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Transient Cortical Blindness with Leptomeningeal Enhancement

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Transient Cortical Blindness with Leptomeningeal Enhancement children with neurofibromatosis type 1: a minute. The patient’s blood pres- longitudinal study. J Pediatr. 1994;125:63- Transient Cortical Blindness sure was controlled with low-dose 66. 3. Balcer LJ, Liu GT, Heller G, et al. Visual loss With Leptomeningeal oral metoprolol. in children with neurofibromatosis type 1 and Enhancement After After the procedure, the patient optic pathway gliomas: relation to tumor lo- Attempted Peripherally complained of progressive visual cation by magnetic resonance imaging. Am J Inserted Central Venous loss, headache, and malaise, which Ophthalmol. 2001;131:442-445. progressed to complete binocular 4. Poussaint TY, Barnes PD, Nichols K, et al. Catheter Placement Diencephalic syndrome: clinical features and visual loss during the ensuing 4 imaging findings. AJNR Am J Neuroradiol. 1997; hours. Ophthalmic examination re- 18:1499-1505. Transient cortical blindness is an in- vealed no light perception vision 5. Dutton JJ. Gliomas of the anterior visual frequent complication of endovas- bilaterally and briskly reactive pu- pathway. Surv Ophthalmol. 1994;38:427-452. 1-3 6. Hoyt WF, Meshel LG, Lessell S, et al. Malig- cular procedures. We describe a pils, without a relative afferent nant optic glioma of adulthood. Brain. 1973; patient who developed transient cor- pupillary defect. The anterior seg- 96:121-132. tical blindness associated with fo- ment, extraocular motility, and di- 7. Djalilian HR, Shah MV, Hall WA. Radio- cal leptomeningeal enhancement on lated funduscopy findings were nor- graphic incidence of multicentric malignant gliomas. Surg Neurol. 1999;51:554-558. contrast-enhanced T1-weighted mal in each eye. Findings from the 8. Van Tassel P, Lee YY, Bruner JM. Synchro- magnetic resonance imaging (MRI) remainder of the neurologic exami- nous and metachronous malignant gliomas: CT following attempted placement of a nation were otherwise normal. findings. AJNR Am J Neuroradiol. 1988;9:725- peripherally inserted central ve- Contrast-enhanced MRI ob- 732. 9. Spoor TC, Kennerdell JS, Martinez AJ, et al. nous catheter (PICC). tained 4 hours after the onset of vi- Malignant gliomas of the optic nerve pathways. sual loss revealed focal leptomenin- Am J Ophthalmol. 1980;89:284-292. Report of a Case. A 57-year-old geal enhancement in the occipital 10. Taphoorn MJ, Willemien AE, de Vries-Knoppert woman with metastatic carcinoma lobes and superior cerebellum WA, et al. Malignant optic glioma in adults. of the colon, which had spread to the (Figure 1). Diffusion-weighted im- J Neurosurg. 1989;70:277-279. 11. Barbaro NM, Rosenblum ML, Maitland CG, et al. liver and peritoneum, was hospital- ages showed no evidence of ische- Malignant optic glioma presenting radiologi- ized for partial small-bowel obstruc- mia, and magnetic resonance angi- cally a ‘cystic’ suprasellar mass: a case report tion. Placement of a PICC for total ography demonstrated normal and review of the literature. Neurosurgery. 1982; parenteral nutrition (TPN) was at- cerebral vasculature. 11:787-789. 12. Condon JR, Rose FC. Optic nerve glioma. Br J tempted with inadvertent cannula- Lumbar puncture showed an el- Ophthalmol. 1967;51:703-706. tion of the brachial artery and infu- evated protein level of 119 mg/dL 13. Gibberd FB, Miller TN, Morgan AD. Glioblas- sion of 10 mL of nonheparinized and a normal glucose level of 81 toma of the optic chiasm. Br J Ophthalmol. 1973; normal saline. The catheter was mg/dL with a normal opening pres- 57:788-791. 14. Hamilton AM, Garner A, Tripathi RC, et al. promptly removed; however, the sure. No atypical cells or white blood Malignant optic nerve glioma. Br J Ophthalmol. patient began to complain of cells were seen. The results for ce- 1973;57:253-264. blurred vision in each eye approxi- rebrospinal fluid cultures and blood 15. Harper CG, Steward-Wynne EG. Malignant op- mately 15 minutes after the at- cultures were negative. Twenty- tic gliomas in adults. Arch Neurol. 1978;35: tempted PICC placement. During four hours after the onset of visual 731-735. 16. Danesh-Meyer HV, Savino PJ, Sergott RC. the procedure, the patient was hy- loss, the patient experienced 2 gen- The prevalence of cupping in end-stage arte- pertensive and tachycardic with a eralized seizures, which were con- ritic and nonarteritic anterior ischemic optic blood pressure of 170/120 mm Hg trolled with intravenous dexameth- neuropathy. Ophthalmology. 2001;108:593- and a heart rate of 120 beats per asone and phenytoin. 598. 17. Abu el-Asrar AM, al Rashaed SA, Abdel Gader AG. Anterior ischaemic optic neuropathy as- sociated with central retinal vein occlusion. Eye. 2000;14:560-562. 18. Repka MX, Savino PJ, Schatz NJ, Sergott RC. Clinical profile and long-term implications of anterior ischemic optic neuropathy. Am J Ophthalmol. 1983;96:478-483. 19. Ischemic Optic Neuropathy Decompression Trial Research Group. Optic nerve decompres- sion surgery for nonarteritic anterior ische- mic optic neuropathy (NAION) is not effec- tive and may be harmful. JAMA. 1995;273: 625-632. 20. Lee AG, Eggenberger ER, Kaufman DI, Man- rique C. Optic nerve enhancement on mag- netic resonance imaging in arteritic ischemic optic neuropathy. J Neuroophthalmol. 1999; 19:235-237. 21. Fivgas GD, Newman NJ. Anterior ischemic op- tic neuropathy following the use of a nasal decongestant. Am J Ophthalmol. 1999;127: 104-106. Figure 1. Sagittal (left) and axial (right) contrast-enhanced T1-weighted magnetic resonance images reveal focal leptomeningeal enhancement (arrows) in the occipital lobes and superior cerebellum, and an old right basal ganglia infarct. (REPRINTED) ARCH OPHTHALMOL / VOL 123, MAY 2005 WWW.ARCHOPHTHALMOL.COM 700 ©2005 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/02/2021 Table. Differential Diagnosis of Leptomeningeal Enhancement Infection Bacterial meningitis Spirochetal meningitis (Lyme disease, neurosyphilis) Tuberculous meningitis Fungal meningitis (Aspergillus, Cryptococcus, Coccidioides) Viral meningitis Cerebrovascular Disorders Areas adjacent to area of early cerebral infarction Subarachnoid hemorrhage Hemosiderin deposition (eg, recurrent subarachnoid hemorrhage) Sturge-Weber syndrome Figure 2. Interval sagittal and axial contrast-enhanced T1-weighted magnetic resonance images after Meningioangiomatosis visual improvement reveal resolution of the contrast enhancement in the occipital lobes. Neoplasia Primary neoplasms (meningioma, During the following week, the pa- sual hallucinations occurred fol- glioblastoma multiforme, lymphoma, tient’s symptoms gradually im- lowing TPN infusion into the right sarcoma, melanoma, melanocytoma) proved. After 72 hours from the time subclavian artery. This patient expe- Metastasis of onset of visual loss, she had light rienced sudden bilateral visual loss Inflammatory Conditions perception in both eyes, and after 5 after the onset of TPN infusion, which Connective-tissue disease days, visual acuity was 20/400 OD improved after several minutes, and Sarcoidosis and 20/800 OS. Nine days after the flashes of light each time her central Wegener granulomatosis initial insult, the patient’s visual acu- line was flushed with normal saline. Demyelinating disease ity was 20/20 OD and 20/30 OS with Ophthalmic examination showed a Vasculitis normal visual fields by confronta- left homonymous hemianopia that Iatrogenic tion, and repeat MRI revealed reso- resolved after 3 days. Magnetic reso- Introduction of foreign substances into lution of the focal leptomeningeal en- nance imaging showed multifocal in- cerebrospinal fluid (eg, blood, chemical agents, contrast material) hancement (Figure 2). A repeat farcts in the occipital and parietal cor- Postoperative enhancement following 5 lumbar puncture revealed a protein tices and in the right cerebellum. craniotomy level of 54 mg/dL, a glucose level of The mechanisms causing visual Post-lumbar puncture 126 mg/dL, and a normal opening loss following contrast and TPN in- pressure. No abnormal cells were fusion remain unclear. However, seen on cytologic examination. several authors have postulated that uting factor was the patient’s el- the hyperosmolarity of these agents evated blood pressure because Comment. Transient cortical blind- may lead to osmotic disruption of the hypertensive encephalopathy may ness following vascular interven- blood-brain barrier and subse- cause transient cortical blindness as- tion has been described primarily af- quent cortical blindness through di- sociated with reversible cerebral 6,7 ter contrast-enhanced coronary, rect neurotoxic effects. Experi- edema on neuroimaging.9 cerebral, and other arterial perfu- mental studies have demonstrated Leptomeningeal enhancement 1-3 sion studies. Inadvertent arterial en- that hyperosmolar agents induce va- may occur from infection, cerebro- try during venous catheterization has sodilation, shrinkage of cerebrovas- vascular disorders, neoplasia, in- resulted in cortical blindness in 2 cular endothelial cells, and wid- flammatory conditions, and iatro- 4,5 8 prior reports. In both of those pa- ened endothelial tight junctions. genic causes10,11 (Table). In our tients, arterial infusion of TPN re- The focal leptomeningeal enhance- patient, the pattern of radiographic sulted in transient bilateral visual loss ment noted on the contrast-en- enhancement could have been at- with occipital lobe abnormalities on hanced MRI in our patient suggests tributed to carcinomatous menin- neuroimaging. In the first report, MRI that disruption of the blood-brain bar- gitis. However,
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