Journal of Neuro-Ophthalmology, June 1991, Volume 11, Issue 2

See-saw nystagmus due to unilateral mesodiencephalic lesion.

See-saw nystagmus is a unique torsional-vertical eye movement disorder with a characteristic appearance. It is a pendular nystagmus with two distinct components: a conjugate torsional component and a disjunctive vertical component. In those cases of see-saw nystagmus in which a focal lesion has been identified, the lesion is usually a bilateral, symmetric lesion located at the mesodiencephalic junction. We report an unusual case of see-saw nystagmus which was due to a strictly unilateral mesodiencephalic lesion. Furthermore, the see-saw nystagmus had, in this case, a jerk wave-form rather than the usual pendular wave-form, with the torsional component of the jerk see-saw nystagmus beating toward the side of the lesion. These observations have an impact upon the localizing and lateralizing significance of torsional nystagmus in general and of see-saw nystagmus in particular.

Journal of Clinical Neuro- ophthalmology 11( 2): 79- 84, 1991. See- Saw Nystagmus Due to Unilateral Mesodiencephalic Lesion G. Michael Halmagyi, M. D. and William F. Hoyt, M. D. © 1991 Raven Press, Ltd., New York See- saw nystagmus is a unique torsional- vertical eye movement disorder with a characteristic appearance. It is a pendular nystagmus with two distinct components: a conjugate torsional component and a disjunctive ver­tical component. In those cases of see- saw nystagmus in which a focal lesion has been identified, the lesion is usually a bilateral, symmetric lesion located at the meso­diencephalic junction, We report an unusual case of see­saw nystagmus which was due to a strictly unilateral mesodiencephalic lesion. Furthermore, the see- saw nystagmus had, in this case, a jerk wave- form rather than the usual pendular wave- form, with the torsional component of the jerk see- saw nystagmus beating to­ward the side of the lesion. These observations have an impact upon the localizing and lateralizing significance of torsional nystagmus in general and of see- saw nystag­mus in particular. Key Words: Nystagmus- See- saw nystagmus- Meso­diencephalic lesions- Wave- forms, From the Eye and Ear Research Unit, Department of Neurol­ogy, Royal Prince Alfred Hospital ( G, M, H,), Sydney, Australia; and Neuro- ophthalmology Unit, Department of Neurosurgery, University of California, San Francisco, California, U. S. A. Address correspondence and reprint requests to Dr. G. M. Halmagyi at Royal Prince Alfred Hospital, Camperdown NSW 2050, Sydney, Australia. 79 See- saw nystagmus is an uncommon but distinc­tive torsional- vertical eye movement disorder. The essential characteristic that distinguishes see- saw nystagmus from other types of torsional- vertical nystagmus is that while the torsional component is conjugate, the synchronous vertical component is disjunctive. Most cases of see- saw nystagmus have a pendular wave- form. Although the precise site of lesion and mechanism of see- saw nystag­mus is not clear, many patients with see- saw nystagmus have large, extrinsic suprasellar lesions ( such as craniopharyngiomas) compressing the mesodiencephalon bilaterally. [ For a review see Miller 1985 ( 1).] In contrast to these cases, we re­port a patient with a strictly unilateral, intrinsic mesodiencephalic lesion, in whom a prominent primary- position see- saw nystagmus was almost the only neurologic abnormality. Furthermore, the see- saw nystagmus in this case had a jerk, rather than the usual pendular wave- form, with the tor­sional component of the quick phases beating to­ward the side of the mesodiencephalic lesion. CASE REPORT A 30- year- old woman presented with right­sided weakness of 16 years' duration and oscillop­sia of 7 years' duration. At age 14 she changed to writing left- handed because of increasing difficul­ties using the right hand. At age 23 she began to complain of oscillopsia, particularly when looking to the right. She consulted an ophthalmologist who noted nystagmus. More recently she had noted headache and dragging of the right leg. On examination she had a mild right hemiparesis af­fecting the arm more than the leg but sparing the face. The most obvious abnormality was a pri­mary- position nystagmus. In the primary position of gaze there was a constant, regular ( 8G- 90 beats/ min), predominantly torsional nystagmus with 80 G. M. HALMAGYI AND W. F. HOYT conjugate left- beating quick phases ( i. e., the tor­sional quick phases rotated the 12 o'clock iris me­ridians toward the patient's left shoulder). The quick phases also had synchronous, disjunctive, vertical, and horizontal components ( Fig. 1). The vertical component of the quick phases was di­rected upward in the right eye and downward in the left eye. The horizontal component of the quick phases was convergent. There was no retraction component in the nystagmus. The frequency and amplitude of the nystagmus increased in the right­ward gaze, decreased in leftward gaze, but was unaltered in upward and in downward gaze. There was no strabismus, no ocular or gaze pare­sis, and no abnormality of head posture. Conver­gence and pupillary reactions were normal. Computed tomography ( CT) and magnetic res­onance imaging ( MRI) revealed a large, calcific le­sion in the left mesodiencephalon, involving the medial thalamus, subthalamus and cerebral pe­duncle ( Fig. 2). There was mild obstructive hydro­cephalus. A biopsy specimen of the lesion showed only gliosis. DISCUSSION The Eye Movements in See- Saw Nystagmus See- saw nystagmus is a torsional- vertical nystagmus in which the torsional component is conjugate and the vertical component is disjunc­tive. The characteristic appearance of the nystag­mus, which resembles that of a see- saw, results from torsional motion of each eye in the same di­rection, combined with vertical motion of each eye in opposite directions. While one eye elevates and intorts, the other eye depresses and extorts. Al­though in most cases the two half- cycles of the nystagmus are of equal speed, giving the nystag­mus a pendular appearance, in some individuals the see- saw nystagmus has a slow phase and a quick phase, giving the nystagmus a jerk appear­ance ( 2,3). The Site of Lesion in See- Saw Nystagmus In some patients with see- saw nystagmus, no focal lesion has been identified in the nervous sys­tem. This group includes patients with congenital see- saw nystagmus ( 4- 6), patients with see- saw nystagmus and ocular abnormalities ( 7), patients with post- traumatic see- saw nystagmus ( 8,9), and patients inadequately investigated by modern standards ( e. g., Maddox's original case ( 10) and Druckman's cases 2 and 3 ( 11)). In patients with see- saw nystagmus and congenital or develop­mental abnormalities of the nervous system such as septo- optic dysplasia ( 12), Chiari malformation ( 13) or Joubert's syndrome ( 14), the relevance of the neural structures involved in the malformation to the mechanism of the see- saw nystagmus is un­certain. In patients with presumed or proven brain stem infarction and see- saw nystagmus, the lesion has been either in the lateral medulla ( e. g., Jen­sen's case 1 ( 15), Daroff's case 2 ( 16), and Mas­taglia's case ( 17)), or at the mesodiencephalic junc­tion ( 2,18- 20). In most patients with see- saw nystagmus in whom an acquired focal lesion has been identified, the lesion has been a large, bilat­eral, symmetrical, extrinsic, suprasellar tumor ~ IG: 1. Sche~ atic , representation of the patient's jerk see- saw nystagmus. The arrows ~ ndlcate the direction and app~ oximate amplitude of the torsional, vertical, and hor­Izont~ 1 components of each qUick phase of the patient's jerk see- saw nystagmus. The amplitude of each component of the qUick phase was estimated from videotape. I Clill Neuro- o1' hthalmol. Vol. 1L No. 2. 1991 A SEE- SAW NYSTAGMUS FIG. 2. Proton density axial ( A) and T1 weighted coronal ( B) MR images showing a mixed signal intensity lesion in the left medial thalamus and midbrain distorting the third ventricle. On the axial sections there appears to be a cystic component anteriorly with a fluid level. B 81 compressing or invading the brain stem at the mesodiencephalic junction ( 11, 16,21- 26). Unilateral Mesodiencephalic Lesions and See- Saw Nystagmus There are 5 single case reports of see- saw nystagmus caused by a unilateral mesodiencepha­lie lesion. Garelli and Gherardini ( 27) reported a patient with Parkinson's disease who, after a series of unilateral stereotactic lesions aimed at the zona incerta, developed what appears to have been a tonic contraversive ocular tilt reaction ( head tor­sion, skew deviation) and see- saw nystagmus. The oculographic records confirm that the vertical com­ponent of the nystagmus was disjunctive, but it is not certain whether the nystagmus had a pendular or a jerk wave- form. Eber et al. ( 2) reported a patient with a large, necropsy- proven, unilateral paramedian mesodi­encephalic infarct, who developed a downgaze­evokl! d see- saw nystagmus, as well as a complete ipsilateral third cranial nerve palsy, an upgaze palsy, and retraction nystagmus. The see- saw nystagmus had a jerk rather than a pendular wave­form and persisted until the patient's death 1 month after the stroke. The direction of the tor­sional and vertical quick phases was not specified in the report. Williams et al. ( 18) reported a patient with a small, CT- proven, unilateral paramedian mesodi-encephalic infarct who developed a transient up­gaze- evoked see- saw nystagmus, as well as bilat­eral first- degree horizontal gaze- evoked, jerk wave- form torsional nystagmus, an abduction­adduction paresis of the contralateral eye, and pos­sibly a tonic contraversive ocular tilt reaction. Kanter et al. ( 19) reported a patient with an MRI­proven, unilateral, paramedian mesencephalic in­farct, who developed a persistent, downgaze­evoked see- saw nystagmus as well as a primary­position upbeat nystagmus. The wave- form of the see- saw nystagmus was not specified. Most recently Ranalli and Sharpe ( 20) reported a patient with a necropsy- proven, unilateral para­median mesodiencephalic infarct who developed what appears to have been a see- saw nystagmus ( Sharpe 1988, personal communication). In the pri­mary position the patient had a dysconjugate tor­sional- vertical jerk nystagmus, with the contralat­eral eye beating upward and the ipsilateral eye ex­torting and beating downward. The patient also had a permanent vertical gaze palsy and a tran­sient ipsilesional skew deviation. The Eye Movements and Site of Lesion in This Case Our patient demonstrated the cardinal feature of see- saw nystagmus, namely, a predominantly tor­sional nystagmus with an additional disjunctive vertical component. Nevertheless, the patient also I Clin Neuro- ophthalmol, Vol. 11. No. 2, 1991 82 G. M. HALMAGYI AND W. F. HOYT demonstrated three unusual features, all of which may bear on the localizing significance and patho­physiological mechanism of see- saw nystagmus: 1. The nystagmus had a jerk rather than a pen­dular wave- form. 2. The nystagmus had an additional disjunctive horizontal component with convergent quick phases. 3. The patient had a unilateral rather than a bi­lateral mesodiencephalic lesion. It should be noted that in our case, just as in at least 2 of the 5 previously reported cases of see­saw nystagmus caused by a unilateral mesodien­cephalic lesion, the see- saw nystagmus has had a jerk rather than a pendular wave- form ( 2,20). Fur­thermore, Dehaene and van Zandijcke ( 3) reported a patient with " see- saw jerk nystagmus" and an adduction paresis, presumably caused by a unilat­eral paramedian mesencephalic infarct near the third nerve nucleus. Differential Diagnosis of See- Saw Nystagmus: Torsional Nystagmus Medullary Lesions Unilateral lesions of the medulla oblongata, par­ticularly lateral medullary infarcts, can cause a jerk wave- form torsional- vertical nystagmus, which may be indistinguishable from the jerk see- saw nystagmus described here ( 17,28). With both uni­lateral medullary lesions and unilateral mesodien­cephalic lesions, the torsional component of the nystagmus is conjugate. The difference in the nystagmus caused by lesions in these two loca­tions is that whereas with unilateral mesodien­cephalic lesions both the vertical and horizontal components are disjunctive, with unilateral med­ullary lesions the horizontal component is conju­gate and vertical component may be disjunctive or conjugate ( 28) ( see Table 1). Furthermore the lateralization of the torsional nystagmus with unilateral medullary lesions is TABLE 1. Comparison of the characteristics of the torsional- vertical nystagmus in patients with unilateral medullary lesions and in patients with unilateral mesodiencephalic lesions generally opposite to the lateralization observed with unilateral mesodiencephalic lesions. Whereas with a unilateral medullary lesion the torsional quick phases generally beat away from the side of the lesion ( 28), with a unilateral mesodiencephalic lesion the torsional quick phases beat toward the side of the lesion. The torsional- vertical nystagmus which occurs with Chiari malformations ( 13) and with syringobulbia ( 29- 31) may also be indistin­guishable from see- saw nystagmus. In these cases the nystagmus may be the result either of medul­lary extension of the syrinx or of medullary com­pression by the cerebellar ectopia. The torsional nystagmus in these cases always has a jerk wave­form; in syringobulbia it beats away from the side of the lesion ( 29,32). The clinical localizing significance of these obser­vations may be summarized as follows: If a patient with pendular see- saw nystagmus has a focal le­sion, then that lesion will be a large, extrinsic su­prasellar lesion compressing the brain stem bilat­erally at the mesodiencephalic junction. If, on the other hand, the see- saw nystagmus has a jerk wave- form, then the patient will have an intrinsic focal brain stem lesion either in the lateral me­dulla- usually on the side opposite the torsional quick phases, or in the mesodiencephalon on the same side as the quick phases. The Mechanism of See- Saw Nystagmus From the clinical and radiologic evidence pre­sented here, it is not possible to be certain about the critical structures which were damaged in or­der to produce a jerk see- saw nystagmus in our patient. Nonetheless, the lesion in this case did involve the medial thalamus, the subthalamus ( in­cluding zona incerta and the fields of Forel), the interstitial nucleus of Cajal, and the rostral inter­stitial nucleus of the median longitudinal fascicu­lus ( riMLF). From clinical and experimental obser­vations, several of these structures are known to be involved in the generation of nystagmus and of torsional eye movements. Damage to these struc­ture~ may have been pertinent to the generation of the Jerk see- saw nystagmus in our case. Nystagmus: Site of lesion quick- phase component Torsional Vertical Horizontal Lateral medulla Conjugate, contraversive Conjugate upbeating or disjunctive Conjugate, contraversive Mesodiencephalon Conjugate, ipsiversive Disjunctive Disjunctive, convergent Interstitial nucleus of Cajal Cl. inical ~~ d experimental lesions in the region of the l~ terShtial nucleus of Cajal in cats, monkeys, and In m~ n produce an ocular tilt reaction [ for a recent r~ vlew see Halmagyi et al. 1990 ( 33)]. The ocul~ r tilt reaction is a postural synkinesis, which conSIsts of conjugate eye torsion, hypotropia ( due felin Neurc. opltthttlliit/ l>, Vol. 11, No. 2, 1991 SEE- SAW NYSTAGMUS 83 to skew deviation) and head tilt, all to the same side. Destructive mesodiencephalic lesions involv­ing the zona incerta or interstitial nucleus of Cajal produce a persistent or tonic contraversive ocular tilt reaction, whereas electrical stimulation and " excitatory" lesions of the same structures pro­duce a paroxysmal or phasic, ipsiversive ocular tilt reaction. The neural drive for the ocular tilt reac­tion probably originates in the otoliths, and then projects via the ipsilateral vestibular nucleus to the contralateral interstitial nucleus of Cajal. The rele­vance of these observations to the mechanism of see- saw nystagmus is that the half cycles of see­saw nystagmus are identical to the eye movement abnormalities in the ocular tilt reaction. Rostral interstitial nucleus of the medial longitudinal fasciculus Recent data from monkey studies indicates that the riMLF is involved in the generation of ipsiver­sive quick phases of torsional vestibular nystag­mus ( 34). Burst neurons in the riMLF fire selec­tively with the ipsilaterally directed vertical and torsional quick phases of vestibular nystagmus. Furthermore, reversible chemical lesions of riMLF not only temporarily abolish all ipsilaterally di­rected torsional quick phases, but also produce a temporary tonic contraversive ocular tilt reaction. While these data seem pertinent to the mechanism of jerk see- saw nystagmus, they are also paradox­ical. They fail to explain why an experimental le­sion of riMLF abolishes ipsiversive torsional quick phases, whereas a clinical lesion ( such as in this case) involving the riMLF actually produces a tor­sional nystagmus with ipsiversive quick phases. Experimental diencephalic nystagmus Electrical stimulation of the mesodiencephalon in rabbits, produces a horizontal nystagmus with contraversive quick phases. Destructive lesions of the optimal stimulation sites- in the medial thala­mus between the lateral geniculate nucleus, the dorsolateral nucleus and the pulvinar- will pro­duce the opposite: a horizontal nystagmus with ipsiversive quick phases. [ For a review see Montandon and Monnier 1964 ( 35).] In our patient with jerk see- saw nystagmus, the medial thalamus was also involved. While there are obvious differ­ences between experimental diencephalic nystag­mus and jerk see- saw nystagmus, the site of the lesion in the two disorders is remarkably similar. The most obvious difference between experimen-tal diencephalic nystagmus and jerk see- saw nystagmus is that jerk see- saw nystagmus is a torsional- vertical nystagmus with only a small, dis­junctive horizontal component, while experimen­tal diencephalic nystagmus is a conjugate horizon­tal nystagmus. This difference cannot be explained simply as a species differences in the alignment and the innervation patterns of the extraocular muscles. It may represent fundamental differences in the three- dimensional organization of the vesti­bulo- ocular reflex in lateral- eyed animals such as the rabbit and in frontal- eyed animals such as man. There is little evidence to suggest a mechanism for the disjunctive horizontal and vertical compo­nents of jerk see- saw nystagmus. Disjunctive hor­izontal quick phases are produced by a lesion in the midbearing pretectum, as in convergence­retraction nystagmus, and the lesion in these cases may be unilateral ( 36). These disjunctive, conver­gent quick phases are similar to the horizontal component of the jerk see- saw nystagmus re­ported here. The precise mechanism of conver­gence nystagmus is obscure but may involve a dis­inhibition of normal reciprocal saccadic mecha­nisms ( 37). The origin of the disjunctive vertical quick phases is also obscure but may indicate a disturbance of a basic pattern of vestibular control of eye movement. Evidence for this lies in the ob­servation that in lateral- eyed animals, angular ac­celeration in roll produces a disjunctive vertical nystagmus in pitch: the eye on the side toward which the animal is accelerated beats downward, whereas the eye on the opposite side beats up­ward. Moreover, thermal stimulation of a single vertical semicircular canal in a lateral- eyed animal also produces a vertical nystagmus with disjunc­tive vertical quick phases ( 38). Despite all these uncertainties about the precise site of lesion and the exact pathophysiological mechanism of jerk see- saw nystagmus, the clinical observation reported here remains valid and use­ful. Jerk see- saw nystagmus can indicate a unilat­eral mesodiencephalic lesion, and the direction of the torsional quick phases indicates the side of the lesion. Jerk see- saw nystagmus needs to be distin­guished from torsional nystagmus caused by uni­lateral medullary lesions; in the latter the lesion is usually on the side opposite the torsional quick phases. Acknowledgment: This study was supported by the National Health and Medical Research Council of Aus­tralia and by the Royal Prince Alfred Hospital Neurology Department trustees. 1Clin Neuro- ophthalmol, Vol. 11. No. 2, 1991 84 G. M. HALMAGYI AND W. F. HOYT REFERENCES 1. Miller NR. Nystagmus and related ocular motility disor­ders. In Walsh & Hoyt's Clinical Neuro- ophthalmology. 4th ed. Baltimore: Williams' & Wilkins, 1985: 907- 8. 2. Eber AM, Rumbach L, Bataillard M, Strubel 0, Collard M. Seesaw nystagmus et troubles oculo- moteurs au cours d'un ramollissement thalamo- pedoncolaire unilateral. Rev Oto­Neuro- Ophthalmologique 1982; 54: 173- 8. 3. Dehaene I, van Zandijcke M. See- saw jerk nystagmus. Neuro- ophthalmology 1984; 4: 261- 3. 4. Bergin OJ, Halpern J. Congenital see- saw nystagmus asso­ciated with retinitis pigmentosa. Ann Ophthalmol 1986; 18: 346- 9. 5. Schmidt 0, Kommerell G. Congenitaler schauleknystag­mus ( Seesaw nystagmus); ein fall mit erhalten Gesichtsfel­dern, vertikaler Blickparese und Kopftremor. Albert von Graefes Arch Klin Exp OphthalmoI1974; 191: 265- 72. 6. Zeit RP, Biglan AW. Congenital seesaw nystagmus. I Pedi­atr Ophthalmol Strabismus 1985; 22: 13- 6. 7. Rucker CWo See- saw nystagmus associated with choroiditis and positive neutralization test for toxoplasmosis. Arch OphthalmoI1946; 35: 301- 2. 8. Fisher NF, Jampolsky A, Scott AB, Morris M, Lehmann S. Traumatic bitemporal hemianopsia. Am I Ophthalmol 1968; 65: 578- 81. 9. Frisen L, Wikkelso O. Post- traumatic see- saw nystagmus abolished by ethanol ingestion. Neurology 1986; 36: 841- 4. 10. Maddox EE. See- saw nystagmus with bitemporal hemiano­pia. Proc R Soc Med 1914; 7: 12- 3. 11. Druckman R, Ellis P, Kleinfeld J, Waldman M. See- saw nystagmus. Arch OphthalmoI1966; 76: 668- 75. 12. Davis GV, Schock JP. Septo- optic dysplasia associated with see- saw nystagmus. Arch OphthalmoI1975; 93: 137- 9. 13. Zimmerman CF, Roach ES, Troost BT. See- saw nystagmus associated with Chiari malformation. Arch Neural 1986; 43: 299- 300. 14. Lambert SR, Kriss A, Gresty MA, Benton S, Taylor D. Joubert syndrome. Arch OphthalmoI1989; 107: 709- 13. 15. Jensen OA. See- saw nystagmus. Br I Ophthalmol 1959; 43: 225- 9. 16. Daroff RB. See- saw nystagmus. Neurology 1965; 15: 874- 7. 17. Mastaglia F. See- saw nystagmus: an unusual sign of brain­stern infarction. I Neurol Sci 1974; 22: 439- 442. 18. Williams 1M, Dickinson P, Ramsay, Thomas L. See- saw nystagmus. Aust NZ JOphthalmoI1982; 10: 19- 25. 19. Kanter OS, Ruff RL, Leigh RJ, Modic M. See- saw nystag­mus and brainstem infarction. Neuro- ophthalmology 1987; 7: 279- 83. 20. Ranalli PJ, Sharpe JA, Fletcher WA. Palsy of upward and , · ¢ ll", N'"-' iH! Pnthnlmol. Vol. 11. No. 2, 1991 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. downward saccadic, pursuit and vestibular movements with a unilateral midbrain lesion. Neurology 1988; 38: 114- 22. Smith JL, Mark VH. See- saw nystagmus with suprasellar epidermoid tumor. Arch OphthalmoI1959; 62: 281- 3. Lourie H. See- saw nystagmus. Arch Neural 1963; 9: 531- 3. Schurr PH. See- saw nystagmus. Proc R Soc Med 1963; 56: 808- 10. Kinder RSL, Howard GM. See- saw nystagmus: an unusual sign of lesions near the third ventricle. Am I DIS ChIld 1963; 106: 331- 2. Drachman DA. See- saw nystagmus. I Neural Neurosurg Psy­chiatlll 1966; 29: 356- 61. Mewis L, Tang RA, Mazow MW. See- saw nystagmus after strabismus surgery. I Pediatr Ophthalmol StrabIsmus 1982; 6: 302- 5. Garelli FF, Gherardini G. Rapporti tra il nistagmo " see­saw" e 10 strabismo verticale " sghembo" ( skew- deviation). Descrizione di un caso. Riv Neural 1972; 42: 137- 62. Morrow MJ, Sharpe JA. Torsional nystagmus in the lateral medullary syndrome. Ann NeuroI1988; 24: 390- 8. Falkenberg K. Zur lokalisation des nystagmus. Deutsche Zeitschrift fur Nervenheilkunde. 1942; 153: 40- 9. Fein JM, Williams ROB. See- saw nystagmus. I Neural Neu-rasurg Psychiatry 1969; 32: 202- 7. . Thrush DC, Foster JB. An analysis of nystagmus In 100 consecutive patients with communicating syringomyelia. I Neural Sci 1973; 20: 381- 6. Thiebaut F, Isch F, Mengus M. Le nystagmus giratoire dans les syndromes retro- olivaires vasculaires et dans la syrin­gobulbie. Rev Oto- Neura- Ophthalmologique 1958; 30: 335- 8. Halmagyi GM, Brandt Th, Dieterich M, Curthoys IS, Stark RJ and Hoyt WF. Tonic contraversive ocular tilt reaction due to unilateral meso- diencephalic lesion. Neurology 1990; 40: 1503- 9. Vilis T, Hepp K, Schwarz U, Henn V. On the generation of vertical and torsional rapid eye movements in the monkey. Exp Brain Res 1989; 70: 1- 11. Montandon P, Monnier M. Correlations of the diencephalic nystagmogenic area with the bulbo- vestibular nystag­mogenic area. Brain 1964; 87: 673- 90. Auerbach SH, DePiero TJ, Romanul F. Sylvian aqueduct syndrome caused by unilateral midbrain lesion. Ann Neural 1982; 11: 91- 4. Ochs AL, Stark L, Hoyt WF, D'Amico D. Opposed adduct­ing saccades in convergence- retraction nystagmus. A pa­tient with Sylvian aqueduct syndrome. Brain 1979; 102: 497­508. De Jong HAA, Goosens HP, Oosterved WJ. Vertical nystag­mus provoked by locally applied calorization at the vertical semicircular canals: a study in pigeon. ORL I Otorhinolo­laryngol Relat Spec 1988; 50: 84- 93.