| OCR Text |
Show Journal of'A] euro- Ophthalmology 21( 1): 1- 7, 2001. © 2001 Lippincott Williams & Wilkins, Inc., Philadelphia Long- term Visual Outcome in Patients With Anterior Visual Pathway Gliomas Gregg S. Gayre, MD, Ingrid U. Scott, MD, MPH, William Feuer, MS, Timothy G. Saunders, MD, and R. Michael Siatkowski, MD Objectives: To investigate the visual outcomes of patients with gliomas of the anterior visual pathway and the clinical features associated with prognosis. Materials and Methods: During retrospective review, demographic and clinical data were abstracted from medical records of patients seen at the Bascom Palmer Eye Institute between January 1, 1970 and December 31, 1998. Results: Of the 42 patients identified, 68% were female, and 55% had neurofibromatosis ( NF) type I. There was no substantial difference in presenting signs, symptoms, and visual acuity between the NF(+) and NF(-) groups except for nystagmus, which was more common in the NF(-) group ( p = 0.014). Throughout follow- up evaluation, vision in the better eye remained stable in both groups, independent of treatment or NF status. Vision in the worse eye often declined, despite treatment. However, binocular visual status, measured as average weighted logMAR ( MAR, minimum angle of resolution) vision, did not change significantly over time, regardless of treatment or NF status. Conclusions: In the NF(+) and NF(-) groups, vision in the better eye remained stable, regardless of treatment, and vision in the worse eye often declined, despite treatment. Binocular visual acuity ( measured as weighted logMAR) did not change significantly over time, regardless of NF status or treatment modality. Key Words: Glioma- Anterior visual pathway- Visual outcome. Gliomas of the anterior visual pathway, with or without contiguous involvement of the hypothalamus, are Manuscript received May 16, 2000; accepted December 5, 2000. Presented in part as a platform presentation at the annual North American Neuro- Ophthalmology Society meeting ( 3/ 14/ 99- 3/ 18/ 99), Snowmass, Colorado. Supported in part by Research to Prevent Blindness, New York, New York. From the Bascom Palmer Eye Institute, Department of Ophthalmology ( GSG, IUS, WF, RMS), University of Miami School of Medicine, Miami, Florida; Charlotte Eye, Ear, Nose, and Throat Associates/ UNC Chapel Hill ( TGS), Charlotte, North Carolina; and the Dean A. McGee Eye Institute, Department of Ophthalmology ( RMS), University of Oklahoma College of Medicine, Oklahoma City, Oklahoma. Address correspondence and reprint requests to R. Michael Siatkowski, MD, Dean A. McGee Eye Institute, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104; e- mail: Rmichael- Siatkowski@ ouhsc. edu. rare tumors that occur most commonly in childhood. They constitute 0.8 to 5.1% of all childhood intracranial tumors and typically appear histologically as low- grade astrocytomas ( 1- 5). Optic gliomas occur commonly in neurofibromatosis ( NF), a multisystem disorder that affects 1 in 3000 to 4000 people. The reported incidence of NF- 1 in patients with optic pathway gliomas ranges from 10 to 70% ( 6- 17). The incidence of optic gliomas in patients with NF- 1 is as high as 15 to 21%, with symptomatic visual loss in approximately 20% of affected people ( 16,18- 20). However, the incidence of progressive neurologic dysfunction appears lower in patients with NF and optic glioma, perhaps suggesting a less aggressive variant of glioma in patients with NF ( 16,21). Considerable controversy exists regarding the natural history and, therefore, the appropriate management of optic gliomas. Some studies advocate surgical resection for symptomatic prechiasmatic tumors and chemotherapy or radiotherapy for symptomatic chiasmal lesions ( 16,22). Other reports have failed to confirm any benefit of therapy with respect to long- term survival or visual function ( 9,16,23- 27). The purpose of this study is to investigate the visual and anatomic outcomes of patients with optic gliomas and to investigate clinical features associated with prognosis. METHODS The study protocol was approved by the University of Miami School of Medicine Institutional Review Board. Records of all patients with optic glioma evaluated at the Bascom Palmer Eye Institute between January 1, 1970 and December 31, 1998 were reviewed. Demographic and clinical data were abstracted from patients' medical records. Proportions were compared with the chi- square test with Yates correction; when expected values were small, exact ( permutation) tests were used. Means were compared by the Student t test; however, when parametric assumptions were violated, the two- sample Wilcoxon test was used. Time to progression was analyzed with the Kaplan- Meier method and the log- rank test was used to assess statistical significance. 2 G. S. GAYRE ETAL. RESULTS Forty- two patients with glioma of the anterior visual pathway were identified. Basic demographic information is summarized in Table 1. Twenty- three of 42 ( 55%) patients had NF- 1. Fourteen percent of the patients presented before age 2 years, 31% between ages 2 and 5 years, 24% between ages 5 and 10 years, and 31% after the age of 10 years. Eighty percent of patients were Caucasian, 15% were Hispanic, and 5% were African- American. Mean duration of follow- up evaluation for all patients was 108.0 months ( range, 3.6^ 23 months). Sixty percent of the patients had been monitored for 5 or more years. In the NF(+) group, 13 of 23 ( 57%) patients had been diagnosed with NF before the detection of optic glioma. Among the 10 of 23 ( 43%) patients diagnosed with NF at or after detection of optic glioma, 70% were diagnosed within 1 month, 80% within 6 months, and 100% within 1 year after diagnosis of optic glioma ( Fig. 1). Common presenting symptoms in both groups were vision loss, headache, and proptosis ( Table 2). Nystagmus was significantly more common in the NF(-) group ( p = 0.014). Typical findings on initial examination for NF(+) and NF(-) patients included decreased acuity, optic atrophy, and visual field defect ( Table 2). The mean age at presentation was 13.7 years for patients with isolated optic nerve involvement and 9.6 years for patients with chiasm/ hypothalamic involvement. This difference was not statistically significant ( p = 0.34). Two patients died during the follow- up period. Although both deaths occurred in the NF(-) group, this result was not statistically significant ( p = 0.20). Neither death was related to glioma or associated complications. As shown in Table 3, there was no significant difference in presenting visual acuity between the NF(+) and NF(-) groups. Among all patients, mean acuity was 20/ 37 in the better eye and less than 20/ 200 in the worse eye. Visual field defects were seen on presentation in both groups. Seven of 19 ( 37%) NF(-) patients and 7 of 23 ( 30%) NF(+) patients had monocular field defects. Five of 19 ( 26%) NF(-) patients and 2 of 23 ( 9%) NF(+) patients had bilateral field loss. The frequency of bilateral deficits was three times higher in the NF(-) group than in the NF(+) group, but this difference was not statistically significant ( p = 0.21). Seven of 19 ( 37%) NF(-) patients and 14 of 23 ( 61%) NF(+) patients had no evidence of visual field defect on initial examination. TABLE 1. Patient demographics NF(-) NF(+) All patients Number of patients 19 23 42 Number ( percent) female 13 ( 68%) 12 ( 52%) 25 ( 60%) Mean ( range) age at presentation ( years) 12.8( 1- 34) 9.8( 0.5- 69) 11.1( 0.5- 69) Family history of NF 0 9( 39%) 9/ 47( 21%) Family history of glioma 0 2 ( 9%) 2 ( 5%) NF, neurofibromatosis. 3 O O. 0 0 11 M 36 4B 60 72 t* « 1M 120 Months since diagnosis FIG. 1. Cumulative proportion of patients without chiasmal involvement versus time since diagnosis of optic glioma. Two of seven NF(-) patients and 5 of 12 NF(+) patients without initial chiasmal involvement progressed to chiasmal involvement during follow- up. Seven of 19 ( 37%) NF(-) patients and 9 of 23 ( 39%) NF(+) patients presented with isolated optic nerve involvement. The frequency of chiasmal involvement at presentation was similar in both the NF(+) or NF(-) groups ( p = 0.99). Two of seven ( 29%) NF(-) patients and five of nine ( 56%) NF(+) patients without initial chiasmal TABLE 2. Presenting signs and symptoms in the NF(+) and NF(-) groups Number (%) of patients Presenting symptoms Gradual vision loss Headache Nystagmus Proptosis Endocrine dysfunction Never developed normal vision Strabismus Visual field defect Nausea/ vomiting Seizure Presenting signs Decreased visual acuity Optic nerve atrophy Afferent pupillary defect Visual field defect Strabismus Nystagmus Proptosis Papilledema Spasmus nutans Endocrine dysfunction Cafe au lait spots Lisch nodules Solitary neurofibroma NF(-) N = 19 11 ( 58%) 7 ( 37%) 5 ( 26%) 3 ( 16%) 3 ( 16%) 1 ( 5%) 1 ( 5%) 1 ( 5%) 1 ( 5%) 0% 12 ( 63%) 10 ( 53%) 10 ( 53%) 9 ( 47%) 5 ( 26%) 4( 21%) 5 ( 26%) 3 ( 16%) 1 ( 5%) 1 ( 5%) 1 ( 5%) 0% 0% NF(+) N = 23 9 ( 39%) 3 ( 13%) 0% 4 ( 17%) 1 ( 4%) 1 ( 4%) 6 ( 26%) 0% 2 ( 9%) 2 ( 9%) 13 ( 57%) 8 ( 35%) 9 ( 39%) 6 ( 27%) 6 ( 26%) 2 ( 9%) 7 ( 30%) 5 ( 22%) 0% 1 ( 4%) 19 ( 83%) 10 ( 44%) 3 ( 13%) p value* 0.35 0.14 0.014 0.99 0.31 0.99 0.11 0.45 0.99 0.49 0.75 0.35 0.54 0.21 0.99 0.38 0.99 0.71 0.45 0.99 < 0.001 0.001 0.24 * Difference between NF(+) and NF(-) groups, assessed with the Fischer Exact Test. NF, neurofibromatosis. / Neuro- Ophthalmol, Vol. 21, No. 1, 2001 ANTERIOR VISUAL PATHWAY GLIOMAS 3 TABLE 3. Presenting visual acuity ( mean vision calculated on the logMAR scale and expressed as a Snellen fraction) NF(-) NF(+) Total p value ( 2 sample t test) Better eye 20/ 46 20/ 31 20/ 37 p = 0.42 Worse eye 20/ 418 20/ 184 20/ 267 p = 0.32 Weighted logMAR 20/ 80 20/ 49 20/ 61 p = 0.26 NF, neurofibromatosis. involvement progressed to chiasmal involvement during follow- up evaluation ( p = 0.32). As seen in Figure 1, five of seven ( 71%) patients who eventually developed chiasmal involvement did so within 12 months after diagnosis, although one NF(-) patient did so after 5 years. Eight of 19 ( 42%) NF(-) patients and 18 of 23 ( 78%) NF(+) patients were initially treated by observation. The majority ( 9/ 12, 75%) of the NF(+) patients who were observed throughout the follow- up period demonstrated anatomic stability without measurable tumor growth. Four of these stable cases were followed for more than 5 years. All three NF(-) patients who were treated by observation similarly demonstrated anatomic stability. Sixteen of 19 ( 84%) NF(-) patients were eventually treated during follow- up, compared with only 10 of 23 ( 43%) NF(+) patients ( p = 0.011). Treatment options included surgical resection, radiation, and chemotherapy. Indications for treatment included decreased vision ( 16 patients, 61%), accelerated tumor growth ( 11 patients, 42%), proptosis ( six patients, 23%), hydrocephalus ( four patients, 15%), need for tissue diagnosis ( five patients, 19%), and/ or endocrine dysfunction ( four patients, 15%). There was no significant difference between the two groups in treatment modality chosen. All ten treated patients in the NF(+) group demonstrated tumor stability after initiation of treatment, as did 12 of 16 ( 75%) patients in the NF(-) group. In total, 22 of 26 ( 85%) treated patients demonstrated anatomic stability, whereas four ( 15%) patients demonstrated progression via serial neu-roimaging ( p < 0.5). Table 4 displays logMAR ( MAR, minimum angle of resolution) visual acuity in the better eye, logMAR visual acuity in the worse eye, and weighted logMAR ( WMAR = 0.75 x better eye acuity + 0.25 x worse eye acuity) acuity changes during follow- up. Patients are divided into NF(+) and NF(-) groups, as well as observed versus treated patients. None of the three acuity measures demonstrated a difference in acuity change by NF status ( best eye, p = 0.79; worst eye, p = 0.86; WMAR, p = 0.77; two- way analysis of variance); however, patients with a larger decrease in worse eye acuity and WMAR acuity were more likely to be treated ( better eye, p = 0.25; worse eye, p = 0.005; WMAR, p = 0.012; two- way analysis of variance). Figure 2A displays the visual fraction of the better eye of all patients plotted against the visual fraction of the worse eye. As demonstrated in this scatter graph, more than half of the patients maintained the acuity needed for a license to drive, as seen in the inner shaded area. Less than 25% of patients were legally blind based on acuity alone ( points beyond outer shaded area). Figure 2B shows a similar plot for final acuity. Overall, there was little change in scatter graphs for presenting and final visual acuities. Figures 3A through 3C display logMAR visual change by length of follow- up evaluation for better eye, worse eye, and WMAR. In the better eyes, only 4 of 42 ( 10%) patients experienced a significant drop in acuity of greater than 0.31 logMAR units ( approximately 2 lines of Snellen acuity); all patients had been followed less than 5 years. Two of these patients were NF(+), three had initial visions better than 20/ 100, and all had been initially observed. In Figure 3B, logMAR acuity of the worse eye of all patients is plotted versus time. On average, logMAR acuity in these eyes decreased by 0.93, about seven lines of vision. However, this decline is significantly affected by 11 patients whose vision declined during an initial period of observation and declined further after treatment. In Figure 3C, weighted average logMAR change of all patients is plotted versus time. On average, weighted average logMAR acuity TABLE 4. LogMAR change in vision Observed NF(-), n = 3 NF(+), n = 13 Treated NF(-), n = 16 NF(+), n = 10 Combined NF(-), n = 19 NF(+), n = 23 Better eye 0 ± ( 20/ 20 in all 3 eyes) - 0.08 ± 0.21 p = 0.4 - 0.10 ± 0.44 - 0.28 ± 0.85 p = 0.5 - 0.08 ± 0.41 - 0.08 ± 0.60 p = 0.5 Worse eye 0.17 ± 0.46 - 0.01 ± 1.07 p = 0.4 - 1.52 ± 1.80 - 1.53 ± 1.24 p = 0.5 - 1.25 ± 1.77 - 0.67 ± 1.36 p = 0.5 Weighted logMAR 0.04 ± 0.12 0.05 ± 0.28 p = 0.4 - 0.45 ± 0.56 - 0.59 ± 0.87 p = 0.5 - 0.37 ± 0.54 - 0.23 ± 0.68 p = 0.5 LogMAR increases of - 0.3, - 0.7, - 1.0, and - 20/ 100, 20/ 200, and 20/ 800, respectively. NF, neurofibromatosis. • 1.5 correspond roughly to a drop from 20/ 20 to 20/ 40, J Neuro- Ophthalmol, Vol. 21, No. 1, 2001 G. S. GAYREETAL. ! i f • - _ = * LP - • J M ID 200 100 • > • : 20> 10 . J°. 1 - i n - i • o ^ T__ • t 8 o r • i • • s T 1 14 1 a - B_ c o 1 i - vr • o : v '< r - b - b % % % % % ° ' \ <*• A PmjKfibiHj VJbrae Eye Acuity %-= " • .= - -" : = awe • : : • : *:•: an M •- S • > c 0 o z • 1 • NF* ONF- * * * ^^% w^^. « % B Final Worse Eye Acu* r FIG. 2. A: Presenting Snellen acuity of the better eye versus that of the worse eye for all patients. More than half of patients have acuity needed for a license to drive, as seen in lighter inner area ( based on Florida requirements of > 20/ 70 acuity in at least one eye). Less than one fourth of patients were legally blind based on acuity alone ( points beyond the outer, darker shaded area, based on Florida requirements of < 20/ 200 acuity OU). B: Snellen acuity of the better eye versus that of the worse eye for all patients at last follow- up. Shaded areas represent the same concept as A. dropped by 0.31, roughly equivalent to a two- line decrease. Once again, these same 11 patients ( see next paragraph) influence this decline. There was no indication of a trend to lose visual acuity, by any of the three acuity measures, among the cases that were followed longer. Eleven of 26 patients ( 42%) were eventually treated after an initial period of observation. Progressive visual loss was an indication for therapeutic intervention in all of these cases, but in addition, six patients demonstrated tumor growth by neuroimaging ( threatening the chiasm in three cases), two patients had severe proptosis, and one patient also developed hydrocephalus. Mean presenting vision in the better eye of this group was 20/ 48. At the time of treatment, mean better- eye vision was 20/ 132; mean better- eye final vision was 20/ 115. Among these patients, vision did not decline significantly in the better eye before treatment ( p = 0.12) or after treatment ( p = 0.8). Mean presenting vision in the worse eye of these 11 patients was 20/ 400. Mean vision at the time of treatment in the worse eye was hand motion, and mean final vision was no light perception. In the worse eye, a significant decline in vision occurred before treatment ( p = 0.018) and also approached significance after treatment ( p = 0.062). In this group of patients, treatment was significantly associated with loss in vision of the worse eye and, therefore, also with weighted average logMAR among the entire treated group. However, because declining visual function was itself an indication for treatment, we cannot determine whether the posttreat-ment visual decline merely reflects a continuation of the process that prompted therapy or whether the treatment itself contributed to the further decline in vision after therapy was completed. In Figure 4A, mean acuity of both eyes in the observed group is plotted versus time. No significant change in vision in either eye was observed. In Figure 4B, mean acuity of both eyes in the treated group is plotted versus time since initiation of treatment. When decline in vision before initiation of treatment is taken into account, visual stability after treatment is observed in both eyes. DISCUSSION Gliomas of the anterior visual pathway are rare tumors and may involve the optic pathway anywhere from the optic disc to the lateral geniculate body ( 28). First reported by von Graefe in 1864 ( 29), optic gliomas comprise 0.6 to 5.1% of all intracranial tumors, 1.7 to 7% of all gliomas, 1.5 to 3.5% of all orbital tumors, and 66% of all primary optic nerve tumors ( 7,15,16,23,30- 36). The clinical behavior of optic gliomas is related not only to their histopathologic characteristics but also to their anatomic extent. When isolated to the optic nerve, gliomas are relatively benign ( 37). However, when chiasmal involvement is present, prognosis is generally believed to be worse ( 4,37). The most important prognostic indicator has been reported to be extent of disease at presentation ( 5,38). In a meta- analysis of 634 published cases of optic glioma, Dutton ( 16) found the mean age of presentation for all patients to be 8.8 years, similar to our finding of 10 years. Twenty- nine percent of patients in Dutton's study had a diagnosis of NF, compared to 57% in our series. According to Dutton ( 16), the majority ( 88%) of patients experiences some degree of visual dysfunction regardless of tumor location. Our data confirm that decreased visual acuity and visual field abnormalities are common. The prevalence of visual loss among our patients may actually be higher than reported; the young age of many of our subjects often made quantitative visual field data difficult to obtain, and some patients were evaluated before the era of modern automated perimetry. However, when weighted average logMAR vision is considered, the majority ( 74%) of patients maintained good visual function ( better than 20/ 70 in at least one eye), regardless of initial anatomic extent or extent of tumor growth. / Neuro- Ophthalmol, Vol. 21, No. 1, 2001 ANTERIOR VISUAL PATHWAY GLIOMAS 5 o or o < O) o ST 1 o £ o o> - 1 or < 120 240 360 Months from glioma diagnosis to last follow- up 480 .5 0.0- -. 5 - 1.0 - 1.5 - 2.0 - 2.5 • • • • % • • • * % • • • ••• • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • 120 240 360 Months from glioma diagnosis to last follow- up 480 FIG. 3. A: Change in logMAR acuity of the better eye of all patients versus time since diagnosis. On average, vision in the better eye remained stable. B: Change in logMAR acuity of the worse eye of all patients versus time since diagnosis. On average, logMAR acuity in the worse eye decreased by 0.88, approximately equal to five lines of vision. C: Change in average weighted logMAR acuity of all patients versus time since diagnosis. On average, weighted average logMAR acuity dropped by 0.31, equivalent to a two- line decrease in vision. Months from glioma diagnosis to last follow- up Throughout the years, great controversy has existed regarding the growth potential of optic gliomas. This dilemma has the greatest clinical consequences when confronting the patient with a glioma of the optic nerve and considering the possibility of posterior extension with chiasmal involvement and contralateral visual loss. Hudson ( 39) and others have argued that optic gliomas represent benign hamartomas with minimal potential for growth. Hoyt and Baghdassarian ( 40) believed that optic gliomas represent congenital nonneoplastic hamartomas with growth potential during early childhood only ( 16,39,40). Recently, however, Massry et al. ( 41) have established convincing evidence of the de novo occurrence of optic pathway gliomas in patients with previously normal neuroimaging. Our study reveals that although chiasmal involvement is common at presentation I 8s Months since treatment O Best eyes • Worse eyes Months since presentation O Best eyes • Worse eyes FIG. 4. A: Mean logMAR acuity of the better and worse eyes in the observed group versus time. No significant change in either eye was observed. B: Mean logMAR acuity of the better and worse eyes in the treated group versus time since initiation of treatment. No significant change in either eye was observed. J Neuro- Ophthalmol, Vol 21, No. 1, 2001 6 G. S. GAYRE ETAL. ( perhaps supporting Hudson's theory), five patients in the NF(+) group and three patients in the NF(-) group demonstrated progression to chiasmal involvement after previously documented isolated optic nerve disease. Progression typically occurred within 1 year of presentation ( 71%). Some of these patients were evaluated before the era of modern imaging studies, and it is possible that some cases of progression may represent original misdiagnosis of unrecognized chiasmal disease because of limited sensitivity of older radiographic testing methods. Considering our data and that of Massry, clinicians should be aware that growth of these tumors is possible. Dutton ( 16) found that among 114 cases of gliomas initially confined to the optic nerve and followed either conservatively or with partial resection, tumor progression was seen in 21%. For chiasmal gliomas followed conservatively, progression was observed in 29% during a follow- up period of 3 to 10 years. In a recent study by Erkal ( 5), 19 of 23 patients treated with radiation therapy at diagnosis of glioma demonstrated no evidence of anatomic tumor progression. In their study, visual improvement was observed in 50% of children with gliomas confined to a single optic nerve, whereas the remainder of the children demonstrated visual stability; vision improved in 34% of children with gliomas involving the chiasm and remained stable in 54% ( 5). Janss et al. ( 42), in 1995, demonstrated anatomic stability in three often patients treated with chemotherapy over a median of 3 years. In our study, anatomic stability was seen in 54% of NF(-) patients and in 100% of NF(+) patients receiving chemotherapy and/ or radiation. In Dutton's study ( 16), vision remained stable in 91% of patients with gliomas isolated to the optic nerve, and was stable or improved in 76.8% of patients with chiasmal tumors managed with observation. In the current study, anatomic stability was noted in 14 of 17 ( 82%) observed patients. The current study is unique in that it provides the most detailed long- term information in the literature regarding visual acuity of patients with optic glioma. In addition, in contrast to a meta- analysis, it carries the advantage of patients followed long term at a single center by a small group of clinicians. We find that visual function ( as measured by average weighted logMAR acuity) was stable in NF(+) and NF(-) groups, and that legal blindness ( based on acuity criteria) occurs in only a minority of these patients. Regarding treatment, vision did not change significantly in the better eye of either the observed or treated groups. However, a significant decline in vision in the worse eye of treated patients occurred before ( prompting treatment) and after treatment in the group of patients in whom treatment was initiated after an initial period of observation. As stated before, we cannot determine what role, if any, treatment played in the continued decline of vision in this subgroup of patients. In summary, in our study population, there was no significant difference in the presenting signs and symptoms of the NF(+) and NF(-) groups, with the exception of nystagmus, which was more common in the NF(-) group. There was no significant difference in presenting visual acuity, visual fields, or anatomic extent of tumor between the NF(+) and NF(-) groups. Chiasmal involvement occurred in both groups ( 26/ 42 patients). If chiasmal involvement was not present initially and did occur ( 7/ 19 patients), it usually did so within the first 12 months after diagnosis. There was no difference in survival outcomes between the NF(+) and NF(-) patients. Based on this retrospective nonrandomized study, we cannot make any specific therapeutic recommendations. However, when treatment was felt to be clinically indicated, it was associated with stability in tumor size in NF(+) and NF(-) groups. Throughout follow- up evaluation, vision in the better eye remained stable in the NF(+) and NF(-) groups, regardless of treatment. Vision in the worse eye often declined, despite treatment. However, binocular visual acuity ( measured as weighted logMAR acuity) did not change significantly over time, regardless of NF status or treatment modality. REFERENCES 1. Alvord EC, Lorton S. Gliomas of the optic nerve or chiasm. Outcomes by patients' age, tumor site, and treatment. J Neurosurg 1998; 68: 85- 98. 2. Borie A, Richardson EP Jr. The biological and clinical behavior of pilocytic astrocytomas of the optic pathways. Brain 1982; 105: 161- 87. 3. Farwell JR, Dohrmann GJ, Flannery JT. Central nervous system tumors in children. Cancer 1977; 40: 3123- 32. 4. Fowler FD, Matson DD. Gliomas of the optic pathways in childhood. J Neurosurg 1957; 14: 515- 28. 5. Erkal HS, Serin S, Cakmak A. Management of optic pathway and chiasmatic hypothalamic gliomas in children with radiation therapy. Radiother Oncol 1997; 45: 11- 5. 6. Christensen E, Ry- Andersen S. Primary tumors of optic nerve and chiasm. Acta Phychiat Neruol Scand 1952; 27: 5- 16. 7. Davis FA. Primary tumors of the optic nerve ( a phenomenon of Von Recklinghausen's disease). A clinical and pathologic study with a report of five cases and a review of the literature. Arch Ophthalmol 1940; 23: 735- 821. 8. Glaser JS, Hoyt WF, Corbett J. Visual morbidity with chiasmal glioma. Arch Ophthalmol 1971; 85: 3- 12. 9. Housepian EM. Management and results of 114 cases of optic glioma ( abstract). Neurosurgery 1977; 1: 67- 8. 10. Hoyt WF, Fletcher WA, Imes RK. Chiasmal gliomas. Appearance and long- term changes demonstrated by computerized tomography. Prog Exp Tumor Res 1987; 30: 113- 21. 11. Lewis RA, Gerson LP, Axelson KA, et al. Von Recklingausen neurofibromatosis. II. Incidence of optic gliomata. Ophthalmology 1984; 91: 929- 35. 12. Manshot WA. Pimary tumors of the optic nerve in von Recklinghausen's disease. Br J Ophthalmol 1954; 38: 285- 9. 13. Marshall D. Glioma of the optic nerve as a manifestation of von Recklinghausen's disease. Am J Ophthalmol 1954; 37: 15- 36. 14. Stern J, DiGiacinto GV, Housepian EM. Neurofibromatosis and optic glioma: clinical and morphological correlations. Neurosurgery 1979; 4: 524- 8. 15. Tenney RT, Laws ER, Young BR, et al. The neurosurgical management of optic gliomas. Results in 104 patients. J Neurosurg 1982; 57: 452- 8. 16. Dutton JJ. Gliomas of the anterior visual pathway. Surv of Ophthalmol 1994; 38: 427- 52. 17. Rush JA, Younge BR, Campbell RJ, et al. Optic glioma: long- term follow- up of 85 histopathologically verified cases. Ophthalmology 1982; 89: 1213- 39. 18. Bognanno JR, Edwards MK, Lee TA, et al. Cranial MR imaging in neurofibromatosis. Am J Radiol 1988; 151: 381- 8. / Neuro- Ophthalmol, Vol. 21, No. 1, 2001 ANTERIOR VISUAL PATHWAY GLIOMAS 7 19. Listernick R, Charrow J, Greenwald M. Emergence of optic pathway gliomas in children with neurofibromatosis type I after normal neuroimaging results. J Pediatr 1992; 121: 584- 7. 20. Lund AM, Skovby F. Optic gliomas in children with neurofibromatosis type 1. Eur J Pediatr 1991; 150: 835- 8. 21. Packer RJ, Bilaniuk LT, Cohen BH, et al: Intracranial visual pathway gliomas in children with neurofibromatosis. Neurofibromatosis 1988; 1: 212- 22. 22. Byers WGM. The primary intradural tumors of the optic nerve ( Fibromatosis nervi optica). Montreal Royal Victoria Hospital Studies 1901; 1: 3- 82. 23. Fowler FD, Matson DD. Gliomas of the optic pathways in childhood. J Neurosurg 1957; 14: 515- 28. 24. Lloyd LA. Gliomas of the optic nerve and chiasm in childhood. Trans Am Ophthalmol Soc 1973; 71: 488- 535. 25. MacCarty CS, Boyd AS, Childs DS. Tumors of the optic nerve and optic chiasm. J Neurosurg 1970; 33: 439- 44. 26. Wagener HP. Gliomas of the optic nerve. Am J Med Sci 1961 ; 237: 238- 61. 27. Wright JE, McDonald WI, Call NB. Management of optic nerve gliomas. Br J Ophthalmol 1980; 64: 545- 52. 28. Tym R. Piloid gliomas of the anterior optic pathways. Brit J Surg 1961; 49: 322- 31. 29. von Graefe A. Geschwulste des Sehenerven. Arch Ophth 1864; 10: 193. 30. Danoff BF, Kramer S, Thompson N. The radiotherapeutic management of optic nerve gliomas in children. Int J Radiat Oncol Biol Phys 1980; 6: 45- 50. 31. Desousa AL, Kalsbeck HE, Mealey J, et al. Diencephalic syndrome and its relation to optico- chiasmatic glioma: review of twelve cases. Neuorsurgery 1979; 4: 207- 9. 32. Matson DD. Gliomas of the optic pathways. In: Neurosurgery of infancy and childhood. 2nd ed. Springfield: Charles C. Thomas, 1969: 523- 36. 33. Weis L, Sagerman RH, King GA, et al. Controversy in the management of optic nerve glioma. Cancer 1987; 59: 1000^ t. 34. Eggers H, Jackobiec FA, Jones IS. Tumors of the optic nerve. Doc Ophthalmol 1976; 41: 43- 128. 35. King DL, Chang CH, Pool JL. Radiotherapy in management of meningiomas. Acta Radiol ( Iher) 1966; 5: 26- 33. 36. Shields JA, Bakewell B, Augsburger JJ, et al. Classification and incidence of space- occupying lesions of the orbit. A survey of 45 biopsies. Arch Ophthalmol 1984; 102: 1601- 11. 37. Gibberd FB, Miller TN, Morgan AD. Glioblastoma of the optic chiasm. Br J Ophthal 1973; 57: 788- 91. 38. Bataini JP, Delanian, S, Ponvert D. Chiasmal gliomas: results of irradiation management in 57 patients and review of literature. Int J Radiol Oncol Giol Phys 1991; 21: 615- 23. 39. Hudson AC. Primary tumors of the optic nerve. Roy Land Ophth HospRep 1912; 18: 317- 439. 40. Hoyt WF, Baghdassarian SA. Optic gliomas of childhood: natural history and rationale for conservative mangagement. Br J Ophthalmol 1969; 53: 793- 8. 41. Massry GG, Morgan CF, Chung SM. Evidence of optic pathway gliomas after previously negative neuro- imaging. Ophthalmology 1997; 104: 930- 5. 42. Janss AJ, Grundy R, Canaan A, et al. Optic pathway and hypo-thalmic/ chiasmatic gliomas in children younger than age 5 years with 6- year follow- up. Cancer 1995; 75: 1051- 9. J Neuro- Ophthalmol, Vol. 21, No. 1, 2001 [VBneurofibromatosis] |
