processor (cerebellum) Vestibular nuclear complex Oculomotor neurons Fig. 1. Schematic drawing illustrating the VOR. Vestibulo-Ocular Reflex 37 labyrinth consists of three SCCs, the cochlea, and the vestibule containing the utricle and saccule). The geometric arrangement of the SCCs allows for detec- tion of head rotation about any axis in space. They are positioned in three nearly orthogonal planes in the head and act as angular accelerometers working in a push-pull arrangement with the other labyrinth (right and left lateral SCC; right anterior and left posterior SCC; left anterior and right posterior SCC). The planes of the SCCs are close to the planes of the extraocular muscles, thus allowing relatively simple neural connections between sensory neurons related to individual canals, and motor output neurons, related to individual ocular muscles (fig. 2) [6]. One end of each SCC is widened in diameter to form an ampulla containing the cupula. The cupula causes endolymphatic pressure dif- ferentials, associated with head motion, to be coupled to the hair cells embed- ded in the cupula. These specialized hair cells are biological sensors that convert displacement due to head motion into neural firing. When hairs are bent toward or away from the longest process of the hair cells, firing rate increases or decreases in the vestibular nerve [7, 8]. The hair cells of the saccule and utricle, the maculae, are located on the medial wall of the saccule and the floor of the utricle. The otolithic membranes are structures similar to the cupulae, but as they contain calcium carbonate crystals called otoconia, they have substantially more mass than the cupulae. The mass of the otolithic membrane causes the maculae to be sensitive to gravity. In contrast, the cupulae normally have the same density as the surrounding endolymphatic fluid and are insensitive to gravity. By virtue of their orientation, the SCC and otolith organs are able to respond selectively to head motion in particular directions [9]. Central Processing of Vestibular Signals The coplanar pairing of canals is associated with a push-pull change in the quantity of SCC output. With rotation in the plane of a coplanar SCC pair, the neural firing increases from tonic resting discharge in one vestibular nerve and decreases on the opposite site. For the lateral canals, displacement of the cupula towards the ampulla (ampullopetal flow) is excitatory, whereas for the vertical canals, displacement of the cupula away from the ampulla (ampullofugal flow) is excitatory (fig. 3). There are certain advantages to the push-pull arrangement of coplanar pairing. First, pairing provides sensory redundancy. If disease affects the SCCs from one member of a pair (e.g. as in vestibular neuritis), the central nervous system will still receive vestibular information about head velocity within that plane from the contralateral member of the coplanar pair. Second, such a pair- ing allows the brain to ignore changes in neural firing that occur on both sides Fetter 38 25º 53º 47º 47º 10 so sr lr ir mr III IV VI ir sr io mr mlf so in lr ra rh rp la lp lh bc bc Fig. 2. The VOR network: corresponding SCCs and the main brainstem connections to the oculomotor nuclei are shown. lr, sr, ir, mr ϭ Left, superior, inferior, medial rectus mus- cle; IO, SO ϭ inferior, superior oblique muscle; III ϭ third nerve nucleus with inferior (ir), superior (sr), medial rectus (mr), and inferior oblique (io) motor neurons; IV ϭ fourth nerve nucleus with superior oblique motor neurons (so); bc ϭ brachium conjunctivum; VI ϭ sixth nerve nucleus with lateral rectus (lr) and internuclear (in) motor neurons; mlf ϭ medial longitudinal fasciculus; la, lh, lp ϭ left anterior, horizontal and posterior SCC; ra, rh, rp ϭ right anterior, horizontal and posterior SCC. (Courtesy of D.A. Robinson, Baltimore.) Vestibulo-Ocular Reflex 39 simultaneously, such as might occur due to changes in body temperature or chemistry. In the otoliths, as in the canals, there is a push-pull arrangement of sensors, but in addition to splitting the sensors across sides of the head, the push-pull processing arrangement for the otoliths is also incorporated into the geometry of the otolithic membranes. Within each otolithic macula, a curving zone, the striola, separates the direction of hair cell polarization on each side. Consequently, head tilt results in increased afferent discharge from one part of a macula, while reducing the afferent discharge from another portion of the same macula [10, 11]. There are two main targets for vestibular input from primary afferents: the vestibular nuclear complex and the cerebellum. The vestibular nuclear complex is the primary processor of vestibular input, and implements direct, fast con- nections between incoming afferent information and motor output neurons. R Resting Inhibition Excitation L Sp/s Fig. 3. With rotation toward the left side, the neural firing increases from tonic resting discharge (shown as horizontal dotted line) in the vestibular nerve of the left lateral canal and decreases in the vestibular nerve of the right lateral canal. During rotation, the head velocity corresponds to the difference in firing rate between SCC pairs. Fetter 40 The erebellum is the adaptive processor – it monitors vestibular performance and readjusts central vestibular processing if necessary [12]. At both locations, vestibular sensory input is processed in association with somatosensory and visual sensory input [5]. The vestibular nuclear complex consists of 4 major nuclei (superior, medial, lateral, and descending) and at least 7 minor nuclei. This large struc- ture, located primarily within the pons, also extends caudally into the medulla. The superior and medial vestibular nuclei are relays for the VOR. The medial vestibular nucleus is also involved in the VSR, and coordinates head and eye movements that occur together. The lateral vestibular nucleus is the principal nucleus for the VSR. The descending nucleus is connected to all of the other nuclei and the cerebellum, but has no primary outflow of its own [13]. The vestibular nuclei are connected via a system of commissures, which for the most part, are mutually inhibitory. The commissures allow information to be shared between the two sides of the brainstem and implements the push-pull pairing of vestibular canals. Extensive connections between the vestibular nuclear complex, cerebellum, ocular motor nuclei, and brainstem reticular acti- vating systems convey the efferent signals to the VOR and VSR effector organs, the extraocular and skeletal muscles [14]. The output neurons of the VOR are the motor neurons of the ocular motor nuclei, which drive the extraocular mus- cles resulting in conjugate movements of the eyes in the same plane as head motion (fig. 2). VOR – Pathology It is crucial to carefully evaluate the eye movements during clinical exam- ination, as the physiological and anatomical substrate of the ocular motor sys- tem is intimately connected with the vestibular system via the VOR. The VOR is responsible for the nystagmus phenomena seen in patients [15]. Caloric stimulation provides perhaps the clearest analogy to what the patient with pathological vertigo and nystagmus experiences. For example, warm stimula- tion of the left ear increases neural activity from the left lateral SCC and there- fore in the left vestibular nerve; it thereby produces not only left-beating horizontal nystagmus but a sense of turning about the body long axis, toward the left. Conversely, cold stimulation of the right ear reduces neural activity in the right lateral SCC, the right vestibular nerve; and by commissural disinhibi- tion it also increases neural activity in the left vestibular nucleus and, there- fore, produces left-beating nystagmus and a sense of turning to the left (the nystagmus always beating toward the side of higher vestibular activity) [16, 17]. In a patient with sudden unilateral loss of peripheral vestibular function Vestibulo-Ocular Reflex 41 (such as in vestibular neuritis), the situation is in some way analogous to a cold caloric stimulus. An example of vertigo due to pathological unilateral increase in vestibular activity is benign paroxysmal positioning vertigo (BPPV), the most common vestibular disorder. With appropriate positioning, there is a sudden brief increase in activity from one SCC. The result is a sudden intense sense of self- rotation in the plane of the activated canal and a nystagmus beating in this plane. For example, if a patient with left posterior canal BPPV is rapidly placed in the provocative left lateral position, there is a sense of self-rotation in a plane halfway between the roll and the pitch plane toward the patient’s left side with a vertical – torsional nystagmus beating upward and with the torsional compon- ent to the lower ear [18–21]. Practical Aspects for Bedside Clinical Evaluation An acute unilateral peripheral vestibular lesion reduces or eliminates input from one or more SCCs and otolith organs on that side. In the acute phase, a complete lesion abolishes the tonic neuronal discharge (resting activity) in the vestibular nerve [22]. The resulting loss of accelerometer function on one side of the head and the imbalance between the tonic inputs on the two sides lead to both spontaneous nystagmus and decreased and asymmetrical dynamic vestibu- lar responses. Thus, there are both static and dynamic imbalances which need to be evaluated. Static Imbalance Spontaneous nystagmus (with the head still) is the hallmark of an imbal- ance in the tonic levels of activity mediating SCC-ocular reflexes. When peripheral in origin, spontaneous nystagmus characteristically is damped by visual fixation and is increased or only becomes apparent when fixation is eliminated. Hence, one must look for spontaneous nystagmus behind Frenzel lenses (magnifying lenses that prevent the patient from using visual fixation to suppress any spontaneous nystagmus) or during ophthalmoscopy (with the opposite eye occluded to prevent fixation). The intensity of nystagmus is com- pared with that observed when the patient is fixing on a visual target. Nystagmus is sometimes seen or even palpated through closed eyelids. Note that during ophthalmoscopy the direction of any horizontal or vertical slow phases is opposite to the direction of the motion of the optic disk. The nystagmus should also be inspected for dependence on the position of the eye in the orbit. Nystagmus arising from a peripheral lesion and most cen- tral lesions is more intense or may be evident only when the eye is deviated in [...]... control of the vestibulo-ocular reflex by the cerebellum J Neurophysiol 1976 ;39 :954–969 Vestibulo-Ocular Reflex 49 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 Brodal A: Anatomy of the vestibular nuclei and their connections; in Kornhuber HH (ed): Handbook of Sensory Physiology The Vestibular System New York, Springer, 1974, vol VI, part 1 Büttner-Ennever JA: Vestibular... Bach-Y-Rita P: The Control of Eye Movements New York, Academic Press, 1971 Suzuki J-I, Tokumasu K, Goto K: Eye movements from single utricular nerve stimulation in the cat Acta Otolaryngol 1969;68 :35 0 36 2 Fernandez C, Goldberg JM, Abend WK: Response to static tilts of peripheral neurons innervating otolith organs of the squirrel monkey J Neurophysiol 1972;6:978–987 Robinson DA: Adaptive gain control of. .. the anatomical on-directions of the SCCs it can be shown that the elicited eye movements are closely aligned with the direction of the offending canal With this proof that also in humans eye movements are produced in the plane of the stimulated SCC, it is possible to deduct which canals are responsible for the direction of eye movements found during vestibular stimulation when parts of the vestibular... direction that is a weighted vector sum of Vestibulo-Ocular Reflex 47 the axes of the involved canals Using this premise, one can stimulate the vestibular system in numerous ways (low- and high-velocity head movements in 3- D, 3- D calorics, and diverse methods of inducing positional nystagmus) and relate the resulting eye movements to the function or dysfunction of single SCCs [44–46] Obviously, in humans... changed in recent years In the last 20 years, there has been a revival of interest in 3- D approaches to the control of eye movements This was boosted by the fact that 3- D eye movement analysis has become practical with the development of the magnetic field search coil technique New analytical approaches have made the mathematics of eye rotations and coordinate transformations more tractable and intuitive... after loss of peripheral sensitivtiy Ann Neurol 1984;16:222–228 Cohen B, Suzuki J: Eye movements induced by ampullary nerve stimulation Am J Physiol 19 63; 204 :34 7 35 1 Suzuki J, Cohen, B: Head, eye, body and limb movements from semicircular canal nerves Exp Neurol 1964;10 :33 3–405 Fetter M, Dichgans J: Vestibular neuritis spares the inferior division of the vestibular nerve Brain 1996;119:755–7 63 Aw ST,... of movement in response to sensory stimulation The visual guidance of saccadic eye movement represents one form of sensory-to-motor transformation that has contributed significantly to our understanding of motor control and sensorimotor processing at large The neural circuitry controlling saccadic eye movements is now understood at a level that is sufficient to link the specific roles of a number of. .. lateral canal variant of BPPV [15] A positioning nystagmus is characteristic of BPPV A transient burst of a mixed vertical (upbeat)-torsional (the superior pole of the globe beats toward Vestibulo-Ocular Reflex 43 the side of the dependent ear) nystagmus, usually appearing after a latency of several seconds and lasting 20 30 s, is characteristic of the inappropriate excitation of the posterior SCC... 1977;85:7– 23 Schuknecht HF: Cupulolithiasis Arch Otolaryngol 1969;90:765–778 Baloh RW, Honrubia V, Jacobson K: Benign positional vertigo Neurology 1987 ;37 :37 1 37 8 Brandt T: Positional and positioning vertigo and nystagmus J Neurol Sci 1990;95 :3 28 Brandt T, Steddin S: Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis or canalolithiasis? J Vestibular Res 19 93; 3 :37 3 38 2... is based on the control of saccade duration by a PV Purkinje cell population signal Copyright © 2007 S Karger AG, Basel One of the major functions of the central nervous system is the generation of movement in response to sensory stimulation Saccadic eye movements represent an example of the sensory guidance of movements that has contributed significantly to our understanding of some of the general . been a revival of interest in 3- D approaches to the control of eye movements. This was boosted by the fact that 3- D eye movement analysis has become practical with the development of the magnetic. ways (low- and high-velocity head movements in 3- D, 3- D calorics, and diverse methods of inducing positional nystagmus) and relate the resulting eye movements to the function or dysfunction of single SCCs. Dodge-ing the issue: Dodge, Javal, Hering, and the measurement of saccades in eye- movement research. Perception 20 03; 32:7 93 804. 2 Wade NJ, Tatler BW: The Moving Tablet of the Eye: The Origins of