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Chiasmatic Arachnoiditis
VOL. 68. NO. 2
IDIOPATHIC STELLATE RETINOPATHY
18. Gallemaerts, V. and Coppez, J. H. : Ophthal moscope picture of albuminurie retinitis without albuminuria. Bull. Soc. Belge Ophtal. 48:25, 1923. 19. Trolowa, W. K.: A case of pseudoalbuminuric retinitis. Russk. Ophth. J. 2:589, 1923. 20. Pascheff, C. : Transitory stellate retinitis. Ber. deutsch. Ophth. Ges. 47 :472, 1928.
345
21. Magitot, M. : Unilateral retinitis azotemic in type without azotemia. Bull. Soc. Ophtal. Paris, 1930, p. 39. 22. Zanen, J. and Meunier, A.: Leber's stellate retinitis (pseudonephritic retinitis). Bull. Soc. Beige Ophtal. 95 :482, 1950.
CHIASMATIC ARACHNOIDITIS A CASE REPORT AND REVIEW J. T E R R E N C E COYLE,
M.D.
Kirkland, Washington
The following case illustrates the value of repeated field examinations and surgical de compression of the optic nerves and chiasm in a patient with tuberculous opticochiasmatic arachnoiditis. CASE REPORT
A 14-year-old Japanese girl was seen on October 23, 1962, because of frontal headaches. Eleven months earlier she had tuberculous meningitis. The infection was treated with isoniazid (INH), strep tomycin and aminosalicylic acid (PAS), but the patient still had a left hemiparesis. Presently she was taking 200 mg of INH and 8.0 gm of PAS a day. Monthly spinal-fluid examinations were negaReprint requests to J. Terrence Coyle, M.D., 515 State Street, Kirkland, Washington 98033.
tive on culture for Mycobacterium tuberculosis but consistently showed 10 to 30 mononuclear cells per cu mm and 50 to 65 mg/100 ce of protein (normal 14 to 45 mg). The ocular examination revealed left homonymous inferior quadrantanopsia (fig. 1), conjugate deviation of the eyes to the left with forced eleva tion of her eyelids (perverse Bell's phenomenon to the left) 1 and an absent optokinetic response on ro tation of the drum to her right.2 Vision could be corrected to 20/20. The initial impression was a de structive lesion involving the right parietal lobe sec ondary to the previous tuberculous meningitis. Three months later, on January 29, the patient was seen because of blurred vision for three days in the left eye. Her acuity was 20/20, R.E., and perception of hand movements at two feet, L.E. The left pupil was slightly dilated and the pupillary response was paradoxic. Ophthalmoscopic examina tion revealed no abnormalities. The visual field of
Fig. 1 (Coyle). Left homonymous inferior quadrantanopsia (5/1000 white) October 23, 1962.
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AMERICAN JOURNAL OF OPHTHALMOLOGY
AUGUST, 1969
Fig. 2 (Coyle). Poorly outlined nasal island of vision, L.E. (5/1000 white) January 29, 1963. the right eye was unchanged from the previous ex amination. The visual field of the left eye was re duced to a small nasal island (fig. 2). Cerebrospinal fluid studies disclosed: protein 55 mg/100 ce, chlo ride 120 meq/1, glucose 60 mg/100 ce and 20 mononuclear cells per cu mm. The colloidal gold curve and the Wassermann test were nonreactive, and no organisms were isolated. The sudden loss of vision, the normal fundi and the prolonged drug therapy suggested a diagnosis of toxic optic neuritis but chiasmatic arachnoiditis had to be ruled out. She was treated with daily doses of 60 mg of prednisone by mouth and 1,000 ßg of vitamin B« intramuscularily. Her INH and PAS were temporarily stopped.
Examinations on February 5, 12 and 18 revealed no changes except for the gradual development of 60 prism diopter left exotropia. On February 22, four weeks after the loss of vision in the left eye, the right superior visual field (fig. 3) in the right eye showed a depression but the acuity remained 20/20. This loss of peripheral field in the uninvolved eye indicated that this was not optic neuritis but more likely a rapidly evolving lesion in the area of the chiasm. The patient was referred to the neurosurgical department of the University of Washington for exploration of the chiasm. Visual field examination on March 2 at the university showed progressive loss of the temporal field and a decrease in acuity
Fig. 3 (Coyle). Beginning loss of superotemporal field, R.E. (5/1000 white) February 22, 1963.
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Fig. 4 (Coyle). Progressive loss of temporal field, R.E. (5/1000 white) March 2, 1963. in the right eye to 20/40 (fig. 4). The left eye still perceived only hand movements. A pneumoencephalogram demonstrated absence of air in the interpeduncular and chiasmatic cisterns. The roentgenologic impression was basal arachnoiditis. On March 8, 1963, a right frontal craniotomy showed that "the optic nerves and chiasm were tightly bound down in a rather vascular and scarred arachnoid. On further exploration, an inflammatory type membrane was found to encompass the chiasm. There was some fear that this represented an active area of tuberculous meningitis. No biopsy was made because of oozing and indistinctness of nor
mal and abnormal tissue. As thorough a resection as possible of the scar tissue binding down the chiasm and optic nerves was performed." * On March 19, 11 days postoperatively, the field of vision, R.E., was once again full, except for the original left inferior quadrantanopsia. Vision had improved to 20/20, R.E., and 20/200, L.E. The visual acuity progressively improved: March 26— 20/20, R.E, 20/70, L.E.; April 2—20/20, R.E., 20/40, L.E. ; April 16—20/20, R.E, 20/25, L.E, and intermittently exotropic; April 30—20/20, R.E, »Report of Dr. Eldon L. Foltz.
Fig. 5 (Coyle). Same as in Figure 1, with the addition of a 10 degree superotemporal field loss. L.E. (5/1000 white) April 30, 1963.
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AMERICAN JOURNAL OF OPHTHALMOLOGY
20/20-2, L.E., and orthophoric. Visual field examina tions revealed that the original quadrantanopsia was unchanged and, in addition, a 10 degree loss of the temporal field, L.E. (fig. S). When last seen in March, 1966, three years later, her acuity and visual fields had remained unchanged. DISCUSSION
Arachnoiditis may have an allergic,3 in fectious or traumatic etiology.4 Meningitis from almost any cause can be followed by chiasmatic arachnoiditis.5 Eighty percent of cases occur in patients under the age of 40 years.4 Symptomatology of arachnoiditis. There are no specific symptoms unless secondary hydrocephalus, damage to the hypothalamus or involvement of the optic nerves and chiasm occur. Many cases of chronic arach noiditis are probably never identified.4 Ophthalmoscopy. The fundi are normal except late when optic atrophy may occur.4 Since arachnoiditis involves the intracranial portion of the optic nerves, thus sparing the central retinal artery and vein, papilledema and venous fullness are not usually seen.5 Indeed, the presence of papilledema, in the absence of hydrocephalus, makes the diagno sis of opticochiasmatic arachnoiditis un likely. Visual fields. The most frequently noted field abnormality is a monocular central scotoma.4'8 It is acute, progressive9 and nonremitting and indicates that the optic nerve rather than the chiasm is the primary site of the disease. Eventually field changes occur in the other eye. The combination of a central scotoma and an atypical hemianoptic defect in the other eye is most suggestive of optico chiasmatic arachnoiditis.10 Pathology. The inflammatory reaction of chiasmatic arachnoiditis, more appropriately call leptomeningitis, involves the pia and arachnoid.5'6 Adhesions, forming between the arachnoid and the underlying pia, may block the free flow of cerebrospinal fluid and produce arachnoidal cysts.4 The central one third of the optic nerve (papulomacular bun dle) is supplied entirely by piai vessels.7 In leptomeningitis, especially in the tuberculous
AUGUST, 1969
form, vasculitis occurs in these vessels, caus ing ischemia of the optic nerve. The rich blood supply7 of the chiasm makes it less likely to be affected. Pneumoencephalography. Pneumoencephalograms may reveal absence of air about the chiasm (the chiasmatic cistern) due to pia-arachnoidal adhesions. At present, pneu moencephalography offers the best method of diagnosing chiasmatic arachnoiditis. Treatment. Since active infection is not present, antimicrobial drugs are usually inef fective. Although chiasmatic archnoiditis ap pears to be a proliferati ve healing process, treatment with systemic corticosteroids is usually unsuccessful. Stripping the inflam matory membrane from the chiasm and optic nerves offers the only effective treatment.11 Prognosis. The prognosis is good be cause : ( 1 ) the circulatory impairment of the intracranial portion of the optic nerve is gradual and incomplete; (2) the ganglioncell layer of the retina is not involved; (3) the pia-arachnoid cicatrization (leptomenin gitis) occurs in the absence of viable infec tive organisms. Even in the presence of optic atrophy, excellent recovery of visual acuity has followed decompression of the optic nerves and chiasm. Patients with less than 20/200 vision for as long as one year have experienced return of 20/30 vision.4 However, the prognosis is poor in syphilitic chiasmatic arachnoiditis,12 possibly because of the chorioretinal involvement. That excep tion may explain the skeptism13 surrounding both the diagnosis of opticochiasmatic arach noiditis and its surgical treatment. SUMMARY
Visual field findings suggested the diagno sis of opticochiasmatic arachnoiditis. Pneumoencephalography supported the diag nosis and surgery verified it. Fourteen months earlier this 14-year-old patient had had tuberculous meningitis. The symptoms ascribed to chiasmatic arachnoiditis result from ischemia of the intracranial portion of the optic nerve secondary to a leptomeningi-
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349
CHIASMATIC ARACHNOIDITIS
5. Lyle, D. J. : Neuro-ophthalmology. Springfield, 111., Thomas, 1954, ed. 2, p. 353. 6. Hogan, M. J. and Zimmerman, L. E. : Ophalmic Pathology, Philadelphia Saunders, 1962, ed. 2, p. 590. 7. Last, R. J. : Wolff's Anatomy of the Eye and Orbit. Philadelphia, Saunders, 1961, ed. 5, p. 349. ACKNOWLEDGMENTS 8. Kestenbaum, A. : Clinical Methods of NeuroI thank Fletcher Pomeroy, M.D., and Robert L. ophthalmologic Examination. New York, Grune Lindemeyer, M.D., for their assistance. and Stratton, 1961, ed. 2, p. 163. 9. Cogan, D. G. : Neurology of the Visual System. REFERENCES Springfield, 111., Thomas, 1966, p. 219. 1. Cogan, D. G. : Neurologic significance of lat 10. Harrington, D. O. : The Visual Fields. St. eral conjugate deviation of the eyes on forced clo Louis ; Mosby, 1964, ed. 2, p. 285. 11. Borromei, A. and Palmieri, L. : Neuro-ophsure of the lids. Arch. Ophth. 39:37, 1948. 2. Smith, J. L. and Cogan, D. G. : Optokinetic thalmological observations on the surgical treatment nystagmus: A test for parietal lobe lesions. Am. J. of Opticochiasmal arachnoiditis. Rev. Oto-neurooftal. 41:233, 1966 Ophth. 48:187, 19S9. 12. Bruetsch, W. : Etiology of optochiasmatic 3. Akamatsu, T. : Talc induced arachnoiditis in arachnoiditis. Arch. Neurol. Psychiat. 59:215, 1948. rabbits. Acta. Soc. Ophth. Jap. 68 :1537, 1964. 13. Merritt, H. : A Textbook of Neurology. Phil 4. Vail, D. : Optochiasmic arachnoiditis. Arch. adelphia, Lea Febiger, 1959, ed. 2, p. 353 Ophth., 20:384, 1938.
tis. Excision of the membrane about the chiasm and optic nerves usually results in rapid recovery of visual acuity and visual fields.
UNILATERAL INTERNAL OPHTHALMOPLEGIA INTRACRANIAL ANEURYSM
WITH
REPORT OF A CASE J O H N W. PAYNE, M.D., AND JOSEPH ADAMKIEWICZ, JR., M.D.
Baltimore, Maryland four months prior to admission, she had had left fronto-temporal headaches which were dull and rather constant and were usually worse in the early morning hours. She no longer noticed any drooping of her eyelids. Awakened the morning of admission by this headache and by pain near the inner canthus, she sought aid in the emergency room. She denied diplopia, blurred vision, episodes of unconsciousness and stiffness in the neck. The neurologic inventory was otherwise unremarkable. Her past history revealed that she had had pri mary syphilis (dark-field positive), which was treat ed in 1946. She was given a second course of therapy in 1957 because serology tests were positive. She stated that one eye had deviated out slightly since childhood. There was no family history of diabetes. CASE REPORT The patient appeared to be a healthy 35-year-old A 35-year-old Negro woman, six months preg woman in her sixth month of pregnancy. General nant, entered the Johns Hopkins Hospital on July physical, obstetric and neurologic examinations were 27, 1965, with complaints of left frontal headache normal. Ocular findings. Vision in the right eye was and left retro-orbital pain. Because of slight drooping of the left upper eyelid six months prior 20/20 with a manifest refraction of a piano sphere. to admission, she had seen an optometrist who In the left eve, vision was 20/50, improved to prescribed +1.0D sph for both eyes. During the 20/20 with a +2.75D sphC+0.75D cyl ax 70°. She was able to read J2 print at 30 cm with her right From the Wilmer Institute and the Division of eye, without an add, but with her left eye could only read J7 print at 30 cm with her manifest cor Neurosurgery, The Johns Hopkins Hospital. Reprint requests to John W. Payne, M.D., 14 rection. She required a +2.5 D add to read J2 West Mount Vernon Place, Baltimore, Maryland print with her left eye at 30 cm. Accommodation in her left eye was, therefore, at least 2.5 diopters 21201.
Involvement of the oculomotor nerve by aneurysms of the circle of Willis usually re sults in blepharoptosis, extraocular muscle weakness and a dilated pupil. Although the presence of pupillary abnormalities is rare, some degree of extraocular muscle weakness and blepharoptosis has invariably been de scribed.1'2 This paper reports an unusual case of intracranial aneurysm in which unilateral internal ophthalmoplegia was the principal feature.
IDIOPATHIC STELLATE RETINOPATHY
18. Gallemaerts, V. and Coppez, J. H. : Ophthal moscope picture of albuminurie retinitis without albuminuria. Bull. Soc. Belge Ophtal. 48:25, 1923. 19. Trolowa, W. K.: A case of pseudoalbuminuric retinitis. Russk. Ophth. J. 2:589, 1923. 20. Pascheff, C. : Transitory stellate retinitis. Ber. deutsch. Ophth. Ges. 47 :472, 1928.
345
21. Magitot, M. : Unilateral retinitis azotemic in type without azotemia. Bull. Soc. Ophtal. Paris, 1930, p. 39. 22. Zanen, J. and Meunier, A.: Leber's stellate retinitis (pseudonephritic retinitis). Bull. Soc. Beige Ophtal. 95 :482, 1950.
CHIASMATIC ARACHNOIDITIS A CASE REPORT AND REVIEW J. T E R R E N C E COYLE,
M.D.
Kirkland, Washington
The following case illustrates the value of repeated field examinations and surgical de compression of the optic nerves and chiasm in a patient with tuberculous opticochiasmatic arachnoiditis. CASE REPORT
A 14-year-old Japanese girl was seen on October 23, 1962, because of frontal headaches. Eleven months earlier she had tuberculous meningitis. The infection was treated with isoniazid (INH), strep tomycin and aminosalicylic acid (PAS), but the patient still had a left hemiparesis. Presently she was taking 200 mg of INH and 8.0 gm of PAS a day. Monthly spinal-fluid examinations were negaReprint requests to J. Terrence Coyle, M.D., 515 State Street, Kirkland, Washington 98033.
tive on culture for Mycobacterium tuberculosis but consistently showed 10 to 30 mononuclear cells per cu mm and 50 to 65 mg/100 ce of protein (normal 14 to 45 mg). The ocular examination revealed left homonymous inferior quadrantanopsia (fig. 1), conjugate deviation of the eyes to the left with forced eleva tion of her eyelids (perverse Bell's phenomenon to the left) 1 and an absent optokinetic response on ro tation of the drum to her right.2 Vision could be corrected to 20/20. The initial impression was a de structive lesion involving the right parietal lobe sec ondary to the previous tuberculous meningitis. Three months later, on January 29, the patient was seen because of blurred vision for three days in the left eye. Her acuity was 20/20, R.E., and perception of hand movements at two feet, L.E. The left pupil was slightly dilated and the pupillary response was paradoxic. Ophthalmoscopic examina tion revealed no abnormalities. The visual field of
Fig. 1 (Coyle). Left homonymous inferior quadrantanopsia (5/1000 white) October 23, 1962.
346
AMERICAN JOURNAL OF OPHTHALMOLOGY
AUGUST, 1969
Fig. 2 (Coyle). Poorly outlined nasal island of vision, L.E. (5/1000 white) January 29, 1963. the right eye was unchanged from the previous ex amination. The visual field of the left eye was re duced to a small nasal island (fig. 2). Cerebrospinal fluid studies disclosed: protein 55 mg/100 ce, chlo ride 120 meq/1, glucose 60 mg/100 ce and 20 mononuclear cells per cu mm. The colloidal gold curve and the Wassermann test were nonreactive, and no organisms were isolated. The sudden loss of vision, the normal fundi and the prolonged drug therapy suggested a diagnosis of toxic optic neuritis but chiasmatic arachnoiditis had to be ruled out. She was treated with daily doses of 60 mg of prednisone by mouth and 1,000 ßg of vitamin B« intramuscularily. Her INH and PAS were temporarily stopped.
Examinations on February 5, 12 and 18 revealed no changes except for the gradual development of 60 prism diopter left exotropia. On February 22, four weeks after the loss of vision in the left eye, the right superior visual field (fig. 3) in the right eye showed a depression but the acuity remained 20/20. This loss of peripheral field in the uninvolved eye indicated that this was not optic neuritis but more likely a rapidly evolving lesion in the area of the chiasm. The patient was referred to the neurosurgical department of the University of Washington for exploration of the chiasm. Visual field examination on March 2 at the university showed progressive loss of the temporal field and a decrease in acuity
Fig. 3 (Coyle). Beginning loss of superotemporal field, R.E. (5/1000 white) February 22, 1963.
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Fig. 4 (Coyle). Progressive loss of temporal field, R.E. (5/1000 white) March 2, 1963. in the right eye to 20/40 (fig. 4). The left eye still perceived only hand movements. A pneumoencephalogram demonstrated absence of air in the interpeduncular and chiasmatic cisterns. The roentgenologic impression was basal arachnoiditis. On March 8, 1963, a right frontal craniotomy showed that "the optic nerves and chiasm were tightly bound down in a rather vascular and scarred arachnoid. On further exploration, an inflammatory type membrane was found to encompass the chiasm. There was some fear that this represented an active area of tuberculous meningitis. No biopsy was made because of oozing and indistinctness of nor
mal and abnormal tissue. As thorough a resection as possible of the scar tissue binding down the chiasm and optic nerves was performed." * On March 19, 11 days postoperatively, the field of vision, R.E., was once again full, except for the original left inferior quadrantanopsia. Vision had improved to 20/20, R.E., and 20/200, L.E. The visual acuity progressively improved: March 26— 20/20, R.E, 20/70, L.E.; April 2—20/20, R.E., 20/40, L.E. ; April 16—20/20, R.E, 20/25, L.E, and intermittently exotropic; April 30—20/20, R.E, »Report of Dr. Eldon L. Foltz.
Fig. 5 (Coyle). Same as in Figure 1, with the addition of a 10 degree superotemporal field loss. L.E. (5/1000 white) April 30, 1963.
348
AMERICAN JOURNAL OF OPHTHALMOLOGY
20/20-2, L.E., and orthophoric. Visual field examina tions revealed that the original quadrantanopsia was unchanged and, in addition, a 10 degree loss of the temporal field, L.E. (fig. S). When last seen in March, 1966, three years later, her acuity and visual fields had remained unchanged. DISCUSSION
Arachnoiditis may have an allergic,3 in fectious or traumatic etiology.4 Meningitis from almost any cause can be followed by chiasmatic arachnoiditis.5 Eighty percent of cases occur in patients under the age of 40 years.4 Symptomatology of arachnoiditis. There are no specific symptoms unless secondary hydrocephalus, damage to the hypothalamus or involvement of the optic nerves and chiasm occur. Many cases of chronic arach noiditis are probably never identified.4 Ophthalmoscopy. The fundi are normal except late when optic atrophy may occur.4 Since arachnoiditis involves the intracranial portion of the optic nerves, thus sparing the central retinal artery and vein, papilledema and venous fullness are not usually seen.5 Indeed, the presence of papilledema, in the absence of hydrocephalus, makes the diagno sis of opticochiasmatic arachnoiditis un likely. Visual fields. The most frequently noted field abnormality is a monocular central scotoma.4'8 It is acute, progressive9 and nonremitting and indicates that the optic nerve rather than the chiasm is the primary site of the disease. Eventually field changes occur in the other eye. The combination of a central scotoma and an atypical hemianoptic defect in the other eye is most suggestive of optico chiasmatic arachnoiditis.10 Pathology. The inflammatory reaction of chiasmatic arachnoiditis, more appropriately call leptomeningitis, involves the pia and arachnoid.5'6 Adhesions, forming between the arachnoid and the underlying pia, may block the free flow of cerebrospinal fluid and produce arachnoidal cysts.4 The central one third of the optic nerve (papulomacular bun dle) is supplied entirely by piai vessels.7 In leptomeningitis, especially in the tuberculous
AUGUST, 1969
form, vasculitis occurs in these vessels, caus ing ischemia of the optic nerve. The rich blood supply7 of the chiasm makes it less likely to be affected. Pneumoencephalography. Pneumoencephalograms may reveal absence of air about the chiasm (the chiasmatic cistern) due to pia-arachnoidal adhesions. At present, pneu moencephalography offers the best method of diagnosing chiasmatic arachnoiditis. Treatment. Since active infection is not present, antimicrobial drugs are usually inef fective. Although chiasmatic archnoiditis ap pears to be a proliferati ve healing process, treatment with systemic corticosteroids is usually unsuccessful. Stripping the inflam matory membrane from the chiasm and optic nerves offers the only effective treatment.11 Prognosis. The prognosis is good be cause : ( 1 ) the circulatory impairment of the intracranial portion of the optic nerve is gradual and incomplete; (2) the ganglioncell layer of the retina is not involved; (3) the pia-arachnoid cicatrization (leptomenin gitis) occurs in the absence of viable infec tive organisms. Even in the presence of optic atrophy, excellent recovery of visual acuity has followed decompression of the optic nerves and chiasm. Patients with less than 20/200 vision for as long as one year have experienced return of 20/30 vision.4 However, the prognosis is poor in syphilitic chiasmatic arachnoiditis,12 possibly because of the chorioretinal involvement. That excep tion may explain the skeptism13 surrounding both the diagnosis of opticochiasmatic arach noiditis and its surgical treatment. SUMMARY
Visual field findings suggested the diagno sis of opticochiasmatic arachnoiditis. Pneumoencephalography supported the diag nosis and surgery verified it. Fourteen months earlier this 14-year-old patient had had tuberculous meningitis. The symptoms ascribed to chiasmatic arachnoiditis result from ischemia of the intracranial portion of the optic nerve secondary to a leptomeningi-
VOL. 68, NO. 2
349
CHIASMATIC ARACHNOIDITIS
5. Lyle, D. J. : Neuro-ophthalmology. Springfield, 111., Thomas, 1954, ed. 2, p. 353. 6. Hogan, M. J. and Zimmerman, L. E. : Ophalmic Pathology, Philadelphia Saunders, 1962, ed. 2, p. 590. 7. Last, R. J. : Wolff's Anatomy of the Eye and Orbit. Philadelphia, Saunders, 1961, ed. 5, p. 349. ACKNOWLEDGMENTS 8. Kestenbaum, A. : Clinical Methods of NeuroI thank Fletcher Pomeroy, M.D., and Robert L. ophthalmologic Examination. New York, Grune Lindemeyer, M.D., for their assistance. and Stratton, 1961, ed. 2, p. 163. 9. Cogan, D. G. : Neurology of the Visual System. REFERENCES Springfield, 111., Thomas, 1966, p. 219. 1. Cogan, D. G. : Neurologic significance of lat 10. Harrington, D. O. : The Visual Fields. St. eral conjugate deviation of the eyes on forced clo Louis ; Mosby, 1964, ed. 2, p. 285. 11. Borromei, A. and Palmieri, L. : Neuro-ophsure of the lids. Arch. Ophth. 39:37, 1948. 2. Smith, J. L. and Cogan, D. G. : Optokinetic thalmological observations on the surgical treatment nystagmus: A test for parietal lobe lesions. Am. J. of Opticochiasmal arachnoiditis. Rev. Oto-neurooftal. 41:233, 1966 Ophth. 48:187, 19S9. 12. Bruetsch, W. : Etiology of optochiasmatic 3. Akamatsu, T. : Talc induced arachnoiditis in arachnoiditis. Arch. Neurol. Psychiat. 59:215, 1948. rabbits. Acta. Soc. Ophth. Jap. 68 :1537, 1964. 13. Merritt, H. : A Textbook of Neurology. Phil 4. Vail, D. : Optochiasmic arachnoiditis. Arch. adelphia, Lea Febiger, 1959, ed. 2, p. 353 Ophth., 20:384, 1938.
tis. Excision of the membrane about the chiasm and optic nerves usually results in rapid recovery of visual acuity and visual fields.
UNILATERAL INTERNAL OPHTHALMOPLEGIA INTRACRANIAL ANEURYSM
WITH
REPORT OF A CASE J O H N W. PAYNE, M.D., AND JOSEPH ADAMKIEWICZ, JR., M.D.
Baltimore, Maryland four months prior to admission, she had had left fronto-temporal headaches which were dull and rather constant and were usually worse in the early morning hours. She no longer noticed any drooping of her eyelids. Awakened the morning of admission by this headache and by pain near the inner canthus, she sought aid in the emergency room. She denied diplopia, blurred vision, episodes of unconsciousness and stiffness in the neck. The neurologic inventory was otherwise unremarkable. Her past history revealed that she had had pri mary syphilis (dark-field positive), which was treat ed in 1946. She was given a second course of therapy in 1957 because serology tests were positive. She stated that one eye had deviated out slightly since childhood. There was no family history of diabetes. CASE REPORT The patient appeared to be a healthy 35-year-old A 35-year-old Negro woman, six months preg woman in her sixth month of pregnancy. General nant, entered the Johns Hopkins Hospital on July physical, obstetric and neurologic examinations were 27, 1965, with complaints of left frontal headache normal. Ocular findings. Vision in the right eye was and left retro-orbital pain. Because of slight drooping of the left upper eyelid six months prior 20/20 with a manifest refraction of a piano sphere. to admission, she had seen an optometrist who In the left eve, vision was 20/50, improved to prescribed +1.0D sph for both eyes. During the 20/20 with a +2.75D sphC+0.75D cyl ax 70°. She was able to read J2 print at 30 cm with her right From the Wilmer Institute and the Division of eye, without an add, but with her left eye could only read J7 print at 30 cm with her manifest cor Neurosurgery, The Johns Hopkins Hospital. Reprint requests to John W. Payne, M.D., 14 rection. She required a +2.5 D add to read J2 West Mount Vernon Place, Baltimore, Maryland print with her left eye at 30 cm. Accommodation in her left eye was, therefore, at least 2.5 diopters 21201.
Involvement of the oculomotor nerve by aneurysms of the circle of Willis usually re sults in blepharoptosis, extraocular muscle weakness and a dilated pupil. Although the presence of pupillary abnormalities is rare, some degree of extraocular muscle weakness and blepharoptosis has invariably been de scribed.1'2 This paper reports an unusual case of intracranial aneurysm in which unilateral internal ophthalmoplegia was the principal feature.