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Show IDlImal of CI"/ I( al Nell",- ophthalmolo.~ 1( 12( 3): 198- 202, 1992. Permanent Homonymous Hemianopias Following Migraine Masato Wakakura, M. D., D. Se. and Yoshiaki Ichibe, M, D. ~ 1992 Raven Press, Ltd., : Two patients with migraine and repetitive visual field defects of homonymous hemianopic type are reported. The visual field defects were confirmed by Goldmann perimetry and automated static perimetry. Neither computed tomography nor magnetic resonance imaging showed abnormal findings. Decreased cerebral blood flow at the left basal ganglion area was the only abnormal finding detected in one patient by 123I_ IMP ( iodoamphetamine)- SPECT ( single photon emission computed tomography), which is applicable to right homonymous hemianopia. A visual field test that includes the current automated static perimetry is important to the diagnosis and the subsequent treatment of patients with migraine, particularly those who have experienced visual negative phenomena. Key Words: Hemianopia- Migraine- Visual negative phenomenon- Automated static perimetry- Single photon emission computed tomography. From the Department of Ophthalmology, Kitasato University, School of Medicine, Sagamihara. Kanagawa. Japan. Address correspondence and reprint requests to Dr. M. Wakakura, Department of Ophthalmology, Kitasato University, School of Medicine, 1- 15- 1, Kitasato, Sagamihara, Kanagwa 228, Japan. 198 Migraine usually affects relatively young people and often occurs without abnormalities detectable by neuro- ophthalmologic examinations. However, there is evidence that a benign clinical course ( 1) is not followed in all cases. Several cases of migraine ischemic optic neuropathy have been reported ( 26). A young, otherwise healthy, woman with migraine was found to have bilateral disk edema and retinal hemorrhage ( 7). Kupersmith et al. ( 8) reviewed 46 complicated migraine patients with visual dysfunction. Lewis et al. ( 9) noted visual field abnormality at a surprisingly high frequency ( 35%) in 60 migraine patients while conducting automated static perimetry. Three of the subjects had homonymous hemianopia. In this study there were two patients with migraine accompanied by repetitive visual negative phenomena of the homonymous hemianopic type. They eventually had permanent retrochiasmal visual field defects. Although migraine cases with permanent visual field loss due to probable or definite retrochiasmal lesion have been mentioned in the older literature ( 10- 12), two similar patients examined by current automated static perimetry and single photon emission computed tomography ( SPECT) are here reported. CASE REPORTS Case 1 The subject was a 24- year- old man with increasi~ gly frequent throbbing headaches affecting parhcularly the right temporal portion, of about 2 months duration. Headaches had recently occurred every day for several hours duration and were sometimes accompanied by nausea and/ or vomiting. One month before, he noted a right visual field defect on awakening. He consulted a private neurosurgeon who found no abnormality by brain computed tomography ( CT). No h\' perten- HEMIANOPIA IN MIGRAINE 199 sion was noted. The visual field defect varied considerably in size from day to day, and complete recovery was never attained. The neurosurgeon referred the patient to Kitasato University Hospital in September 1989. Visual acuity was 20/ 20 OU, and Goldmann perimetry showed incongruous right homonymous hemianopia with macular sparing. Plain and enhanced brain CT showed no abnormal findings. Spin echo magnetic resonance imaging ( MRl) by 0.5 tesla indicated no abnormal findings on Tl- weighted or T2- weighted images with tomographic slices of 10 mm in width. No gadolinium enhancement was performed. Without treatment, the field appeared to have recovered in mid- October. Goldmann perimetry showed significant improvement in the visual field of each eye, but the right field defect was shown to persist by both the 30- 2 threshold program of the Humphrey Visual Field Analyzer and conventional Goldmann perimetry. At the end of October, examinations were conducted at the Department of Medicine because of sinus tachycardia and arrhythmia, which had developed suddenly at midnight. The symptoms were transient and the cause unknown. Echocardiography indicated normokinesis. Several days later, severe throbbing headache occurred again, and the patient went to bed. On the following morning, he noted the right visual field defect of each eye to have enlarged. He was subsequently hospitalized at our department. Blood tests showed mild liver dysfunction ( glutamic- oxaloacetic transaminase 30 IU/ L, glutamicpyruvic transaminase 54 lUlL), mild hyperlipidemia ( cholesterol 247 mg/ dl, triglyceride 264 mgl dl), and RA (+). The results of an erythrocyte sedimentation test ( 10 mm/ h), negative C- reactive protein and negative antinuclear antigen failed to give any indication of vasculitis. The maximum platelet aggregation rate examined by 2.25 fLM adenosine diphosphate showed 58%, this being slightly high ( normal 30- 55%). SPECT, using a tracer, N- isopropyl- p-[ 1231) iodoamphetamine ( IMP), was conducted, following essentially the same method described by Schlake et al. ( 13). In brief, 20 minutes following an intravenous administration of 123I_ lMP, 64 early scan images were obtained with a rotation gamma camera ( General Electric MaxiCamera 400ACT). The imaging time per image was 40 seconds, and each examination took 35 minutes. Late scan was also done 4 hours after the tracer administration. The early scan facilitated the assessment of regional cerebral blood flow ( rCBF) ( 14) and indicated decreased CBF in the left basal ganglion area ( Fig. 1). CBF in the bilateral occipital portions, however, appeared normal or to have slightly increased. The patient was given aspirin ( 250 mg/ day) and Inderal ( 2 tablets/ day). Severity of the headaches subsequently abated somewhat. However, the vi- IR FIG. 1. Early scan image of [ 1231liodoamphetamine single photon emission computed tomography in Case 1. ( A); Transverse and ( 8) coronal sections. Arrows indicate decreased tracer uptake by left basal ganglion area. J Clill Nellro- ophthalmol, Vol. 12, No. 3, 1992 200 M. WAKAKURA AND Y. ICHIBE sual field defect again tluctuated, and, finally, a condition of permanent right homonymous hemianopia developed. Neither MRI nor SPECT in March 1990, at the time the headaches ceased, showed abnormal findings except for possibly increased CBF in both occipital areas, according to SPECT. Dynamic CT in June showed no abnormality. The time course of the visual field is shown in Fig. 2. Case 2 The subject was a 39- year- old woman who had had occasionally throbbing headaches of the frontal or temporal portion for approximately 10 years duration. The family history was negative for migraine headaches. She had no hypertension. At the end of October 1987, she felt deep right orbital pain and transient visual loss in both eyes. The symptoms were relatively quickly relieved, but a right visual field defect was noted. She consulted an ophthalmologist. Right homonymous hemianopia was detected by an automated static perimeter. CASE 1 989 Sep. Goldmann perimetry conducted 2 days later showed slight depression of the right visual field of each eye. The patient was referred to the Department of Ophthalmology, Kitasato University Hospital on November 9,1987. At that time, the patient felt she had the complete recovery of the visual field of each eye. Goldmann perimetry showed normal findings as did also brain CT. The patient had no visual symptoms afterward, although, on some occasions, there were headaches. On September 30, 1989, the patient had a strong throbbing left temporal headache for several hours. Two days later, the headache disappeared, but darkness of the right half- field was noted. Visual acuity was 20/ 20 OU. The 30- 2 threshold program of Humphrey Field Analyzer showed decreased sensitivity of the right lower field in each eye. Blood tests that indicated determination of the erythrocyte sedimentation rate, platelet aggregation, titer of antinuclear antigen and immunoglobulins showed no abnormality. MRI indicated normal findings. 1231- IMP- SPECT showed no defi- Oct. ' Nov. D'ec. Mar. FIG. 2. Clinical time course of visual field defect in Case 1. , elm NCliro- oplllll1llmol, Vol. 12, No. 3, 1992 HEMIANOPIA IN MIGRAINE 201 nitely abnormal findings, but there was indication of what appeared to be slightly increased bilateral occipital CBF. The visual field showed right homonymous hemianopia wit!, macular sparing on September 28, 1989. The time course of each field is shown in Fig. 3. During follow- up for 1 year, the fields significantly improved, but permanently decreased sensitivity persisted in the right peripheral field of each eye. DISCUSSION Homonymous hemianopic visual field defects in the patients discussed here indicated retrochiasmaI lesions. At least 13 patients with migraine, along with probable or definite retrochiasmal visual field defects, have been reported ( 8,10- 12). Two relatively old patients ( a 60- year- old woman and a 54- year- old woman) of Hollenhorst ( 11) and one patient ( a 47- year- old man) of Connor ( 12) appeared to have late- onset migraine headaches. These may have been secondary to agerelated vascular disease of the brain. The remaining 10 reported patients, as well as our 2 patients, are quite likely typical cases in which, etiologically, there is a direct relationship between migraine headaches in young patients and retrochiasmallesions. Unlike the previously reported cases, our two cases are characterized by initially transient but ultimately permanent visual field defects. The reason why the visual fields fluctuated over months to years is unknown, since no lesion could be found by computed tomography, magnetic resonance imaging, or dynamic computed tomography. Decreased cerebral blood flow in the left basal ganglion area detected by single photon emission Oct .11967 CASE 2 .. :. t". · .- • • ,- 1. • !' ..'" , · ' · :; h; · . i=:"~~ · · ...~. ~ ~ :. ' t-:~"-'. I'--'.,.:..: : I • ,. f' ~' P -. . - 26- 0ct I Oct 01989 4 ti. ,_ :' 1 " -: I FIG. 3. Clinical time course of visual field defect in Case 2. 14- 0ct 28- 0ct I Clill Neuro- ophthalmol. Vol. 12, No. 3. 1992 202 M. WAKAKURA AND Y. ICHIBE computed tomography in Case 1 was the only objective finding, indicating possibly decreased flow of the left posterior cerebral artery or its branches. Although this is not direct evidence for left occipital hypocirculation, decreased flow of the left posterior cerebral artery is consistent with the right homonymous hemianopia noted in this patient. Prolonged, relatively mild, hypoperfusion to the responsible area may have caused fluctuation of visual field defects and pathologic changes undetectable by presently available means. The permanent visual field defects may have been due to intolerance of prolonged hypoperfusion. Occipital lobe arteriovenous malformations ( 10,15) should also be considered for differential diagnosis in our two cases. However, in addition to CT and MRI, dynamic CT, shown to be useful for detecting cerebral vascular anomalies ( 16), failed to indicate any abnormality in the occipital area. SPECT showed somewhat slightly increased CBF in the bilateral occipital areas, but these findings are not an actual indication of the presence of occipital lobe arteriovenous malformations. Brain angiography was not performed for the following reasons: other neurological symptoms were absent, there was continued good visual acuity, and there was insufficient indication for surgery. There was no scintillating scotoma ( visual positive phenomenon) preceding temporally visual negative phenomenon or visual field loss in our cases. In only one case of Symonds ( 10), did scintillating scotoma appear to have continued after visual field loss. Similar continuity has been noted in a case with metastatic melanoma ( 17). A temporally visual negative phenomenon was demonstrated in 8 of the 10 reported ( 8,10- 12) patients and our 2 patients. The visual negative phenomenon may thus be more important as a warning sign for organic disease. Current automated static perimetry facilitated the detection of transient and permanent visual field defects, as also noted by Lewis et al. ( 9). Study of the central field has also been found clinically useful for patients showing visual negative phenomena, even after subjective " , .: ~ '( If 1:!. No. 3. 1991 symptoms have subsided and in the absence ul objective findings ( CT, MRI, SPECT). In conclusion, since migraine headaches do . not always follow a benign clinica~ co. urse, ~ xammation should be made of the static Visual held, particularly for patients with such headaches and visual negative phenomena. Acknowledgment: Dr. Toshimasa Fukuda is gratefully acknowledged for having referred Case 2 to our department. REFERENCES 1. McDonald WI, Sanders MD Migraine complicated by isch-aemic papillopathy. Lallcet 1971; 2: 521- 3. .. 2. Weinstein jM, Feman 5S. IschemiC ophc neuropathy 10 mI-graine Arch Ophthalmol1982; 100: 1097- 1100. .. 3 Cowan CL, Knox DL. Migraine optic neuropathy 10 mI-graine. AIlIl Ophthalmol1982; 14: 164-- t>... .. 4. Corbett JJ. euro- ophthalmic comphcahons of mlgrame and cluster headaches Neurol Clin 1983; 1: 97:>- 95. 5 O'Hara M, O'Connor PS. Migrainous optic neuropathy. I Clill Nellro- ophthalmol 1984; 3: 85- 9. 6. Wakakura M Visual field defects and migraine. Gallaka 1991; 33: 911-- 8. 7. Victor OJ, Welch RB. Bilateral retinal hemorrhages and disk edema in migraine. Am I Ophthalmol 1977; 84: 555- 8. 8. Kupersmith Mj, Warren FA, Hass WK. The non- benign aspects of migraine. Neuro- opllthalmology 1986; 7: 1- 10. 9. Lewis RA, Vijayan N, Watson C, Keltner J, johnson CA. Visual field loss in migraine Ophthalmology 1989; 96: 321~. 10. Symonds C. Migrainous variants. Trans Med Soc Lond 1952; 67237- 50. 11. Hollenhorst RW. Ocular manifestations of migraine: report of - I cases of hemianopia. Mayo Clill Proc 1953; 28: 686-- 93. 12. Connor RCR. Comphcated migraine: a study of permanent neurological and \' isual defects caused by migraine. Lancet 1962; 2: 1072- 5. 13. Schlake H- P, Bottger IG, Grotemeyer K- H, Husstedt IW. Brain imaging with '~ JI- IMP- SPECT in migraine between attacks. Headache 1989; 29: 34+- 9. 1- 1. Kuhl DE, Barrio jR, Hung SC, et al. Quantifying local cerebral blood ! low by N- isopropyl- p-[ I~ JIJiodoamphetamine ( IMP) tomography. I ?' JllcI Med 1982; 23: 196-- 203. 15. Troost BT, Newton TH. Occipital lobe arteriovenous malformations: clinical and radiologic features in 26 cases with comments on differentiation from migraine. Arch Ophthalmol 1975; 93: 25~. 16. Handa J, Matsuda M, Nakasu Y, Nakasu S, Morioka Y. Dvnamic computed tomography and functional imaging in cerebral vascular anomalies. Surg NellroI1983; 19: 497- 507. 17. Weinstein jM, Appen RE, Houston L, ZuRhein G. Recurrent scintillating scotoma and homonymous hemianopia due to metastatic melanoma. I Clill Neuro- ophthalmol 1987; 7: 155- 60. |
