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Show ]. Clin. Neuro-ophth.l/nHl/. I: 120 -133, 1081. Bitemporal Hemianopsia in Basilar Artery Aneurysm JAMES A. RUSH, MD. GENE A. BALIS, MD. CHARLES G. DRAKE, MD., LA.C.S. Abstract A lO-year-old boy had a 4-month history of blurred visio~ and severe occipital headaches. Visual acuity was diminished bilaterally, but ophthalmoscopy was normal, and the Correct diagnosis was delayed until inferior bitemporal defects were found. Cranial CT scans and vertebral angiograms demonstrated a giant aneurvsm at the bifurcation of the basilar artery. Bitemporal hemianopsia occurring in children is usually due to craniopharyngioma or chiasmal glioma. To the best of our knowledge, this is the first report of a patient whose chiasmal syndrome was due to a basilar artery aneurysm and whose visual deficit improved after occlusion of the aneurysm. Introduction Visual loss is a well-known occurrence in patients who have intracranial aneurysms of the anterior cerebral circulation I but infrequently results from aneurysms of the basilar artery. Blindness has resulted from third ventricular obstruction by a basilar artery aneurysm that caused chronic papilledema and optic atrophy,~but chiasmal compression by a basilar artery aneurysm is rare. Bitemporal field defects have been noted in two cases of basilar artery aneurysm, J.l but we could find no previous, well-documented report of a basilar artery aneurysm causing a chiasmal syndrome. Case Report A lO-year-old boy was seen here for evaluation of headache and blurred vision of 2 months' duration. He had been well until November 10, 1979, when a presumed adenoviral gastroenteritis was diagnosed. Intramuscular injections of staphage vaccine were administered, but photophobia, blurred vision, and increasingly frequent occipital headaches occurred; the last were less severe when he reclined. On December 4, 1979, results of a From the Department~ of Ophthalmology (JAR) ~nd Nl'uro,urgery (GAB). UniverSity of South F10rldJ Coll(,g(, of M('dlun(', Tampa. Florida; and Unlv(,f',ly Ho_p,tal (CCD). L,.ndon. Ontario, Canada. June 1981 neurological and general physical examination were normal. Visual acuity was 20/30 in the right eye and 20/40 in the left, ophthalmoscopic examination was normal, and no cause for the visual loss was found. A skull roentgenogram and an electroencephalogram were normal, and a presumed postviral encephalitis was diagnosed. Blurred vision continued, and on January 3. 1980, an ophthalmologist found a visual acuity of 20/100 in the right eye and 20/200 in the left. Ophthalmoscopy was normal, visual field testing was inconclusive, and the visual loss was attributed to "optic neuritis" related to the preceding viral encephalitis. The patient was examined by one of us (JAR) on January 21, 1980. Interruptions were frequent because of the patient's insistence on lying prone in order to relieve an occipital headache. The best corrected visual acuity was 20/60 in the right eye and 20/200 in the left eye. The pupils were normal; no afferent pupillary defect was present. The Poltient failed to identify eight HRR pseudoisochromatic plates in the right eye and 14 in the left eve Confrontation finger counting fields were full. Ocular rotations were performed normally without nystagmus, and the optokinetic responses were symmetrical. Slit lamp biomicrosopy olnd ophthalmoscopy were normal. Visual field eXolmination revealed an inferior bitemporal field depression olnd central scotoma of the left eve (Fig. I) A neurosurgical consultolnt found norm.l1 ((.mi.l1 nerve function, other tholn the visUoll k'ss.•md nl' limb weakness in ol neurologicollly int.lct poltient. Routine serum hematologic and chemistry v.llues were normal. A computerized axial tomL)gr.lm l,f the head revealed ol 2-cm strongly enh.mcing lesion posterior and superior to the sella (Fig. 2), olnd a right femoroll retrogr.lde angiogr.m1 den1l1nstr.lted a giant, bilnbed aneurysm at the bifurc.ltion l,f the basilar .utery (Fig. J). Clip occlusion l,f the dist.ll basil.H artery trunk W.1S successfully performed by one of us (CeO) on February t" I qso, and resulted in complete thrombosis of the aneurysm (Fig. 4). Nystagmus in lateral gaze was temporarily present postoperatively. On June 5, 1980, visual acuity was 20/25 in both eyes, .md ophthalmoscopy was normal. Visual field testing showed resolution of the central scotoma of 129 B.1Si 1.1 r Anl'lI ryslll v= 6'18 (20/60 ) uo Figure I. FIeld, show .I smJII, dense centrJI scotomJ of the left eye with relJtive, inferior temporJI qUJdrJntic defects bllJterJlly, more extensive on the left. Figure 2. Computed JxiJI tomogrJm of the heJd .lfter injection of (ontr.!st medium showing .I 2-(m, strongly enhJncing lesion in the posterior supr.lsell.H r('~ion. Journal of Clinical Neuro-ophthalmology Rush, Balis, Drake figure 3. Preoperative lateral vertebral angiogram showing d giant, bilobed aneurysm of the basilar bifurcation. enveloping the origin of the posterior cerebral and superior cerebellar arteries. The anterior sac extends superior to the sella. Figure 4. Postoperdtive anteroposterior vertebral angillgr.lm shc1wing occlusilln of the b.lsilar artery by a SUl\itd clip. the left eye and the right-sided inferotemporal defect; the inferior temporal defect of the left eye persisted. Comment Vertebrobasilar aneurysms constitute 8-15% of all intracranial aneurysms4 and usudlIy rupture, June 1981 causing subarachnoid hemorrhage.-H ; Vertebrobasilar aneurysms that do not bleed can simulate tumors, compressing the brain stem and cerebellum, causing pdlsies of crdnidl nerves 3 dnd 6, dnd other cduddl crdnidl nerves, as well dS atdxid dnd pyramiddl tract signs.'-B Aneurysms of the posterior circulation occur most frequently on the basilar artery, where its 131 Basilar Aneurysm bifurcation is the preferential site for development of s.1Ccular .1I1eurysms.:I -'; Since saccular aneurysms form at .1 congenital defect in the elastic and muscle byers of blood vessel wall, they CJn be found in young p.ltients who m.1Y have no evidence of atherosclerosis. 1<I The youngest reported patient we could find who had a saccular aneurysm of the basil.H bifurcation was an I I'Y.I-year-old boy who, like most young people who have intracranial aneurysms (but unlike our la-year-old male patient), had a subarachnoid hemorrhage. I I An interesting though unexplained observation is the male predominance in children who have intracranial aneurysms; an approximate 2:1 male ratio is reported in several large series. 12-14 Severe headaches were prominent in our patient and occur in most cases of vertebrobasilar aneurysms, with',-7 or without2. !. subarachnoid hemorrhage. Some authors7emphasized that suboccipital headaches that are aggravated by head motion indicated the aneurysmal nature of posterior fossa lesions in their patient; our patient, who insistently lay prone on the floor for relief of his headache, confirms the validity of their clinical generalization. The most alarming symptom produced by the aneurysm in our patient was the bilateral visual loss. Reference to visual loss caused by basilar artery aneurysms in reports from eye hospitals has been sparse. I. 10 Walsh knew of one case and stated that it was difficult to visualize a basilar artery aneurysm involving the chiasm. I In a large neurosurgical practice, Drake found only one case of bitemporal visual field loss occurring in patients who had giant aneurysms of the basilar bifurca- 'j tion.' Bitemporal defects in children are most likely caused by a craniopharyngioma or a chiasmal glioma. Iii In children who have a craniopharyngioma, frontal headaches, visual loss and temporal field defects are common, and suprasellar calcification is typically present on plain skull roentgenograms. 17 Our patient, whose clinical features superficially simulated those of craniopharyngioma, had normal skull roentgenograms. Moreover, a cranial computed tomogram (CT) scan was atypical for a craniopharyngioma: the posteriorly situated, noncystic, suprasellar mass in our patient had marked contrast enhancement and was noncalcified. A confident CT scan diagnosis of craniopharyngioma requires the visualization of two of the following characteristics of a centrally placed suprasellar lesion: cyst formation, calcification, and contrast enhancement. 1M The possibility of a chiasmal glioma was also considered in our patient, although there were no signs of neurofibromatosis or hypopituitarism, two common associated findings in gliomas of childhood. Furthermore, nystagmus, strabismus, and opti\ disc pall(lr, frequent findings in patients with ,h",·.m.ll ~~I")111.1S,I!1 were absent; and headaches, which infrequently occur in cases of chiasmal glioma, were prominent. These clinical features and a normal skull film-plain skull roentgenograms are abnormal in over 80% of patients with chiasmal gliomas2°-diminished the likelihood that a glioma had caused the visual acuity and field loss in our patient. Rarely, pituitary adenomas occur in children under IS years of age21 ; they typically have diminished acuity and headaches/I, 22 but the occurrence of a normal skull roentgenogram (as in our patient) is uncommon in cases of pituitary adenoma.23 Nonetheless, a pituitary tumor should be excluded in all cases of chiasmaI compression, and in our patient the cranial CT scan demonstrated a posterior suprasellar lesion. This case demonstrates that a patient who has an unruptured basilar artery aneurysm presents a difficult diagnostic problem. Previous examples of such cases have simulated cerebellopontine angle or brain-stem tumors,4-M but we emphasize that a giant basilar bifurcation aneurysm that projects superiorly and anteriorly can cause a chiasmal syndrome mimicking sellar or suprasellar tumors. We found, like previous authors,4. 7. M that vertebral angiography is a requisite for an accurate diagnosis that may be impossible on clinical evaluation alone. Without surgical treatment the mortality of vertebrobasilar aneurysms is as high as 80%/4 but neurologic surgery has improved the prognosis in most cases, and direct clipping of the aneurysm25 or ligation of the basilar artery trunk26 have been successfully performed. In a recent series of giant basilar bifurcation aneurysms,) almost two-thirds of the patients undergoing either aneurysmal clipping or basilar artery occlusion had good or excellent results. Our patient's giant aneurysm of the basilar bifurcation was amenable to surgical therapy because a large left posterior communicating artery that provided excellent collateral flow was present. Surgical therapy preserved vision and prevented the eventual likelihood of life-threatening subarachnoid hemorrhage. References 1. Walsh, F.B.: Visual field defects due to aneurysms at the circle of Willis. Arch. Ophthalmol. 71: 15-27, lQb4. 2. )efferson, G.: Further concerning compression of the optic pathways by intracranial aneurysms. Clin. Neurosurg. 1: 55-103, 1953. 3. Drake, e.G.: Giant intracranial aneurysms: Experience with surgical treatment in 174 patients. Clin. Neurosurg. 26: 12-95, 1979. 4. Duvoisin, R.e., and Yahr, M.D.: Posterior fossa aneurysms. Neurology IS: 231-241, 1965. 5. Hook, 0., Norlen, G., and Guzman, J,: Saccular aneurysms of the vertebral-basilar arterial system. A report of 28 cases. Acta Neural. Scand. 39: 271-303, 1963. 6. Sharr, M.M, and Kelvin, F.M.: Vertebrobasilar aneu- Journal of Clinical Neuro-ophthalmology rysms. Experiel1(e with 27 (,Ises. fur. NI'Ufll/. 10: 12Q-143, IQ73. 7. Yas"in, H.E., ,1Ild Alpers. B.I.: Aneurysm uf the vertebr,11 artery. Repl1rt uf ,I l',ISl' in whi,:h the ,1I1eurysm simul,lted ,I tunlllr llf the pl1sll'ril1r fnss,l. Arch. Neufll/. Ps\'ch. 51: 271-27('>, 11l44. 8. Mich,u'l. W.F.: rllstt'ri,'r f"SS.1 ,lIwurvsms simul,ltil1~ tumllrs. I. Nt'unl/. Nt'un'sur~. I's\'l·hi.ltr\, 37: 21/1223, 11l74. ll. Trobe, JD., el.lser, 1.5, ,111.1 QUl'l1l'N, R.C.. Is"I,lted ocultlnllltllr p.u,llvsis. The pn,dul'l "f s,ln'ul.u ,lnd fusif,'rm .1Ileul1·sms "f the b,lsil.u .uterv. Arch. <. )phth. l/nwl. 96: 123('>- 1240, 1117t\. 10. Nijens"hn. D.E, 5,ll'z. R.I. ,111.1 Rl'.lh,ln, T.I.: C1il1il'al sihnifi(.1I1ce "f b,lSiI.u ,uterv .lIlt'urvsms. Nt'un,l<,~v 2-1: 301-305. 11l74. II. M.ltS')I1. D.D.: Il1tr,lrr,lIli.11 ,lrteri,ll .1I1eurvsms in childh""d. I. .\'·eun"ur~. 23: 57/1-5t\3, Illt)5' 12. Patel. A.~ ...111.1 Ril'h.uds"I1. A.E.: Ruptured intracrani. 11 aneur"sm, in the fir,t two decades of life. ). .'·eur,'surg. 35: 571-57('>, 11l71. 13. Loc"lsley, H.B.: Natural historv of subar,lChnoid hem,)rrh,lge. intrarrani.ll aneurysms and arteriovenous malformati,'ns. B,lsed on ('>.3b/l cases. I. Neurosurg. 25: 21 11-230, 1000. 14. Amacher, AL.. and Dra"e, CG.: The results of operJting upon cerebral aneurysms and angiomas in children and adolescents. I. Cerebral aneurysms. Child's Brain 5: 151-105. 1079. IS. Dailey. E.j., Holloway, 1.A., Murto. R,E., and Schlezinger. :-.1.5.: Evaluation of ocular signs and symptoms in cerebral aneurysms. Arch. Ophtha/mol. 71: 463-474. 1964. 10. Duke-Elder, S: System of Ophthalmology, Vol. XII. Henry Kimptom, London, 1971. p. 297. 17. Kennedy, H.B. and Smith. R.j.5.: Eye signs in cran- June 1981 Rush, B.llis. Drake iopharyngioma. Br. /. Ophth.Jlnwl. 59: b89-695, 11l75. 1/1. Fitz, CR.. Wortzman, C., H.Jrwo(,d-Nash. D.C, Holg. lll', R.C.. Barry. I.K., .md Bllldt, D.W.: Computed tnmogr.lphy in craniopharyngioma. f?adio/ogy 127: b87-bO I. 1078. Ill. Chutnri,ln, A.M., Schwartz, I.F.. Evans, R.A., ,md Clrtl'r, S,: Optic glioma in children. N('uro/ogy 14: /l3-115, IliM. 20. Dndgl', H.W., Lnve. '.e., Craig, W. McK., Dockerty. M.B.. Kearns, T.I'., Holman, CB.. and Hayles, A.B.: Gliomas of the optic nl'rves. Arch. Nl'uro/. 79: b07b21, 1%8. 21. Hnllenhorst, R.W., and Youngl', B.R.: Ocular manifestatinns produced by adenoma" of the pituitary gland: An.llysis of 1,000 cases. [xcerpta Med. Int. Congr. Ser, 303: 53-64, 1973. 22. Crombie. A.L.: Ophthalmologic aspects of piluit.lry tumors. In Pituitary and Parapituitary Tumors, j Harkinston and M. Banna. Eds. W.B. Saunders. Philadelphia, 1978, pp. 80-97 23. Wilson, P., and Falconer. M.A.. Patterns of visual failure with pituitary tumors. Clinical and radiological conditions. Br. ). Ophtha/mol. 52: 94-1 10, 1968. 24, Pool. j.L.: Surgical attack on intracranial aneurysms. In fntracranial Aneurysms and Subarachnoid Hemorrhage, W.S. Fields, and A.L. Sahs, Eds. Charles C Thomas, Springfield, III. 1965, pp. 459-466. 25. Drake. CG.: Bleeding aneurysms of the basilar artery: Direct surgical management in four cases. }. Neurosurg. 18: 230-238,1961. 26. Mount, L.A., and Tavares, I.M.: Ligation of basilar artery bifurcation. ]. Neurosurg. 14: Ib7-170, 1962. Write for reprints to: james A. Rush. M.D., 12901 North 30th Street, Tampa, Florida 33012. 133 |
