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Show f. Clin. Neuro-ophthalmol. 3: 49-51, 1983. Monocular Rotary Nystagmus JORGE C. KATTAH, MD. STANLEY L. COHAN, MD. WILLIAM CAHILL, M.D. MICHAEL BUAS, PhD. Abstract A patient with transient monocular rotary-vertical nystagmus demonstrated decreased gain of vertical pursuit and normal vestibulo-ocular reflex on electrooculogram. A supranuclear brain stem lesion, resulting in lack of monocular inhibition of oculomotor neurons, is postulated on the basis of these findings. A 62-year-old man with a history of hypertension, myocardial infarction, and late latent lues noted sudden onset of blurring of vision and a pulling sensation behind the right eye. He also complained of light-headedness and gait instability and was admitted to the hospital for further evaluation. While the general physical examination was unremarkable, the neurologic examination demonstrated a slightly wide-based gait and mild rightsided ataxia. Neuro-ophthalmologic examination showed intermittent monocular, intorting, rotatory- vertical movement of the right eye. It was present in all directions of gaze but most prominently looking down and to the left where it became primarily vertical. In addition, he had a decreased blinking rate. Vertical optokinetic nystagmus and vestibulocular reflex were normal. The neuro-ophthalmologic examination was otherwise normal. The ataxia and gait instability cleared within the first day of hospitalization, but the abnormal movements of the right eye persisted for 2 more days. Neurologic workup included a normal CT scan of the head. Cerebrospinal fluid was obtained under normal pressure and revealed no cells, a glucose of 80 mg%, and a protein of 60 mg%. Cerebrospinal fluid serology was nonreactive. On the fifth day of hospitalization, the patient was discharged with improvement of his neurologic deficit and remains symptom-free to date. From the Department of Neurology and the Department of Bioengineering, Georgetown University Medical School, Washington, D.C March 1983 Methods and Results Conventional electro-oculogram recording of horizontal and vertical eye movements was obtained the night of admission. The equipment used have been described previously. 1 Vestibulo-ocular reflex was tested in the dark. The patient was asked to fixate on a distant static target as his chair followed a sinusoidal oscillation. The oblique vestibulo- ocular reflex gain was obtained by asking the patient to tilt the head 45 ° to the right and left from midposition, as the chair oscillated. In the primary position of gaze, the patient showed primary position nonrhythmic, pendular rotatory, and vertical monocular oscillations in the right eye with an average frequency of 2-3 Hz and an amplitude in the vertical and horizontal planes of 6°, respectively. When the patient fixated on an eccentric target, the oscillation became strictly vertical with an amplitude of 12°, and the nystagmus components in this position were pendular, with an average velocity of 35° /second (Fig. 1). Horizontal saccades were tested following a sequence described previously.l The saccades were normometric and had normal velocity and latency. While the gain of horizontal pursuit was 1.0, vertical pursuit showed decreased gain (0.6). The gains of horizontal and oblique vestibulo-ocular reflex were normal. The rest of the electro-oculogram was unremarkable. Discussion Dissociated nystagmus refers to a group of disorders in which the nystagmoid movements of the two eyes differ in amplitude and/or direction. This definition includes patients with monocular nystagmus. A large variety of clinical conditions have been associated with monocular nystagmus. Spasmus nutans is probably the most common cause c Chiasmal and optic nerve gliomas and other suprasellar mass lesions have been reported in association with rotatory, vertical, or horizontal monocular nystagmus.:l . 4 In most of these cases, decreased visual acuity in the affected eye was noted in addition to significant local mass effect. Monocular visual loss without other known abnormalities has been reported in association with horizontal or 49 Monocular Rotary Nystagmus RighI Lell Up I ~_......--- + 15' O~",dR~Hb-,- -:::><__--"""'===--~----- _ I ~owo I ''',----~~~~:::::=:.... '''"I'-'~ --== Down I f:~ ~.",,-;::y::;,W' 0500 1000 1500 2000 2500 3000 3500 4000 4500 5000 Figure I. Electr<'-ocul"gram~ Eve movement5 were recorded for 5 5ecl) nds uSing electrt1CulogrJphv. RH: Right hOflwntal. LH: Left hl)rizontal. RY: R.ght verlic.,I. LY: Left vert.Lll. The patient was instructed to look at J target located 50 to the left of fi'ation In the hl,<izl'ntJI meridi.m~ Obser\'e .1 monl)(ular, pnmarilv verticJI pendulM nY5tagmus in the right eve. verticill monocular nystagmus. 1-'7 In these Cdses, a supranuclear system for monocular contral of fixation dependent on visual cues initiated in the same eye has been postulated. Yee believes that this supranuclear control system could involve the vergence system, the only oculomotor control sys~ tem known to produce monocular movements." This possibility, however, seems unlikely, since there is no evidence at present that the vergence system is involved in the generation or control of vertical eye movements." Horizontal monocular nystagmus has recently been reported as an ictal phenomena in a patient with photosensitive epilepsy. x Animal experiments have demonstrated brain stem sites where electrical stimuli lead to monocular nystagmus.~ Brain stem lesions in humans can also cause monocular nystagmus. 111-1 I Duane described two patients with monocular rotatory nystagmus similar to ours. Ie. II One of them with an apparent brain stem lesion, had a diagnosis of general paresis. Initially, this patient had been in coma for 3 weeks~ Delirium, gait ataxia, and dysarthria were noted as the patient regained co~- so sciousness; 1 year later, monocular rotatory nystagmus was f~undIe The second patient had a long-standing history of intermittent vertical diplopia and had been aware of involuntary, periodic monocular oscillations for several years. With the exception of monocular rotatory nystagmus, no other abnormalities were found."l Circumduction nystagmus has been reported in patients with multiple scierosis.1 4 These cases are of interest because the nystagmus necessarily involved vertical as well as horizontal monocular movements. In none of these reports was a precise lOCation for the causative lesions apparent. Monocular eye movements attributable to the action of the superior oblique muscle have been described as superior oblique myokymia.l"-I~ Patients with superior oblique myokymia tend to have chronic courses of intermittent oscillopsia and resting hyperphoria in the affected eye. Characteristically the movements are of high frequency and low amplitude, often requiring ophthalmoscopic eXamination to be identified. Electromyographic studies revealed few abnormal interference pattern units in the superior oblique muscle which were Journal of Clinical Neuro-ophthalmology consistent with a lesion in the region of the fourth nerve nucleus. Simultaneous recordings in the inferior oblique muscle were normal. IS In our case, the monocular rotatory nystagmus was similar in character to that described in superior oblique myokymia, but differs in the greater amplitude of the eye movements and their nearly continuous occurrence during the acute episode. The normal gains on the horizontal and oblique vestibulo-ocular response suggest that a supranuclear lesion was responsible for the production of the nystagmus seen in our patient. Maintenance of steady fixation is the result of burst neuron inhibition by pause cells located in the medial pontine reticular formation.~" Lesions involving this group of cells could result in unsteady fixation and involuntary saccadic horizontal, vertical, and oblique eye movements."" Although this inhibitory influence is likely to be binocular in nature, monocular interrruption of this prenuclear inhibitory mechanism could result in monocular nystagmus. Finally, considering the brief duration and complete reversibility of the monocular nystagmus in this case, it is likely that transient ischemia was the main etiologic factor. References Ledley, R.5., Rotolo, L.S, and Kattah, j.C: Computerized electroculography (CEOG). Proceedings of 31st Annual Conference in Engineering in Medicine and Biology. The Alliance for Engineering in Medicine and Biology Publishers, Bethesda, Maryland, 1978, p. 100. 2. Donin, j.F.: Acquired monocular nystagmus in children. Can.]. Ophthalmol. 2: 212-215, 1%7. 3. Schulman, jA., Shults, W.T., and jones, jM: Monocular vertical nystagmus as an initial sign of chiasmal glioma. Am.]. Ophthalmol. 87: 87-90, 1979. 4 Udvarhely, GB., Khodadoust, A.A., and Walsh, F.B.: Gliomas of the optic nerve and chiasm in children: An unusual series of cases. Clin. Neurosurg. 13: 204237,19b6. 5 Yee, RD., jelks, G.W., Baloh, R.W, and Honrubia, V.: Uniocular nystagmus in monocular visual loss. March 1983 Katt,lh, et al. Ophthalmology 86: 511-518, 1079. b. Miller, N.R.: Discussion of presentation by Dr. Robert D. Yee, et al. Ophthalmology 86: 519-522,1979. 7. Dufour, A., Guccione, G, and Ramburino, V: Considerations electronystagmographiques sur deux cas de nystagmus monoculaire. Rev. Otaneuro-ophthalmol. 44: 125-132, /on 8. jacome, D.A., and Fitzgerald, R.. Monocular ictal nystagmus. Arch. Neurol. 39: b53-b57, 1982. 9. jampe!, R.S.: Experimental monocular nystagmus in the monkey. Arch. Ophthalmol. 70: 587, 1963. 10. Cogan, D.G: Dissociated nystagmus with lesions in the posterior fossa. Arch. Ophthalmol. 70: 121-128, 1963. 11. Nathanson, M., Bergman, P.S., and Bender, M.S.: Monocular nystagmus. Am.]. Ophthalmol. 40: 685b92, 1955. 12. Duane, A.. Unilateral and other unusual forms of nystagmus. NY. State]. Med. 5: 245-249, 1905. 13. Duane, A.: Unilateral rotary nystagmus. Trans. Am. Ophthalmol. Soc. 11: b3-b7, 190b. 14. Castaigne, P., Chain, F, Pierrot-Deseilligny, C, and Larmande, P.: Le nystagmus de circumduction monoculaire. Rev. Neurol. (paris) 135: 51-57,1979. 15. Hoyt, W.F., and Keane, j.R: Superior oblique myokymia. Arch. Ophthalmol. 84: 461-467, 1970. 16. Clarke, E.: A case of apparent intermittent overaction of the left superior oblique. Br. Orthopt. ]. 23: Ilb117,196b. 17. Susac, j.O., Smith, j.L, and Schatz, N.j.: Superior oblique myokymia. Arch. Neurol. 29: 432-434, 1973. 18. Roper-Hall, G, and Burde, R.M.: Superior oblique myokymia. Am. Orthapt.]. 28: 58-b3, 10 78. 19 Grainger, KM.R., ,md Gubbay, S.5.: Superior oblique myokymia. Proc. Aust. Assoc. Neural. 12: 27-29, 1975. 20. Keller, E.L.: Participation of medial pontine reticular formation in eye movement generation in monkey. J Neurophysiol. 37: 31l,-332, 1074. Acknowledgment This work was supported in part by a grant from the Strauss Found,ltion. Write ft'r reprints to: Jorge C Kattah. MD. 3800 Reservoir Ro,ld, NW., Washington. D.C 20007. 51 |
