Journal of Neuro-Ophthalmology, September 1988, Volume 8, Issue 3

Seesaw nystagmus. Role of visuovestibular interaction in its pathogenesis.

Elevation and intorsion of one eye and synchronous depression and extorsion of the other eye characterize a half cycle of seesaw nystagmus. Reversal of these movements constitutes the second half cycle, forming the "seesaw"-like movements. Based on analysis of the ocular oscillation characteristics of the cases of seesaw nystagmus reported in the literature, including the two new cases we present, we postulate that seesaw nystagmus is another type of ocular oscillation brought about by an unstable visuovestibular interaction control system. Nonavailability of retinal error signals to the inferior olivary nucleus essential for vestibuloocular reflex adaptation due to complete chiasmal dissection makes the system less stable. This system instability is further accentuated by the pursuit feedback element. The intact inferior olivary nucleus-nodulus connections in seesaw nystagmus would explain the 180 degrees phase difference that distinguishes it from the midline form of oculopalatal myoclonus, where these connections are likely disrupted.

Journal ofClilliCl1I Nffiro-ophllwlmology 8(3): 171-177.1988. Seesaw Nystagmus Role of Visuovestibular Interaction in Its Pathogenesis Tsutomu Nakada, M.D., and Ingrid L. Kwee, M.D. 1988 Raven Press. Ltd .• New York Elevation and intorsion of one eye and synchronous de­pression and extorsion ot the other eye charactenze a half cycle of seesaw nystagmus. Reversal of these move­ments constitutes the second half cycle, forming the "seesaw"-like movements. Based on analysis of the oc­ular oscillation characteristics of the cases of seesaw nystagmus reported in the literature, including the two new cases we present, we postulate that seesaw nys­tagmus is another type of ocular oscillation brought about by an unstable visuovestibular interaction control system. NonavailabiJity of retinal error signals to the in­ferior olivary nucleus essential for vestibuloocular reflex adaptation due to complete chiasmal dissection makes the system less stable. This system instability is further accentuated by the pursuit feedback element. The intact inferior olivary nucleus-nodulus connections in seesaw nystagmus would explain the 1800 phase difference that distinguishes it from the midline form of oculopalatal myoclonus, where these connections are likely disrupted. Key Words: Nystagmus, seesaw- Visuovestibular in­teraction. . From the Clinical Oculomotor Laboratory, Veterans Admin­Istration Medical Center, Martinez, and Department of Neu­rology. University of California, Davis, California. Address correspondence and reprint requests to Dr. T. Na­kada at Department of Neurology, University of California, Davis, Veterans Administration Medical Center, 150 Muir Road, Martinez. CA 94553, U.S.A. 171 In 1914, Maddox described curious ocular oscil­lations in a 53-year-old carriage builder who had bitemporal hemianopsia and coined these move­ments "seesaw nystagmus" (1). Elevation and in­torsion of one eye and synchronous depression and extorsion of the other eye characterize a half cycle. Reversal of these movements constitute the second half cycle, forming the "seesaw"-like eye movements. The frequency of the oscillations of Maddox's patient with the eyes in primary posi­tion was 1521min and 204/min on upgaze. The ver­tical distance of excursion of each eye was -1 mm and increased on downgaze. To date, -30 cases have appeared in the literature. The majority of these cases conform to Maddox's original descrip­tion. Despite efforts by many authors, the underlying mechanism of seesaw nystagmus has remained obscure. Because of its frequent association with visual symptoms, especially bitemporal hemi­anopsia, disturbance of visual input has been thought to playa main role in its pathogenesis (2). On the other hand, because seesaw nystagmus has been reported in patients with brainstem le­sions in the absence of any visual deficits, certain authors believe that disturbance of visual input is not essential in its pathogenesis (3). Instead, dys­function of the ocular counterrolling system is postulated to be responsible for its pathogenesis. In our recent work on oculopalatal myoclonus, we introduced a model of visuovestibular interac­tion involving the inferior olivary nucleus- me­diated vestibuloocular reflex adaptation mecha­nism, and hypothesized that instability of this vi­suovestibular interaction control system resulting from inferior olivary nucleus degeneration may be the underlying mechanism in the pathogenesis of the type of ocular oscillation seen in oculopalatal myoclonus (4). Retinal error signals essential to this adaptation mechanism reach the inferior oli- 172 T. NAKADA AND I. L. KWEE vary nucleus through the accessory optic tract in­dependent of the geniculocortical projection (5). Theoretically, nonavailability of these retinal error signals can similarly result in system instability. We studied two cases of seesaw nystagmus and performed an extensive review of the literature in attempt to delineate its pathogenesis with respect to the role of the visuovestibular interaction con­trol system. METHODS Eye movements were recorded by a video re­cording system. Each frame of the recording was analyzed sequentially in freeze-frame as well as in slow motion. Torsional eye movements were rec­ognized by following an identifiable marker on the iris individualized for each patient. Vertical and horizontal eye movements were further monitored by an infrared photoelectric cell eye movement re­cording system (Eye Track Model 210, Applied Science Laboratories). CASE REPORTS Case 1 A 41-year-old man was referred to the clinical oculomotor laboratory because of ocular oscilla­tions. The patient sustained severe head injury 20 years prior, which resulted in incomplete, bitem­poral hemianopsia and anosmia. Ten years after the injury he sought medical attention for spells of short lapses of memory and fainting sensation. He also noted worsening of the bitemporal hemi­anopsia. No ocular oscillations were noted at that time. The patient was released without any treat­ment. He returned 5 years later with the complaint of blurred vision. Neurological examination re­vealed classic seesaw nystagmus with symmetric ocular oscillations at -ISO/min. The nystagmus became smaller and faster on upgaze, and larger and slower on downgaze. The patient had less dif­ficulty with reading on downgaze. The nys­tagmus, as monitored with an infrared photoelec­tric cell eye monitoring system for vertical oscilla­tions, disappeared in the dark. Visual acuity was 20/40 and 20/20 for the right and left eyes, respec­tively. The patient had complete bitemporal hemi­anopsia. Extraocular movements were full. The rest of the neurological examination was entirely normal. Computed tomography revealed frontal ,-"'nh,11I"'m,11acia. The brainstem appeared to be 1Clirl Neuro-llpJr'halmol. \ '",. ~ . ....0 ',. _ .,~. FIG. 1. Case 1. Computed tomography scan showing frontal encephalomalacia. The brainstem appears in­tact. Case 2 A 57-year-old man with long-standing posttrau­matic headache was referred to the clinical oculo­motor laboratory because of seesaw nystagmus. The patient sustained severe head injury 34 years earlier, which resulted in complete bitemporal hemianopsia. Subsequent ophthalmology follow­up 10 ye~rs later revealed seesaw nystagmus. NeurologIcal examination showed classic seesaw nystagmus with symmetric ocular oscillations at -140/min. The nystagmus became smaller and faster on upgaze, and larger and slower on down­gaze. !he nystagmus, as monitored with a photo­electnc cell eye-monitoring system for vertical oscillations, disappeared in the dark. The best cor­rected visual acuity was 20/80 and 20/20 for the right and left eyes, respectively. Extraocular move­ments were full. The patient had severe bitem­por. al h~mianopsia. The rest of the neurological ex­ammation ~as ~nremarkable. Nuclear magnetic reson~nce Ima~mg revealed bifrontal encephalo­malaCIa and mild hydrocephalus. The brainstem appeared intact (Fig. 2). LITERATURE REVIEW Table 1 summarizes the cases reported in the lit­erature. Overall, of the patients whose visual SEESAW NYSTAGMUS: VISUOVESTIBULAR INTERACTION 173 FIG. 2. Case 2. (A) Magnetic resonance imaging showing large left frontal encephalomalacia. (B) Mag­netic resonance imaging showing that the brainstem appears intact. status is known, including our two cases (31 cases), -70% (21/31) exhibited visual symptoms. None of the reported cases had complete blind­ness. If the cases with significant asymmetry or other oculomotor deficits are excluded, >95% of patients (total 20 patients) had visual symptoms. AU but two of these 20 patients had bitemporal hemianopsia. RESULTS The prototype case of seesaw nystagmus can be described as follows. Ocular oscilJations are sym­metric and are reminiscent of ocular counterrolling produced by head tilt about an anteroposterior axis in the center between the two eyes (Fig. 3). The nystagmus becomes smaller and faster on up­gaze, and larger and slower on downgaze. The nystagmus disappears in the dark or with eye clo­sure. The onset of the nystagmus is insidious. The nystagmus is almost always accompanied by bi­temporal hemianopsia. DISCUSSION The vestibuloocular reflex receives selective in­hibitory control from the ipsilateral floccular Pur­kinje cells at the level of the vestibular nucleus. This inhibition is exerted on only one of each of the two vestibuloocular reflex pathways con­verging on the individual extraocular muscles (6) (Table 2). As a result, unilateral floccular disinhibi­tion of the vestibuloocular reflex creates a unique tonic imbalance of the vestibuloocular reflex, which can produce torsional eye movements sim­ilar to those observed in the lateral form of oculo­palatal myoclonus (Fig. 4). These torsional move­ments are primarily a consequence of the disin­hibited anterior semicircular canal-originated vestibuloocular reflex activities that produce con­traction of the ipsilateral superior rectus and con­tralateral inferior oblique muscles and relaxation of their antagonists (4,7). The vertical to-and-fro pen­dular oscillation of eyes observed in the midline form of oculopalatal myoclonus is thought to rep­resent bilateral disease (4). Similar bilateral oscilla­tions, but 1800 out of phase, should in theory pro­duce the eye oscillations characteristic of seesaw nystagmus (8). More than 95% of the cases with classic, sym­metric, seesaw nystagmus reported in the litera­ture, including OUf two cases (total of 20 cases), were associated with visual symptoms. All but two of these patients had bitemporal hemianopsia. Indeed, recovery from bitemporal hemianopsia re­sults in disappearance of seesaw nystagmus (9). It appears, therefore, that disruption of the crossing fibers at the chiasm plays a major role in the pathogenesis of seesaw nystagmus. On the other hand, because total blindness does not produce seesaw nystagmus and seesaw nystagmus disap­pears with eye closure or in the dark, preservation of geniculocortical function appears to be a second necessary factor for the generation of seesaw nys­tagmus. Inferior olivary nudeus- mediated vestibulo­ocular reflex adaptation has been studied exten­sively in the rabbit (10). The inferior olivary nu­cleus uses visual information for the vestibulo- , 011I Neurtro/lhthalmol, V,'1. 8, No.3. 1988 TABLE 1. Cases of seesaw nystagmus reported in the literature Patient Visual acuity Age Visual Reference (years) Sex Cause R L field Comment Maddox (1) 53 M ? 6/24 6/24 BH 152/min. faster on upgaze Rucker (18) 51 M Choroiditis 20/60 3/60 Isles 128/min. ?asymmetric Larsen (19) 4 M Oligodendroglioma ? ? ? Chiasmal lesion, brainstem compression Jensen (20) 55 M Brainstem 6/18 6/18 ? ?MLF. divergent strabismus infarct 66 M Brainstem 6/18 6/18 NL ?MLF, divergent strabismus infarct Mark (9) 10 F Suprasellar 20/200 20/30 BH Smaller on upgaze, larger on epidermoid downgaze; disappeared postoperatively with improved field and acuity 10 M Hypothalamic ? ? BH glioma Lourie (21) 43 M Chromophobe 5/200 20/200 BH Smaller on upgaze. larger on adenoma downgaze Kinder (22) 8 M Craniopharyngioma 20/100 CF BH Shurr (23) 7 F Craniopharyngioma NL NL BH 4/min, disappeared postoperatively with improved field 51 F Chromophobe 6/60 6/60 BH adenoma Arnott (2) 15 F Craniopharyngioma 6/36 6/12 BH 160/min Slatt (24) 32 M Childhood 20/70 20/200 NL Faster/smaller on upgaze. slower and febrile larger on downgaze illness Daroff (25) 66 F Chromophobe 20/200 20/50 BH Larger on downgaze adenoma 68 M Brainstem 20/20 20/20 NL ?MLF, asymmetric infarct Drachman (26) 65 F Chromophobe 20/60 20/60 BH adenoma Druckman (27) 41 F Cran iopharyngioma 20/100 20/100 BH 34 M Childhood 20/50 20/100 NL 70-120/min febrile illness 17 F Difficult LP 20/200 ? Mixed nystagmus birth 35 M ?MS ? ? ? Mixed nystagmus Eber (28) 62 M Brainstem ? ? ? infarct Fein (29) 41 F Syringobulbia? 20/30 20/20 NL Fasterlsmaller on upgaze; slowerl larger on downgaze Schmidt (30) 20 F Trauma 0.5 1.0 BH 50-70/min, faster on downgaze; disapeared with eye closure 37 M Trauma 1.0 10 BH 30-70/min 52 M Trauma 1.0 10 BH 30-60/min; disappeared with eye closure Arnott' (39) ? M Trauma ? ? BH Disappeared with eye closure Regli (31) 34 F ?Congenital 1.0 1.0 NL Faster on upgaze, disappeared with eye closure Garelli (32) 50 M Stereotactic 5/10 CF NL Largerlslower on downgaze surgery for parkinsonism Mastaglia (33) 73 F Brainstem ? ? NL Acute onset. disappeared within 3 infarct days Rych (34) 23 F Degeneration 0.1 0.05 Al 240-300/min; ?MLF of cone; aminoaciduria Davis (35) 20 F Septooptic 20/100 20/20 BH dysplasia Williams (36) 7 F ? NL NL NL Asymmetric 33 F Thalamic ? ? ? Acute onset; disappeared within 3 infarct days; ?MLF Mewis (37) 7 F Craniopharyngioma 20/80 20/80 BH Zimmerman (38) 19 F Chiari 20/25 20/40 NL Asymmetric malformation ~~. bite~por~1 hemi~nopsia;NL•. normal; Al. altitudinal hemianopsia; MLF. medial longitudinal fasciculus syndrome; MS. ;n -,.\I,'j~'" Sr-,,(HOSIS: LP. light perceptlon;- CF, count fingers. , firsl Cd::C N),1:, :€:jJ0r1ed previously (2). T. NAKADA AND I. L. KWEE 175 FIG. 3. Schematic presentation of see-saw nys­tagmus. The anteroposterior torsional axis is located halfway between the two eyes (X). ocular reflex adaptation. These retinal error signals reach the inferior olivary nucleu through two dis­crete pathways independent of the geniculocor­tical projections (5). Projections from the eye con­tralateral to the inferior olivary nucleus cross at the optic chiasm and enter the ipsilateral accessory optic tract. After relays at the nucleus of the optic tract as well as the dorsal and lateral terminal nu­cleus, these projection descend through the brainstem to the caudal part of the dorsal cap of the inferior olivary nucleus. The second pathway arises from the eye ipsilateral to the inferior oli­vary nucleus, enters the contralateral accessory optic tract, and crosses again in the posterior com­missure. After relay at a cell group located ventro­medial to the red nucleus, it descends through the brainstem to the rostral part of the dorsal cap of the inferior olivary nucleus. The caudal part of the dorsal cap projects to Purkinje cells, which inhibit horizontal semicircular canal-originated vestibu­loocular reflex activities, while the rostral part of the dorsal cap projects to those Purkinje cells in- TABLE 2. Vestibuloocular reflex pathways and their floccular inhibition Canals Extraocular muscles Floccular inhibition Anterior Excitatory I-Superior rectus Yes c-Inferior oblique Yes Inhibitory i-Inferior rectus Yes c-Superior oblique Yes Horizontal Excitatory i-Medial rectus Yes c- Lateral rectus No Inhibitory i-lateral rectus Yes c-Medial rectus No Posterior Excitatory i-Superior oblique No c-Inferior rectus No Inhibitory i-Inferior oblique No c-Superior rectus No i, Ipsilateral; c. contralateral. Based on Ito et al. (6). FIG. 4. Schematic presentation of the lateral form of oculopalatal myoclonus. The axis is located lateral to the outer canthus of the eye (X). hibiting anterior semicircular canal-originated vestibuloocular reflex activities (5). In humans, visual tracking is dominated by the pursuit system. Development of the fovea and geniculo-cortical projections was accompanied with the development of a binocular arrangement and chiasmal hemidecussation. The accessory optic tract pathway is retained in humans inde­pendent of the geniculocortical pathway. The pathways discussed earlier that convey retinal error signals to the inferior olivary nucleus for ves­tibuloocular reflex adaptation are likely to be sim­ilar to those of other animals (11,12). Therefore, chiasmal dissection can be expected to disrupt the retinal error signals to the inferior olivary nucleus but still retain the signals for the pursuit system. NonavaiJabiJity of retinal error signals essential for vestibuloocular reflex adaptation renders the vi­suovestibular control system less stable. This in­stability is further accentuated by the pursuit feed­back element (8). Recent physiological studies indicate that the cerebellar nodulus governs the vestibuloocular re­flex phase control (5,13). Lesions of the nodulus result in marked vestibuJoocular reflex phase ad­vancement without significant concomitant changes in vestibuloocular reflex gain (13). It is now known that the nodulus receives collateral input from the inferior olivary nucleus climbing fibers projecting to the flocculus (14). Integrity of inferior olivary nucleus-nodulus connections may be responsible for the observed 1800 phase differ­ence in the bilateral oscillations of seesaw nys­tagmus. In contrast, the in-phase bilateral oscilla­tions in the midline form of oculopalatal myoc­lonus likely reflect disruption of these connections. Electrical stimulation of the nodulus Purkinje cell produces powerful inhibition on the activities of the reciprocal connections of the ves­tibular and fastigial nuclei (15). Therefore, these structures may contribute to nodulus control of the vestibuloocular reflex phase. Of interest is the fact that activities of the otolith- ocular reflex, I ClIII ".''''''1'1111''''11101. 1'01. S. Nil. 3, 1938 176 T. NAKADA AND I. L. KWEE which is responsible for the tonic phase of ocular counterrolling (16) is also under weak but definite inhibitory control of nodulus Purkinje ceUs (15). The role of the interstitiaJ nucleus of CajaJ in the development of seesaw nystagmus is unclear. Al­though electrical stimulation of the interstitial nu­cleus of Cajal produces ocular counterroUing, and a case of the disappearance of seesaw nystagmus by stereotactic destruction of the interstitial nu­cleus of Cajal has been reported (3,17), its role in the generation of seesaw nystagmus remains to be defined. Data in support of interstitial nucleus of CajaI involvement in the generation of seesaw nystagmus, therefore, must be considered incon­clusive. We present the hypothesis that seesaw nys­tagmus is yet another type of ocular oscillation brought about by an unstable visuovestibular in­teraction control system due to nonavailability of retinal error signals for the vestibuloocular reflex adaptation mechanism. The condition produces bilateral, 1800 out-of-phase oscillations of floccular Purkinje cells. Because the final product of the vi­suovestibular interaction control system is eye ve­locity, the velocity of ocular 0 cillations in seesaw nystagmus should likely remain essentially con­stant. Therefore, the product of the oscillation wavelength and the angular velocity will be con­stant. Indeed, the majority of the cases, including our two, exhibited changes in ocular oscillation characteristics on vertical gaze consistent with those predicted by the hypothesis, being smaller and faster on upgaze and larger and slower on downgaze. Acknowledgment: This study was supported by grants from the NIH (GM 37197) and the Veterans Ad­ministration Research Service. REFERENCES I. Maddox EE. See-saw nystagmus with bitemporal hemi­anopia. Proc R Soc Med 1914:7:12-3. 2. Arnoll EJ. Vertical see-saw nystagmus. Trail; O,'i11lmlll",1 5<Jc UK 1964;84:251-7. 3. Miller NR. 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