The caverno-apical triangle: anatomic-pathological considerations and pictorial review

    The Caverno-apical Triangle: Anatomic-pathological Considerations and Pictorial Review Jared Narvid MD, Jason F. Talbott MD, PhD, Christine M. Glastonbury MD PII: DOI: Reference:

S0899-7071(15)00222-3 doi: 10.1016/j.clinimag.2015.08.005 JCT 7899

To appear in:

Journal of Clinical Imaging

Received date: Revised date: Accepted date:

9 March 2015 4 August 2015 12 August 2015

Please cite this article as: Narvid Jared, Talbott Jason F., Glastonbury Christine M., The Caverno-apical Triangle: Anatomic-pathological Considerations and Pictorial Review, Journal of Clinical Imaging (2015), doi: 10.1016/j.clinimag.2015.08.005

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ACCEPTED MANUSCRIPT The Caverno-apical Triangle: Anatomic-pathological Considerations and Pictorial Review

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Jared Narvid MD, Jason F. Talbott MD PhD, Christine M.Glastonbury MD Division of Neuroradiology

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Department of Radiology and Biomedical Imaging

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University of California, San Francisco San Francisco, CA

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Correspondence to: Jared Narvid, MD

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Neuroradiology

Tel: 415-353-1863

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FAX: 415-353-8606

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San Francisco, CA 94143-0628

[email protected]

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505 Parnassus Avenue, L-352

ACCEPTED MANUSCRIPT Abstract: Background: The caverno-apical triangle (CAT) is defined from the components that define its contours: the cavernous sinus and the orbital apex. A wide range of pathologies arise from the space between the cavernous sinus and the orbital apex. Object: To better define radiologically this critical anatomic landmark and establish an organized approach for image analysis to help generate focused differential diagnoses and accurately characterize lesions found

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on imaging Conclusion: We have identified common imaging characteristics of frequently encountered lesions and

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divided them into specific categories to facilitate creation of logical and focused differential diagnoses.

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Keywords: cavernous sinus, orbital apex, skull base

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Introduction The caverno-apical triangle (CAT) is defined from its shape and the components that delineate its contours: the cavernous sinus and the orbital apex. A wide range of pathologies may arise from the space between the cavernous sinus and the orbital apex. Detection and appropriate characterization of pathology at the caverno-apical triangle remains vital as pathology can affect critically important structures often progressing intracranially and within the orbit. Moreover, this region remains a challenging location for operative biopsy and the procurement of tissue diagnosis. Accordingly, the informed radiologist can guide clinical management by alerting clinicians to the involvement of local anatomic structures and by generating an appropriate differential diagnosis. Despite this, the caverno-apical triangle has not been previously described in the literature as a distinct anatomic landmark and because of its small size, can be readily overlooked on imaging. Clinical findings of CAT lesions are variable including orbital apex and cavernous sinus syndromes but these lesions can also be asymptomatic. Moreover, the clinically important anatomic relations in this area may result in high morbidity. CT and MRI are complementary in formulating limited differential and sometimes precise diagnoses and in defining the relationship with adjacent neurovascular structures to guide the surgical approach. As a broad range of lesions can occur here, our purpose is to better define radiologically this critical anatomic landmark and establish an organized approach for image analysis to help generate focused differential diagnoses and accurately characterize lesions found on imaging.

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Normal Anatomy and Contents The CAT forms part of the anteromedial aspect of the middle cranial fossa. Its name is defined from the components that define its contours: the cavernous sinus and the orbital apex. This triangular shaped region is formed by the cavernous sinus anterior to Meckel cave and extends to the superior orbital fissure (SOF) where the III, IV, Vi, and VI cranial nerves enter the orbital apex superolateral to optic nerve (Figure 1). The bony confines of the CAT are formed by the greater and lesser wings of the sphenoid bone which project transversely from the sphenoid corpus, bending superiorly in their anterior portion and contain foramina through which the cranial nerves exit. The lesser wings are two thin triangular plates of bone arising from the anterior aspect of the sphenoid bone. The inferior surface constitutes a portion of the superior wall of the orbit and overhangs the superior orbital fissure, the elongated opening between the wings. The posterior CAT is formed at the anterior cavernous sinus in the plane of the carotico-clinoid foramen (Henle) [1]. The posterior roof of the CAT is formed by the surgical carotico-oculomotor triangle at the level of the anterior clinoid process [2]. More noteworthy is an understanding of the anatomic relationships between the anterior cavernous sinus and its connecting foramina that serve as neurovascular channels to the orbit and thus permit egress of pathology along natural anatomic conduits. The SOF is situated between the greater and lesser wings and body of the sphenoid bone. At the fissure, the dura covering the middle fossa and cavernous sinus blends into the periorbita of the orbital apex and the annular tendon of Zinn from which the extraocular muscles arise [3]. The lateral margin of the SOF and CAT, sometimes referred to as the horizontal meningeal limb is covered by the frontotemporal dural fold [4]. It is important to note, however, that the foramen for the ophthalmomeningeal vein (Hyrtl) is situated in the greater wing and may form the lateral CAT, usually connecting the lateral half of the orbit with cerebral veins and cavernous sinus. A meningolacrimal artery may also pass through this foramen and supply lacrimal territory [5]. The anterior CAT is formed as an osseous tunnel for the numerous neurovascular structures entering the orbital apex and associated with the annulus of Zinn and posterior muscle cone [6]. Clinical Presentation of Lesions: Symptoms associated with CAT lesions are myriad but can be absent as well. Involvement of the anterior cavernous sinus can produce cranial neuropathies equivalent to the cavernous sinus syndrome. Various combinations of Horner’s syndromes, oculomotor palsy and facial sensory loss can be seen [7]. Similarly, the orbital apex syndrome has been described wherein ophthalmoplegia is

ACCEPTED MANUSCRIPT combined with optic nerve dysfunction [8]. All such symptoms may be accompanied by ophthalmologic red flags pointing to a retro-bulbar lesion [9].

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Materials and Methods A database of exemplary lesions is maintained by the UCSF Department of Radiology and Biomedical Imaging as a collaborative effort between Laboratory for Radiological Informatics and AGFA Medical Imaging, UCSF Digital Teaching File. Subsequent to query of this database, electronic medical records of patients presenting to the tertiary referral center, UCSF, and the San Francisco General Hosital were reviewed. This study qualified for exempt/waived requirement for informed consent under UCSF institutional review board guidelines.

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Range of Pathological Lesions of the CAT

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From our collection of cases from 3 hospitals, and on review of the available literature we created an imaging guide to creating a differential diagnosis of the common and unusual CAT lesion (Table 1). The table may be of value for reminding radiologists of the varied pathologies and specific features of each.

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Meningiomas

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Parasellar meningiomas account for 5-10% of meningiomas, and these are also the most frequent tumor in the cavernous sinus [10]. At CT and MRI examination they usually show a broad dural basis and strong enhancement (Figure 2). They are iso-hyperintense on T2-weighted imaging and markedly hyperintense on arterial spin labeling (ASL) [11]. However, psammomatous meningiomas can be heavily calcified and lack contrast enhancement and ASL hyperintensity. These meningiomas characteristically are dense on CT images. FLAIR images may also demonstrate expansion of the anterior cavernous sinus and loss of hyperintense clinoidal and apical fat (Figure 3). They may demonstrate mass effect by constricting the lumen of the ICA, a relatively specific sign [12]. Adjacent hyperostosis is characteristic. Meningiomas that involve the CAT are more difficult to excise given their concomitant involvement of both cavernous sinus and orbital apex [13,14]. Those meningiomas within the CAT which present operative risk are increasingly treated with stereotactic or conformal fractionated radiation therapy. When tumor is within close proximity to the optic nerve, high dose single fraction radiosurgery is contraindicated secondary to the high risk of radiation induced optic neuropathy (RION) [15]. Thus, the anatomic location within the CAT may inform treatment options. Peripheral nerve-sheath tumors (schwannomas) Schwannomas comprise 1% of all neoplasms of the orbital apex [16]. They are typically slow growing masses which are sharply circumscribed and extend along the axis of the involved nerve (Figure 4). Schwannomas are typically hyperintense on T2-weighted images with heterogeneous contrast enhancement (Figure 5). A particularly useful differentiating feature is that the enhancement occurs in regions of low T2 and iso-intense T1 signal [17]. Within the CAT, these lesions tend to enlarge the vertical neural limb of the SOF with smooth bony erosion which distorts their normal spindle appearance into that of an hourglass (Figure 6). Perineural Tumor Spread Perineural tumor spread (PNTS) is a well-recognized pathological behavior of many head and neck (HN) cancers, and represents the dissemination of tumor from the primary site via the nerve and neural sheath as a mode of metastasis. The common HN culprits include cutaneous squamous cell and basal cell carcinoma and melanoma (particularly desmoplastic melanoma), mucosal primary tumors such as squamous cell carcinoma and nasopharyngeal carcinoma, salivary gland malignancies (especially adenoid cystic carcinoma), and lymphoma. Among patients with PNTS, 40%

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may be asymptomatic which puts the onus on the radiologists to be vigilant to its presence [18]. Detection of PNTS has important therapeutic implications either directing the surgeon to additionally involved areas or permitting recognition of unresectable disease. PNS most often occurs along the branches of the trigeminal nerves (CNV) and facial nerve (CNVII). Within the context of the CAT, two anatomically and pathologically distinct subtypes of PNTS can be distinguished. First, CNV1 divides into the nasociliary, frontal, and lacrimal nerves just before it enters the orbit via the SOF. Forehead skin tumors such as basal cell carcinoma thus can spread via the frontal nerve toward the CAT (Figure 7). These can extend intracranially through the SOF. Following orbital exenteration, careful evaluation of the CAT is critical for identifying potential recurrence on surveillance imaging (Figure 8). Second, PNTS can involve branches of CNV2 extending intracranially along foramen rotundum. Typical malignancies that involve CNV2 are cutaneous malignancies, mucosal squamous cell malignancies, and minor salivary gland tumors. Knowledge of the site of primary tumor allows for careful examination of the appropriate local nerves for enhancement, nerve thickening, and foraminal enlargement. On the other hand, involvement of the CAT can alert the radiologists to look for cutaneous malignancies of the eye, nose, and cheek; tumors of the maxillary or ethmoid sinuses; tumors of the palate and nasopharynx; and involvement of pterygopalatine fossa.

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Inflammatory Processes Neurosarcoid

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Sarcoidosis is an idiopathic inflammatory disorder characterized histopathologically by noncaseating granulomas and epitheliod proliferation [19]. Up to 80% of patients affected by systemic sarcoid will have involvement of the orbit, often involving the orbital apex and CAT [20]. Thickening of the optic nerve can be seen with characteristic low T2 inflammatory changes (Figure 9). Optic nerve involvement, uveal involvement, and nodular pachymeningeal thickening are findings that are most specific for sarcoid. In addition, orbital sarcoid and idiopathic orbital inflammatory disease often present as enlargement and enhancement of the lacrimal glands. A CAT lesion with lacrimal changes should raise suspicion for these diagnoses. Granulomatosis with polyangitis (GPA)

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Granulomatosis with polyangitis (previously known as Wegener granulomatosis) has a predilection for the upper and lower respiratory tracts and kidneys, although patients frequently exhibit HN manifestations (72-99% of cases) and less commonly CNS disease (22-54%)[21] [22]. Although the diagnosis of patients with systemic disease is supported by the often elevated ANCA/anti-PR3, patients with chronic isolated head and neck manifestations lack autoantibodies, thereby raising the stakes for radiologic diagnosis [21]. Like sarcoid, chronic inflammation can give rise to T2 hypointense inflammatory/fibrous tissue (Figure 10). Unlike sarcoid, GPA often produces sinonasal bony destructive changes not typical of other lesions centered in the CAT [23]. Idiopathic orbital inflammatory disease (IOI) Idiopathic orbital inflammatory disease, also previously known as pseudotumor, is an autoimmune phenomenon of unclear etiology consisting of orbit inflammation with infiltration of myofibroblasts and spindle cells [24]. There are six different distributions of inflammation in orbital pseudotumor, defined by the anatomic structures that are involved: the dacritis form affects the lacrimal glands, the myositis form (the most common) affects the muscles, the neuritis form affects the optic nerve sheath, the apical form affects the posterior orbit, the episcleral form affects the anterior orbit, and the diffuse form affects the entire orbit. When occurring at the orbital apex and cavernoapical triangle this entity has been termed Tolosa–Hunt syndrome [25]. Tolosa-Hunt syndrome is a painful ophthalmoplegia caused by inflammation of the cavernous sinus or SOF. It has been proposed to be the result of exaggerated immunological process triggered

ACCEPTED MANUSCRIPT by viral or bacterial infection [26]. Accordingly, these inflammatory processes can involve the CAT beginning either within the orbital apex or anterior cavernous sinus (Figure 11) and extending into the pterygopalantine fossa (Figure 12). Infection

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Invasive fungal sinusitis most commonly occurs in the setting of uncontrolled diabetes (6080%) or in patients otherwise immune-compromised by neutropenia or HIV [27]. Aspergillus and mucormycosis constitute the overwhelming majority of responsible fungal organisms. Clinically, headache and facial pain are typically out of proportion to the clinical evaluation and the often subtle imaging findings. Ulceration of the nasal cavity or eschar are specific clinical and radiologic signs [28]. Prompt treatment is necessary to avoid vision loss and death and includes intravenous amphotericin B, surgical debridement, and sometimes hyperbaric oxygen therapy and/or orbital exenteration. On MRI, signal intensity is variable on T1- and T2- weighted sequences due to varying degrees of edema and fungal elements Invasive disease appears as hypointense masses on T1and T2-weighted sequences that lack enhancement on post-contrast sequences (Figure 13) [29] [30] [31]. Hypointense signal often reflects necrotic, devitalized tissues associated the angioinvasive nature of invasive fungal disease [32]. In addition, invasion into the cavernous sinus can compromise the cavernous carotid artery giving rise to infective pseudoaneurysms [33]. CT may also show osteolysis at the sphenoid wall, optic strut, and SOF. Vascular

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Complex orbitofacial arteriovenous malformations can be seen as a part of the cerebro-facial metameric syndromes (CAMSs) as originally described and common to cases involving arteriovenous malformations of the brain and orbit (Bonnet-Dechaume-Blanc or Wyburn-Mason syndrome) [34]. These often involve abnormal high-flow vascularity extending through the CAT to involve both orbit and brain. However, this appearance can also been found in dural arteriovenous fistulae of the orbital apex often supplied by the meningolacrimal artery and draining to the superior ophthalmic vein (Figure 14) [35].

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Cavernous sinus fistulas, like all arteriovenous fistulas, represent abnormal communications between arterial and venous blood circulations, either directly between the ICA lumen and the cavernous sinus or indirectly between branches of the ICA and /or ECA and the cavernous sinus. The former direct connection between ICA and cavernous sinus are termed carotid cavernous fistulas (CCFs), whereas communications linking the cavernous sinus and dural arterial supply are more aptly termed dural arteriovenous fistulas (DAVF) of the cavernous sinus. Although both direct CCFs and DAVFs may cause similar symptoms, namely pulsating exophthalmos, they represent in terms of etiology and pathogenesis entirely different lesions [36]. Direct CCFs arise either traumatically or via rupture of a spontaneous cavernous carotid aneurysm; while numerous etiologies have been suggested for DAVFs including hormonal, coagulopathic/thrombotic, and traumatic possibilities [37]. Nevertheless, both types may produce expansion and contrast enhancement on both CT and MRI of the CAT. Intracranial extracerebral hemangiomas arising from the cavernous sinus are rare lesions. They are well demarcated, expansive, T2 hyperintense and can be prone to severe intraoperative bleeding which as raised interest in Gamma Knife radiosurgery as a treatment [38]. As such, preoperative diagnosis is critical [39] although differentiation from meningioma can be challenging [40]. A profoundly and homogenous T2 CAT lesion with heterogenous enhancement should raise the possibility of a cavernous sinus cavernous hemangioma (CSCH) [41] (Figure 15). Conclusion Accurate characterization and categorization of pathology at the caverno-apical triangle is clinically relevant, as CAT lesions may cause both intraorbital and intracranial morbidity. We have

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identified common imaging characteristics of the most frequently encountered lesions at our institution and divided them into specific categories to facilitate creation of logical and focused differential diagnoses. The clinically important anatomical relations in this area mean that pathology may result in high morbidity, and surgical access is also difficult for pathological diagnosis. The CAT should be carefully evaluated on CT / MR, particularly when patients have symptoms of CN III, IV or VI neuropathy, orbital pain or altered visual acuity.

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Table 1: Differentiating features of CAT lesions by CT and MR.

CN III, IV, V, VI involvement

Cavernous Sinus involvement

Enhancement

Meningioma Schwannoma

Uninvolved Involved

Variable Variable

Homogenous Peripheral/Target

Perineural tumor spread

Involved

Involved

Involved

Involved

Uninvolved

Sarcoid AVM

b

Lesional T2 signal intensity Iso Variable

Dural Tail Extension to orbit

Homogenous

Absent

Primary site

Iso

Homogenous

None

EOM/Sclera

Iso

Variable

Homogeneous

None

Face

Low

Variable

Variable

Homogeneous

None

Lacrimal/Uveal

Low

Uninvolved

Variable

Serpentine

None

Vascular pouch

Low

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GPA

Hyperostotic Smooth lytic

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a

Extra-CAT abnormality

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IOI

Bony Changes on CT

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Lesion

Figures

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a. Idiopathic orbital inflammation (formerly orbital pseudotumor). b. Granulomatosis with polyangiitis (formerly Wegener’s granulomatosis).

Figure 1. Anatomy of the caverno-apical triangle (CAT). Left, illustration of the right CAT (red triangle) which includes the anterior cavernous sinus (blue) and the orbital apex. Upper Right, labeled ex vivo skull base, superolateral view. 1) anterior clinoid 2) sphenoid ridge 3) optic strut 4) optic canal 5) superior orbital fissure 6) planum sphenoidale 7) chiasmatic sulcus 8) tuberculum sellae 9) pituitary fossa 10) dorsum sellae 11) posterior clinoid 12) carotid sulcus 13) foramen rotundum 14) foramen ovale 15) middle clinoid. Lower Right, axial post-contrast T1 MR; Lower Left, axial noncontrast CT illustrating the CAT. The CAT forms part of the anteromedial aspect of the middle cranial fossa. Its name is defined from its shape and the components that define its contours: the cavernous sinus and the orbital apex. This triangular shaped region is formed by the cavernous sinus anterior to Meckel’s cave, and extends to the superior orbital fissure (SOF) where cranial nerves 3, 4, 5¹ & 6 enter the orbital apex, superolateral to the optic nerve.

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Figure 2. CAT Meningioma. A 36-year-old female who initially presented to the ED with nonspecific visual changes and headache. Initial MRI performed in 2003 demonstrates early subtle T2 asymmetry (A) on axial T2-weighted image and contrast enhancement (B) on axial T1-weighted postcontrast image within the CAT on the left (yellow arrows). This MRI exam was interpreted as “normal” at an outside institution. Follow-up MRI including axial FIESTA (C) and sagittal post-contrast T1 (D) sequences performed 10 years later reveals conspicuous progression of tumor involving the anterior CAT where the cavernous dura blends into the apical periorbita and annulus of Zinn (yellow arrow); yet equally shows the orbital apex as a conduit to the inferior orbital fissure (red arrow).

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Figure 3. CAT meningioma. Axial FLAIR images (A,B) demonstrate loss of clinoidal and apical (yellow arrows in A and B respectively) fat as a clue to a CAT lesion on FLAIR in this 57-year-old female who presented with left ptosis.

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Figure 4. CAT Schwannoma. A 14-year-old male with left oculomotor palsy underwent MRI which revealed a spindle shaped lesion with intermediate T2 signal intensity on axial T2-weighted image (A, yellow arrow) and homogenous enhancement (B, yellow arrow) on axial T1-weighted post contrast image centered at the SOF suggestive, although not diagnostic for schwannoma. Arc susceptibility artifact projecting over the orbits and skull base related to dental hardware (braces).

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Figure 5. CAT Schwannoma. A 43 year-old male with known vestibular schwannoma presents for routine surveillance imaging. A. Subtle T2 hyperintense oval mass at the left CAT is centered along the superior orbital fissure on axial T2-weighted image. B. Characteristic enhancement on axial T1weighted post-contrast image in areas that lack T2 hyperintensity is noted, a characteristic feature of schwannoma, asymptomatic and incidentally noted in this case.

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Figure 6. CAT neurofibroma in patient with neurofibromatosis 1 (NF-1). 20-year-old female with NF-1 presents with progressively enlarging CAT and orbital mass. This neurofibroma shows heterogenous T2 (A) on axial T2-weighted image and contrast-enhancement (B) with “waisting” (yellow arrows) at the CAT on a axial T1-weighted post-contrast image. Figure 7. Basal cell carcinoma (BCC) with perineural spread (PNS) into the CAT. A 55 year old female patient with newly diagnosed BCC undergoes MRI to evaluate for deep extension of tumor. Asymmetrical enhancement at the left CAT (A, red triangle) along with medial canthal enhancement suggests a primary cutaneous lesion (yellow arrow in B) and perineural tumor within the inferior orbital fissure (red arrow in B), both images are axial T1-weighted post-contrast. The lesion at the CAT is the “tip of the iceberg” as the tumor extends to the pterygopalatine fossa (C) and along vidian (yellow arrow D) and maxillary nerves (red arrow D). Orbital involvement of the infraorbital nerve is seen on coronal T1 post contrast image (yellow arrow E) as a route of spread toward the CAT; coronal T1weighted post-contrast images.

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Figure 8. Basal cell carcinoma (BCC) recurrence in the CAT following orbital exenteration. After orbital exenteration the first clue to recurrence can be asymmetrical soft tissue in the CAT (red triangle); axial T1-weighted post-contrast image.

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Figure 9. Neurosarcoid involving the CAT. A 49-year-old female presents with double vision and known lung disease. Left CAT asymmetry (A, red triangle) extends into the orbital apex (B) on postcontrast T1 axial images. Coronal T2-weighted (C) and T1-weighted post-contrast images (D) show T2 hypointense enhancing tissue within the SOF and orbital apex (red arrows in C and D). These findings should prompt search for optic nerve involvement, uveal involvement, and nodular pachymeningeal thickening, relatively specific signs of sarcoid.

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Figure 10. Granulomatosis with polyangiitis (GPA) involving the CAT. Nonspecific loss of T1 fat signal (A, yellow arrow) within the left CAT on axial pre-contrast T1-weighted image, a subtle clue to inflammatory changes and enhancement on post-contrast T1-weighted image (B) associated with biopsy-proven GPA in this 55-year old male who presented with left vision loss. . Figure 11. Idiopathic orbital inflammatory (IOI) disease involving the CAT. Post-contrast CT (A) for this 19-year old female with right retro-orbital pain and diplopia shows subtle asymmetry (yellow arrow) without bony changes as seen to better advantage within the right CAT on T1-weighted axial post-contrast MR (B). The patient’s severe right retro-orbital pain and response to steroids corroborated the diagnosis of pseudotumor.

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Figure 12. Idiopathic orbital inflammatory (IOI) disease involving the CAT. 27 year old female presented with left orbital pain. Asymmetrical enhancement in the left CAT on axial T1-weighted postcontrast MR images (A, red triangle) reveals more extensive inflammation into the PPF, orbital apex and pterygomaxillary fissure (B, yellow arrow).

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Figure 13. Chronic invasive fungal infection in the CAT. A 63 year-old female with multiple medical problems was hospitalized for septic shock, altered mental status, and left-sided vision loss. Axial T2-weighted image (A) shows subtle fullness and low signal in the left CAT (yellow arrow) with sinus mucosal thickening on axial CT images (B) and frank osteolysis at the sphenoid sinus and SOF (C, yellow arrows). This T2-hypointense soft tissue is associated with low ADC values on axial MR (D, yellow arrow) diffusion imaging. The constellation of clinical history, mucosal disease, bone erosion, and T2 hypointensity is highly suggestive of invasive fungal infection.

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Figure 14. Dural arteriovenous fistula (DAVF) of the CAT. A 33 year old man presented loss of visual acuity. Axial pre-contrast T1-weighted images (A, B) show loss of left CAT fat signal and a ovoid low intensity lateral apical lesion (yellow arrows) with avid enhancement on the axial T1weighted post contrast image (C, yellow arrow). Digital subtraction angiography with left external carotid injection shows the middle meningeal artery filling a venous pouch which drains forward to the SOV, diagnostic of a dural arteriovenous fistula.

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Figure 15. Cavernous sinus cavernous hemangioma (CSCH) of the CAT. 45 year old female who presented with dizziness and headache. Axial FLAIR (A) and T2 (B) images show homogenous hyperintense circumscribed lesion at the right CAT which avidly enhances (C) on coronal T1-weighted post-contrast image. The lesion was biopsied and found to be a cavernous hemangioma.

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ACCEPTED MANUSCRIPT 40. Hasiloglu ZI, Asik M, Kizilkilic O, Albayram S, Islak C. Cavernous hemangioma of the cavernous sinus misdiagnosed as a meningioma: a case report and MR imaging findings. Clin Imaging. 2013;37:744–6.

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Figure 15