Neuroimaging of Meckel’s cave in normal and disease conditions

Insights into Imaging, Apr 2018

Meckel’s cave is a dural recess in the posteromedial portion of the middle cranial fossa that acts as a conduit for the trigeminal nerve between the prepontine cistern and the cavernous sinus, and houses the Gasserian ganglion and proximal rootlets of the trigeminal nerve. It serves as a major pathway in perineural spread of pathologies such as head and neck neoplasms, automatically upstaging tumours, and is a key structure to assess in cases of trigeminal neuralgia. The purpose of this pictorial review is threefold: (1) to review the normal anatomy of Meckel’s cave; (2) to describe imaging findings that identify disease involving Meckel’s cave; (3) to present case examples of trigeminal and non-trigeminal processes affecting Meckel’s cave. Teaching points • Meckel’s cave contains the trigeminal nerve ganglion and rootlets between the prepontine cistern and cavernous sinus. • Assessment is essential for perineural spread of disease and trigeminal neuralgia. • Key imaging: neural enhancement, enlargement, perineural fat/CSF effacement and skull base foraminal changes.

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Neuroimaging of Meckel’s cave in normal and disease conditions

Neuroimaging of Meckel's cave in normal and disease conditions Ajay Malhotra 0 1 2 3 4 5 6 Long Tu 0 1 2 3 4 5 6 Vivek B. Kalra 0 1 2 3 4 5 6 Xiao Wu 0 1 2 3 4 5 6 Ali Mian 0 1 2 3 4 5 6 Rajiv Mangla 0 1 2 3 4 5 6 Elias Michaelides 0 1 2 3 4 5 6 Pina Sanelli 0 1 2 3 4 5 6 Dheeraj Gandhi 0 1 2 3 4 5 6 0 Orlando Health , Orlando, FL , USA 1 Department of Radiology and Biomedical Imaging, Yale School of Medicine , Box 208042, Tompkins East 2, 333 Cedar St, New Haven, CT 06520-8042 , USA 2 Ajay Malhotra 3 Department of Radiology, University of Maryland Medical Center , Baltimore, MD , USA 4 Northwell Health , Great Neck, NY , USA 5 Department of Surgery (Otolaryngology) and Department of Pediatrics, Yale School of Medicine , New Haven, CT , USA 6 State University of New York Upstate Medical University , Syracuse, NY , USA Meckel's cave is a dural recess in the posteromedial portion of the middle cranial fossa that acts as Faconduit for the trigeminal nerve between the prepontine cistern and the cavernous sinus, and houses the Gasserian ganglion and proximal rootlets of the trigeminal nerve. It serves as a major pathway in perineural spread of pathologies such as head and Oneck neoplasms, automatically upstaging tumours, and is a key structure to assess in cases of trigeminal neuralgia. ThOepurpose of this pictorial review is threefold: (1) to review the normal anatomy of Meckel's cave; (2) to describe imaging findings that identify disease involving Meckel's cave; (3) to present case examples of trigeminal and non-trigeminal processResaffecting Meckel's cave. P hyperintense cerebrospinal fluid (CSF)-containing structure holds tremendous importance in neuroimaging-its effacement or abnormal enhancement may herald otherwise occult infectious, inflammatory, congenital or neoplastic lesions. Its careful assessment can lead to early detection of perineural spread of malignancy with significant prognostic and therapeutic implications. Meckel's cave; Trigeminal; Neuralgia; Perineural C; Skull base - Teaching points Meckel’s cave contains the trigeminal nerve ganglion and rootlets betweDenthe prepontine cistern and cavernous sinus. E Assessment is essential for perineural spread of disease and trigeminal neuralgia. Key imaging: neural enhancement, enlargement, perineural fat/CSF effacement and skull base foraminal changes. T E R R Introduction Meckel’s cave is a natural mouth-shaped aOperture in the medial portion of the middle cranial fossa that acts as a key conduit for the largest cranial nerve, Cthe trigeminal nerve (CN V). It connects the cavernoNussinus to the prepontine U cistern of the posterior fossa. This tiny parasellar T2* Anatomy Meckel’s cave is an aperture within petrous apex’s meningeal dura propria and periosteal layers measuring 4 × 9 mm wide at its opening and 15 mm in length [10]. The cave is shaped like an open-ended three-fingered glove pointing anterosuperomedially (Fig. 1). The palm of the glove rests within a bony indentation of the petrous apex (impressio trigemini) and contains the semilunar-shaped Gasserian ganglion of the trigeminal nerve. The fingers of the glove, superior to inferior, contain the three postganglionic rootlets that comprise the “tri-” of the trigeminal nerve—ophthalmic (V1), maxillary (V2) and mandibular (V3), which provides sensory innervation to the face and motor function for mastication. The cuff of the glove or the entrance of the cave, the porus trigeminus, is between the superior and inferior petrosal sinuses and contains the trigeminal nerve with an arachnoid sheath [21]. The internal carotid artery precavernous segment courses inferomedial to the cave. Anteriorly, lies the cavernous sinus, with its lateral wall superomedial to the cave [18]. Trigeminal nerve (CN 5) branches V1 and V2, oculomotor nerve E (CN 3) and trochlear nerve (CN 4) course within a dural sheath that comprises cavernous sinus lateral wall itself. V1 exits through the superior orbital fissure with the oculomotor, Rtrochlear and the abducens nerves (CN 6), and receives sensoRryinput from the eye, orbit and forehead. V2 exits through foramen rotundum, an imaging landmark in the sphenoid bone sOuperolateral to the vidian canal, and receives sensory input fCrom the maxilla, palate, upper lip, cheek, nasal cavity, nose and nasopharynx. V3 exits inferiorly between Meckel’s cave Nand the cavernous sinus through the foramen ovale, couUrsing down towards the mandible, F O O R P and receives sensory input from the chin, lower lip, floor of mouth, tDongue, scalp and meninges, and gives motor output to the masticator muscles (masseter, medial pterygoid, lateral pter E ygoid, temporalis), tensor veli palatini and tensor tympani. TPerineural vascular plexus surrounds the Gasserian ganglion Cand proximal V2 and V3 rootlets, resulting in normal findings of thin mild enhancement [23]. Imaging modalities and imaging technique Magnetic resonance imaging (MRI) is preferred to assess Meckel’s cave, its contents and relationship with adjacent structures. Dedicated, high-resolution images from the orbital apex through the prepontine cistern are obtained. Parallel imaging and high-field 3-T MRI depict fine anatomical detail, Neoplastic - Schwannomas - Meningiomas Malignant - CSF spread of primary CNS malignancies - Lymphoma - Perineural spread Miscellaneous Non-intrinsic lesions of Meckel’s cave that - Petrous apFexmucocele may compress of invade Meckel’s cave - Pituitary macroadenoma O O cave. The MRI protocol should include imaging in three siveness of a lesionR.Multi-detector helical CT acquisition in especially the cranial nerves and walls of the Meckel’s base foramina, thereby providing information about aggresplanes with T1- and T2-weighting, short-tau inversion re- the axial plane Pwith reformats in the sagittal and coronal covery (STIR) and gadolinium-enhanced T1-images with planes are routinely displayed as 3-mm slices, with thinner fat suppression. STIR, which is not based on frequency- sub-millDimetre slices available as needed. selective pulses, is preferred for more homogeneous fat E suppression at the skull base [4]. High-resolution heavily T T2-weighted volumetric sequences can demonstrate the Imaging indications and key features cisternal course of the cranial nerves as well as the tri-C geminal rootlets and ganglion within Meckel’s cave [5E].A Skull base imaging specifically evaluating Meckel’s cave is thin-section (3 mm), small field of view (FOV) (16– most frequently performed for assessing for trigeminal peri18 cm), fast spin echo, T1-weighted sequence is Rbest to neural spread of head and neck malignancy and trigeminal depict bone marrow invasion and assess fat pRlanes at the neuralgia. Trigeminal neuropathy may present as facial pain, pressed T1-weighted high-resolution, smOallFOV images trismus. Meckel’s cave may be involved in a spectrum of skull base. Intravenous gadolinium-enhanced fat-sup- numbness and weakness of muscles of mastication, and even depict meningeal invasion and perineCural spread and max- pathologies: congenital, infectious, inflammatory, vascular or imise tumour contrast against adNjacent structures. neoplastic lesions (Tables 1 and 2). Key imaging features of Computed tomography (CT) better defines the bony anat- pathology of Meckel’s cave are moderate enhancement greatomy of the skull base and the Uthin cortical margin of the skull er than the perineural vascular plexus, nerve enlargement with Fig. 2 Perineural spread of tumour. Coronal T2 (a), axial C+ (b), coronal C+ (c), coronal C+ (d). A 60-year-old man with right CN V symptoms. Expansile T2 hypointense, enhancing lesion filling the right Meckel’s cave extending through the foramen ovale and along V2 in the foramen rotundum Fig. 3 Perineural spread of tumour. A 45-year-old man with left facial pain and numbness. CT showing enhancing soft tissue along the course of left CN V, expanding into the foramen rotundum (a), infraorbital foraEmen R (b) and foramen ovale (c). Posteriorly, the enhancing tumour extends to perineural fat plane effacement, osseous foraminRalerosion or enlargement, and trigeminal cistern CSF effOacement. Any enhancement of the trigeminal nerve posteriorly, within the cisternal segment or root entry zone, is a Cspecific sign of pathological enhancement. Foraminal Nassessment holds a greater U role in assessing for retrograde perineural spread, which can occur discontinuously, with cisternal/root entry zone enhancement portending a worse prognosis [15]. Fig. 4 Diffuse infantile pontine glioma (a) with significant increase in size on the 3-month study (b) with perineural spread along left CN V into Meckel’s cave D E T F O O R P Cthe left Meckel’s cave. Rapid expansion on follow-up MRI (d) with intense uptake on positron emission tomography (PET) (e) in left CN V including foramen ovale (arrow) Trigeminal disease Perineural spread Perineural spread from skin and head-and-neck malignancies can occur along the trigeminal and facial nerves. Its presence has marked implications for staging and treatment of otolaryngological malignancies, automatically upstaging tumours to 123 124 125 126 127 128 spread along nerves communicating with facial nerve branches such as the greater superficial petrosal/vidian nerves near the pterygopalatine fossa and auriculotemporal nerve near the temporomandibular joint. Squamous cell carcinoma is the most common cause of perineural spread given its large prevalence, but adenoid cystic carcinomas of the minor salivary glands have the highest incidence [17] (Figs. 2 and 3). Brainstem tumours can also rarely spread anteriorly through CN V (Fig. 4). Trigeminal neuralgia Although trigeminal neuralgia is a clinical diagnosis, neuroimaging may be performed for confirmation in viral/ idiopathic aetiologies and Ftoassess for treatable neurovascular compression. Viral aetiologies, including herpes zoster and simplex Oviruses, involve the Gasserian ganglion, where they cOanlie dormant. Mild enhancement of the ganglion is non-specific and difficult to distinguish from normal peRrineural vascular plexus; however, cisternal/root ePntry zone enhancement is specific. Herpes rhombencephalitis asymmetric enhancement in the clinical contDextof reactivation has characteristic imaging findings E(Fig. 5). Tappropriate clinical context with trigeminal cisternal/root Neurovascular compression can be suggested in the Centry zone deformation from a vascular loop such as the superior cerebellar artery or anterior inferior cerebellar artery [9]. Persistent trigeminal artery, the most common persistent fetal carotid-basilar anastomosis, normally runs through a dural foramen located immediately medial to the Meckel’s cave (Fig. 6). Rarely, a vascular loop may be associated with trigeminal neural arteriovenous malformation, where symptoms may be from the malformation itself or nerve compression/deformation from enlarged feeding and draining vessels [11] (Fig. 7). Microvascular decompression is an effective treatment for these cases, although stereotactic radiosurgery has also been used, especially in the context of arteriovenous malformation (AVM). Non-vascular/idiopathic causes of trigeminal neuralgia are treated with anticonvulsants, antispasmodics E R perioral numbness for 2 weeks—vesicular rash. Tubular Renhancement Fig. 5 Herpes zoster reactivation. A 62-year-old woman with right extending to Meckel’s cave O along the right CN V from origin through cisternal segment and C Committee Cancer staging manNual[12]. Maxillary nerve T3 in the most recent eighth edition of American Joint (V2) perineural spread occurs Ufrom primary tumours in the midface skin, maxilla, upper lip and palate. Mandibular nerve (V3) perineural spread occurs from tumours in the lower face, mandible, masticator space and parapharyngeal space. Trigeminal perineural involvement may also occur from Fig. 6 Persistent trigeminal artery. Vascular channel connecting the left internal carotid artery and the basilar artery, and running through the medial aspect of Meckel’s cave Fig. 7 Trigeminal AVM. A 58-year-old man with right facial neuralgia. Axial T2 (a) and axial C+ (b) showing abnormal serpentine vasculature along cisternal segment of right CN V extending into Meckel’s cave on DSA (c)—arteriovenous shunting from right anterior inferior cerebellar artery (AICA) with prominent draining vein Fig. 8 Trigeminal schwannoma. Coronal C+ (a), axial T2 (b), axial T1 (c), axial C+ (d): expansile enhancing mass in the right Meckel’s cave with a large, lobulated cystic component along the cisternal segment of the right CN V Fig. 9 Schwannoma of Meckel’s cave in a patient with neurofibromatosis type 2. Axial T2 (a), axial C+ (b), coronal C+ (c) showing an enhancing lesion within the right Meckel’s cave. Note additional bilateral vestibular schwannomas D E T C E R R O C N U F O O R P Fig. 1E2Sarcoidosis. Axial T1 (a), axial T2 (b), axial T1 C+ (c). A 53Tyear-old woman with facial pain and numbness. Enhancing, T2 hypointense lesions symmetrically involving the bilateral Meckel’s Cc a v e . C h e s t X - r a y ( d ) — b i l a t e r a l h i l a r a n d m e d i a s t i n a l lymphadenopathy. Follow-up (e)—complete resolution avid enhancement. Nerve sheath tumours may be isolated or syndromic, in phacomatoses such as neurofibromatosis (Fig. 9). Neurofibromatosis should be considered in cases of multiple nerve sheath tumours and dural ectasia (Fig. 10). Leptomeningeal metastases, most frequently from breast and lung malignancies, result in linear segmental enhancement, usually in the setting of disseminated disease [22]. Fig. 11 Lymphoma. Axial T2 (a), axial C+ (b), CT (c). Bilateral CN VI palsy and right facial pain. Mottled appearance of clivus and petrous apices on CT—caused by T2 hypointense, enhancing infiltrating lesion. Post treatment (d, e)—complete resolution and botox. Radiosurgery (gamma knife) is reserved for medically refractory symptoms. Enhancement without expansion can be transient or persistent following stereotactic radiosurgery [16]. Neoplastic, inflammatory and other Predictably, the most common neoplasm of MeckeRl’scave is a trigeminal nerve sheath tumour, schwRannoma and neurofibroma. Nerve sheath tumours result in nerve and foraminal enlargement, demonstrate T2 Ohyperintense signal with moderate-to-intense heterogCeneous enhancement. A dumbbell shape provides specificity, with the waist at constricting foramina (Fig. 8). NIncontrast, meningiomas often display T2 hypointenUsesignal and show uniform, Fig. 14 Meningioma (extrinsic). Axial T2 (a), T2 SPACE (b), axial T1 (c), axial C+ (d). Right petroclival T2 hypointense, enhancing mass invading the right Meckel’s cave. Postoperative residual enhancing lesion in the right Meckel’s cave and abutting basilar artery (e) Lymphoma can result in neural involvement from either perineural invasion or leptomeningeal disease [2]. Lymphoma can cause dural tail, but absence of hyperostosis helps differentiate it from meningioma (Fig.11). Sequences that highlight CSF such as T2 SPACE or CISS play an important part in helping detect CSF disseminated malignancies. The normal high T2 signal of CSF maybe replaced by low signal from malignant E lesions. Inflammatory aetiologies such as sarcoidosis have more nodular enhancement than other leptomeningReal diseases due to granulomas and can involve the Rtrigeminal nerve. Symmetrical involvement of Meckel’s cave is rarely reported [13] (Fig. 12). NeurosarcoidOosis is rare without pulmonary manifestations and Cfacial nerve involvement is more common [6, 19]. Additionally, involvement of pituitary hypothalamic axis cNanhelp point towards the correct diagnosis. U Diffuse cranial nerve marked enlargement can be seen in chronic inflammatory demyelinating polyneuropathy (CIDP), F O O R neurofibromatoPsisand hereditary sensory motor neuropathies (HSMNs). HSMN type I (Charcot-Marie-Tooth disease) demonstrates Dno significant enhancement nor leptomeningeal dis E ease [3] (Fig. 13). Diagnosis is frequently known from genetic testing of the autosomal-dominant characteristic clinical hisTtory of distal weakness and absent reflexes beginning in the Csecond decade. CIDP demonstrates diffuse enhancement and neurofibromatosis demonstrates more defined mass lesions and numerous additional findings such as plexiform fibromas and sphenoid wing dysplasia. Non-trigeminal disease Meckel’s cave, being composed of dura, is subject to meningiomas. Meningiomas may originate in the dura mater in or around Meckel’s cave (Fig. 14). Rarely, the tumours can be confined within the cave and arise from the trigeminal nerve [8]. Additionally, the cave may also be invaded by non-neural processes such as posterior extension of F pituitary macroadenoma and orbital inflammatory disease. Meckel’s cave. Such large tuOmours are associated with sellar Lesions of adjacent bone and other structures may extrin- expansion, ICA encasement without extrinsic compression, sically compress the canal, best assessed on thin coronal sphenoid sinus extensiOon,and are relatively homogeneous T2-weighted imaging. Examples include petrous apex, and moderately T2R-hyperintense. from ocular nerve sheath tumours and internal carotid ar- also be seen iPnTolosa Hunt, a variant of orbital inflampetroclival fissure and clival diseases, osseous expansion Posterior extension of pathology to Meckel’s cave can tery (ICA) aneurysms. matory disease (orbital pseudotumour) involving the or Thin, high-resolution, three-dimensional constructive bital apDexthat extends posteriorly into the cavernous siinterference in steady state imaging can distinguish the sec- nus E[7]. Patients present with painful ophthalmoplegia and ond most common primary neoplasm in Meckel’s cave, Tcavernous fullness, asymmetric enhancement and ICA peripheral with enhancing dural tail, arising from the duralC Osseous processes compressing Meckel’s cave involve meningioma, from nerve sheath tumour. Meningiomas are narrowing (Fig. 16). reflections comprising the cave’s margins, while neErve the petrous apex, petroclival fissure and clivus. Petrous sheath tumours will be more central within the cavRe,grow- apex cephalocele is usually an incidental finding, reflecting ing along the course of the nerve. Calcifications and T2- benign ballooning of the arachnoid space communication hypointensity in meningiomas are additional dRistinguishing with Meckel’s cave. Fluid distended Meckel’s cave has an findings (Fig. 15). O enlarged porus trigeminus notch and a smooth expansile Pituitary macroadenomas can be invasive, contiguously cystic space in the anteromedial petrous apex [20] extending from the sella, through the Ccavernous sinus, to (Fig. 17). Findings may reflect intracranial hypertension, N U Fig. 16 Tolosa-Hunt syndrome. Axial T1 C+ (a, b), axial T2 (c), coronal C+ (d). A 23-year-old woman with acute onset of painful left diplopia. Asymmetric enhancing tissue in left cavernous sinus extending to Meckel’s cave and through the foramen ovale (b, d). Follow-up—complete resolution (e) Insights Imaging similar to empty sella, and is associated with spontaneous CSF leaks due to dehiscence [1]. Signal characteristics follow CSF, with FLAIR suppression. Petrous apex mucoceles have a similar appearance but do not connect to Meckel’s cave; rather, they compress it, resulting in symptoms. Cholesterol granulomas are T1 hyperintense, demonstrate susceptibility and no FLAIR suppression. Congenital cholesteatomas and epidermoids both demonstrate restricted Fig. 18 Epidermoid. Expansion of left Meckel’s cave by a left cerebellopontine angle mass on axial T2 (a), showing no enhancement (b) and restricted diffusion (c). Postoperative residual tissue in left Meckel’s cave (d, e) T C E R R O C N U diffusion, incomplete FLAIR Osuppression and no enhancement, but congenital chOolesteatomas are localised to the petrous apex, while epidermoids are in the cerebellopontine R angle/prepontine cistern and are much more proliferative, extending into mPultiple cisterns and encasing the basilar artery [14] (Fig. 18). Petroclival/petrooccipital fissure chondroid lesions deDmonstrate characteristic imaging features on CT with rings Eand arcs calcifications (Fig. 19). Clival chordomas Fig. 19 Chondrosarcoma. Axial T2 (a), axial T1 (b), axial T1 C+ (c), CT (d). A 61-year-old woman with effacement of the right Meckel’s cave by an expansile petrous apex mass that is hyperintense on T2, hypointense on T1 and shows avid enhancement on post contrast image. CT shows features of slow growing lesion. Note preserved Meckel’s cave on the left Fig. 20 Bilateral cavernous ICA aneurysms. Axial C+ (a), coronal T2 (b), CT (c) and (d). A 73-yearold woman with left facial pain. Bilateral cavernous enhancing, partially calcified lesions encroaching the Meckel’s cave— left greater than right F O O R P D E T demonstrate extensive bony destruction, marked T2-Caneurysms and dissections may cause carotid-cavernous hyperintensity, haemorrhagic and calcific susceptibility, Eand fistulas. honeycomb enhancement pattern. They can be distinguished from pituitary macroadenoma by lack of sellar mass, Rsparing of the sphenoid sinus and signal characteristicRs.There are Conclusions isolated case reports of intradural chordomas of the Meckel’s cave and paraganglioglioma. O Meckel’s cave contains the trigeminal nerve ganglion and prox Aneurysms of the petrous and caCvernous segments of imal rootlets, situated between the prepontine cistern and the the close proximity (Fig. 20). TNhese segments are demar- Meckel’s cave are effacement of CSF signal in Meckel’s cave, the ICA can result in mass effect on Meckel’s cave given cavernous sinus. Key imaging features of pathology of cated by the petrolingual liUgament. Ruptured aneurysms moderate enhancement greater than the perineural vascular in either location do not cause subarachnoid haemor- plexus, nerve enlargement with perineural fat plane effacement rhage as they are extradural, but cavernous ruptured and osseous foraminal erosion or enlargement. Neural 332223 pathologies include nerve sheath tumours, perineural tumour 11. 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Ajay Malhotra, Long Tu, Vivek B. Kalra, Xiao Wu, Ali Mian, Rajiv Mangla, Elias Michaelides, Pina Sanelli, Dheeraj Gandhi. Neuroimaging of Meckel’s cave in normal and disease conditions, Insights into Imaging, 2018, 1-12, DOI: 10.1007/s13244-018-0604-7