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Show ORIGINAL CONTRIBUTION Fourth Nerve Palsy, Homonymous Hemianopia, and Hemisensory Deficit Caused by a Proximal Posterior Cerebral Artery Aneurysm Jennifer K. Hall, MD, Dina A. Jacobs, MD, Tammy Movsas, MD, and Steven L. Galetta, MD A 21- year- old man developed an ipsilateral fourth nerve palsy, contralateral hemianopia, and contralateral hemisensory deficit as manifestations of a proximal right posterior cerebral artery aneurysm. This unusual constellation of signs reflects the involvement of the structures that run in the ambient cistern. The fourth nerve palsy and homonymous hemianopia are attributed to compression by the aneurysm. The hemisensory loss is ascribed to compromise of thalamoperforate arteries emanating from a thrombosed portion of the aneurysm. ( JNeuro- Ophthalmol 2002; 22: 95- 98) Cisterns are CSF- filled spaces with membranous borders that surround the brainstem. The ambient cistern lies dorsolateral to the midbrain. Structures contained within this cistern include the posterior cerebral artery ( PCA), the anterior choroidal artery, the optic tract, and the trochlear nerve ( 1,2). The PCA runs through the ambient cistern, giving off thalamic perforating arteries and anterior and posterior temporal branches. The trochlear nerve emerges dorsally from the midbrain medial to the superior cerebellar peduncle and courses anteriorly through the ambient cistern. The optic tract courses posteriorly around the cerebral peduncles, through the ambient cistern, to the lateral geniculate nucleus of the thalamus, with some fibers passing to the pretectal nucleus. We report a patient who presented with a fourth nerve palsy, contralateral hemianopia, and contralateral hemisensory deficit owing to a proximal PCA aneurysm. CASE REPORT In May 2000, a 21- year- old previously healthy man presented with the acute onset of left- sided numbness and a decrease in vision. During the preceding year, the patient Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Address correspondence to Steven L. Galetta, MD, Department of Neurology, 3 East Gates, 3400 Spruce Street, Philadelphia, PA 19104, USA had had constant bifrontal throbbing headaches associated with nausea. On the day prior to admission, he developed numbness of the left arm lasting for 1 hour. As the day progressed, he experienced a severe headache associated with nausea and vomiting. One hour later, he noted the onset of visual blurriness in his left visual field, left arm numbness, and intermittent vertical diplopia worse in left gaze. The patient had no known past medical problems and was on no medications. His family history was significant for fatal cerebral aneurysms in an 18- month- old cousin and his maternal grandfather. His neurologic examination on presentation to the neurosurgery service was significant for a left homonymous hemianopsia. There was intermittent rhythmic jerking of his left arm. He had decreased sensation to light touch in his left face, arm, and leg. Brain magnetic resonance imaging revealed a partially thrombosed aneurysm originating from the proximal right PCA ( Fig. \ A and E) and an acute infarct involving the right thalamus ( Fig. \ C). No subarachnoid hemorrhage was present. A lumbar puncture was normal. A cerebral angiogram ( Fig. 2A) confirmed the presence of a 2- cm partially thrombosed aneurysm at the right P2/ P3 segment. The aneurysm lay just distal to the takeoff of the posterior temporal artery. The right PI segment was hypoplastic. There was a fetal origin of the right PCA, which derived from the right internal carotid artery. There was collateral filling of the right PCA from the left PCA. The patient underwent intracranial coil embolization of the PCA aneurysm with sacrifice of the parent vessel. A postembolization angiogram ( Fig. IE) demonstrated good closure of the aneurysm with preservation of the right posterior temporal artery located proximal to the aneurysm. Neuro- ophthalmic examination performed immediately after embolization revealed 20/ 20 visual acuity in OU. The patient could identify only 3/ 10 Ishihara color plates OD and 2/ 10 OS but had a history of congenital color blindness. Confrontation fields revealed a mildly incongruous left homonymous hemianopia, which was later confirmed by Goldmann perimetry ( Fig. 3). Also present was a mild right hypertropia that increased in left gaze and on right „ JNeuro- QpMhqlxnoL. Vol. 22, Nn. t2, 2002 „ , „ , . , . , . DOI: 1O. 1O97/ O1. WNQ. 0OOOO18242.84472.33 ., 95 , Copyright © Lip pincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. JNeuro- Ophthalmol, Vol. 22, No. 2, 2002 FOURTH NERVE PALSY, HOMONYMOUS HEMIANOPIA, AND HEMISENSORY DEFICIT head tilt. Pupils reacted briskly to light bilaterally, and there was no afferent pupillary defect. Ophthalmoscopy was normal. The left homonymous hemianopia resolved within several months, as did the right hypertropia and left hemisensory deficit. The patient had a normal follow- up computerized perimetry in October 2000. FIG. 1. A: Axial T2 magnetic resonance imaging ( MRI) demonstrates a right posterior cerebral artery aneurysm ( arrow) compressing the posterolateral aspect of the right midbrain. B: Axial gradient echo MRI reveals signal of old clotted blood in a partially thrombosed aneurysm. C: Axial FLAIR MRI demonstrates a right thalamic infarct ( arrow). DISCUSSION We report a patient with a right fourth nerve palsy, left homonymous hemianopia, and left hemisensory deficit as manifestations of a proximal right PCA aneurysm. Figure 4 demonstrates the relationship of the aneurysm to the „ V6 , , „ , , , „ . . © 2002 Lippincott Williams & Wilkins , Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. HALL ETAL. FIG. 2. A: Cerebral angiogram reveals a 2- cm partially thrombosed aneurysm at the P2/ P3 segment ( arrow). B: Posternbolization angiogram demonstrates nonfilling of the coiled aneurysm ( arrow). adjacent structures in the ambient cistern. The patient's left hemisensory deficit was due to a right thalamic infarction. Although the thalamic perforators usually branch off from the parent PC A proximal to the location of this patient's aneurysm, it is likely that the perforators were located distal to the aneurysm because of the hypoplastic PI segment. These perforators were either compressed by the aneurysm or, more likely, occluded by partial thrombosis within the aneurysm. The intermittent rhythmic tremor of his left arm was probably caused by ischemia to the ventrolateral nucleus of the thalamus. Copyright © Lippincott Williams & Wilkins. JNeuro- Ophthalmol, Vol. 22, No. 2, 2002 120 105 90 73 60 120 105 90 75 60 240 255 170 383 300 240 255 270 285 3O0 LEFT RIGHT FIG. 3. Goldmann visual fields reveal an incongruous left homonymous hemianopia. The right fourth nerve palsy and left incongruous homonymous hemianopia were probably caused by aneurysmal compression of adjacent pathways ( Fig. 4). Visual field loss due to optic tract lesions is unusual. In a series of 100 patients with homonymous hemianopsias, Smith ( 3) reported that only 3% were due to optic tract lesions. He noted that tract hemianopsias were very difficult to diagnose by perimetry. The author's clues to picking up a FIG. 4. Drawing of the lateral brainstem demonstrates compression of the optic tract medially and the fourth cranial ( trochlear) nerve laterally by a proximal posterior cerebral artery ( PCA) aneurysm. nauthorized reproduction of this article is prohibited. JNeuro- Ophthalmol, Vol. 22, No. 2, 2002 FOURTH NERVE PALSY, HOMONYMOUS HEMIANOPIA, AND HEMISENSORY DEFICIT tract lesion were " extreme incongruity, a negative optokinetic response, and evidence of neurologic disease in neighboring structures" ( 3). Two other series have reviewed the optic tract syndrome ( 4,5). Savino etal. ( 4) documented 21 patients with lesions of the optic tract. They reiterated the importance of associated neurologic findings in identifying the optic tract as the site of the lesion ( 4). Without other associated neurologic findings, it would be easy to attribute a homonymous hemianopia to another location in the retrochiasmal visual pathway. Savino et al. ( 4) also noted that the classic tract field defect was extremely incongruous ( 4). The associated neurologic findings in their series included headache, change in cognition, sixth nerve palsy, hemiparesis, and paresthesias ( 4). None of the patients in their series had the same constellation of symptoms as our patient. Newman and Miller ( 5) described a series of 10 patients with optic tract lesions. They noted that an afferent pupillary defect ( APD) would not be observed unless there was significant asymmetry in the degree of visual field loss between the two eyes ( 5). Therefore, the absence of an APD in our patient does not preclude an optic tract lesion. Their series did report one patient with an arteriovenous malformation ( AVM) in the right ambient cistern who presented with a left homonymous hemianopia, left hemiparesis, and left hemisensory loss, but no fourth nerve involvement was noted. Another patient in that series with an AVM in the ambient cistern presented with a mild fourth nerve palsy. However, a hemianopia did not develop until after surgical resection of the AVM ( 5). Ohtsuka et al. ( 6) described another case of bilateral fourth nerve palsies secondary to an arachnoid cyst of the quadrigeminal cistern with extensive compression of both ambient cisterns. The young age of our patient and the location of his aneurysm are two other noteworthy features. The incidence of intracranial aneurysms has been reported as approximately 3% in people age 20 years and younger ( 7). PC A aneurysms are generally uncommon ( 7- 9), accounting for only 0.26% to 1.0% of intracranial aneurysms ( 9). Of these, only 13% are PC A aneurysms occurring distal to the posterior temporal branch ( 9). However, in the pediatric population, higher frequencies of aneurysms located in the posterior circulation have been noted ( 10). Meyer et al. ( 10) found a rate of 46% in their study of 24 aneurysms in patients aged 18 years or younger. However, large series have not substantiated this observation ( 10). Meyer et al. ( 10) also observed a male predominance among pediatric intracranial aneurysm patients. REFERENCES 1. Rhoton AL Jr. Cerebellum and fourth ventricle. Neurosurgery 2000; 47: S7- 27. 2. Morris P. The posterior cerebral artery. In Morris P, ed. Practical Neuroangiography. Baltimore: Williams and Wilkins, 1997: 193- 202. 3. Smith JL. Homonymous hemianopia: a review of one hundred cases. Am J Ophthalmol 1962; 54: 616- 23. 4. Savino PJ, Paris M, Schatz NJ, et al. Optic tract syndrome: a review of 21 patients. Arch Ophthalmol 1978; 96: 656- 63. 5. Newman SA, Miller NR. Optic tract syndrome: neuro-ophthalmologic considerations. Arch Ophthalmol 1983; 101: 1241- 50. 6. Ohtsuka K, Hashimoto M, Nakamura Y. Bilateral trochlear nerve palsy with arachnoid cyst of the quadrigeminal cistern. Am J Ophthalmol 1998; 125: 268- 70. 7. de Sousa AA, Dantas FL, Neto AP, et al. Giant posterior cerebral artery aneurysm in a 4- year- old child. Surg Neurol 1996; 45: 31- 5. 8. Gerber CJ, Neil- Dwyer G. A review of the management of 15 cases of aneurysms of the posterior cerebral artery. Br JNeurosurg 1992; 6: 521- 7. 9. Simpson RK, Parker WD. Distal posterior cerebral artery aneurysm: case report. J Neurosurg 1986; 64: 669- 72. 10. Meyer FB, Sundt TM, Fode NC, et al. Cerebral aneurysms in childhood and adolescence. J Neurosurg 1989; 70: 420- 5. _ 9o . „ . © 2002 Lippincott Williams & WUkins , Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. |
