ct and mri assessment in differential diagnosis and ...€¦ · -review petrous apex (pa) anatomy...

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CT and MRI assessment in differential diagnosis andsurgical planning of the petrous apex lesions

Poster No.: C-1785

Congress: ECR 2010

Type: Educational Exhibit

Topic: Head and Neck

Authors: F. Piludu, S. Gaudino, T. Tartaglione, G. M. Di Lella, A. M.Costantini, F. R. Quaglio, E. Pravatà, F. Bussu, C. Colosimo;Rome/IT

Keywords: petrous apex ( PA), Non-Neoplastic / Neoplastic lesions, CT/ MRI

DOI: 10.1594/ecr2010/C-1785

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Learning objectives

-Review petrous apex (PA) anatomy and its content in a simple and schematicway, taking account of normal anatomical variants (e.g. asymmetric marrow spacedevelopment)

-Point-out technical CT & MR requirement to work out the appropriate imaging protocol

-Illustrate Non-Neoplastic (e.g. cholesterol granuloma, cholesteatoma, primarymucocele), inflammatory (e.g.apical petrositis) and dysplastic (e.g. Pagets disease)PA lesions

-Illustrate Neoplastic PA Lesions (e.g. metastasis, rhabdomyosarcoma, endolymphaticsac tumour) arising in PA

-Design an imaging algorithm to assist in differential diagnosis

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Images for this section:

Fig. 1

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Background

Management of PA pathology poses a unique challenge even to the most seasoned skullbase surgeons. Its central location in the skull base with surrounding critical neural andvascular structures make surgical approaches anything but a trivial matter.

Orientering: How Not To Get Lost

The PA is the most medial portion of the temporal bone with a pyramid-shaped structureobliquely positioned within the skull base.

•The PA apex is located anteromedially and the PA base posterolaterally.

•PA is positioned between the inner ear structures laterally, petrosphenoid fissureanteriorly, and petro-occipital fissure medially.

•Its anterosuperior portion forms the floor of the middle cranial fossa while theposterosuperior portion constitutes the anterior wall of the posterior cranial fossa.

•The base of the pyramid is the otic capsule, semi-canal of the tensor tympani and thepetrous carotid artery.

•The superior surface or -meatal planed - extends from the arcuate eminence to theprecavernous carotid artery and Meckel's cave.

•The posterior surface faces the cerebello-pontine angle and begins laterally at thecommon crus/vestibular aqueduct and ends medially at Dorello's canal and petroclinoidligament.

•The inferior aspect contents the jugular fossa and inferior petrosal sinus.

Channels

The petrous carotid and the internal auditory canal are the largest one, whereasthe Dorello's, singular, and arcuate canals are markedly smaller and not constantlyvisualized. When viewed from above a parallel line, drawing through the internal auditorymeatus divides PA into larger anterior (principally consisting of bone marrow or air cells)and a smaller posterior (derived from the dense bone of the otic capsule) compartments.

Pneumatization

Approximately 33% of people have pneumatized petrous apices, (4% -7%asymmetrically). In the adult, temporal bone pneumatization is divided into five generalareas:

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•middle ear

•squamomastoid (mastoid)

•petrous apex

•perilabyrinthine

•accessory air cells

In 35% of patients,the petrous apex is pneumatized by infralabyrinthine, anterior,superior, posteriormedial, or subarcuate tracts that directly communicate with the mastoidor middle ear cleft. These tracts provide direct ''pathways'' for diseases to spread fromthe mastoid or middle ear cavity to the petrous apex.

Surgical approches

Traditionally, the most common approaches to the PA lesions are: infracochlear,subtemporal, infralabyrinthine, subarcuate and sinodural angle approaches,supracochlear, retrosigmoid, infratemporal, transnasal endoscopic, translabyrinthine,transotic and transcochlear.

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Fig. 1

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Fig. 2

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Imaging findings OR Procedure details

MRI plays an essential role in:

• characterizing lesions.• evaluating lesions relationship with PA "contents".

Multidetector CT is complementary to MRI in evaluating PA lesions . It is the method ofchoice to image the osseus architetture of PA "container". CT exam:

• asses bone changes (bone structures: sclerosis, erosion or invasion).• Defines the proximity of PA lesions to IAC, otic capsule, ICA.

Angiographic exams (conventional angiography, magnetic resonance angiography/venography, computed tomography angiography/venography) should be taken inaccount in PA lesions compressing, invading, or abutting ICA, jugular bulb, and inferior/superior petrosal sinus.

CT and MRI are complementary to reduce differential diagnosis list and to propose thecorrect diagnosis. Imaging investigations are preeminent for the surgical approach andallow the detection of pseudolesions ("leave me alone")

We Illustrate the most common Non-Neoplastic and Neoplastic PA Lesions and certainrare/tricky case.

1. NON-NEOPLASTIC PA LESIONS

-Asymmetric pneumatization: unilateral petrous apex air cells occurring concurrentlywith a marrow-filled petrous apex in the contralateral temporal bone.

•Imaging CT >>> MR: CT rarely leads to an incorrect interpretation. Bone algorithm canensure lack of mass effect/bony erosion & no worrisome changes to trabeculae = BESTDIAGNOSTIC CLUE!!

•MRI is more confusing because the nonpneumatized petrous apex shows variable signalintensity depending on a patient's age. Lesion is 1st suspected without fat saturation(fat-sat sequences confirm "leave me alone nature" without CE on T1 C+ FAT-SAT- wi ).

•DDX: Cholesteatoma, cholesterol granuloma, mucocele, apical petrositis.

(CT recommended to assess surrounding anatomic landscape!!!!!)

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Fig.: Asymmetric pneumatization. Unilateral left PA air cells (arrows) occurreconcurrently with a marrow-filled right PA (arrowheads). Ax/Cor CT can ensure lack ofmass effect/bony erosion and no worrisome changes to trabeculae.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Giant air cell: a petrous apex air cell that is larger than 1.5 cm in largest diameter.

•Imaging CT >>> MR.

•DDX: small PA mucocele when it is completely filled with fluid (CT recommended toassess surrounding anatomic landscape!!!!)

-Arachnoid granulations: also included in PA lesion from some authors.

•On CT/MRI follow the attenuation of CSF. CT demonstrates no disruption of the cortex .No/capsule-like CE.

•DDX: epidermoid cysts or metastases (CT recommended to assess surroundinganatomic landscape!!!).

-Petrous apex effusion: usually considered a "leave me alone lesion". It is mostcommonly discovered as an incidental finding on routine imaging studies ("retained" or"trapped" fluid).

•Imaging CT >>>MRI. CT shows opacified PA cells without trabecular loss & withoutexpansion = BEST DIAGNOSTIC CLUE!! CT through temporal bone area is used tosort out rare surgical lesions of PA from far more common but incidental TF-PA.

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•MR signal intensity is low on T1-wi, high on T2-wi. No CE of PA or adjacent meninges.

•DDX: Cholesteatoma, cholesterol granuloma, mucocele and apical petrositis (CTrecommended to assess surrounding anatomic landscape!!!!!).

Fig.: Effusion. Ax and Cor T2 wi show high signal (CSF-like) within the rigth PA(arrows) and mastoid air cell system. Internal PA bony trabeculae seen as subtle lowsignal lines are preserved.

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References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Trauma: Recently the temporal bone fractures are divided into two major categories:petrous and nonpetrous fractures to better correlate with clinical symptoms andprognosis (higher incidence of complications observed in petrous apex fractures).

•Imaging: CT >>>MRI.

•CT is required to depict fractures = BEST DIAGNOSTIC TOOL!!

•MRI is required for eventually involvement of VII c.n., of the inner ear, CSF leak.

•CTA/MRA are mandatory to detect traumatic carotid artery dissections when fracturesextend into or through the petrous carotid canal.

•CAVE: pseudofractures!!!!!!

•DDX: extrinsic sutures-fissures (occipitomastoid, petrooccipital, temporoparietal),intrinsic fissures (petrotympanic & petrosquamosal, tymapanosquamosus &tympanomastoid), intrinsic channels (mastoid, inferior tympanic, petromastoid canal)

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Fig.: Fracture. Ax CT reveals trasverse fracture (arrows) extending from posteriorpetrous surface and involving coclea (A). Tricky case: Petromastoid canal & Temporalbone fracture (B).References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Petrous segment ICA aneurysm: Etiology: Post-traumatic, congenital, orpostinfectious. Aneurysm rupture results in massive hemorrhage either from the noseor ear, with no reports of intracranial bleeding.

•Imaging: MRA, CTA demonstrate complex expansive mass of petrous ICA canal withinternal flow = BEST DIAGNOSTIC CLUE!!

•CT: focal or fusiform enlargement of petrous ICA canal; curvilinear calcification inaneurysm wall; may appear destructive with extension into adjacent structures.

•RM: ovoid or fusiform complex signal mass: if thrombus is present = predominantlyhyperintense on T1-wi with peripheral hemosiderin rim on T2-wi (onionskin

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appearance), may "bloom" on T2* GRE/DWI. Otherwise Flow-void (like in other siteaneurysm)

•DSA: for endovascular treatment (not for diagnosis!!)

•DDX: aberrant internal carotid artery (artery enter more posterolaterally than oppositenormal side on MRA/CTA), cholesterol granuloma ( complex PA mass with T1 & T2signal), glomus tympanicum paraganglioma (CE coclear promontory mass), glomusjugulare paraganglioma (CE mass extending up from jugular foramen into middle earcavity), schwannoma of jugulare foramen ( diffusely CE tubular mass following cranialnerve course).

-Aberrant internal carotid artery malformation (aICA): rare vascular congenitalmalformation of the PA, caused by regression of the cervical internal carotid artery duringembryogenesis. As explained by Moret et al, the aICA represents an enlarged inferiortympanic artery anastomosing with an enlarged caroticotympanic artery.

•Imaging CT>>>MR. On CT images it can be recognized by markedly more posteriorlateral extension of the petrous carotid canal that is contiguous with an enlarged inferiortympanic canaliculus. Always view axial and coronal images (don't stop at first slice!!):absent carotid foramen and petrous ICA segment, thinning and remodeling of bonesurrounding middle ear.

•CAVE!!! MRI does not reliably identify aberrant ICA.

•DDX: on coronal images DDX: glomus tumor (misinterpretation = disaster due touncontrollable bleeding or cerebral infarction of potential biopsy or removal), cholesterolgranuloma (MRI+DWI+CM), aneurysm (ICA canal expansion on CT).

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Fig.: Intriguing case. MRI shows right mastoid and PA effusion, but MRI can't identifythe aberrant right ICA and diagnosis of glomus tumor was posed. On CT it's easy torecognize the right aberrant ICA (more posterior and lateral than the right one) with anenlarged inferior tympanic canaliculus. Angiograms confirm diagnosis of aberrant ICA.References: IM Vallone, MD and A. Cerase, MD, UOC Neuroimmagini eNeurointerventistica, Dipartimento di Neuroscienze, AOUS, Policlinico

-Petrous apex meningocele/ PA Arachnoid cyst (PAC): centered in the anteriorpetrous apex is thought to arise from the protrusion of arachnoid or dura from Meckel'scave (MC diverticulum).

•Imaging MR>>>CT (CSF density/intensity lesion of PA which is in continuity with MeckelCave):Thin sections, high resolution, multiplanar T2 wi make diagnosis = BESTIMAGING TOOL!!!.

•On CT smooth, (noninvasive) bony scalloping of PA. No CE of PA or adjacentmeninges.

•DDX: cholesteatoma (no connection to MC, DWI, CE), cholesterol granuloma (internalcontents do not suppress on FLAIR), apical petrositis (clinical setting of otomastiditis;thick CE-rim; thick meningeal CE), MC trigeminal schwannoma (dense CE), effusion (allcortical margins intact on NECT).

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Fig.: Petrous apex meningocele/ Arachnoid cyst. CT (A;B) shows smooth, noninvasivebony escavation of left PA. On ax T2 wi (C) lesion demostrates same intensity of CSFand direct communication with MC. No CE is evident after contrast administration (D).References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Petrous apex mucoceles (PAM): probably caused by postinflammatory obstruction.More commonly in the paranasal sinuses, occasionally in the PA.

Imaging: CT+MRI>>MRI>>>CT.

•CT: indistinguishable from cholesterol granulomas:

-Smooth bone erosion with loss/erosion of osseous septae, fluid-like density

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•MRI: may differentiate PAM from cholesterol granulomas:

Characteristically low to intermediate signal intensity on T1-wi (high water content).No evidence of CE.

•CAVE!!!!! Extensive peripheral CE may suggest superinfection (mucopiocele)

•DDX: cholesterol granuloma (high signal on T1 wi/T2wi), effusion (no loss or erosion ofosseous septae; cortex & trabeculae intact on CT), cephalocele (continuity to MC)

Fig.: Mucoceles. CT shows smooth bone erosion with loss/erosion of osseous septae,fluid-like density (A). Notice the presence of fluid-fluid level with declive portion ofthe lesion hyperintense on T1 wi and hipointense on T2 wi (B;E). Antideclive portionappears isointense to CSF on T2 wi and slightly hyperintense to CSF on T1 wi (C;D).Fluid-fliud level is due to different protein content.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

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-Cholesterol granuloma: intraosseous cyst filled with dark, viscous, chocolatebrown fluid and granulation tissue. Two etiologic hypothesis: Classical hypotesis:granulation tissue forms secondary to repeated haemorrhage, leading to expansive PAlesions. Recent hypotesis: mucosal penetration into PA exposes marrow which leadsto sustained/repeated microhaemorrhage.

Imaging: MRI >>>CT

•MRI: high T1& T2 signal (high T2 signal on FLAIR) in expansive PA mass. No internalCE.

•CT: evaluates bony erosion & invasion of contiguous structures.

•MRA: to assess encasement of petrous ICA.

CAVE!!!! Lesion with high T1 signal appeared bright on TOF-MRA mimics aneurysm.

DDX: asymmetric fatty marrow (non expansive fat density on CT; suppressed withfat-sat MR techniques); cholesteatoma (rim-CE); effusion (opacified air cells; cortex& trabeculae intact on CT ); apical petrositis (thick rim-CE; meningeal thickness andCE); ICA aneurism (internal flow void on MRI T1& T2; Heterogeneous CE on T1 C+);chordoma/chondrosarcoma (destructive lesion at clivus or petro-occipital fissure withcondroid matrix on CT; Heterogeneous internal CE )

Fig.: Cholesterol granuloma. CT (A) demonstrates an expansive mass involving thePA; there is no evidence of bony erosion. Tipically T1 wi (B) and T2 wi (D;E) show anhyperintense lesion with mass effect on the right prepontine cistern. No CE is seen (C).

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References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Cholesteatoma (Chol-PA): classified as acquired or congenital. PA is more commonlyaffected by congenital cholesteatomas that arise from aberrant ectoderm, trapped withinthe PA during embryogenesis.

•Imaging: MRI>>>CT

•MRI: (Thin Ax & Cor slices) expansive mass with low T1& high T2/FLAIR signal.Restricted diffusion (# DWI) is characteristic. No/mild rim CE.

•CT: low-density expansive mass that determinates smooth bone erosion. Largerlesions erode regionally (horizontal petrous ICA, otic capsule, IAC, jugular foramen).CT scan must be extended from skull base to cover all temporal bone. Always includecoronal reconstructions.

•MRA: to asses petrous ICA

•DDX: effusion (non expansive opacified PA air cells on CT), apical petrositis (septicpatient unless already with antibiotics; dural thickening & CE), cholesterol granuloma(previous history of chronic otomastoiditis common; high signal on T1/T2); mucocele(may exactly mimic cholesteatoma except NO DWI # ); petrous ICA aneurysm (MRA/CTA!!).

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Fig.: Cholesteatoma. Two cases of PA cholesteatoma: notice on CT low-densityexpansive masses that demonstrate smooth bone erosion. Ax/Cor T2 wi demonstrateexpansive hyperintense lesions; post-gadolinium T1-wi reveal mild rim-CE .References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Inflammatory pseudotumor (IP): rare, locally aggressive (extensive bony erosions),mimics neoplastic lesion or aggressive infection. IP may involve the facial nerve and thelabyrinthine and otic capsule, without specific imaging features .

The final diagnosis is made after biopsy/surgical resection.

•Imaging MRI>>>CT. Focal thickening of meninges, isointense on T1 wi, iso-hypointense on T2 wi. On T1 C+ diffusely CE focal area of meningeal thickening (ifunderlying bone invasion on T1 C+ fat-sat).

•CT: underlines bone erosion.

•MRA: when ICA narrowing may occur

•DDX: apical petrositis, osteomyelitis, meningeal NH lymphoma/metastasis, chordoma/chondrosarcoma.

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-Petrous apicitis: results from spread of infection to PA through preformed air-cell tractsin the temporal bone (++Haemophilus influenzae, Streptococcus pneumoniae, and B-hemolytic streptococcus species).

•Imaging: MRI+CT>>MR>>>CT

•MRI: asymmetric fluid signal on T1-wi and T2-wi within air cells of PA &mastoid complex.If abscess occur, high T2 signal focus centered in PA.

Always fat-sat after gadolinium injection to image intracranial complications: -epiduralabscess, -parenchimal brain abscess, -skull base osteomyelitis.

•CT: in early stage: opacification of PA air cells. In advanced stage: COALESCENCEof PA air cells (lysis of internal bony trabeculae, permeative cortical erosion & fistulizationto labyrinthin).

•MRA/CTA: when involvement of adjacent skull base arteries is suspected

•DDX: cholesteatoma (low T1 signal; no meningeal CE); effusion (non expansiveopacified PA air cells on CT; usually low T1/ high T2 signal; no meningealCE ); cholesterol granuloma (high T1/T2 signal); chordoma/chondrosarcoma (lacksacute infectious symptoms; infiltrative heterogeneous CE mass of clivus or petro-occipital fissure); metastasis/NH lymphoma (lacks acute infectious symptoms; infiltrativeinhomogeneous CE PA mass).

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Fig.: Petrous apicits. MRI show fluid signal on T1-wi and T2-wi in right and left air cellsof PA & mastoid complex (arrows). Post-contrast T1-wi (with fat-sat) demonstrate CE(arrowheads) on the right mastoid and extension into right cavernous sinus, and skullbase osteomyelitis (arrowheads), prevalent on the right sideReferences: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Fibrous dysplasia: a benign lesion (characterized by excessive remodelling of bone)that may involve the petrous apex. It is classically divided into the rarer polyostotic formand the more common monostotic form.

•Imaging: CT >>>MRI.

•CT is enough to make correct diagnosis (axial views) = BEST DIAGNOSTIC TOOLto define demineralization (early phase), ''ground glass'' appearance (intermediatephase), extreme bone thickening (late phase).

•MRI: any signal intensity on T1/T2 wi reflects the different degrees of fibrousand cystic components (low attenuation on T1/T2 wi :high degree of mineralization).Heterogeneous CE on T1 C+ with possible meningeal CE.

•DDX: otosyphilis, osteoradionecrosis, osteogenesis imperfecta.

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-Langerhans cell histiocytosis (LCH): idiopathic neoplasm caused by proliferationof mature eosinophils and specialized bone marrow -derived Langerhans cells-. +++eosinophilic granuloma. Frontal and temporal bones are the most commonly affectedregions in the skull.

•Imaging: CT >>>MRI

•CT = BEST DIAGNOSTIC MODALITY: bony lesion with variable appearance ("punchedout", irregular/sclerotic margins, fragment of bone within soft tissue) and focal or diffusebone changes

•CAVE!!!!!!: CECT or MR help differentiate inflammatory mastoid lesions from LCH

•MRI: Iso- to hypointense soft tissue mass on T1-wi; hyper- to isointense on T2-wi.Heterogeneously CE +/- intracranial extradural extension (always FAT-SAT T1 C+)

•DDX: cholesteatoma (no CE); cholesterol granuloma (preceded by history of cronic earinfections; Hyperintense on T1 wi); otomastoiditis (clinical symptoms that respond toantibiotics) inflammatory pseudotumor, petrous apicitis.

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Fig.: Langerhans cell histiocytosis. Ax CT shows destructive bilateral PA masseswith permeative bone changes (A). After steroid treatment, 2 years later, notice thecomplete healing.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

2. NEOPLASTIC (Benign) PA LESIONS

-PA Hemangioma: benign vascular tumour arising from capillaries around facialnerve , most commonly in area of geniculate. Site of occurrence GENICULATEFOSSA>>internal auditory canal fundus >> posterior genu facial nerve.

•Imaging MR>>>CT: on T1 wi mixed signal lesion with foci of low signal within lesionmatrix (ossific matrix), on T2 wi high signal lesion with foci of low signal. CM: avid CE

•CT: (Ax & Cor planes) amorphous "honeycomb" bone changes (highlycharacteristic!!!!!!!!!!), poorly marginated lesion of geniculate fossa.

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•DDX: cholesteatoma (no CE, DWI restricted), facial schwannoma, perineural parotidmalignancy on CN7.

Fig.: Hemangioma. Ax/Cor CT images show a poorly marginated mass of geniculatefossa with typical amorphous "honeycomb" bone changes (arrows), post gadoliniumT1-wi demonstrate avid CE with foci of low signal (arrows).References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

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Fig.: TRICKY CASE. tiny lesion located in right PA with high signal on T2 wi (A, B). T1wi after contrast demonstrate faint, rim CE (C, D). Hypothesis of VII cn schwannomais not supported by the lesion location that appears slightly eccentric respect togeniculate fossa(D). Other possible hypotheses are hemangioma or cholesteatoma(DWI non usefull due to the small lesion dimension!!). MRI follow-up has beenrequested.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Schwannoma (Schw): does not arise within the PA but it involves PA from directextension. It originates from cranial nerves VIII>VII>V>IV and VI; vestibular division ismost commonly involved. Acoustic schwannoma might extend laterally into the labyrinthor into the middle ear cavity via the round or oval window. Isolated involvement of thelabyrinthine structures of the vestibule, semicircular canals, or cochlea also has beendescribed.

•Imaging MR>>>CT: Signal intensity is low on T1-wi, high on T2-wi. CE is markedand inhomogeneous when larger. When filling up the IAC it typically resembles an "icecream cone".

DDX mostly depends on the origin of the schwannoma:

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1. Vestibular: most commonly arises from superior vestibular branch, around thevestibular ganglion, near the fundus of the IAC.

•DDX: metastases, lymphoma (lesions number), meningioma (dural-based).

2. Facial: geniculate ganglion>> 2°/3° segment.

•DDx: cholesteatoma (restricted diffusion on DWI, no CE), glomus tympanicumparaganglioma (pulsatile mass + clinical symptoms, angiographic blush).

3. Trigeminal: within the Meckel's cave.

•DDX : meningioma, perineural spread (via V3) .

Fig.: VIII cn schwannoma. Illustration from Diagnostic Imaging, head and neck(Harnsberger et al.) When filling up the IAC schwannoma typically resembles an "ice

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cream cone". Signal intensity is low on T1-wi, heterogeneous but predominant high onT2-wi. SSFP better demonstrate enlarging IAC mass. CE is marked and homogenous.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

Fig.: V nc schwannoma. T2-wi and post-gadolinium T1-wi demonstrate solid, welldefined mass centered in the Meckel cave, containing cystic componentsReferences: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

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Fig.: Two cases of VII cn schw arising from different cn segment. TRICKY CASE:unless MRI characteristics of lesion in C should appear similar to A and B, it is aperineural spread of parotid cancer (*)References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Meningioma: involves the petrous apex region arising from cerebellopontine angle(extending into the internal auditory canal) and petroclival ligament (affecting the fifth andsixth cranial nerves or entering the Dorello's canal).

•Imaging MRI >>>CT.

• MRI: isointense or slight hypointense on T1-wi , isointense to hyperintense on T2-wi, may "bloom" on T2* GRE. CE is homogenous with accompanying dural tails (+C:Ax & Cor thin section!!) with the shape of a"mushroom head"

•CAVE!!!! Atypical and malignant meningiomas are rare, with tendency to show restricteddiffusion (DWI).

•CT Ax & Cor: internal calcification, bone reaction and hyperostotic-sclerotic bonechanges.

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•DDX: sarcoidosis (often multifocal, look for infundibular stalk involvment), acoustic-trigeminal and facial schwannoma (no dural tails and meningeal reaction),leptomeningeal metastasis (multifocal meningeal involvment), primary meningeallymphoma, pseudotumor (rare diffuse meningeal thickening & CE).

Fig.: Meningioma. Illustration from Diagnostic Imaging, head and neck (Harnsbergeret al.) Ax graphic, T2-wi and post-gadolinium T1-wi demonstrate large meningiomacausing mass effect on brainstem and cerebellum. Notice homogenous CE withaccompanying dural tails ("mushroom head"!!!).References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

-Chordoma (Ch): rare tumor, originated from embryologic remnants of the notochord. Itis midline lesion that occurs anywhere from the clivus to the sacrum with approximatelyone third involving the clivus.

•Imaging MRI>>>CT

•MR : hypointense to isointense destructive midline mass on T1-wi (small foci ofhyperintensity for haemorrhage or mucoid materiale) , hyperintense on T2-wi (small fociof hypointensity forcalcification, haemorrhage or mucoid materiale), on T2* GRE focal #signal. CE with a characteristic ''honeycomb'' pattern.

•CT: locally destructive lesion centered at the clivus, with lytic bone destruction andtrue calcifications (chondroid chordoma variant)

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•MRA: encasement & displacement of vessel

•DDX: chondrosarcoma (chondroid calcification> 50%), plasmacytoma (T2 signal usually#), metastatic tumour (destructive mass that can be anywhere; often multiple enhancing),inflammatory pseudotumor, petrous apicitis, osteomyelitis.

Fig.: TRICKY CASE. Ax CT (A; D) show locally destructive lesion containingcalcifications. Mass appears hyperintense on T2-wi (B) and hypointense on T1-wi (E)with outlying ring of CE (C;F). EXCEPTION to the rule: in this case the lesion is notmidline, it arises from R-PA, extending into the clivus.References: Courtesy of A. Cerase. MD, UOC Neuroimmagini e Neurointerventistica,Dipartimento di Neuroscienze, AOUS, Policlinico "Santa Maria alle Scotte", Siena, Italy.

3. NEOPLASTIC (Malignant) PA LESIONS

-Chondrosarcoma (Csa): rare malignancy (account for less than 1% of intracranialneoplasms) arising from embryologic cartilage rests along the sphenopetroclival fissure.Five different histologic subtypes:

-conventional, -clear cell, -myxoid,-mesenchymal, -dedifferentiated.

•Imaging: CT+MR

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•CT: characteristic CHONDROID CALCIFICATION in tumour matrix (>50%); greaterthan 50% and bone destruction

•MR: hypointense to intermediate destructive mass located at petro-occipital fissure onT1 wi, hyperintense on T2 wi (foci of hypointensity for calcification). Heterogeneously-CE

•MRA, MRV mandatory. Pre-operative DSA with test occlusion.

•DDX: vs cholesteatoma ( no CE), meningioma (not typically destructive on CT; CE with"dural tail"); chordoma (hallmarks to differentiate Ch from Csa: should be midline locationof Ch and lateral location of Csa; # internal calcification; # invasive bone changes inpetro-occipital fissure); metastasis (destructive mass that can be anywhere; often multipleenhancing), plasmacytoma (more midline within clivus; T2 signal usually #) inflammatorypseudotumor, petrous apicitis, osteomyelitis.

- Metastasis (Mets): commonly in patients between 50 and 70 y.o. PA is the mostcommonly involved site in the temporal bone. The mechanisms for metastatic tumorinvolvement include haematogenous spread from distant tumors or leukemia/lymphoma,direct extension via an extra or intracranial neoplasm, and extension from leptomeningealmetastastic location. Most common primitive tumor is adenocarcinoma.

•Imaging: MRI+NECT>>MR>>CT

• MRI & CT: signal/density depends on the primary tumor. CE in most case(fat sat onT2-wi and on T1-wi after gadolinium: CAVE!!!!!!).

• CT show significant bone destruction

•DDX: cholesteatoma, plasmacytoma, inflammatory pseudotumor, petrous apicitis,osteomyelitis, chordoma/chondrosarcoma.

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Fig.: Metastasis. Ax T2 wi (A) reveals area of inhomogeneous high signal fillingthe right PA, post gadolinium Ax/CorT1 wi (B;C) show diffuse CE. Notice adjacentenhancing fat of the clivus and of VIII c.n (arrow in C).References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

- Endolymphatic sac tumor (EST): rare tumour , specific to the PA. EST arises fromthe proximal rugose portion of the endolymphatic sac located halfway between the IACand jugular foramen, along the posterior aspect of the temporal bone.

•Imaging: both CT & MR are necessary. Characteristic findings: intratumoral bonespicules (CT), high signal foci within tumor matrix (T1-wi)

•NECT: aggressive, soft tissue mass that erodes posterior wall of temporal bone.

•CAVE!!!!!!!!!: always look at posterolateral jugular foramen/posterior wall of IAC

•MRI: hyperintense foci within tumour on T1-wi (along tumour margin if <3cm; withintumour if> 3 cm); flow voids (if> 2cm). Heterogeneous CE.

•MRA to asses external carotid branches feed lesion; MRV to evaluated sigmoid sinus(occluded by larger tumors)

•DDX: cholesterol granuloma (long term sequelae of chronic otitis media; high signalon T1wi involves entire lesion); glomus paraganglioma (pulsatile tinnitus; rarely involvesretrolabyrinthine temporal bone; high signal foci on T1 MR rare; high velocity flowvoids present); schwannoma of jugular foramen (uniform CE, intramural cysts possible);meningioma of jugular foramen-CPA cistern (CE mass on T1 C+, lacks flow voids)inflammatory pseudotumor, petrous apicitis, osteomyelitis.

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Fig.: Endolymphatic sac tumor. Lesion shows high signal on T2 wi (A), withinhyperintense foci on T1-wi B), typically located in the posterior petrous ridge. Postgadolinium T1 wi (C) reveals heterogeneous CE. Notice the involvement of the internalauditory canal. Axial CT and 3D VR reconstruction (D, E) show typical permeative bonechanges of ELST; notice the involvement of internal auditory canal.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

IMAGING ALGORITHM

First, we propose an imaging algorithm to assist in differential diagnosis, based on:

• First: recognize "origin" of lesion: within PA vs involvement from adjacentstructures

• Second: PA size: normal vs expanded• Third: pattern of growth: aggressive vs. non aggressive• Fourth: Imaging characterization by signal intensity/CT density/CE

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Fig.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

Then, application of the algorithm to the most common (and clinically relevant) PAlesions has been shown.

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Fig.References: F. Piludu; Department of Bioimaging and radiological Sciences, UCSC,Rome, ITALY

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Fig. 1

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Conclusion

As a consequence of improved diagnostic imaging modalities, otologists haveencountered a steadily increasing number of PA lesions . Imaging plays a critical rolein the evaluation of patients with petrous apex abnormalities because this area is notdirectly visible on clinical examination and is difficult to access for percutaneous biopsy.

A knowledge of the anatomy and its variations is essential so as not to mistake ananatomic variation or ''no-touch'' lesion for a lesion that requires surgical interventionand rational and systematic approach to use CT and MRI, along with the history andphysical examination is mandatory and essential to support the differential diagnosisand the surgical planning.

In fact advances in diagnostic imaging and different microsurgical techniqueshave made the management of petrous apex pathology less daunting for modernskull base surgeons.

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Personal Information

References

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ct and mri assessment in differential diagnosis and ...€¦ · -review petrous apex (pa) anatomy...

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