Journal of Neuro-Ophthalmology, June 1996, Volume 16, Issue 2

Recurrent Chiasmal Apoplexy due to Cavernous Malformation

We report a case of chiasmal apoplexy due to a cavernous malformation (CM). Surgery was delayed because of the patient's advanced pregnancy, and nearly complete recovery of vision occurred spontaneously. Recurrent hemorrhage prompted surgical extirpation. The patient was left with a residual deficit. The literature pertaining to chiasmal apoplexy and CMs is reviewed. Nearly half of the reported cases of chiasmal CM had recurrent hemorrhages. The co-occurrence of hemorrhage from CM and pregnancy is too rare to merit any conclusions about cause and effect.

Journal of Nemo- Ophthalmology 16( 2): 99- 106, 1996. > 1996 Lippincott- Raven Publishers, Philadelphia Recurrent Chiasmal Apoplexy due to Cavernous Malformation Judith E. A. Warner, M. D., Joseph F. Rizzo III, M. D., Eugene W. Brown, M. D., and Christopher S. Ogilvy, M. D. We report a case of chiasmal apoplexy due to a cavern­ous malformation ( CM). Surgery was delayed because of the patient's advanced pregnancy, and nearly complete recovery of vision occurred spontaneously. Recurrent hemorrhage prompted surgical extirpation. The patient was left with a residual deficit. The literature pertaining to chiasmal apoplexy and CMs is reviewed. Nearly half of the reported cases of chiasmal CM had recurrent hem­orrhages. The co- occurrence of hemorrhage from CM and pregnancy is too rare to merit any conclusions about cause and effect. Key Words: Chiasmal apoplexy- Cavernous malforma­tion- Pregnancy- Recurrent hemorrhage- Surgery. Chiasmal apoplexy is a rare event, often caused by a vascular malformation. Patients typically present with sudden visual loss, often with head­ache. There are 29 cases in the literature of chias­mal apoplexy ( 1- 23), the majority attributable to cavernous malformations ( CM), which are low flow, angiographically occult, vascular malforma­tions with no intervening neural tissue. We present a case of a pregnant patient who experi­enced recurrent visual loss and spontaneous re­covery from a CM of the chiasm. The natural his­tory of these lesions is reviewed, and the role of surgery is discussed. Manuscript received March 14, 1995; accepted October 20, 1995. From the Departments of Ophthalmology and Neurology, University of Utah, Salt Lake City, Utah ( J. E. A. W.); Depart­ments of Ophthalmology ( J. F. R.) and Radiology ( E. W. B.), Bos­ton, Massachusetts; and Harvard Medical School, Massachu­setts Eye and Ear Infirmary, Department of Neurosurgery, Massachusetts General Hospital ( C. S. O.), Boston, Massachu­setts, U. S. A. Address correspondence and reprint requests to Dr. Judith E. A. Warner, Assistant Professor of Ophthalmology and Neu­rology, Moran Eye Center, University of Utah, 50 North Med­ical Drive, Salt Lake City, UT 84132, U. S. A. CASE REPORT A 32- year- old right- handed legal secretary was 4.5 months pregnant when she developed " trou­ble seeing my computer." She was only able to see letters that were directly ahead of her, and she had to move her head around in order to read. There were no associated symptoms. Past medical his­tory was not significant. Examination on the second day revealed visual acuity of 16/ 20 OD and 16/ 20 OS. She was able to read 12/ 12 Ishihara color plates OU, but reported " 10%" red desaturation OS. Amsler grids had a " fuzzy patch" inferotemperally OU. External ex­amination, intraocular pressure, pupils, extraocu­lar movements, dilated funduscopy, and neuro­logic testing were normal. Visual field testing showed an inferotemperal defect that respected the vertical meridian OD, and an inferotemperal defect that crossed the vertical meridian OS ( Fig- 1). Magnetic resonance imaging ( MRI) showed a 1.3 cm mass within the chiasm and enlargement of the adjacent optic nerves. The mass was of mixed signal on short Tl weighted images, with areas of hyperin- 99 100 J. E. A. WARNER ET AL. , t a8 a _ B ' 5 i . I H 11 B • • - » ' ' ' T" 1 7- f-ii n 12 „ IP. FIG. 1. Automated static perimetry, Humphrey 120 point program, performed on the day of presentation, demon­strating bitemporal defects. tensity and hypointensity. On T2 weighted im­ages, the lesion was hypointense due to T2 short­ening. This appearance was consistent with acute and subacute hemorrhage ( Fig. 2). Cerebrospinal fluid was clear and colorless without xanthochro­mia, with protein of 23 mg/ dl, glucose of 62 mg/ dl, 127 RBC/ mm3 and 2 WBC/ mm3. Cerebral angiog­raphy was normal. Surgery was planned, but was deferred because of concerns about the patient's advanced pregnancy. Over the next year, the patient's vision recov­ered completely with the exception of subtle bitemporal defects ( Fig. 3). She had an uneventful Cesarean section delivery. Serial MRIs showed that the chiasmal mass had become smaller, with resolution of the Tl bright, T2 dark areas ( Fig. 4). At 13 months after her initial presentation, a rou­tine MRI showed evidence of subclinical rehemor-rhage. At 15 months after her initial presentation, she returned because of headache and a sudden change in her vision. The only change in her ex­amination was increased density of the inferotem-peral defects, which crossed the midline OS. MRI showed evidence of a new hemorrhage, with ex­tension above the chiasm ( Fig. 5). Over the next several days, she reported further decline in her vision OS, and neurosurgical intervention was un­dertaken. A left pteronial craniotomy was used to expose the left optic nerve and chiasm. The chiasm was enlarged and had a purple discoloration in the left superior aspect. A 3- mm incision was made over the abnormal area, clotted blood was aspirated, and a vascular malformation was revealed. Bipolar coagulation was used to shrink the lesion, allow­ing gross total resection. Pathologic evaluation re­vealed a CM, with many thin- walled sinusoids, evidence of new and old hemorrhage, and no in­tervening neural or glial tissue ( Fig. 6). Neuro- ophthalmic evaluations over the next 8 months revealed stable visual acuity of 16/ 15 OD and 16/ 70 OS, normal color vision, a left afferent pupillary defect, and dense bilateral inferotemp-eral field defects ( Fig. 7). The patient developed bilateral optic disc pallor. Follow- up MRI 2 months postoperatively showed almost complete resolu­tion of the chiasmal lesion, with minimal residual T2 susceptibility and enhancement of the left optic nerve. The chiasm regained a near normal contour ( Fig. 8). DISCUSSION Vascular malformations of the anterior visual pathway include CM, ( cavernous angioma) ve­nous angioma, and arteriovenous malformation ( AVM). There are 29 reported cases of chiasmal apoplexy, only 15 with pathology described as CM ( 2- 13,23,24). Some lesions are referred to as " ve­nous angiomas" ( 1,14,16), but are probably more accurately classified as CMs because of the absence of intervening neural tissue. Several cases of chi­asmal apoplexy are attributed to AVM ( 5,10,14,17, 22), a high flow vascular anomaly. Most of these had normal angiograms, more suggestive of CM. Some reports lacked details of pathology, but the / Neuro- Ophthalmol, Vol. 16, No. 2, 1996 CHIASMAL APOPLEXY AND CAVERNOUS MALFORMATION 101 descriptions are consistent with CM ( 18- 21). Table 1 gives an outline of the cases as well as some of the clinical and pathologic features. The course of the patient presented here is typ­ical for a CM of the chiasm. Most patients present in their third or fourth decade with sudden visual loss. Men and women are affected equally. Typi­cally, the events are apoplectic, but there have been several cases in which vascular malforma­tions have acted as expansile mass lesions. For in­stance, Burnbaum ( 18) reported a man with pro­gressive visual loss with apoplectic episodes. Pa­thology was not obtained, but the gross descrip- FIG. 2. MRI at initial presentation. A: T1- weighted sagittal image showing an enlarged hyperintense ch­iasm. B: T1- weighted coronal image showing the hy­per- and hypointense mass within the chiasm. C: T2- weighted coronal showing marked hypointensity within the chiasm. tion of a " blue domed cyst" is typical of CMs seen at craniotomy. Malik and colleagues ( 24) described a 4- year- old boy with slowly progressive visual loss. The vessels in the vascular malformation were " thickened and hyalinized," somewhat atyp­ical for CM, but other family members had more classic lesions. Steiger gives a convincing argu­ment that cavernous angiomas can act as expansile mass lesions in the cerebral cortex, with slowly progressive neurologic deficit ( 25). The course of the patient presented here is in­structive because of the well- documented relaps-ing- remitting course. Not surprisingly, misdiag- / Neuro- Ophthatmol, Vol. 16, No. 2, 1996 202 /. E. A. WARNER ET Ah. 30° : H h . 30" SO5 J 1- , r. v."" i r 30° gi-; FIG. 3. Automated static perimetry, Humphrey 30- 2 program, performed 1 year after initial presentation showing mild residual deficits. noses, such as optic neuritis ( 2,4,16,19), migraine ( 3), and retinal tear ( 1), have been made due to the pattern of abrupt visual loss with recovery. Of the 17 cases of CM or venous angioma, seven patients had two or more apoplectic events prior to surgery ( 1- 3,8,11,12,16). Of the 30 cases of chiasmal vas­cular malformations or hemorrhages, 12 had recur­rent visual loss. In the recent literature, it is almost impossible to find a patient who is not taken im-t | at i\ i lWtttt 1 •- - !••>: I- £ w- • • - s i n r n ' i M T j^ f A fljP r ft T *** . X i • i i 1 t , B ^ ^ • ^ • i , ' < * t \ * r ^ j / mWl i % 1 r FIG. 4. T1- weighted MRI 1 year after presentation showing considerable resolution of the chiasmal en­largement, with some residual T1 hypointensity on co­ronal images. mediately to surgery. Steinberg ( 11) reported on one woman in whom the diagnosis of vascular malformation was made. She was observed for 18 months before visual deterioration prompted sur­gical extirpation. Our patient not only had a sec­ond episode of visual loss, but also, while visually stable, had evidence of fresh hemorrhage on rou­tine MRI. There have been several analyses of large series' of patients with cerebral CM. One series of 57 pa­tients with CM ( 26), with a mean follow- up of 26 months, reported clinically significant hemorrhage at presentation in seven patients. One patient had recurrent hemorrhage, but four had been treated surgically. Thus, one of three untreated patients presenting with hemorrhage had clinically signifi­cant rehemorrhage. Kattapong ( 27) reported a 2 month to 6- year follow- up interval. Of 14 patients with 67 lesions, four had growth in the malforma­tion size and seven developed new lesions. Extrap­olation from the literature to predict chiasmal CM behavior is problematic because of the small num­bers of cases and limited clinical information. In these series, however, the tendency for recurrent hemorrhage or expansion of the mass is evident. The chiasm is unusual in that, frequently, the pa­tient is acutely aware of minor fluctuations in vi­sion. Serial visual field testing allows for precise documentation of progression and regression. If the natural history of CM is to rebleed at a low rate, perhaps a CM in the chiasm will cause a more clinically apparent deficit with a lower threshold. As our patient experienced, visual deficit can ac­crue with successive hemorrhages. Evidence of acute and chronic hemorrhage is characteristic in pathologic and radiologic studies / Neuro- Ophthalmol, Vol. 16, No. 2, 1996 CHIASMAL APOPLEXY AND CAVERNOUS MALFORMATION 103 FIG. 5. T1 weighted ( A) co­ronal and ( B) axial ( with gadolinium) MRI images 15 months after presentation, showing recurrent hemor­rhage. of CMs ( 12,25,28,29). Earlier neuro- imaging meth­ods were insensitive to this diagnosis because of the presence of a hemorrhagic mass on imaging studies, with angiographic silence. Routine angi­ography does not reveal the vascular nature of CMs. Modern neuro- imaging permits an accurate diagnosis at first presentation. MRI is the preferred imaging technique due to its capability to show old and new blood products ( 11,28). Demonstration of high flow within the lesion raises the possibility of AVM. In 1976, Voight and Yasargil ( 30) suggested re­moval of surgically accessible cortical CMs. Many cortical lesions can be removed with low morbidity, given current stereotactic methods. Some centers use lasers to coagulate and shrink lesions, attempt­ing to minimize damage to surrounding structures ( 11). As surgical techniques develop, the definition of " surgically accessible" becomes broader, and most CMs in the chiasm reported in recent years have been treated with surgical extirpation. There are no reports of long- term follow- up of patients operated on for chiasmal CMs, but resection is thought to be curative. Most patients who have undergone surgery for CM either improved or remained unchanged post­operatively ( see Table 1). Decompression of the he­matoma is thought to be the mechanism of early im­provement. In reviewing surgical results, the out­come is somewhat dependent upon the nature of the lesion. High- flow malformations seem to have a greater potential for recurrent hemorrhages. Lavin FIG. 6. Photomicrograph ( x10) show­ing typical CM with dilated thin- walled sinuses. No intervening neural or glial tissue is seen. J Neuro- Ophthalmol, Vol. 16, No. 2, 1996 104 }. E. A. WARNER ET AL. 3U'- • • l l * ' f t M p ; <%% S • •-•': *' i :•'•: • fl^^ ilif^ S!;^ , : : ; ; : : ; : : : : : . : ; : ; t ^ < ^ ? ^ a FIG. 7. Automated static perimetry, Humphrey 30- 2 program, 8 months postoperatively, showing residual de­fects OU. et al. ( 5) reported on one patient in whom a high-flow chiasmal AVM was operated on after two ep­isodes of visual loss. The patient had several sub­sequent events that prompted a second attempt at resection. Tien and colleagues ( 12) reported on a patient who had progressive visual loss following biopsy of a CM, suggesting that gross total resec­tion should be the goal. The influence of pregnancy on the behavior of vascular malformations is controversial. Robinson and colleagues ( 31,32) reviewed the relationship FIG. 8. MRI 2 months after surgery showing resolution of the chiasmal enlargement on T1 coronal images. Minimal gadolinium enhancement is seen at the oper­ative site. between subarachnoid hemorrhage, aneurysm, AVM, and pregnancy, and found that the risk of hemorrhage was increased during pregnancy. Pregnancy was thought to increase the rate of hemorrhage from AVMs, particularly during " high risk" times of early pregnancy, labor, and delivery. The increased risk was believed to be due to increased cardiac output. Recently, more con­servative estimates ( 33) have not shown an in­creased risk of hemorrhage from AVM during pregnancy. This information may or may not be relevant for CMs. Only three instances of hemorrhage from chias­mal CMs associated with pregnancy have been re­ported. Maruoka et al. ( 7) reported on a woman with chiasmal apoplexy occurring 10 days postpar­tum. Reilly and colleagues ( 10), however, found a CM of the optic nerve and chiasm causing sudden visual disturbance in a 36 year- old woman who had been " either pregnant or breast- feeding for the preceding 8 years." Thus, she was " at risk" and asymptomatic for many years before the apo­plectic event. One of the series of cortical CM ( 26) found that two of six women presenting with overt hemorrhage were in the first trimester of preg­nancy. Given the age group of patients typically affected by CM, this may not be significant. Our patient had her first hemorrhage while in her fourth month of pregnancy, not generally consid­ered a high- risk period. Her second symptomatic hemorrhage occurred 10 months after she deliv­ered. These cases do not confirm or refute an as­sociation between pregnancy and the risk of hem­orrhage from a chiasmal CM. In summary, this case illustrates several interest­ing points about chiasmal CMs. First, substantial / Neuro- Ophthalmol, Vol. 16, No. 2, 1996 CHIASMAL APOPLEXY AND CAVERNOUS MALFORMATION 105 TABLE 1. Summary of reported cases of chiasmal apoplexy and vascular malformations No. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 Author ( ref) Carter ( 1) Corboy ( 2) Hassler ( 3) Hwang ( 4) Lavin ( 5) Lavin ( 5) Lavin ( 5) Manz ( 6, 15) Maruoka ( 7) Mohr ( 8) Regli ( 9) Reilly ( 10) Reilly ( 10) Steinberg ( 11) Steinberg ( 11) Tien ( 12) Zentner ( 13) Hankey ( 14) Hankey( 14) Hufnagel( 16) Roski( 17) Burnbaum ( 18) Holt ( 19) Maitland ( 20) Maitland ( 20) Maitland ( 20) Riishede ( 21) Malik ( 24) Lejeune ( 22) Castel ( 23) Initial Dx Retinal tear Optic neuritis Migraine Optic neuritis Chiasmal Syndrome vs hysteria Optic neuritis Age 48 44 24 42 43 37 27 30 24 30 28 31 36 58 33 32 35 26 36 39 37 43 33 26 23 63 20 4 26 23 Sex F F F M M M F M F M F F F M F F M M F F M M M M F F F F F F Malformation type VA CA CA CH CA AVM, angio(-) AVM, angio(-) CH/ VA CH CH CA AVM, angio (-) CA CA CA CH CA ( tract) VA AVM, angio (-) VA AVM, angio(-) Blue domed cyst, blue fluid Bulging chiasm, filled cyst Blue domed cyst Enlarged blue ch blood Mass in chiasm, i blood Enlarged brown i clotted blood , viscous amber fluid , blood iasm, clotted chiasm, CA " hyalinized thickened vessels" AVM CA No. of events ( interictal period) 2 ( 3 yr) 3 ( 7 yr, 2 yr) 2 ( 3 yr) 1 1 5 ( 6 mo, 30 mo, 2 wk, 12 mo) 1 1 1 > 3 ( 18 mo, 2 mo, 2 mo) 1 1 1 1 2 ( 18 mo) Fluctuation for 9 yr 1 1 1 3 ( 7 yr, 2 yr) 2 ( 6 mo) 2 ( 23 mo) 3 ( 1 mo, 24 mo) 1 1 Unknown Unknown Progressive 1 1 Outcome Improved after surgery No change after surgery Worsened visual field defect after surgery Improved after fine needle aspiration No changes OS, worse OD after surgery 2 improved after surgery, 3 improved spontaneously Improved after surgery Improved after surgery No change after surgery Improved after survery Improved after surgery Improved after surgery Improved after surgery No change after surgery Improved after surgery Radiation decreased fluctuation Improved after surgery Surgery, no follow- up Improved after surgery Improved after surgery Improved after surgery Improved after aspiration Aspiration, radiation, deterioration 2 yr later ( optic neuritis?) Improved after surgery Improved after surgery No information Improved after surgery No change after surgery Improved after surgery No change after surgery AVM, arteriovenous malformation; CM, cavernous malformation; CA, cavernous angioma; CH, cavernous hemangioma; VA, venous angioma. improvement in vision may occur spontaneously, probably due to resorption of a small hematoma. Second, these lesions have a tendency to recurrent hemorrhages, often within 1- 2 years. Third, sur­gery can improve or maintain vision, although there is not enough follow- up data to know wheth­er surgery prevents recurrence. Surgical improve­ment is predicated on pathology consistent with CM, since high- flow AVMs may be more likely to rebleed. Finally, there is insufficient evidence to confirm an association between pregnancy and hemorrhage from chiasmal CMs. Acknowledgment: Supported, in part, by a grant from Research to Prevent Blindness, Inc., New York, NY, U. S. 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