Cavernous malformations of the optic pathway and hypothalamus: analysis of 65 cases in the literature

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  • 1 Department of Neurological Surgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Neurological Institute of New Jersey, Newark, New Jersey; and Departments of
  • | 2 Neurological Surgery and
  • | 3 Pathology, Oregon Health & Science University, Portland, Oregon
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Object

Cavernous malformations (CMs) of the optic pathway and hypothalamus (OPH) are extremely rare. Patients with these lesions typically present with chiasmal apoplexy, characterized by sudden visual loss, acute headaches, retroorbital pain, and nausea. Surgical removal is the recommended treatment to restore or preserve vision and to eliminate the risk of future hemorrhage. However, the anatomical location and eloquence of nearby neural structures can make these lesions difficult to access and remove. In this study, the authors review the literature for reported cases of OPH CMs to analyze clinical and radiographic presentations as well as surgical approaches and neurological outcomes.

Methods

A MEDLINE/PubMed search was performed, revealing 64 cases of OPH CMs. The authors report an additional case in the study, making a total of 65 cases. Each case was analyzed for clinical presentation, lesion location, radiographic features, treatment method, and visual outcome.

Results

In 65 patients with OPH CMs, the optic chiasm was affected in 54 cases, the optic nerve(s) in 35, the optic tract in 13, and the hypothalamus in 5. Loss of visual field and acuity was the most common presenting symptom (98%), followed by headache (60%). The onset of symptoms was acute in 58% of patients, subacute in 15%, and chronic progressive in 26%. Computed tomography scans revealed hyperdense suprasellar lesions, with calcification visible in 56% of cases. Magnetic resonance imaging typically demonstrated a heterogeneous lesion with mixed signal intensities suggestive of blood of different ages. The lesion was often surrounded by a peripheral rim of hypointensity on T2-weighted images in 60% of cases. Minimal or no enhancement occurred after the administration of gadolinium. Hemorrhage was reported in 82% of cases. Most patients were surgically treated (97%) using gross-total resection (60%), subtotal resection (6%), biopsy procedure alone (6%), biopsy procedure with decompression (23%), and biopsy procedure followed by radiation (2%). Those patients who underwent gross-total resection had the highest rate of visual improvement (85%). Two patients were treated conservatively, resulting in complete blindness in 1 patient and spontaneous recovery of vision in the other patient.

Conclusions

Cavernous malformations of the OPH are rare and challenging lesions. Gross-total resection of these lesions is associated with favorable visual outcomes. Emergent surgery is warranted in patients presenting with chiasmal apoplexy to prevent permanent damage to the visual pathway.

Abbreviations used in this paper:

CM = cavernous malformation; GTR = gross-total resection; OPH = optic pathway and hypothalamus; STR = subtotal resection.

Object

Cavernous malformations (CMs) of the optic pathway and hypothalamus (OPH) are extremely rare. Patients with these lesions typically present with chiasmal apoplexy, characterized by sudden visual loss, acute headaches, retroorbital pain, and nausea. Surgical removal is the recommended treatment to restore or preserve vision and to eliminate the risk of future hemorrhage. However, the anatomical location and eloquence of nearby neural structures can make these lesions difficult to access and remove. In this study, the authors review the literature for reported cases of OPH CMs to analyze clinical and radiographic presentations as well as surgical approaches and neurological outcomes.

Methods

A MEDLINE/PubMed search was performed, revealing 64 cases of OPH CMs. The authors report an additional case in the study, making a total of 65 cases. Each case was analyzed for clinical presentation, lesion location, radiographic features, treatment method, and visual outcome.

Results

In 65 patients with OPH CMs, the optic chiasm was affected in 54 cases, the optic nerve(s) in 35, the optic tract in 13, and the hypothalamus in 5. Loss of visual field and acuity was the most common presenting symptom (98%), followed by headache (60%). The onset of symptoms was acute in 58% of patients, subacute in 15%, and chronic progressive in 26%. Computed tomography scans revealed hyperdense suprasellar lesions, with calcification visible in 56% of cases. Magnetic resonance imaging typically demonstrated a heterogeneous lesion with mixed signal intensities suggestive of blood of different ages. The lesion was often surrounded by a peripheral rim of hypointensity on T2-weighted images in 60% of cases. Minimal or no enhancement occurred after the administration of gadolinium. Hemorrhage was reported in 82% of cases. Most patients were surgically treated (97%) using gross-total resection (60%), subtotal resection (6%), biopsy procedure alone (6%), biopsy procedure with decompression (23%), and biopsy procedure followed by radiation (2%). Those patients who underwent gross-total resection had the highest rate of visual improvement (85%). Two patients were treated conservatively, resulting in complete blindness in 1 patient and spontaneous recovery of vision in the other patient.

Conclusions

Cavernous malformations of the OPH are rare and challenging lesions. Gross-total resection of these lesions is associated with favorable visual outcomes. Emergent surgery is warranted in patients presenting with chiasmal apoplexy to prevent permanent damage to the visual pathway.

Abbreviations used in this paper:

CM = cavernous malformation; GTR = gross-total resection; OPH = optic pathway and hypothalamus; STR = subtotal resection.

Cavernous malformations are low-flow vascular lesions, which are typically angiographically occult. On histological examination, the wall of the vascular channels consists of a single layer of endothelial cells that lacks any muscle cells. These lesions are well circumscribed with no intervening brain parenchyma,33,53 having an incidence of 0.3 to 0.7% in the general population and representing 10–20% of all vascular malformations.43,50 The distribution of CMs within the CNS is proportional to the volume of the various compartments. Most occur in the supratentorial compartment (80%), followed by the infratentorial compartment (15%); the remaining 5% occur in the spinal cord. Cavernous malformations of the OPH are extremely rare, representing 1% or less of all CMs.21 The earliest reported lesion was described in 1979 by Klein et al.29

Patients with CMs of the OPH typically present with chiasmal apoplexy, characterized by sudden visual disturbance, headache, retroorbital pain, and nausea.36 Apoplectic symptoms are frequently preceded by transient blurred vision and headache weeks or months beforehand. Although some episodes are self-limiting, permanent damage can occur from neural compression of the optic nerve, chiasm, or tract. Surgical removal is the recommended treatment to restore or preserve vision, to decompress the visual apparatus, and to eliminate the risk of future hemorrhages. However, the anatomical location and eloquence of intrinsic neural structures can make these formidable lesions difficult to surgically access and remove. In this study, we evaluated 65 cases of OPH CMs in the literature, including a newly reported case from our institution. We also analyzed the clinical and radiographic characteristics and reviewed the surgical approaches and neurological and visual outcomes of OPH CMs.

Methods

A biomedical literature search for OPH CMs confined to the English language was performed using the MEDLINE/PubMed search engine. The search included the following key words: “cavernous malformation,” “cavernoma,” “cavernous hemangioma,” “cavernous angioma,” combined with “optic nerve,” “optic chiasm,” “optic tract,” and “hypothalamus,” for all possible combinations. All relevant articles pertaining to CMs of the OPH were reviewed. Additional cases were identified in the references of these articles, that is, references to articles that did not show up on the initial PubMed search. A total of 64 OPH CM cases were identified.2,8–10,12–15,18,19,21,22,25–27,29–31,36–42,46–48,51,52,57–64,67,68 We also report an additional case in this paper, making a total of 65 cases that were reviewed. Each case was analyzed for clinical presentation, lesion location, radiographic features, surgical treatment, and neurological and visual outcome (Table 1).

TABLE 1:

Literature review of 65 patients with OPH CMs*

Authors & YearAge (yrs), SexClinical PresentationLesion LocationTreatmentOutcome
Arrué et al., 199936, Macute visual loss, headacheOCobservationimproved
36, Mprogressive visual loss, headacheOC, LOTSTRimproved
55, Facute visual loss, headacheOC, LONGTRimproved
Castel et al., 198923, Facute visual loss, headacheOCGTRimproved
Cerase et al., 201030, Ffluctuating visual lossLONsteroidsworsened
Christoforidis et al., 200038, Msubacute visual disturbance, headacheOCGTRNA
Corboy & Galetta, 198944, Facute visual loss, headacheOC, LON, LOTBxstable
Deshmukh et al., 200334, Msubacute visual lossOC, LONGTRimproved
29, Facute visual lossOC, LONGTRimproved
28, Fprogressive visual loss, headacheOCGTRimproved
29, Facute visual lossOCGTRimproved
Escott et al., 200140, Fcardiac arrestOCNANA
Ferreira & Ferreira, 19928, Macute visual loss, headacheOC, LONGTRstable
Glastonbury et al., 200325, Facute visual loss, headacheOC, RONGTRNA
Hankey & Khangure, 198736, Fsubacute visual lossOC, LONGTRimproved
26, Msubacute visual loss, headacheOCGTRimproved
Hasegawa et al., 199554, Facute visual loss, headache, unsteady gait, convulsionhypothalamusSTRstable
Hassler et al., 19892124, Fprogressive visual loss, headacheRONGTRimproved
16, Msubacute visual lossOC, RONGTRimproved
35, Macute visual loss, headacheROTGTRimproved
Hassler et al., 19892024, Ffluctuating visual loss, headacheRONGTRimproved
Hempelmann et al., 200738, Mprogressive visual loss, confusion, lethargyOCGTRimproved
Hufnagel & Cobbs, 198830, Facute visual loss, headacheOCGTRimproved
Hwang et al., 199342, Macute visual loss, headacheOC, LON, LOTBxDimproved
Iwai et al., 199931, Facute visual loss, headacheOC, RONGTRimproved
Kehagias, 200327, Mfluctuating visual lossOC, RONGTRNA
Klein et al., 197930, Msubacute visual loss, headacheOC, LON, RON, ROTBxDimproved
Kurokawa et al., 200127, Fprogressive visual loss, headachehypothalamusGTRstable
Lehner et al., 200639, Facute visual loss, headacheOC, LOTGTRimproved
Lejeune et al., 199026, Facute visual loss, headacheOCBxDimproved
Maitland et al., 198226, Macute visual loss, headache, nausea, vomitingOCBxDimproved
23, Facute visual loss, headacheOC, LON, RONBxDimproved
63, Fsubacute visual loss, headacheOCBxDNA
15, Fprogressive visual loss, headacheOC, LONBxDworsened
Malik et al., 19924, Facute visual lossOC, LONSTRstable
Manz et al., 197930, Macute visual loss, headacheOC, RON, ROTBxDimproved
Maruoka et al., 198824, Facute visual lossOC, RONGTRimproved
Mizoi et al., 199240, Mprogressive visual losshypothalamusGTRimproved
60, MdementiahypothalamusGTRimproved
Mizutani et al., 198136, Facute visual loss, headacheOC, LONBxDimproved
26, Macute visual lossOC, LON, LOTBxDNA
Mohr et al., 198530, Macute visual loss, confusion, lethargyOC, LON, LOTBxDstable
Muta et al., 200614, Mprogressive visual lossLON, RONBxstable
Newman et al., 200816, Macute visual loss, headacheOC, LONGTRimproved
Ozer et al., 200715, Macute visual lossOC, LONGTRimproved
Paladino et al., 200158, Fprogressive visual loss, headacheOC, RONSTRimproved
Regli et al., 198928, Facute visual loss, headacheOCGTRimproved
Reilly & Oatey, 198631, Facute visual loss, headacheOC, LON, LOTBxDimproved
36, Facute visual loss, headacheOC, LONBxDimproved
Shaikh et al., 200242, Macute visual lossOC, LON, RONGTRimproved
Shibuya et al., 199518, Fsubacute visual lossOCGTRimproved
60, Fsubacute visual loss, headacheOC, RONGTRimproved
Son et al., 200839, Facute visual loss, headache, nauseaOCGTRstable
Steinberg et al., 199058, Macute visual loss, nauseaOC, ROTBxDstable
33, Facute visual loss, headacheOC, RONGTRimproved
Suarez et al., 199441, Mprogressive visual loss, headacheOCBxNA
52, Mprogressive visual loss, headacheOC, RONBxNA
Tien & Dillon, 198932, Ffluctuating visual lossOCBx & radstable
Wang et al., 200362, Fprogressive unsteady gait, LE weaknesshypothalamusGTRstable
Warner et al., 199632, Facute visual loss, headacheOCGTRimproved
Yoshimoto & Suzuki, 198637, Macute visual lossOCBxDimproved
43, Msubacute visual lossOC, RON, ROTGTRworsened
27, Facute visual loss, headacheOC, RONGTRimproved
Zentner et al., 198935, Macute visual loss, headacheROTGTRimproved
present case50, Fprogressive visual lossOCGTRimproved

* Bx = biopsy; BxD = biopsy with decompression; LE = lower extremity; LON = left optic nerve; LOT = left optic tract; NA = not applicable; OC = optic chiasm; rad = radiation; RON = right optic nerve; ROT = right optic tract.

Results

Among the 65 cases of OPH CMs, 60 lesions arose from the optic pathway and 5 from the hypothalamus. The optic chiasm was affected in 54 cases, the optic nerve(s) in 35, the optic tract in 13, and the hypothalamus in 5. Three cases occurred as a third ventricular mass. One case of a hypothalamic CM extended into the thalamus, and another extended into the basal ganglia. Among the 65 cases were 36 females and 29 males. The average age was 34 years (range 4–63 years). The majority of cases (73%) occurred in patients in their 2nd to 4th decade of life.

Clinical Characteristics

The most common presenting symptom was visual deficit (98%), including visual acuity loss, visual field deficit, or both. Bitemporal hemianopia was the most prevalent pattern of visual field loss from chiasmal involvement (16 cases [25%]), followed by homonymous hemianopia from optic tract involvement (12 cases [18%]). An afferent pupillary defect was present in 17 cases (26%). Sixteen patients (25%) experienced prior episodes of visual disturbance, and 7 (11%) of these had long-term fluctuation of their visual symptoms. Thirty-nine patients (60%) presented with a headache or retroorbital pain, and 15 of them (38%) had a history of headaches. Five patients presented with confusion, 4 with nausea, 2 with lethargy, 2 with gait disturbance, and 1 with endocrine disturbance. The onset of symptoms was acute (chiasmal apoplexy) in 38 patients (58%), subacute in 10 (15%), and progressive in 17 (26%). Nineteen of the 38 patients (50%) presenting with chiasmal apoplexy had prior episodes of acute headache and visual loss.

Radiographic Characteristics

In 39 patients with preoperative CT scans, the OPH CMs appeared as suprasellar hyperdense masses. Fifty-six percent of these lesions had calcification. Cerebral angiography studies for 33 patients did not reveal any arterial feeding vessels or early draining veins suggestive of arteriovenous malformations. Magnetic resonance imaging data were available for 52 patients, including T2 gradient echo scans in 32 instances. In 46 cases (88%), the lesion was described as heterogeneous with mixed signal intensities suggestive of different ages of blood. This appearance was often described as a “popcorn-like” lesion. A peripheral rim of hypointensity (hemosiderin ring) on T2-weighted images was reported in 31 cases (60%). Minimal or no enhancement occurred after the intravenous administration of Gd. Lesions of the optic nerve or tract tended to appear as a thickened nerve with an increase in diameter that was best seen on coronal images. Lesions of the chiasm or hypothalamus were characterized as focal and round suprasellar masses. Acute hemorrhage was reported in 35 patients (54%). Evidence of old or chronic bleeding, often discovered intraoperatively, was found in 18 patients (28%). Additional cerebral CMs were found in 10 patients (15%), including the patient newly described in this study. In this new case, there were multiple CMs within the OPH region: 1 from the optic chiasm and 1 from the left optic tract. Two patients presented with a subarachnoid hemorrhage, and 2 with intraventricular hemorrhage. Lesion sizes ranged from 0.5 to 4.0 cm.

In 22 (34%) of 65 patients, the initial preoperative radiographic diagnosis was difficult to make, and a CM was not suspected as the initial diagnosis. The differential diagnosis most commonly included craniopharyngioma, optic neuritis, or optic glioma.

Surgical Treatment and Outcomes

Most patients (97%) were treated surgically. Gross-total resection was performed in 39 cases (60%), STR in 4 (6%), biopsy procedure alone in 4 (6%), biopsy procedure with decompression of the hemorrhage in 15 (23%), and biopsy procedure followed by radiation in 1 case. Forty-three (75.4%) of 57 patients with outcome data experienced improvement in vision, 11 had stable vision (19.3%), and 3 had worsening vision (5.3%). For those who underwent GTR, 85% had visual improvement, 12% had no change, and 3% had worsened vision (Table 2). Of the 4 patients who underwent STR, 2 had visual improvement and 2 had no change. Biopsy procedure alone resulted in stable vision in 2 patients; there was no visual outcome data in the other 2 patients.61 Biopsy procedure with decompression resulted in a 77% rate of visual improvement, 15% visual stabilization, and 8% visual worsening. Biopsy procedure followed by radiation therapy resulted in visual stabilization in 1 patient.

TABLE 2:

Visual outcomes in patients with OPH CMs*

Treatment (no. of cases)% w/ Visual Improvement (no.)% w/ Visual Stabilization (no.)% w/ Visual Worsening (no.)No. w/ No Outcome Data
GTR (39)85 (30)12 (4)3 (1)4
STR (4)50 (2)50 (2)
Bx alone (4)100 (2)2
BxD (15)77 (10)15 (2)8 (1)2
Bx w/ rad (1)100 (1)
nonsurgical treatment (2)50 (1)50 (1)
overall (65)75.4 (43)19.3 (11)5.3 (3)8

* Percentages are based on patients with outcome data. — = not applicable.

A variety of operative approaches were used for the surgical removal of OPH CMs. An anterolateral approach (pterional, orbitozygomatic, or frontotemporal) was used in 76% of patients, and a midline transcranial approach (transbasal subfrontal or transbasal interhemispheric) in 17%. One patient underwent a frontoparietal approach, 1 a transcortical transventricular approach, and 1 an eyebrow keyhole craniotomy approach. There were 9 reports of opening the lamina terminalis (including our new case) to access the CM within the third ventricle.

Two patients were not treated surgically.2,8 One was treated with prednisone and acetazolamide for presumed optic neuritis with a fluctuating clinical course that ended in total blindness in 1 eye. The other patient was treated conservatively with observation for an unresectable lesion and experienced spontaneous total recovery of vision without surgical intervention. The duration of follow-up was available for just 26 cases described in the literature, with an average of 8 months (range 1 month–4 years).

Illustrative Case

History and Examination

This 50-year-old woman presented with progressive visual loss in both eyes (worse on the right) with a left temporal visual field deficit. Magnetic resonance imaging revealed a heterogeneously enhancing suprasellar mass involving the optic chiasm (Fig. 1). Gradient-echo sequences demonstrated blooming consistent with old hemorrhage. The radiographic diagnosis was consistent with a suprasellar CM of the optic chiasm located within the third ventricle. The patient also had an asymptomatic CM in the dorsal brainstem with an associated deep venous anomaly. Because the patient was losing vision in her right eye, resection was recommended.

Fig. 1.
Fig. 1.

Preoperative sagittal (A), coronal (B), and axial (D) post-Gd T1-weighted and axial gradient-echo (C) MR images demonstrating a heterogeneously enhancing suprasellar CM of the optic chiasm. Because the lesion was located within the third ventricle, a translamina terminalis approach was required to remove the lesion. Gradient-echo sequence (C) showing blooming consistent with hemosiderin deposition. There is an associated venous angioma located in the right posterolateral mesencephalon (D).

Operation

A right pterional transsylvian approach was used to expose the optic chiasm, optic nerves, and suprasellar cistern. The chiasm appeared tinged with brown, consistent with old hemosiderin; however, no obvious CM was visible within the surgical exposure. The lamina terminalis was, therefore, opened to explore the third ventricle. Within the ventricle, an abnormal mulberry-like lesion consistent with a CM was noted. The lesion, which extended to the right optic chiasm, was totally resected via careful microdissection with preservation of the optic chiasm and optic nerves. Further exploration of the third ventricle revealed another separate CM arising from the left optic tract, which was surgically removed. Complete resection was achieved for both lesions.

Postoperative Course

Pathological examination confirmed that both lesions were CMs (Fig. 2). Each malformation was surrounded by reactive changes including inflammation, fibrosis, and hemosiderin. Immunohistochemical staining was positive for CD34, indicating the endothelial lining of the CM. Elastin stain was negative, indicating the absence of an arterial component and thereby ruling out an arteriovenous malformation.

Fig. 2.
Fig. 2.

Histopathological examination of the suprasellar lesion. A: Photomicrograph demonstrating the CM with red blood cells dispersed in the field. B: Photomicrograph showing the surrounding reactive changes including inflammation, fibrosis, and hemosiderin. C: Immunohistochemical staining showing positivity of CD34, indicating the endothelial lining of the CM. D: Histochemical staining showing negativity to elastin, indicating the absence of an arterial component to distinguish the CM from an arteriovenous malformation. H & E (A and B), original magnification × 100 (A and B) and × 200 (C and D).

Postoperatively, the patient's visual acuity improved to 20/20 in the left eye and 20/50 in the right eye. The left temporal field deficit remained stable. There were no neurological deficits. Follow-up MR imaging studies at 2 years demonstrated complete removal of the CMs without any evidence of recurrence (Fig. 3).

Fig. 3.
Fig. 3.

Postoperative sagittal (A), axial (B), and coronal (C) post-Gd T1-weighted and coronal T2-weighted (D) MR images demonstrating complete resection of the optic chiasm CM. The optic chiasm is decompressed and well visualized on the coronal views (C and D). The associated venous angioma is again shown in the right posterolateral aspect of the mesencephalon (B).

Discussion

Cavernous malformations have an incidence of 0.3–0.7% in the general population,43,50 with < 1% of CMs appearing in the OPH region.21 Most patients present with symptoms in their 2nd–4th decade of life.54 There is generally no sex predilection, but hemorrhage reportedly occurs more frequently in females than in males (36 females: 25 males1). Optic pathway and hypothalamic CMs are usually brought to clinical attention by visual deterioration. Chiasmal apoplexy is the most common clinical presentation, characterized by sudden visual disturbance, headache, retroorbital pain, and nausea. Apoplectic symptoms are often preceded by transient blurred vision and headaches that occur weeks or months beforehand. Symptoms can also occur in a chronic or progressive manner with intermittent episodes of headache and visual loss. Chiasmal apoplexy is nearly always associated with acute hemorrhage.2 Transient or progressive symptoms are likely to result from recurrent episodes of hemorrhage and lesion growth;8 however, the fluctuation of visual symptoms may not necessarily be associated with radiographic documentation of hemorrhage.50

Natural History

The natural history of OPH CMs specifically is not clear, as most reported cases have been surgically treated. Nonetheless, we can attempt to extrapolate the natural history from data acquired in cerebral and brainstem CMs. The rate of hemorrhage for CMs, in general, ranges from 0.7% to 3.1% per year.43,54 Prior hemorrhage is a risk factor for subsequent bleeding, as rehemorrhage rates for cerebral CMs have been found to range from 3.8% to 22.9%.1,28 There is evidence that the rehemorrhage rate for an untreated bleed is high in the first 2–3 years but decreases thereafter.4 Although the hemorrhage and rehemorrhage rates for OPH CMs are not known, they are generally thought to be higher than those for cerebral lesions.31,44 A large study of brainstem CMs revealed a 5% per year hemorrhage rate and a 30% per year rehemorrhage rate.50 Other authors have reported brainstem rebleed rates of 17.7% per year with up to more than 1 hemorrhage per year.6,55 The significantly higher rebleed rates seen with brainstem CMs may be partially due to the eloquent nature of the surrounding tissue. Therefore, each bleeding event is likely to result in a clinically apparent neurological deficit. It is reasonable to consider OPH CMs in a similar fashion with a higher rebleed rate because of the eloquent location of the visual apparatus. Therefore, each hemorrhagic event is likely to result in a symptomatic visual deficit.

Neuroimaging Studies

Magnetic resonance imaging is the most sensitive and specific imaging modality for identifying CMs.53 These lesions usually appear as areas of mixed signal intensity with a hypointense rim. A typical “popcorn” appearance is characteristic of hemorrhagic components of different ages. Minimal or no enhancement occurs after the intravenous administration of Gd. Lesions of the optic nerve or tract may appear as nerve thickening on coronal views, whereas lesions in the chiasm or hypothalamus often appear as focal and round masses. Gradient-echo sequences are particularly sensitive to small hemorrhages and are ideal for detecting the presence of additional lesions in patients with multiple CMs.31 The hemosiderin rim appears particularly dark on T2 gradient-echo sequences.66 It is notable that peripheral hypointensity was not found in more than one-third of the cases providing detailed MR imaging information. The absence of the hemosiderin rim may have resulted from blood washout by CSF.47 On CT scans, OPH CMs appear as areas of hyperdensity with or without calcification and can sometimes mimic the appearance of a tumor or thrombosed aneurysm.58 Angiography does not typically show any pathological vessels. In some cases, however, an associated venous angioma (developmental venous anomaly) can be visualized.20,21

Differential Diagnosis

The differential diagnosis includes optic glioma, craniopharyngioma, meningioma, arteriovenous malformation, venous angioma, thrombosed aneurysm, pituitary apoplexy, and optic neuritis.9,39,44 Optic gliomas can cause enlargement of the optic nerve or chiasm but usually do not exhibit signs of hemorrhage.47 Intense enhancement after contrast administration is common for these lesions.23 Meningiomas of the optic nerve sheath typically appear as tram-tracking patterns of enhancement around the nerve.65 Craniopharyngiomas can appear cystic and/or solid with calcification on CT and typically enhance after contrast administration.11 Arteriovenous malformations and aneurysms can be distinguished from CMs by their visibility on angiography. Venous angiomas are commonly associated with brainstem CMs and may have a role in inducing their formation.5 Both contrast-enhanced MR imaging and angiography are useful in revealing associated venous angiomas (Fig. 1). The symptoms of pituitary apoplexy may resemble chiasmal apoplexy but can be distinguished by the presence of ocular paresis from cavernous sinus compression.45 Optic neuritis, which can cause acute visual loss, appears as an intensely enhanced optic nerve on fat-suppressed post-Gd T1-weighted MR imaging.3,8

Surgical Treatment, Timing, and Visual Outcomes

Gross-total resection is the gold standard of treatment, as any residual malformation can be at risk for rebleeding.12,22,31,44,47,59 Biopsy procedure alone is not recommended because of the risk of further bleeding and visual worsening.12,47 While decompression without complete resection has resulted in visual improvement, this stratThe lack of long-term follow-up data makes it difficult to evaluate rebleed rates or the durability of visual improvement following decompression or STR. Currently, there are not enough data to favor stereotactic radiosurgery as a primary treatment for OPH CM. The role of radiosurgery for CMs in general is still controversial. Recent evidence suggests that the risk of recurrent hemorrhage may be reduced after radiosurgery;35 however, radiation-related complications are greater for CMs than for arteriovenous malformations, even when adjusting for lesion size and radiation dosage.49 In cases of chiasmal apoplexy in which emergent surgical decompression of the optic apparatus is warranted, radiation therapy may not be the ideal form of treatment.

The timing for surgical intervention in OPH CMs may differ from that for malformations in other locations. For brainstem CMs in general, it has been advised to wait until 2 symptomatic hemorrhages have occurred before attempting resection. This strategy is based on the reasoning that only then will the risk of surgery be less than the risk of any morbidity associated with a subsequent hemorrhage.17 In some cases, however, earlier intervention may be more appropriate for OPH CMs.12,22,47 In patients with chiasmal apoplexy, emergent surgery (usually within 24 hours) is warranted to avoid permanent compressive damage to the visual pathway.31 Rapid diagnosis is important, as even total visual loss can improve if decompression of the optic apparatus is achieved promptly.46

Despite the critical location, excellent surgical outcomes can be achieved. Ninety-four percent of the patients treated surgically in the present study experienced visual improvement or stabilization. Visual acuity and visual field improved simultaneously most of the time. In the present study, the highest rate of visual improvement (85%) was achieved in those who underwent GTR (Table 2). Only 2 patients experienced worsening of their vision after total resection.

Surgical Approach

Lesions of the OPH present an operative challenge because of their deep and eloquent location in the brain. The optimal surgical approach should provide maximal exposure of the optic chiasm with the shortest distance to the lesion while using minimal brain retraction. One should be prepared to open the lamina terminalis and explore the third ventricle, as some of these malformations are located intraventricularly. In our case included in the present study, the lesion was not visualized on initial exposure of the optic chiasm until the lamina terminalis was entered. Access to the lamina terminalis can be achieved using anterolateral approaches (pterional, supraorbital, or orbitozygomatic) and midline approaches (transbasal subfrontal, or transbasal interhemispheric). The majority of cases reviewed in this study involved an anterolateral approach (45% frontotemporal, 42% pterional, and 13% orbitozygomatic). The orbitozygomatic approach is a natural extension of the pterional approach and offers a wider exposure, shorter distance to the target, and more inferior-to-superior viewing trajectory.16,56 The major disadvantage of anterolateral approaches to the lamina terminalis is the lack of midline orientation and lack of visualization of the ipsilateral wall of the third ventricle. In a midline approach to the lamina terminalis, both walls of the third ventricle and hypothalamus are well visualized for direct microdissection of the lesion.34

Conclusions

Cavernous malformations of the OPH are rare and challenging lesions. In cases of chiasmal apoplexy, emergent surgical removal is indicated to prevent permanent visual damage. Gross-total resection of these malformations is associated with favorable visual outcomes.

Disclosure

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author contributions to the study and manuscript preparation include the following. Conception and design: Liu, Delashaw. Acquisition of data: Liu, Lu, Raslan, Gultekin. Analysis and interpretation of data: all authors. Drafting the article: Liu, Lu, Raslan. Critically revising the article: Liu, Lu. Reviewed final version of the manuscript and approved it for submission: Liu, Delashaw. Statistical analysis: Liu.

Acknowledgments

The authors express their appreciation and thanks to Shirley McCartney, Ph.D., for editorial assistance, and Andy Rekito, M.S., for illustrative assistance.

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    Cerase A, , Franceschini R, , Battistini S, , Maria Vallone I, , Penco S, & Venturi C: Cavernous malformation of the optic nerve mimicking optic neuritis. J Neuroophthalmol 30:162131, 2010

    • Search Google Scholar
    • Export Citation
  • 9

    Christoforidis GA, , Bourekas EC, , Baujan M, , Drevelangas A, & Tzalonikou M: Neuroradiology case of the day. AJR Am J Roentgenol 175:888890, 2000

    • Search Google Scholar
    • Export Citation
  • 10

    Corboy JR, & Galetta SL: Familial cavernous angiomas manifesting with an acute chiasmal syndrome. Am J Ophthalmol 108:245250, 1989. (Erratum in Am J Ophthalmol 108:619, 1989)

    • Search Google Scholar
    • Export Citation
  • 11

    Curran JG, & O'Connor E: Imaging of craniopharyngioma. Childs Nerv Syst 21:635639, 2005

  • 12

    Deshmukh VR, , Albuquerque FC, , Zabramski JM, & Spetzler RF: Surgical management of cavernous malformations involving the cranial nerves. Neurosurgery 53:352357, 2003

    • Search Google Scholar
    • Export Citation
  • 13

    Escott EJ, , Rubinstein D, , Cajade-Law AG, & Sze CI: Suprasellar cavernous malformation presenting with extensive subarachnoid hemorrhage. Neuroradiology 43:313316, 2001

    • Search Google Scholar
    • Export Citation
  • 14

    Ferreira NP, & Ferreira MP: Optic nerve apoplexy caused by a cavernous angioma: case report. Neurosurgery 30:262264, 1992

  • 15

    Glastonbury CM, , Warner JEA, & MacDonald JD: Optochiasmal apoplexy from a cavernoma. Neurology 61:266, 2003

  • 16

    Gonzalez LF, , Crawford NR, , Horgan MA, , Deshmukh P, , Zabramski JM, & Spetzler RF: Working area and angle of attack in three cranial base approaches: pterional, orbitozygomatic, and maxillary extension of the orbitozygomatic approach. Neurosurgery 50:550557, 2002

    • Search Google Scholar
    • Export Citation
  • 17

    Gross BA, , Batjer HH, , Awad IA, & Bendok BR: Brainstem cavernous malformations. Neurosurgery 64:E805E818, 2009

  • 18

    Hankey GJ, & Khangure MS: Chiasmal apoplexy due to intrachiasmatic vascular malformation rupture. Aust N Z J Med 17:444446, 1987

  • 19

    Hasegawa H, , Bitoh S, , Koshino K, , Obashi J, , Kobayashi Y, & Kobayashi M, et al.: Mixed cavernous angioma and glioma (angioglioma) in the hypothalamus—case report. Neurol Med Chir (Tokyo) 35:238242, 1995

    • Search Google Scholar
    • Export Citation
  • 20

    Hassler W, , Zentner J, & Petersen D: Cavernous angioma of the optic nerve. Case report. Surg Neurol 31:444447, 1989

  • 21

    Hassler W, , Zentner J, & Wilhelm H: Cavernous angiomas of the anterior visual pathways. J Clin Neuroophthalmol 9:160164, 1989

  • 22

    Hempelmann RG, , Mater E, , Schröder F, & Schön R: Complete resection of a cavernous haemangioma of the optic nerve, the chiasm, and the optic tract. Acta Neurochir (Wien) 149:699703, 2007

    • Search Google Scholar
    • Export Citation
  • 23

    Hollander MD, , FitzPatrick M, , O'Connor SG, , Flanders AE, & Tartaglino LM: Optic gliomas. Radiol Clin North Am 37:5971, ix, 1999

  • 24

    Hufnagel TJ, & Cobbs WH: [Microangioma and optochiasmatic apoplexy. Description of an anatomo-clinical entity associating spontaneous hemorrhages of the anterior optic pathways and rupture of cryptic vascular anomalies.]. J Fr Ophtalmol 11:8184, 1988. (Fr)

    • Search Google Scholar
    • Export Citation
  • 25

    Hwang JF, , Yau CW, , Huang JK, & Tsai CY: Apoplectic optochiasmal syndrome due to intrinsic cavernous hemangioma. Case report. J Clin Neuroophthalmol 13:232236, 1993

    • Search Google Scholar
    • Export Citation
  • 26

    Iwai Y, , Yamanaka K, , Nakajima H, & Miyaura T: Cavernous angioma of the optic chiasm—case report. Neurol Med Chir (Tokyo) 39:617620, 1999

    • Search Google Scholar
    • Export Citation
  • 27

    Kehagias DT: A case of headache and disordered vision: cavernous hemangioma of the optic chiasm (2003:8b). Eur Radiol 13:25522553, 2003

    • Search Google Scholar
    • Export Citation
  • 28

    Kim DS, , Park YG, , Choi JU, , Chung SS, & Lee KC: An analysis of the natural history of cavernous malformations. Surg Neurol 48:918, 1997

  • 29

    Klein LH, , Fermaglich J, , Kattah J, & Luessenhop AJ: Cavernous hemangioma of optic chiasm, optic nerves and right optic tract. Case report and review of literature. Virchows Arch A Pathol Anat Histol 383:225231, 1979

    • Search Google Scholar
    • Export Citation
  • 30

    Kurokawa Y, , Abiko S, , Ikeda N, , Ideguchi M, & Okamura T: Surgical strategy for cavernous angioma in hypothalamus. J Clin Neurosci 8:Suppl 1 106108, 2001

    • Search Google Scholar
    • Export Citation
  • 31

    Lehner M, , Fellner FA, & Wurm G: Cavernous haemangiomas of the anterior visual pathways. Short review on occasion of an exceptional case. Acta Neurochir (Wien) 148:571578, 2006

    • Search Google Scholar
    • Export Citation
  • 32

    Lejeune JP, , Hladky JP, , Dupard T, , Parent M, , Hache JC, & Christiaens JL: [Opticochiasmatic apoplexy.]. Neurochirurgie 36:303307, 1990. (Fr)

    • Search Google Scholar
    • Export Citation
  • 33

    Little JR, , Awad IA, , Jones SC, & Ebrahim ZY: Vascular pressures and cortical blood flow in cavernous angioma of the brain. J Neurosurg 73:555559, 1990

    • Search Google Scholar
    • Export Citation
  • 34

    Liu JK, , Christiano LD, , Gupta G, & Carmel PW: Surgical nuances for removal of retrochiasmatic craniopharyngiomas via the transbasal subfrontal translamina terminalis approach. Neurosurg Focus 28:4 E6, 2010

    • Search Google Scholar
    • Export Citation
  • 35

    Lunsford LD, , Khan AA, , Niranjan A, , Kano H, , Flickinger JC, & Kondziolka D: Stereotactic radiosurgery for symptomatic solitary cerebral cavernous malformations considered high risk for resection. Clinical article. J Neurosurg [epub ahead of print February 19, 2010. DOI: 10.3171/2010.1.JNS081626]

    • Search Google Scholar
    • Export Citation
  • 36

    Maitland CG, , Abiko S, , Hoyt WF, , Wilson CB, & Okamura T: Chiasmal apoplexy. Report of four cases. J Neurosurg 56:118122, 1982

  • 37

    Malik S, , Cohen BH, , Robinson J, , Fried A, & Sila CA: Progressive vision loss. A rare manifestation of familial cavernous angiomas. Arch Neurol 49:170173, 1992

    • Search Google Scholar
    • Export Citation
  • 38

    Manz HJ, , Klein LH, , Fermaglich J, , Kattah J, & Luessenhop AJ: Cavernous hemangioma of optic chiasm, optic nerves, and right optic tract. Virchows Arch A Pathol Anat Histol 383:225231, 1979

    • Search Google Scholar
    • Export Citation
  • 39

    Maruoka N, , Yamakawa Y, & Shimauchi M: Cavernous hemangioma of the optic nerve. Case report. J Neurosurg 69:292294, 1988

  • 40

    Mizoi K, , Yoshimoto T, & Suzuki J: Clinical analysis of ten cases with surgically treated brain stem cavernous angiomas. Tohoku J Exp Med 166:259267, 1992

    • Search Google Scholar
    • Export Citation
  • 41

    Mizutani T, , Goldberg HI, , Kerson LA, & Murtagh F: Cavernous hemangioma in the diencephalon. Arch Neurol 38:379382, 1981

  • 42

    Mohr G, , Hardy J, & Gauvin P: Chiasmal apoplexy due to ruptured cavernous hemangioma of the optic chiasm. Surg Neurol 24:636640, 1985

  • 43

    Moriarity JL, , Wetzel M, , Clatterbuck RE, , Javedan S, , Sheppard JM, & Hoenig-Rigamonti K, et al.: The natural history of cavernous malformations: a prospective study of 68 patients. Neurosurgery 44:11661173, 1999

    • Search Google Scholar
    • Export Citation
  • 44

    Muta D, , Nishi T, , Koga K, , Yamashiro S, , Fujioka S, & Kuratsu JI: Cavernous malformation of the optic chiasm: case report. Br J Neurosurg 20:312315, 2006

    • Search Google Scholar
    • Export Citation
  • 45

    Nawar RN, , AbdelMannan D, , Selman WR, & Arafah BM: Pituitary tumor apoplexy: a review. J Intensive Care Med 23:7590, 2008

  • 46

    Newman H, , Nevo M, , Constantini S, , Maimon S, & Kesler A: Chiasmal cavernoma: a rare cause of acute visual loss improved by prompt surgery. Pediatr Neurosurg 44:414417, 2008

    • Search Google Scholar
    • Export Citation
  • 47

    Ozer E, , Kalemci O, , Yücesoy K, & Canda S: Optochiasmatic cavernous angioma: unexpected diagnosis. Case report. Neurol Med Chir (Tokyo) 47:128131, 2007

    • Search Google Scholar
    • Export Citation
  • 48

    Paladino J, , Rotim K, , Pirker N, , Gluncić V, , Jurić G, & Kalauz M: Minimally invasive treatment of cavernous angioma of the optic chiasm: case report. Minim Invasive Neurosurg 44:114116, 2001

    • Search Google Scholar
    • Export Citation
  • 49

    Pollock BE, , Garces YI, , Stafford SL, , Foote RL, , Schomberg PJ, & Link MJ: Stereotactic radiosurgery for cavernous malformations. J Neurosurg 93:987991, 2000

    • Search Google Scholar
    • Export Citation
  • 50

    Porter RW, , Detwiler PW, , Spetzler RF, , Lawton MT, , Baskin JJ, & Derksen PT, et al.: Cavernous malformations of the brainstem: experience with 100 patients. J Neurosurg 90:5058, 1999

    • Search Google Scholar
    • Export Citation
  • 51

    Regli L, , de Tribolet N, , Regli F, & Bogousslavsky J: Chiasmal apoplexy: haemorrhage from a cavernous malformation in the optic chiasm. J Neurol Neurosurg Psychiatry 52:10951099, 1989

    • Search Google Scholar
    • Export Citation
  • 52

    Reilly PL, & Oatey PE: Optic nerve apoplexy. Report of two cases. J Neurosurg 64:313316, 1986

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    Rigamonti D, , Drayer BP, , Johnson PC, , Hadley MN, , Zabramski J, & Spetzler RF: The MRI appearance of cavernous malformations (angiomas). J Neurosurg 67:518524, 1987

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    Robinson JR, , Awad IA, & Little JR: Natural history of the cavernous angioma. J Neurosurg 75:709714, 1991

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    Samii M, , Eghbal R, , Carvalho GA, & Matthies C: Surgical management of brainstem cavernomas. J Neurosurg 95:825832, 2001

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    Shibuya M, , Baskaya MK, , Saito K, , Suzuki Y, , Ooka K, & Hara M: Cavernous malformations of the optic chiasma. Acta Neurochir (Wien) 136:2936, 1995

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    Steinberg GK, , Marks MP, , Shuer LM, , Sogg RL, , Enzmann DR, & Silverberg GD: Occult vascular malformations of the optic chiasm: magnetic resonance imaging diagnosis and surgical laser resection. Neurosurgery 27:466470, 1990

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    Suarez B, , Carlier R, , Gilbert D, , Parker F, , Lacroix C, & Doyon D: Suprasellar cavernous haemangioma: an important differential diagnosis in the diencephalic tumours. Eur Radiol 4:470473, 1994

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    Tien R, & Dillon WP: MR imaging of cavernous hemangioma of the optic chiasm. J Comput Assist Tomogr 13:10871088, 1989

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    Wang CH, , Lin SM, , Chen Y, & Tseng SH: Multiple deep-seated cavernomas in the third ventricle, hypothalamus and thalamus. Acta Neurochir (Wien) 145:505508, 2003

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    Warner JE, , Rizzo JF III, , Brown EW, & Ogilvy CS: Recurrent chiasmal apoplexy due to cavernous malformation. J Neuroophthalmol 16:99106, 1996

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    Wilms G, , Lammens M, , Marchal G, , Van Calenbergh F, , Plets C, & Van Fraeyenhoven L, et al.: Thickening of dura surrounding meningiomas: MR features. J Comput Assist Tomogr 13:763768, 1989

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    Wurm G, & Fellner FA: Implementation of T2*-weighted MR for multimodal image guidance in cerebral cavernomas. Neuroimage 22:841846, 2004

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    Yoshimoto T, & Suzuki J: Radical surgery on cavernous angioma of the brainstem. Surg Neurol 26:7278, 1986

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    Zentner J, , Grodd W, & Hassler W: Cavernous angioma of the optic tract. J Neurol 236:117119, 1989

  • View in gallery

    Preoperative sagittal (A), coronal (B), and axial (D) post-Gd T1-weighted and axial gradient-echo (C) MR images demonstrating a heterogeneously enhancing suprasellar CM of the optic chiasm. Because the lesion was located within the third ventricle, a translamina terminalis approach was required to remove the lesion. Gradient-echo sequence (C) showing blooming consistent with hemosiderin deposition. There is an associated venous angioma located in the right posterolateral mesencephalon (D).

  • View in gallery

    Histopathological examination of the suprasellar lesion. A: Photomicrograph demonstrating the CM with red blood cells dispersed in the field. B: Photomicrograph showing the surrounding reactive changes including inflammation, fibrosis, and hemosiderin. C: Immunohistochemical staining showing positivity of CD34, indicating the endothelial lining of the CM. D: Histochemical staining showing negativity to elastin, indicating the absence of an arterial component to distinguish the CM from an arteriovenous malformation. H & E (A and B), original magnification × 100 (A and B) and × 200 (C and D).

  • View in gallery

    Postoperative sagittal (A), axial (B), and coronal (C) post-Gd T1-weighted and coronal T2-weighted (D) MR images demonstrating complete resection of the optic chiasm CM. The optic chiasm is decompressed and well visualized on the coronal views (C and D). The associated venous angioma is again shown in the right posterolateral aspect of the mesencephalon (B).

  • 1

    Aiba T, , Tanaka R, , Koike T, , Kameyama S, , Takeda N, & Komata T: Natural history of intracranial cavernous malformations. J Neurosurg 83:5659, 1995

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  • 2

    Arrué P, , Thorn-Kany M, , Vally P, , Lacroix F, , Delisle MB, & Lagarrigue J, et al.: Cavernous hemangioma of the intracranial optic pathways: CT and MRI. J Comput Assist Tomogr 23:357361, 1999

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  • 3

    Atkins EJ, , Biousse V, & Newman NJ: The natural history of optic neuritis. Rev Neurol Dis 3:4556, 2006

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    Barker FG II, , Amin-Hanjani S, , Butler WE, , Lyons S, , Ojemann RG, & Chapman PH, et al.: Temporal clustering of hemorrhages from untreated cavernous malformations of the central nervous system. Neurosurgery 49:1525, 2001

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    Batra S, , Lin D, , Recinos PF, , Zhang J, & Rigamonti D: Cavernous malformations: natural history, diagnosis and treatment. Nat Rev Neurol 5:659670, 2009

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    Bruneau M, , Bijlenga P, , Reverdin A, , Rilliet B, , Regli L, & Villemure JG, et al.: Early surgery for brainstem cavernomas. Acta Neurochir (Wien) 148:405414, 2006

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  • 7

    Castel JP, , Delorge-Kerdiles C, & Rivel J: [Cavernous angioma of the optic chiasm.]. Neurochirugie 35:252256, 1989. (Fr)

  • 8

    Cerase A, , Franceschini R, , Battistini S, , Maria Vallone I, , Penco S, & Venturi C: Cavernous malformation of the optic nerve mimicking optic neuritis. J Neuroophthalmol 30:162131, 2010

    • Search Google Scholar
    • Export Citation
  • 9

    Christoforidis GA, , Bourekas EC, , Baujan M, , Drevelangas A, & Tzalonikou M: Neuroradiology case of the day. AJR Am J Roentgenol 175:888890, 2000

    • Search Google Scholar
    • Export Citation
  • 10

    Corboy JR, & Galetta SL: Familial cavernous angiomas manifesting with an acute chiasmal syndrome. Am J Ophthalmol 108:245250, 1989. (Erratum in Am J Ophthalmol 108:619, 1989)

    • Search Google Scholar
    • Export Citation
  • 11

    Curran JG, & O'Connor E: Imaging of craniopharyngioma. Childs Nerv Syst 21:635639, 2005

  • 12

    Deshmukh VR, , Albuquerque FC, , Zabramski JM, & Spetzler RF: Surgical management of cavernous malformations involving the cranial nerves. Neurosurgery 53:352357, 2003

    • Search Google Scholar
    • Export Citation
  • 13

    Escott EJ, , Rubinstein D, , Cajade-Law AG, & Sze CI: Suprasellar cavernous malformation presenting with extensive subarachnoid hemorrhage. Neuroradiology 43:313316, 2001

    • Search Google Scholar
    • Export Citation
  • 14

    Ferreira NP, & Ferreira MP: Optic nerve apoplexy caused by a cavernous angioma: case report. Neurosurgery 30:262264, 1992

  • 15

    Glastonbury CM, , Warner JEA, & MacDonald JD: Optochiasmal apoplexy from a cavernoma. Neurology 61:266, 2003

  • 16

    Gonzalez LF, , Crawford NR, , Horgan MA, , Deshmukh P, , Zabramski JM, & Spetzler RF: Working area and angle of attack in three cranial base approaches: pterional, orbitozygomatic, and maxillary extension of the orbitozygomatic approach. Neurosurgery 50:550557, 2002

    • Search Google Scholar
    • Export Citation
  • 17

    Gross BA, , Batjer HH, , Awad IA, & Bendok BR: Brainstem cavernous malformations. Neurosurgery 64:E805E818, 2009

  • 18

    Hankey GJ, & Khangure MS: Chiasmal apoplexy due to intrachiasmatic vascular malformation rupture. Aust N Z J Med 17:444446, 1987

  • 19

    Hasegawa H, , Bitoh S, , Koshino K, , Obashi J, , Kobayashi Y, & Kobayashi M, et al.: Mixed cavernous angioma and glioma (angioglioma) in the hypothalamus—case report. Neurol Med Chir (Tokyo) 35:238242, 1995

    • Search Google Scholar
    • Export Citation
  • 20

    Hassler W, , Zentner J, & Petersen D: Cavernous angioma of the optic nerve. Case report. Surg Neurol 31:444447, 1989

  • 21

    Hassler W, , Zentner J, & Wilhelm H: Cavernous angiomas of the anterior visual pathways. J Clin Neuroophthalmol 9:160164, 1989

  • 22

    Hempelmann RG, , Mater E, , Schröder F, & Schön R: Complete resection of a cavernous haemangioma of the optic nerve, the chiasm, and the optic tract. Acta Neurochir (Wien) 149:699703, 2007

    • Search Google Scholar
    • Export Citation
  • 23

    Hollander MD, , FitzPatrick M, , O'Connor SG, , Flanders AE, & Tartaglino LM: Optic gliomas. Radiol Clin North Am 37:5971, ix, 1999

  • 24

    Hufnagel TJ, & Cobbs WH: [Microangioma and optochiasmatic apoplexy. Description of an anatomo-clinical entity associating spontaneous hemorrhages of the anterior optic pathways and rupture of cryptic vascular anomalies.]. J Fr Ophtalmol 11:8184, 1988. (Fr)

    • Search Google Scholar
    • Export Citation
  • 25

    Hwang JF, , Yau CW, , Huang JK, & Tsai CY: Apoplectic optochiasmal syndrome due to intrinsic cavernous hemangioma. Case report. J Clin Neuroophthalmol 13:232236, 1993

    • Search Google Scholar
    • Export Citation
  • 26

    Iwai Y, , Yamanaka K, , Nakajima H, & Miyaura T: Cavernous angioma of the optic chiasm—case report. Neurol Med Chir (Tokyo) 39:617620, 1999

    • Search Google Scholar
    • Export Citation
  • 27

    Kehagias DT: A case of headache and disordered vision: cavernous hemangioma of the optic chiasm (2003:8b). Eur Radiol 13:25522553, 2003

    • Search Google Scholar
    • Export Citation
  • 28

    Kim DS, , Park YG, , Choi JU, , Chung SS, & Lee KC: An analysis of the natural history of cavernous malformations. Surg Neurol 48:918, 1997

  • 29

    Klein LH, , Fermaglich J, , Kattah J, & Luessenhop AJ: Cavernous hemangioma of optic chiasm, optic nerves and right optic tract. Case report and review of literature. Virchows Arch A Pathol Anat Histol 383:225231, 1979

    • Search Google Scholar
    • Export Citation
  • 30

    Kurokawa Y, , Abiko S, , Ikeda N, , Ideguchi M, & Okamura T: Surgical strategy for cavernous angioma in hypothalamus. J Clin Neurosci 8:Suppl 1 106108, 2001

    • Search Google Scholar
    • Export Citation
  • 31

    Lehner M, , Fellner FA, & Wurm G: Cavernous haemangiomas of the anterior visual pathways. Short review on occasion of an exceptional case. Acta Neurochir (Wien) 148:571578, 2006

    • Search Google Scholar
    • Export Citation
  • 32

    Lejeune JP, , Hladky JP, , Dupard T, , Parent M, , Hache JC, & Christiaens JL: [Opticochiasmatic apoplexy.]. Neurochirurgie 36:303307, 1990. (Fr)

    • Search Google Scholar
    • Export Citation
  • 33

    Little JR, , Awad IA, , Jones SC, & Ebrahim ZY: Vascular pressures and cortical blood flow in cavernous angioma of the brain. J Neurosurg 73:555559, 1990

    • Search Google Scholar
    • Export Citation
  • 34

    Liu JK, , Christiano LD, , Gupta G, & Carmel PW: Surgical nuances for removal of retrochiasmatic craniopharyngiomas via the transbasal subfrontal translamina terminalis approach. Neurosurg Focus 28:4 E6, 2010

    • Search Google Scholar
    • Export Citation
  • 35

    Lunsford LD, , Khan AA, , Niranjan A, , Kano H, , Flickinger JC, & Kondziolka D: Stereotactic radiosurgery for symptomatic solitary cerebral cavernous malformations considered high risk for resection. Clinical article. J Neurosurg [epub ahead of print February 19, 2010. DOI: 10.3171/2010.1.JNS081626]

    • Search Google Scholar
    • Export Citation
  • 36

    Maitland CG, , Abiko S, , Hoyt WF, , Wilson CB, & Okamura T: Chiasmal apoplexy. Report of four cases. J Neurosurg 56:118122, 1982

  • 37

    Malik S, , Cohen BH, , Robinson J, , Fried A, & Sila CA: Progressive vision loss. A rare manifestation of familial cavernous angiomas. Arch Neurol 49:170173, 1992

    • Search Google Scholar
    • Export Citation
  • 38

    Manz HJ, , Klein LH, , Fermaglich J, , Kattah J, & Luessenhop AJ: Cavernous hemangioma of optic chiasm, optic nerves, and right optic tract. Virchows Arch A Pathol Anat Histol 383:225231, 1979

    • Search Google Scholar
    • Export Citation
  • 39

    Maruoka N, , Yamakawa Y, & Shimauchi M: Cavernous hemangioma of the optic nerve. Case report. J Neurosurg 69:292294, 1988

  • 40

    Mizoi K, , Yoshimoto T, & Suzuki J: Clinical analysis of ten cases with surgically treated brain stem cavernous angiomas. Tohoku J Exp Med 166:259267, 1992

    • Search Google Scholar
    • Export Citation
  • 41

    Mizutani T, , Goldberg HI, , Kerson LA, & Murtagh F: Cavernous hemangioma in the diencephalon. Arch Neurol 38:379382, 1981

  • 42

    Mohr G, , Hardy J, & Gauvin P: Chiasmal apoplexy due to ruptured cavernous hemangioma of the optic chiasm. Surg Neurol 24:636640, 1985

  • 43

    Moriarity JL, , Wetzel M, , Clatterbuck RE, , Javedan S, , Sheppard JM, & Hoenig-Rigamonti K, et al.: The natural history of cavernous malformations: a prospective study of 68 patients. Neurosurgery 44:11661173, 1999

    • Search Google Scholar
    • Export Citation
  • 44

    Muta D, , Nishi T, , Koga K, , Yamashiro S, , Fujioka S, & Kuratsu JI: Cavernous malformation of the optic chiasm: case report. Br J Neurosurg 20:312315, 2006

    • Search Google Scholar
    • Export Citation
  • 45

    Nawar RN, , AbdelMannan D, , Selman WR, & Arafah BM: Pituitary tumor apoplexy: a review. J Intensive Care Med 23:7590, 2008

  • 46

    Newman H, , Nevo M, , Constantini S, , Maimon S, & Kesler A: Chiasmal cavernoma: a rare cause of acute visual loss improved by prompt surgery. Pediatr Neurosurg 44:414417, 2008

    • Search Google Scholar
    • Export Citation
  • 47

    Ozer E, , Kalemci O, , Yücesoy K, & Canda S: Optochiasmatic cavernous angioma: unexpected diagnosis. Case report. Neurol Med Chir (Tokyo) 47:128131, 2007

    • Search Google Scholar
    • Export Citation
  • 48

    Paladino J, , Rotim K, , Pirker N, , Gluncić V, , Jurić G, & Kalauz M: Minimally invasive treatment of cavernous angioma of the optic chiasm: case report. Minim Invasive Neurosurg 44:114116, 2001

    • Search Google Scholar
    • Export Citation
  • 49

    Pollock BE, , Garces YI, , Stafford SL, , Foote RL, , Schomberg PJ, & Link MJ: Stereotactic radiosurgery for cavernous malformations. J Neurosurg 93:987991, 2000

    • Search Google Scholar
    • Export Citation
  • 50

    Porter RW, , Detwiler PW, , Spetzler RF, , Lawton MT, , Baskin JJ, & Derksen PT, et al.: Cavernous malformations of the brainstem: experience with 100 patients. J Neurosurg 90:5058, 1999

    • Search Google Scholar
    • Export Citation
  • 51

    Regli L, , de Tribolet N, , Regli F, & Bogousslavsky J: Chiasmal apoplexy: haemorrhage from a cavernous malformation in the optic chiasm. J Neurol Neurosurg Psychiatry 52:10951099, 1989

    • Search Google Scholar
    • Export Citation
  • 52

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