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Show ]. C1in. Neuro-ophth<l/mo/. 2: 193-195, 1982. Ocular Bobbing and Unilateral Pontine Hemorrhage Report of a Case BARRETT KATZ, M.D.* WILLIAM F. HOYT, M.D. JEANNETTE TOWNSEND, M.D. Abstract Ocular bobbing is most frequently recognized in patients with large central pontine hematomas. We report a case of ocular bobbing that occurred in a patient with a focal unilateral hemorrhage in the pons. Ocular bobbing is a unique disorder of eye movements that is characterized by an abrupt, spontaneous, and usually conjugate jerking of the eyes downward, followed by their slow return to midposition. Attention was first directed to this entity by Fisher, l.2 and its clinical prevalance was first defined by Susac et al} who stressed the diversity of diseases associated with it and the differing clinical settings in which it may be encountered. They described observations of monocular bobbing due to superimposed oculomotor paresis, of typical bobbing associated with a paralysis of both reflex and spontaneous horizontal eye movements, and of atypical cases in which the bobbing was neither associated with coexisting paralysis of horizontal gaze nor explainable by concomitant cranial nerve palsies. Additional variants have since been documented. Daroff described reverse bobbing, in which the primary movement is a rapid, conjugate jerking of the eyes upward from midposition, followed by a slow return.4 Knobler et al. described inverse bobbing, in which a slow downward movement of the eyes is followed by a delayed, then quick return to midposition." The spectrum of clinical settings in which ocular bobbing occurs has expanded as well. Initially recognized as a sign of From the Neuro-ophthalmology Unit, Departments of Neurological Surgery, Neurology, Ophthalmology, and the DepJrtment of Pathology, School of Medicine, University of C.,lifornia, San Francisco. 'Dr. Katz's current address: Departments of Ophthalmology, Neurology, and Neurosurgery, University of Arizona, Arizona Health Sciences Center, Tucson, Arizona. September 1982 extensive pontine destruction,I.2 it has since been observed in cases of metabolic encephalopathies, obstructive hydrocephalus, presumptive vertebrobasilar insufficiency,3 pontine gliomas,6 cerebellar hemorrhage with brain stem compression/ multiple sclerosis,S and in a case of bromism.9 It has been observed following trauma/ and has also been reported to occur in association with leigh's necrotizing encephalomyelopathy,IO alpha coma, opsoclonus-myoclonus, and convergence spasm. l ] We report a case of ocular bobbing that developed after the patient had a subarachnoid hemorrhage. Pathological examination documented a restricted unilateral pontine hematoma. Case Report A 57-year-old woman came to the emergency room at our institution with a 3-day history of headache of sudden onset, vomiting, and diplopia on horizontal gaze. She had been seen previously in the outpatient clinic for treatment of severe hypertension, and was receiving chronic anticoagulant therapy for multiple episodes of deep vein thrombosis. She had compensated congestive heart failure and chronic renal failure, and had been diagnosed as having a hydralazine-induced lupuslike anticoagulant syndrome. When first examined, her blood pressure was 210/110, her respiration was regular, and her temperature was normal. She was alert, albeit sleepy, and manifested Kernig's and Brudzinski's signs, but no dysarthria or posturing. There was a Babinski response on the left. She had a mild left hemiparesis, normal sensory functioning, and no evidence of truncal or appendicular ataxia. The ophthalmic examination revealed normally reactive pupils (3 mm), and examination of ocular motility showed bilateral deficits of abduction, the deficit in the right eye being greater than in the left. The results of laboratory evaluations, including a hemogram and an SMA-12 panel, were normal, except for a blood urea nitrogen of 38 and a creatinine level of 2.4. The prothrombin time was 193 Ocular Bobbing 19.5 seconds (normal: 10.5-12.5 seconds) and the partial thromboplastin time was 48.6 seconds (normal: 24-38 seconds). The woman was admitted to the hospital. A computerized tomography scan of less than ideal quality suggested the presence of subarachnoid blood in the ambient cisterns. A lumbar puncture (opening pressure, 270 mm of water) yielded frankly xanthochromic cerebrospinal fluid (CSF). Analysis showed 20,000 RBCjmm, and 300 WBCj mm with a polymorphonuclear response; the level of protein in the CSF was 110 mg%; the glucose value was 50 mg%. Her anticoagulation was reversed with the infusion of fresh frozen plasma. She was treated prophylactically with phenytoin and phenobarbital, and placed at bed rest. Over the ensuing 24 hours, her level of consciousness decreased. She manifested a gaze palsy to the right, and disturbed abduction of the left eye. On the third hospital day, she was noted to have spontaneous, fast eye movements into downward gaze, followed by a slow return of the eyes to midposition. On her fifth hospital day, she was stuporous. She had a dense left hemiparesis and normally reactive pupils (2 mm). She also had ocular bobbing, consisting of downbeating jerks from midposition with slow return occurring at an irregular rate and of a variable amplitude. She had a pontine-type palsy on right gaze, a mild deficit of abduction of the left eye, and a peripheral facial paresis on the right side. Her stupor progressed to periods of coma inter-spersed with lucid intervals. The ocular bobbing persisted intermittently for 5 days, then disappeared. During the next 2 weeks, her neurological status stabilized and fuIl consciousness was restored. She was left with a dense left hemiparesis and gaze palsy to the right; abduction of the left eye returned. A four-vessel cerebral angiogram performed on the 14th hospital day revealed no abnormalities. Her general medical condition deteriorated, with the progression of renal failure, decompensation of heart function, frank pulmonary edema, refractive hypertension, and sepsis. Over the ensuing weeks, she suffered multiple cardiac arrests. She died 47 days after she was admitted to the hospital. A postmortem examination revealed massive cardiomegaly and a severe transmural infarction of the left ventricle. Several pulmonary infarcts secondary to emboli were found. External examination of the brain revealed hemosiderin staining and evidence of old hemorrhage in the right cerebellopontine angle. Coronal sections of the brain demonstrated small remote infarcts in the putamen and thalamus on the right. An organizing hematoma was found in the caudal portion of the basis pontis on the right. It extended from the level of the sixth nerve nucleus and middle cerebeIlar peduncle to the cerebeIlopontine angle (Fig 1). Microscopic examination showed that the lesion involved the seventh nerve nucleus, pontine fibers, and portions of the descending corticospinal tracts. Neovascularization, macrophages, and scattered astrocytes Figure I. Org~llizing hern"tom~ found in the caudal portion of the basis pontis on Ih" ri~hl side. Journal of Clinical Neuro-ophthalmolo2V surrounded the hematomel. The tissue immediately adjacent to the cavity was infc1rcted. The left basis pontis and both sixth nerve nuclei were normal. Although the blood held dissected into the subarachnoid space in the cerebellopontim' angle, there was no dissection into the fourth ventricle. The cerebellar hemispheres and vestibul.1r nuclei were normal. Mild atherosclerotic changes were found in the basilar arteries, but no severe c1rteriosclerotic changes were seen in parenchyma. Discussion This case is unusual because of the restricted nature of the pontine hematoma and the ocular bobbing that occured. Mohr et all~ described two cases of atypical ocular bobbing in the setting of partial pontine hematoma. Both patients survived, so pathological definition was not afforded. Hammeroff et al. described ocular bobbing appearing in association with brain stem trauma.? Their patient had evidence of multifocal disease, although the pons itself was asymmetrically involved. There were contusions of the right half of the pons and medulla and associated subarachnoid blood. Contusive hemorrhage was also seen in the left ventral half of the caudal medulla, but there was no mention of such lesions on the left side of the pons. This patient manifested signs of unilateral pontine dysfunction, with a gaze palsy to the right. Ice water stimulation of the left canal evoked a sluggish and incomplete deviation of the eyes to the left. During seizure activity, however, there was persistent and complete deviation of the eyes to the left, suggesting relative preservation of the paramedian pontine reticular formation and rostral brain stem medial longitudinal fasciculus, and physiologic integrity of the left side of the pons. This is also the case in our patient. We have rejected the possibility that anticonvulsants had any role to play in our patient's case of ocular bobbing, as the measured levels of both phenytoin (5 mcg/ml) and phenobarbital (12 mcg/ ml) in the blood were minimal when the bobbing was observed. We presume that the deficit of abduction on the left side in this patient was the September 1982 Katz, Hoyt, Townsend result of subarachnoid hemorrhage and increased intracranial pressure; the pathological examination documented a focal, unilateral lesion of the pons. References I. Fisher, CM.: Clinical syndromes of cerebral hemorrhage. In /959 Houston Symposium on Pathogenpsis and Treatmpnt of Cprpbrovascu/ar Diseasp, W.5. Field, Ed. Charles C Thomas, Springfield, 1961, pp. 318-342. 2. Fisher, CM.: Ocular bobbing. Arch. Neural. 11: 543-546, 1964. 3. Susac, J.O., Hoyt, W.F., Daraff, R.B., et .II.: Clinical spectrum of ocular bobbing. /. Neural. Neurosurg. Psychiatry 33: 771-775, 1970. 4. Daroff, R.B., Troost, B.T., and 01'11'0550, L.F.: Nystagmus and related ocular oscillations. In Neuraophthalmology, ).5. Glaser, Ed. Harper and Row, Hagerstown, 1978, pp. 219-240. 5. Knobler, R.L., Somasundaeram, M., and Schutta, H.5.: Inverse ocular bobbing. Ann. Neural. 9: 195-197, 1981. 6. Daroff, R.B., and Waldman, A.L.: Ocular bobbing. /. Neural. Neurasurg. Psychiatry 28: 375-377, 1965. 7. Hammeroff, S.B., Garcia-Mullin, R., and Eckholdt, J.: Ocular bobbing. Arch. Ophthalmol. 82: 774-780, 1969. 8. Ash, P.R., and Keltner, J.L.: Neuro-ophthalmic signs in pontine lesions. N. Med. 58: 304-320, 1979. 9. Paty, D.W., and Sherr, H.: Ocular bobbing in bromism. Neuralogy 22: 526-527, 1972. 10. Baril, A.: Leigh's necrotizing encephalomyelopathy: Neuro-ophthalmic abnormalities. Arch. Ophthalmol. 85: 438-442, 1971. 11. Boddie, H.G.: Ocular bobbing and opsoclonus. /. Neural. Neurasurg. Psychiatry 35: 739-742, 1972. 12. Kase, C.S., Maulsby, G.O., and Mohr, J.P.: Partial pontine hematomas. Neurology 30: 652-655, 1980. Acknowledgment The authors thank Dr. Dale Bredesen, who brought this case to our attention. Write for reprints to: William F. Hoyt, MD., c/o Department of Neurological Surgery, The Editorial Office, 350 Parnassus, Suite 807, San Fr.mcisco, California 94117. 195 |
