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Show JOIITllal of Clinical Nellro-oplrtlwlmology 7(4): 241-243. 1987. Slow-Upward Ocular Bobbing Thomas J. Goldschmidt, M.D., and Michael Wall, M.D. ~ 1987 Raven Press, Ltd., l':ew York A patient with a previously undescribed spontaneous arrhythmic vertical eye movement termed Slow-upward ocular bobbing is reported. The patient had a one-anda- half syndrome due to pontine infarction. A simplified scheme for describing the variations of ocular bobbing is proposed based on the velocity and direction of the initial eye movement. Key Words: Ocular bobbing-Eye movements-Oneand- a-half syndrome-Cerebrovascular disease. From the Departments of Neurology and Psychiatry (T.J.G., M.W.) and Ophthalmology (M.W.). Tulane University Schoo! of Medicine, New Orleans, Louisiana. Address correspondence and reprint requests to Dr. M. Wall at Tulane University School of Medicine, Department of Neurology and Psychiatry, 1415 Tulane Avenue, New Orleans, LA 70112, U.SA 241 Ocular bobbing as first described by Fisher (1) is a spontaneous vertical ocular oscillation characterized by a brisk-downward eye movement with a slow return to midposition. Reverse ocular bobbing is an oscillation characterized by a brisk-upward eye movement from the primary position with a slow return to midposition. Inverse bobbing (ocular dipping) is distinguished by a slowdownward movement with a fast return to midposition. We report a patient with an eye movement abnormality characterized by a conjugate slow-upward eye movement followed by a fast-downward movement to the primary position. This phenomenon could be termed "inverse-reverse" or "converse" ocular bobbing. Because of the taxing overabundance of terms in the literature describing ocular bobbing, we propose that this variant be named slow-upward bobbing and that the ocular bobbing nosology be simplified. CASE REPORT A 59-year-old right-handed black woman with a history of poorly controlled hypertension and non-insulin-dependent diabetes mellitus presented with a chief complaint of right-sided weakness and difficulty speaking. Her past history was significant for a stroke, occurring 1 year prior to admission. This was associated with a minimal right hemiparesis and was due to infarction of the posterior limb of the left internal capsule. On examination the patient was afebrile with a pulse of 96 beats/min and respirations of 24/min. The blood pressure was 1701100 mm Hg. Her speech was dysarthric. She understood instructions and followed simple commands. Her neurologic examination showed a left lower motor neuron type facial palsy and right flaccid hemiplegia. A right Babinski sign was present. Tendon reflexes were brisker on the right side and ankle jerks were decreased bilaterally. Her gag re- 242 T.]. GOLDSCHMIDT AND M. WALL flex was depressed with poor palate elevation bilaterally. There was slight tongue deviation to the left. A right exotropia was present in the primary position. There was complete left gaze paresis. On gaze to the right her left eye came near to but did not cross the midline. There was horizontal jerk nystagmus in her right eye, which was able to abduct fully. The right pupil was 2 mm; left pupil 3 mm, both round and reactive to light. Right eyelid ptosis of moderate degree was present. Funduscopic examination revealed background diabetic retinopathy. On day 2 of hospitalization the patient was noted to have full or at other times incomplete conjugate slow-upward deviation of her eyes from the midposition. The duration of the upward movement was -1 s. The eyes remained in upgaze for from <1 to -4 s. This movement was followed by a conjugate fast component downward that varied in velocity and returned the eyes to midposition. At other times the vertical movement appeared pendular. Eyelid retraction occurred in synchrony with the slow-upward movement. The bobbing movement was unrelated to blinking, eyelid closure, or performance of a Bell's phenomenon. She was unable to control the movement. It occurred at a rate of approximately 10-15 times/min. The episodes of bobbing lasted up to -45 s and continued throughout the day. There were periods of 15-30 s between episodes of bobbing. Oculocephalic reflexes failed to overcome gaze limitation with head turning to right. Rotation of the head to the left produced abduction of the right eye with the left eye maintaining a midline position. Cold caloric testing with the head 30° above horizontal produced slow deviation of both eyes to either irrigated side with a horizontal jerk nystagmus in the opposite direction. Head computed tomography showed a low-density area in the right basis pontis. DISCUSSION Slow-upward ocular bobbing completes the initial direction and velocity spectrum of observed conjugate ocular bobbing variations. Our patient had a one-and-a-half syndrome due to an ischemic lesion in the right basis pontis noted on computed tomography. She had clinical findings consistent with a left pontine lesion. Since the cold caloric responses were normal, we propose the lesion involved the left paramedian pontine reticular formation at the pontomedullary junction and at least JClin Neuro-ophthalmol, Vul. ;, Nul, )~S; partially spared the sixth nerve nucleus. The clinicopathologic correlation for this formulation has been reviewed by Kommerell et a1. (2). Ocular bobbing was first described by Fisher in 1964 (1). It is characterized by intermittent, usually conjugate, brisk downward eye movements of several millimeters from the primary position. This movement is followed by a slow return to primary position. A slight rotary component is sometimes present, and paralysis of horizontal gaze is characteristic (typical ocular bobbing). Excursions occur 2-12 times per minute (1), and the rate can increase with caloric stimulation (3). The eyes may remain in the downward position for as long as 10 s (3). Ocular bobbing occurs in both comatose and awake patients. It is unrelated to breathing, blinking, or extensor posturing. The reported etiologies of ocular bobbing are parenchymal pontine lesions (infarction, hemorrhage, glioma, central pontine myelinolysis, posterior inferior cerebellar artery aneurysm, and multiple sclerosis) (1,3-11). In addition, indirect brainstem compression from cerebellar hemorrhage or infarction can cause ocular bobbing (12). The term atypical ocular bobbing (3) is defined as the occurrence of bobbing without complete loss of horizontal eye movements. It is attributed to extrapontine lesions, i.e., cerebellar infarction or hemorrhage, leptomeningitis, bromism, and metabolic encephalopathy (1,3,13-18). Inverse ocular bobbing (ocular dipping) is characterized by a slow-downward ocular deviation that is followed by a quick return of the eyes to midposition. Extreme downgaze can be maintained for up to 10 s with the entire pupil obscured beneath the lower lid. Rates up to 20 cycles/min occur. Brainstem horizontal gaze reflexes are usually intact. Additionally, the rapid upward component has been associated with phasic contraction of the orbicularis oculi muscles. Inverse ocular bobbing is thought to be due to anoxic encephalopathy (14-17). Another "bobbing" phenomenon is termed "reverse bobbing." It is portrayed by a fast-upward phase followed by a slow return to the midposition. It occurs with pontine hemorrhage and metabolic encephalopathy (19,20). Ocular bobbing with absent horizontal eye movements (typical ocular bobbing) is associated with parenchymal pontine lesions or results indirectly from compression of pontine structures. Bobbing without total paralysis of horizontal eye movements (atypical ocular bobbing) (3), however, can be produced by a larger variety of pathologic insults. The lack or presence of horizontal eye movements can be incidental to the ocular SLOW-UPWARD OCULAR BOBBING 243 TABLE 1. Ocular bobbing-proposed terminology REFERENCE Acknowledgments: The authors thank Dr. Michael Rosenberg for his helpful comments. oscillation. This is documented in a case described by Susac et aL where the ocular motility disturbance evolved from atypical to typical bobbing (3). Since the absence of voluntary and reflex horizontal eye movements on examination localizes the lesion to the lower dorsal pons, using the prefixes typical or atypical adds little to our nosology. Also, confusion can result due to other "atypical" bobbing types [monocular (3), pretectal pseudobobbing (21)]. We suggest there is little to be gained, other than probability of pontine localization, from the adjectives typical or atypical and propose we drop this terminology. To simplify the nomenclature used to describe ocular bobbing variations, we propose a classification based on the direction and speed of the initial ocular movement (Table 1). For example, the case reported here is termed slow-upward bobbing. Using this nomenclature, reverse bobbing is fastupward bobbing and inverse bobbing is slowdownward bobbing. This descriptive terminology simplifies classification until the presently unknown pathophysiology of ocular bobbing is clarified. Ocular bobbing Reverse Inverse (dipping) Converse Pretectal pseudobobbing Bobbing movement Fast-downward, bilateral eye movement with slow return to midposition Fast-upward eye movement with slow return to midposition Slow-downward eye movement with fast return to midposition Slow-upward eye movement with fast return to midposition Downward and inward oscillations with fast downstroke Proposed terminology Fast-downward bobbing or ocular bobbing Fast-upward ocular bobbing Slow·downward ocular bobbing Slow-upward ocular bobbing Pretectal pseudobobbing 1. Fisher CM. Ocular bobbing. Arch NCliro/1964;11:543-6. 2. Kommerell G, Henn Y, Liicking CH. Unilateral lesion of the paramedian pontine reticular formation. Loss of rapid eye movements with preservation of vestibular ocular reflex and pursuit. Neuro-ophthalmo 1987;7:93-8. 3. Susac JO, Hoyt WF, Daroff RB, Lawrence W. Clinical spectrum of ocular bobbing. / NClirol Neliroslirg Psychiatry 1970;33:771-5. 4. Hammeroff SB, Garcia-Mullin R, Eckholdt J. Ocular bobbing. Arch Ophtha/mol 1969;82:774-80. 5. Daroff RB, Waldman AL. Ocular bobbing. / Nellrol Nellroslirg Psychiatrt/ 1965;28:375-7. 6. Nelson JR, Johnston CH. Ocular bobbing. Arch Nellro/ 1970;22348-56. 7. Katz B, Hoyt WF, Townsend J. Ocular bobbing and unilateral pontine hemorrhage. / Clill Nellro-ophtha/mol 1982;2:193-5. 8. Ash PR, Keltner JL. Neuro-ophthalmic signs in pontine lesions. Medicinc (Baltimore) 1979;58:304-19. 9. Zegers De Beyl 0, Flament-Durand L Borenstein S, Brunko E. Ocular bobbing and myoclonus in central pontine myelinolysis. I NCliro/ Neliroslirg Psychiatry 1983;46:564-5. 10. Kase CS, Maulsby GO, Mohr JP. Partial pontine hematomas Nellrologlf 1980;30:652-5. 11. Osenbach RK, Blumenkopf B, McComb B, Huggins MJ. Ocular bobbing with ruptured giant distal posterior inferior cerebellar artery aneurysm. Slirg Nellro/1986;25:149-52. 12. Rosenberg ML. Spontaneous vertical eye movements in coma. Ann NellroI1986;20:635-7. 13. Paty OW, Sherr M. Ocular bobbing in bromism. Nellrologlf 1972;22:526-7. 14. Knobler RL. Somasundarum M, Schutta HS. Inyerse ocular bobbing. Ann Nell1'ol 1981;9:194-7. 15. Ropper AH. Ocular dipping in anoxic coma. Arch Nellrol 1981;38:297-9. 16. Stark SR, Masucci EF, Kurtzke JF. Ocular dipping. Nellrology 1984;34:391-3. 17. Safron AB, Berney J. Synchronism of reverse ocular bobbing and blinking: Am f OpllthaI111011983;95:401-2. 18. Drake ME, Erwin CW, Massey EW. Ocular bobbing in metabolic encephalopathy: clinical pathologic and electrophvsiologic study. NClirologl/1982;32:1029-31. 19. Brusa A, Firpo MP, Massa S, Piccardo A, Bronzini E. Typical and reyerse bobbing: a case with localizing value. fllr NClI1'011984;23:151-5. 20. DeHoff RB, Troost BT, Dell'Osso LF. In: Glaser JS, ed. Nellro-ophthallllologi/. Hagerstown: Harper and Row, 1978. 21. Keane J. Pretectal pseudobobbing, tive patients with "Y" pattern convergence nystagmus. Arch Nellr,,1 1985;42: 592-4. |