Malignant Optic in
a
Glioma 70-Year-Old Patient
Riri S. Manor, MD; Jacob Israeli, MD; Uriel Sandbank, MD
On general physical examination, the patient looked younger than his age and appeared to be in excellent physical condi¬ tion. The neurological examination, how¬ ever, revealed signs of mild right hemipa¬ resis with a slight motor weakness in the right limbs, brisker reflexes on the same side, and a Babinski sign on the right side. There was also a slight hypesthesia on the same
\s=b\ In a
70-year-old man with glioma of optic nerves and tracts, the initial symptom was a unilateral loss of vision that progressed rapidly and was followed by amaurosis of both eyes. All diagnostic radiological procedures were negative. the
Four months after the onset of the
disease, the patient developed hemiplegia, became comatose, and died. Postmortem examination revealed a glioblastoma multiforme of both optic nerves, chiasma, and optic tracts that extended posteriorly into the left thalamus and medical geniculate body. The tumoral thickening of the optic nerves was absent in the intracanalicular part, a finding that concurred with the normal radiological appearance of the optic foramen. Glioblastoma multiforme of the optic pathways should be included in the differential diagnosis of acute visual failure in elderly people, even though the final diagnosis may be possible only at postmortem examination.
(Arch Ophthalmol 94:1142-1144, 1976) is only a small number of adult cases of optic glioblastoma found in the neuro-ophthalmological literature. On the basis of the cases previously reported, as well as an additional five seen by them, Hoyt et al1 recently defined the clinical and pathologic nature of this tumor, which is distinctly different from glioma of the optic nerve occurring in younger persons. They found that the syn¬ drome of this malignant optic glioma of adulthood is characterized by: (1) occurrence in middle-aged men; (2) initial signs and symptoms that may
There
Accepted for publication
Nov 11, 1975. From the departments of ophthalmology (Dr Manor), neurosurgery (Dr Israeli), and pathology (Dr Sandbank), Beilinson Medical Center, Tel Aviv University Medical School, Petah Tikva, Israel. Reprint requests to the Department of Ophthalmology, Beilinson Medical Center, Petah Tikva, Israel (Dr Manor).
mimic those of optic neuritis; (3) to total blindness within five to six weeks; and (4) a fatal end within several months. We observed a case of glioblastoma multiforme of the optic pathways in a 70-year-old patient. This case is of particular interest because the tumor occurred in a patient of advanced age as compared with its usual occurrence in middle-aged people. At this age, the differential diagnosis was also differ¬ ent, being more suggestive of tempo¬ ral arteritis than of optic neuritis.
progression
REPORT OF A CASE A vigorous 70-year-old man was in excel¬ lent health and still able to work full time as a manual laborer when he began to notice a progressive decrease in the vision of the right eye, accompanied by headaches in the frontal area. The only notable aspect of his medical history was craniocerebral trauma incurred during the war 24 years before. He failed to consult a physician with the onset of symptoms, but within the next two months there was also a rapid decrease in the vision of the left eye, and he was finally referred to us. On his first examination, the findings were as follows. There was no light perception in the right eye and a visual acuity of only 1/18 in the left eye. Only the inferior nasal quadrant of the left visual field was present. Appla¬ nation tonometry was 14 mm in both eyes. Ophthalmoscopically, there was a very slight temporal pallor of both optic discs. The nasal border of the right optic disc was blurred. The retinal veins were not congested and the arteries appeared to be in very good condition considering his age, ie, there was no narrowing or visible arteriosclerotic change. Ophthalmodynamometry showed equal values in both eyes, corresponding to his normal brachial arterial pressure values. Ocular motility was normal. The right pupil was nonreactive to light. There was no exophthalmos, and the temporal arteries were not bulg¬ ing, tense, red, or painful.
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
side.
In laboratory examinations, the hematocrit reading, leukocyte count, sedimenta¬ tion rate, urinalysis, and serum glucose, bilirubin, protein, cholesterol, and alkaline phosphatase levels were all normal. The cerebrospinal fluid (CSF) and blood were negative for syphilis. In the CSF, the glucose levels and blood cell count were within normal limits, but the protein level was high (126 mg/100 ml). The electroen¬
cephalogram,
brain scan, angiographie studies of both carotid arteries, and pneumoencephalography all failed to reveal any pathologic findings. X-ray films of the skull and orbita, and tomography of the orbita and the optic canals were also nega¬ tive. The optic foramina were normal and of equal size. Three weeks later, the left eye also became definitely amaurotic. Both pupils were wide open and nonreactive to light. The border of the right optic disc became sharp. There was the same slight temporal pallor of the optic discs. The contrast between the almost normal appearance of the discs and the amaurosis was striking. Aside from the amaurosis and the mild right hemiparesis, there were no other neurological signs of a further evolution of the disease. Four months after the onset of the ocular complaints, the right hemipare¬ sis suddenly developed into hemiplegia and the patient became comatose and died the
following day.
PATHOLOGIC FINDINGS
Lesions were found in the anterior visual pathway. Both optic nerves, optic chiasma, and tracts were thick¬ ened and infiltrated by a hard, reddish gray tissue (Fig 1). The right optic nerve measured 10 mm in diameter (normal size, 4 to 5 mm) and was thicker than the left optic nerve, which measured 7 mm in diameter. Only in the optic canal area were the optic nerves of normal size, appearing
"strangulated."
There was no anterior invasion of the eyeballs by the tumor. Posteriorly, it extended into the midbrain and hypothalamus, invading the cerebral
Fig 1.—Macroscopic appearance of glioma of both optic nerves, optic chiasma, and optic tracts viewed from below. Note "stran¬ gulated" portion of optic nerves in optic canal area (arrow).
Fig 2.—Cross-section
to left.
Fig
and
3.—Note mixture of areas with well-differentiated astrocytes areas with anaplastic hyperchromatic cells (hematoxylin-
eosin, original magnification
250).
peduncle down into the substantia nigra. Medially, it extended to the wall of the cerebral aqueduct (Fig 2). Laterally, the medial geniculate body was invaded, but the lateral genicu¬ late body was unaffected. The pons was
of brain
showing posterior spread
Fig 4.—Low-power view of tumor. There proliferation with hyperplasia of endothelial eosin, original magnification 100).
Fig 5.—Detail of Fig 4, showing areas of necrosis with pseudopalisading of tumor cells (hematoxylin-eosin, original magnifi¬ cation x250).
tumor-free.
HISTOPATHOLOGIC FINDINGS
The tumor was composed of a mixture of areas with well-differen-
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
of tumor
is strong vascular cells (hematoxylin-
tiated astrocytes and highly cellular areas with anaplastic hyperchromatic cells (Fig 3). Areas of necrosis with pseudopalisading of the tumor cells could be seen. There was strong vascular proliferation, with hyperplasia of the endothelial cells (Fig 4 and
5). COMMENT The various etiologic factors that may be involved in acute unilateral visual failure were studied by Wihlein and Rucker,- who found that in 34.8% of the cases, the lesions involved the retrobulbar portion of the optic nerve. Among these lesions, tumors of the optic nerve or optic chiasma were second in frequency. In the case reported herein, the clinical onset was also manifested as an acute unilateral visual loss. The rapid evolution with involvement of the contralateral eye and subsequent amaurosis in a 70year-old patient was suggestive of a temporal arteritis. This diagnosis, however, was excluded by the normal appearance of the temporal arteries, the absence of headaches, the normal erythrocyte sedimentation rate, and the lack of response to steroids. Furthermore, all of the complex neuroradiological examinations failed to reveal any pathologic features, so that there was no choice but to allow time to bring the diagnosis to light. The nonenlargement of the intracanalicular portion of the optic nerve and of its surrounding canal is not surprising in view of the rapidity with which the tumor spread, as well as the bone resistance of the optic canal in adulthood. As is well known, gliomatous tumors of the optic nerve may extend through the chiasma and optic tract to the hypothalamus. There may also be an invasion of the optic chiasma and optic nerves by neighboring gliomas.'" "' In our case, there was an involvement of the left side of the brain stem and of left hypothalamic nuclei. As already noted, there are very few cases of glioblastoma multiforme of the anterior optic pathways in adults or elderly patients. A 56-yearold patient was reported by Martin and Cushing.6 Foerster and Gagel7
a 30-year-old patient who developed blindness, epileptic tempo¬ ral lobe seizures, and polydipsia, and
described
who died nine months after the onset of the ocular symptoms. Levitt8 reported the case of a 43-year-old woman with a vascular glioma, in whom there was a progressive loss of vision during the course of many years. Saebo9 reported a 43-year-old wo¬ man with unilateral exophthalmos, progressive loss of vision, and increas¬ ing intraocular pressure on the same side. There was also a mushroomshaped disc protrusion, but the roentgenologic analysis showed no patho¬ logic findings. Four months later, the left optic foramen appeared to be enlarged, and when the left eye was enucleated, a glioblastoma multiforme was discovered. The patient died a year later with generalized cerebral
symptoms.
Condon and Rose10 reported the of a 79-year-old woman with a tumor of the optic nerves, but histo¬ logically, this proved to be an astrocy-
case
toma.
Mattson and Peterson41 described the case of a 59-year-old woman with a dimness of vision in one eye that progressed to blindness and a rapid loss of vision in the contralateral eye six weeks later, accompanied by polyuria, polydipsia, and hemiparesis. The roentgenologic examinations failed to reveal any lesion. Four months after the onset of ocular symptoms, the patient died in a coma¬ tose state. Postmortem examination revealed the presence of a glioblas¬ toma multiforme in both optic nerves, chiasma, optic tracts, the hypothala¬ mus, left temporal lobe, left cerebral peduncle, and pons. This case is very similar to the case we have reported herein regarding symptoms, time of evolution, normal roentgenologic ap¬ pearance, and autopsy findings. In the five cases of malignant optic glioma in adulthood recently de¬ scribed by Hoyt et al,1 as in some of the previously reported cases, there was a progressive swelling of one optic disc with superimposed venous and then arterial occlusion. When the tumor reached the distal segment of the second optic nerve, the corre-
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
sponding disc
also became edema¬
tous. In
our case, there was only a blur¬ ring of the nasal border of the right disc. During the following three weeks, this nasal border became sharp and a slight temporal pallor of both
discs could be detected. Since this patient was first seen by us only two months after the onset of the ocular symptoms, it may be that we missed the stage of papilledema. Hoyt et al1 claim that in these cases, the papil¬ ledema is not the expression of increased intracranial pressure, but a phenomenon secondary to the local occlusion of vessels (induced by the adventitial and endothelial changes in this highly malignant tumor). In an elderly patient, the occurrence of blindness with a rapid evolution from an edematous optic disc to optic atrophy may further confuse the diag¬ nosis with that of temporal arteritis. In spite of all the modern diagnostic procedures available, it is still very difficult to diagnose these extremely rare cases of malignant optic glioma. In fact, there is only a single case described in the literature (case 2 of Hoyt et al's series1) in which the diag¬ nosis was made prior to craniotomy or postmortem examination. References 1. Hoyt WF, Meshel LG, Lessel S, et al: Malignant optic glioma of adulthood. Brain 96:121-133, 1973. 2. Wihlein A, Rucker CW: The neurosurgeon's role in acute visual failure. Arch Ophthalmol 60:223-229, 1958. 3. Jefferson G, Pollak E, Yates O: Invasion of the optic chiasma and optic nerves by neighbouring gliomas. J Neurol Neurosurg Psychiatry 20:234-235, 1957. 4. Jefferson G: Invasion of optic chiasm and optic nerves by cerebral gliomas. Trans Ophthalmol Soc UK 79:463, 1959. 5. Hoyt WF, Piovanetti E, Malamud N, et al: Cranio-orbital involvement in glioblastoma multiforme. Neurochirurgia 15:1-8, 1972. 6. Martin P, Cushing H: Primary gliomas of the chiasma and optic nerves. Arch Ophthalmol 52:209-241, 1923. 7. Foerster 0, Gagel O: Ein Fall von Sog Gliom des Nervus opticus-spongioblastoma multiforme ganglioides. Z Neurol Psychiat 146:335-336, 1931. 8. Levitt JM: Tumor of optic chiasm and optic nerves. Arch Ophthalmol 18:91-94, 1937. 9. Saebo J: Primary tumors of the optic nerve (glioblastoma multiforme). Br J Ophthalmol 33:701-708, 1949. 10. Condon JR, Rose FC: Optic nerve glioma. Br J Ophthalmol 51:703-706, 1967. 11. Mattson RH, Peterson EW: Glioblastoma multiforme of the optic nerve. JAMA 196: 799-800, 1966.
a
Glioma 70-Year-Old Patient
Riri S. Manor, MD; Jacob Israeli, MD; Uriel Sandbank, MD
On general physical examination, the patient looked younger than his age and appeared to be in excellent physical condi¬ tion. The neurological examination, how¬ ever, revealed signs of mild right hemipa¬ resis with a slight motor weakness in the right limbs, brisker reflexes on the same side, and a Babinski sign on the right side. There was also a slight hypesthesia on the same
\s=b\ In a
70-year-old man with glioma of optic nerves and tracts, the initial symptom was a unilateral loss of vision that progressed rapidly and was followed by amaurosis of both eyes. All diagnostic radiological procedures were negative. the
Four months after the onset of the
disease, the patient developed hemiplegia, became comatose, and died. Postmortem examination revealed a glioblastoma multiforme of both optic nerves, chiasma, and optic tracts that extended posteriorly into the left thalamus and medical geniculate body. The tumoral thickening of the optic nerves was absent in the intracanalicular part, a finding that concurred with the normal radiological appearance of the optic foramen. Glioblastoma multiforme of the optic pathways should be included in the differential diagnosis of acute visual failure in elderly people, even though the final diagnosis may be possible only at postmortem examination.
(Arch Ophthalmol 94:1142-1144, 1976) is only a small number of adult cases of optic glioblastoma found in the neuro-ophthalmological literature. On the basis of the cases previously reported, as well as an additional five seen by them, Hoyt et al1 recently defined the clinical and pathologic nature of this tumor, which is distinctly different from glioma of the optic nerve occurring in younger persons. They found that the syn¬ drome of this malignant optic glioma of adulthood is characterized by: (1) occurrence in middle-aged men; (2) initial signs and symptoms that may
There
Accepted for publication
Nov 11, 1975. From the departments of ophthalmology (Dr Manor), neurosurgery (Dr Israeli), and pathology (Dr Sandbank), Beilinson Medical Center, Tel Aviv University Medical School, Petah Tikva, Israel. Reprint requests to the Department of Ophthalmology, Beilinson Medical Center, Petah Tikva, Israel (Dr Manor).
mimic those of optic neuritis; (3) to total blindness within five to six weeks; and (4) a fatal end within several months. We observed a case of glioblastoma multiforme of the optic pathways in a 70-year-old patient. This case is of particular interest because the tumor occurred in a patient of advanced age as compared with its usual occurrence in middle-aged people. At this age, the differential diagnosis was also differ¬ ent, being more suggestive of tempo¬ ral arteritis than of optic neuritis.
progression
REPORT OF A CASE A vigorous 70-year-old man was in excel¬ lent health and still able to work full time as a manual laborer when he began to notice a progressive decrease in the vision of the right eye, accompanied by headaches in the frontal area. The only notable aspect of his medical history was craniocerebral trauma incurred during the war 24 years before. He failed to consult a physician with the onset of symptoms, but within the next two months there was also a rapid decrease in the vision of the left eye, and he was finally referred to us. On his first examination, the findings were as follows. There was no light perception in the right eye and a visual acuity of only 1/18 in the left eye. Only the inferior nasal quadrant of the left visual field was present. Appla¬ nation tonometry was 14 mm in both eyes. Ophthalmoscopically, there was a very slight temporal pallor of both optic discs. The nasal border of the right optic disc was blurred. The retinal veins were not congested and the arteries appeared to be in very good condition considering his age, ie, there was no narrowing or visible arteriosclerotic change. Ophthalmodynamometry showed equal values in both eyes, corresponding to his normal brachial arterial pressure values. Ocular motility was normal. The right pupil was nonreactive to light. There was no exophthalmos, and the temporal arteries were not bulg¬ ing, tense, red, or painful.
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
side.
In laboratory examinations, the hematocrit reading, leukocyte count, sedimenta¬ tion rate, urinalysis, and serum glucose, bilirubin, protein, cholesterol, and alkaline phosphatase levels were all normal. The cerebrospinal fluid (CSF) and blood were negative for syphilis. In the CSF, the glucose levels and blood cell count were within normal limits, but the protein level was high (126 mg/100 ml). The electroen¬
cephalogram,
brain scan, angiographie studies of both carotid arteries, and pneumoencephalography all failed to reveal any pathologic findings. X-ray films of the skull and orbita, and tomography of the orbita and the optic canals were also nega¬ tive. The optic foramina were normal and of equal size. Three weeks later, the left eye also became definitely amaurotic. Both pupils were wide open and nonreactive to light. The border of the right optic disc became sharp. There was the same slight temporal pallor of the optic discs. The contrast between the almost normal appearance of the discs and the amaurosis was striking. Aside from the amaurosis and the mild right hemiparesis, there were no other neurological signs of a further evolution of the disease. Four months after the onset of the ocular complaints, the right hemipare¬ sis suddenly developed into hemiplegia and the patient became comatose and died the
following day.
PATHOLOGIC FINDINGS
Lesions were found in the anterior visual pathway. Both optic nerves, optic chiasma, and tracts were thick¬ ened and infiltrated by a hard, reddish gray tissue (Fig 1). The right optic nerve measured 10 mm in diameter (normal size, 4 to 5 mm) and was thicker than the left optic nerve, which measured 7 mm in diameter. Only in the optic canal area were the optic nerves of normal size, appearing
"strangulated."
There was no anterior invasion of the eyeballs by the tumor. Posteriorly, it extended into the midbrain and hypothalamus, invading the cerebral
Fig 1.—Macroscopic appearance of glioma of both optic nerves, optic chiasma, and optic tracts viewed from below. Note "stran¬ gulated" portion of optic nerves in optic canal area (arrow).
Fig 2.—Cross-section
to left.
Fig
and
3.—Note mixture of areas with well-differentiated astrocytes areas with anaplastic hyperchromatic cells (hematoxylin-
eosin, original magnification
250).
peduncle down into the substantia nigra. Medially, it extended to the wall of the cerebral aqueduct (Fig 2). Laterally, the medial geniculate body was invaded, but the lateral genicu¬ late body was unaffected. The pons was
of brain
showing posterior spread
Fig 4.—Low-power view of tumor. There proliferation with hyperplasia of endothelial eosin, original magnification 100).
Fig 5.—Detail of Fig 4, showing areas of necrosis with pseudopalisading of tumor cells (hematoxylin-eosin, original magnifi¬ cation x250).
tumor-free.
HISTOPATHOLOGIC FINDINGS
The tumor was composed of a mixture of areas with well-differen-
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
of tumor
is strong vascular cells (hematoxylin-
tiated astrocytes and highly cellular areas with anaplastic hyperchromatic cells (Fig 3). Areas of necrosis with pseudopalisading of the tumor cells could be seen. There was strong vascular proliferation, with hyperplasia of the endothelial cells (Fig 4 and
5). COMMENT The various etiologic factors that may be involved in acute unilateral visual failure were studied by Wihlein and Rucker,- who found that in 34.8% of the cases, the lesions involved the retrobulbar portion of the optic nerve. Among these lesions, tumors of the optic nerve or optic chiasma were second in frequency. In the case reported herein, the clinical onset was also manifested as an acute unilateral visual loss. The rapid evolution with involvement of the contralateral eye and subsequent amaurosis in a 70year-old patient was suggestive of a temporal arteritis. This diagnosis, however, was excluded by the normal appearance of the temporal arteries, the absence of headaches, the normal erythrocyte sedimentation rate, and the lack of response to steroids. Furthermore, all of the complex neuroradiological examinations failed to reveal any pathologic features, so that there was no choice but to allow time to bring the diagnosis to light. The nonenlargement of the intracanalicular portion of the optic nerve and of its surrounding canal is not surprising in view of the rapidity with which the tumor spread, as well as the bone resistance of the optic canal in adulthood. As is well known, gliomatous tumors of the optic nerve may extend through the chiasma and optic tract to the hypothalamus. There may also be an invasion of the optic chiasma and optic nerves by neighboring gliomas.'" "' In our case, there was an involvement of the left side of the brain stem and of left hypothalamic nuclei. As already noted, there are very few cases of glioblastoma multiforme of the anterior optic pathways in adults or elderly patients. A 56-yearold patient was reported by Martin and Cushing.6 Foerster and Gagel7
a 30-year-old patient who developed blindness, epileptic tempo¬ ral lobe seizures, and polydipsia, and
described
who died nine months after the onset of the ocular symptoms. Levitt8 reported the case of a 43-year-old woman with a vascular glioma, in whom there was a progressive loss of vision during the course of many years. Saebo9 reported a 43-year-old wo¬ man with unilateral exophthalmos, progressive loss of vision, and increas¬ ing intraocular pressure on the same side. There was also a mushroomshaped disc protrusion, but the roentgenologic analysis showed no patho¬ logic findings. Four months later, the left optic foramen appeared to be enlarged, and when the left eye was enucleated, a glioblastoma multiforme was discovered. The patient died a year later with generalized cerebral
symptoms.
Condon and Rose10 reported the of a 79-year-old woman with a tumor of the optic nerves, but histo¬ logically, this proved to be an astrocy-
case
toma.
Mattson and Peterson41 described the case of a 59-year-old woman with a dimness of vision in one eye that progressed to blindness and a rapid loss of vision in the contralateral eye six weeks later, accompanied by polyuria, polydipsia, and hemiparesis. The roentgenologic examinations failed to reveal any lesion. Four months after the onset of ocular symptoms, the patient died in a coma¬ tose state. Postmortem examination revealed the presence of a glioblas¬ toma multiforme in both optic nerves, chiasma, optic tracts, the hypothala¬ mus, left temporal lobe, left cerebral peduncle, and pons. This case is very similar to the case we have reported herein regarding symptoms, time of evolution, normal roentgenologic ap¬ pearance, and autopsy findings. In the five cases of malignant optic glioma in adulthood recently de¬ scribed by Hoyt et al,1 as in some of the previously reported cases, there was a progressive swelling of one optic disc with superimposed venous and then arterial occlusion. When the tumor reached the distal segment of the second optic nerve, the corre-
Downloaded From: http://archopht.jamanetwork.com/ by a Osaka University User on 06/17/2015
sponding disc
also became edema¬
tous. In
our case, there was only a blur¬ ring of the nasal border of the right disc. During the following three weeks, this nasal border became sharp and a slight temporal pallor of both
discs could be detected. Since this patient was first seen by us only two months after the onset of the ocular symptoms, it may be that we missed the stage of papilledema. Hoyt et al1 claim that in these cases, the papil¬ ledema is not the expression of increased intracranial pressure, but a phenomenon secondary to the local occlusion of vessels (induced by the adventitial and endothelial changes in this highly malignant tumor). In an elderly patient, the occurrence of blindness with a rapid evolution from an edematous optic disc to optic atrophy may further confuse the diag¬ nosis with that of temporal arteritis. In spite of all the modern diagnostic procedures available, it is still very difficult to diagnose these extremely rare cases of malignant optic glioma. In fact, there is only a single case described in the literature (case 2 of Hoyt et al's series1) in which the diag¬ nosis was made prior to craniotomy or postmortem examination. References 1. Hoyt WF, Meshel LG, Lessel S, et al: Malignant optic glioma of adulthood. Brain 96:121-133, 1973. 2. Wihlein A, Rucker CW: The neurosurgeon's role in acute visual failure. Arch Ophthalmol 60:223-229, 1958. 3. Jefferson G, Pollak E, Yates O: Invasion of the optic chiasma and optic nerves by neighbouring gliomas. J Neurol Neurosurg Psychiatry 20:234-235, 1957. 4. Jefferson G: Invasion of optic chiasm and optic nerves by cerebral gliomas. Trans Ophthalmol Soc UK 79:463, 1959. 5. Hoyt WF, Piovanetti E, Malamud N, et al: Cranio-orbital involvement in glioblastoma multiforme. Neurochirurgia 15:1-8, 1972. 6. Martin P, Cushing H: Primary gliomas of the chiasma and optic nerves. Arch Ophthalmol 52:209-241, 1923. 7. Foerster 0, Gagel O: Ein Fall von Sog Gliom des Nervus opticus-spongioblastoma multiforme ganglioides. Z Neurol Psychiat 146:335-336, 1931. 8. Levitt JM: Tumor of optic chiasm and optic nerves. Arch Ophthalmol 18:91-94, 1937. 9. Saebo J: Primary tumors of the optic nerve (glioblastoma multiforme). Br J Ophthalmol 33:701-708, 1949. 10. Condon JR, Rose FC: Optic nerve glioma. Br J Ophthalmol 51:703-706, 1967. 11. Mattson RH, Peterson EW: Glioblastoma multiforme of the optic nerve. JAMA 196: 799-800, 1966.
