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Show Journal of Neuro- Ophthalmology 16( 1): 33- 35, 1996. © 1996 Lippincott- Raven Publishers, Philadelphia Occipital Lobe Infarction from a Carotid Artery Embolic Source Laura J. Baker, M. D., Steven L. Galetta, M. D., Robert W. Hurst, M. D., Eric L. Zager, M. D., and Eric C. Raps, M. D. Cerebral infarcts related to internal carotid artery ( ICA) occlusive disease usually occur in the distribution of the middle cerebral artery or middle cerebral- anterior cerebral artery regions. Posterior cerebral artery distribution infarcts resulting from internal carotid disease are rare. Occipital lobe infarction with visual field defects has been reported in association with anomalous vascular connections within the circle of Willis, including persistent trigeminal artery ( 1) and persistent fetal origin of the posterior cerebral artery from the ICA ( 2,3). Conversely, a small or absent ipsilateral posterior communicating artery is a risk factor for stroke in patients with ICA occlusion ( 4). We report the MRI and angiographic findings for a patient with middle cerebral and posterior cerebral artery distribution infarcts of similar age ipsilateral to an ICA dissection and a prominent posterior communicating artery. A 49- year- old hypertensive man developed a severe right- sided headache involving his ear, upper neck, and temporal area. This was associated with nausea, vomiting, and lightheadedness. The next day, he noted " fluttering lights" in his left visual field. A magnetic resonance imaging ( MRI) scan of the brain performed 3 weeks later demonstrated subacute hemorrhagic infarcts in the right operculum and right medial temporal- occipital cortex ( Fig. 1A and B). From the Departments of Neurology ( L. J. B., S. L. G., E. C. R.), Neurosurgery ( E. L. Z.), and Interventional Neuroradiology ( R. W. H.), University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, U. S. A. Address correspondence and reprint requests to Dr. Steven L. Galetta, Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce St., Philadelphia, PA 19104, U. S. A. Neuro- ophthalmic examination and Goldmann perimetry disclosed a complete left homonymous hemianopsia. Visual acuity, pupillary, ocular motility, and funduscopic examinations were normal. There were no other neurologic signs. A transthoracic echocardiogram with bubble study failed to demonstrate right- to- left shunting or a cardiac source of emboli. Laboratory evaluation for vasculitus and hypercoagulable state was normal. Four- vessel cerebral angiography was performed. Injection of the right common carotid artery showed marked tortuosity and a > 90% stenosis in the proximal cervical segment of the internal carotid artery ( Fig. 2A). The differential diagnosis at that time included carotid artery dissection versus focal atherosclerosis. Significant anterograde ( anterior- to- posterior) flow through a prominent right posterior communicating artery was also noted ( Fig. 2B). Left vertebral artery injection demonstrated slow filling of the right posterior cerebral artery as compared with the left, suggestive of right Pa segment hypoplasia ( Fig. 2C). The patient was treated with warfarin for 6 weeks. Repeat carotid ultrasound and carotid angiography showed normalization of the previously noted right ICA stenosis. This patient presented with simultaneous middle cerebral and posterior cerebral artery distribution embolic infarcts with an ipsilateral internal carotid lesion as the only detectable source. In retrospect, the rapid resolution of the critical stenosis with warfarin therapy provides compelling evidence that a carotid artery dissection was the most likely cause of the patient's initial headache and embolic infarctions. We conclude that in the presence of a large pos- 33 FIG. 1. Magnetic resonance imaging ( MRI) of the brain. Axial T^ weighted gadolinium- enhanced images ( TR = 500, TE = 11) demonstrate hemorrhagic infarction of the right operculum ( A) and right medial temporal- occipital cortex ( B). Gyriform enhancement in these areas ( arrows) indicates the subacute nature of both infarcts. A .• * !£ FIG. 2. Four- vessel cerebral angiogram. Right common carotid artery injection demonstrates a > 90% stenosis ( arrow) of the proximal internal carotid artery ( A) and significant anterograde flow through a prominent right posterior communicating artery ( arrow) ( B). Slow filling of the right posterior cerebral artery after left vertebral artery injection ( arrow) suggests PT segment hypoplasia ( C). 1 / Neuro- Ophthalmol, Vol. 16, No. 1, 1996 OCCIPITAL LOBE INFARCTION 35 terior communicating artery, carotid artery dissection may cause embolic infarction in the territory of the posterior cerebral artery. Carotid athero-occlusive disease or dissection with coincidental anomalies in the posterior circulation should be considered in the differential diagnosis of vertebrobasilar infarction. Our report emphasizes the importance of contrast cerebral angiography in detecting and defining these vascular abnormalities and confirms that serial studies may be necessary to reach a definitive diagnosis of carotid dissection. REFERENCES 1. Gasecki AP, Fox AJ, Daneault N. Bilateral occipital infarctions associated with carotid stenosis in a patient with persistent trigeminal artery. Stroke 1994; 25: 1520- 23. 2. Pessin MS, Kwan ES, Scott RM, Hedges TR. Occipital infarction with hemianopsia from carotid occlusive disease. Stroke 1989; 20: 409- 11. 3. Pessin MS, Lathi ES, Cohen MB, Kwan ES, Hedges TR, Caplan LR. Clinical features and mechanism of occipital infarction. Ann Neurol 1987; 21: 290- 9. 4. Schomer DF, Marks MP, Steinberg GK, et al. The anatomy of the posterior communicating artery as a risk factor for ischemic cerebral infarction. N Engl J Med 1994; 330: 1565- 70. / Neuro- Ophthalmol, Vol. 26, No. 1, 1996 |
