Findings and procedure details
Malignant Tumors
Squamous Cell Carcinoma (SCC)
Most common malignant tumor of the temporal bone, typically arising in the external auditory canal or middle ear1. On high-resolution CT, it often manifests as aggressive, “moth-eaten” bone destruction with possible extension into the mastoid air cells or petrous apex.
Fig 1: Malignant SCC.
CT images show soft tissue mass of the left temporal bone (a), complete destruction of the bone (b) due to SCC of the external ear. The contrast enhancement is seen mostly on the edges of the lesion, and the central part is mostly filled with tumoral necrosis.
MRI usually reveals an irregular, heterogeneously enhancing soft-tissue mass, with perineural invasion or intracranial extension in advanced cases.Metastatic Disease
Metastases can originate from breast, lung, prostate, and kidney malignancies. On CT, these lesions may appear lytic or sclerotic, involving sites like the middle ear, mastoid, or petrous apex. MRI findings vary but commonly show an enhancing mass that may impinge on critical structures (e.g., internal auditory canal, facial nerve canal) and present with hearing loss or cranial neuropathies.
Fig 2: Metastases.
Brain MRI shows high T2 signal lesion of the left petrous apex (a). The lesion shows strong contrast enhancement (b).
Chordoma
Malignant tumors that arise from notochordal remnants, typically midline involving the clivus and extending into the petrous apex2. CT imaging reveals lytic bone destruction, while MRI shows lobulated, T2-hyperintense masses with heterogeneous enhancement, often demonstrating soft-tissue extension into adjacent structures.
Fig 3: Chordoma.
MRI demonstrates a midline osteolytic clival mass with T2/FLAIR hyperintensity (a, b), T1 hypointensity (c), iso DWI (d), iso/low ADC (e), and heterogeneous enhancement on post-contrast images (f), consistent with a chordoma.
Chondrosarcoma
Malignant cartilaginous tumors that commonly affect the petroclival fissure. CT reveals a calcified matrix within lytic bone lesions (a in Figure 4.), and MRI demonstrates lobulated masses with high T2 signal intensity and marked enhancement, often distinguishing them from other skull base tumors.
Fig 4: Chondrosarcoma.
Imaging reveals an off-midline mass centered in the left petro-occipital synchondrosis, with calcified matrix within lytic bone destruction on CT (a). MRI shows a high T2/FLAIR signal (b, c), restriction diffusion on DWI (d, e), and strong post-contrast enhancement (f).
Pituitary macroadenoma
An unusual case of pituitary macroadenoma extending bellow the sella, infiltrating the clivus and the right petrous apex.
Fig 5: Pituitary macroadenoma infiltrating petrous apex.
MRI images of pituitary macroadenoma extending below the sella. The tumor shows high intensity on T2 (a,c), low T1 (b) and shows strong contrast enhancement (d,e,f).
The macroadenoma usually shows low T1 and high T2 signal with homogenous enhancement on MRI.Endolymphatic Sac Tumor
Endolymphatic sac tumors are rare, often slow-growing but locally aggressive lesions arising from the endolymphatic sac in the posterior petrous temporal bone. They may occur sporadically or in association with von Hippel–Lindau disease. On CT, they appear as lytic lesions that can expand or erode bone. MRI characteristically demonstrates a heterogeneous mass with variable signal intensities due to hemorrhagic or cystic components, and strong enhancement.
Fig 6: Endolymphatic sac tumor.
Images show a left temporal expansile mass with lytic bone destruction in an infiltrative or "moth-eaten" pattern, with central calcific spiculation on CT (a,b).
On MRI, the lesion is heterogeneous with hyperintense T2 cystic components (c) and T1 hemorrhagic areas (d), with strong, heterogeneous enhancement and intracranial extension on post-contrast images (e,f). Findings are consistent with endolymphatic sac tumor in a patient suspected of having von Hippel Lindau syndrome.
Symptoms may include hearing loss, tinnitus, and vertigo.
Benign Tumors and Masses
Cholesteatoma
Though not a true neoplasm, cholesteatomas are expansile collections of keratinizing squamous epithelium, often originating in the Prussak space, that can erode bone and require surgical removal. On CT, they appear as a non-enhancing soft-tissue mass in the middle ear or mastoid, frequently causing scutum or ossicular destruction.
Fig 7: Cholesteatoma.
CT images of a young patient with left sided ear pain and hearing loss show a soft tissue mass centered in Prussak space and epitympanum that surrounds the slightly demineralized ossicles with erosion of scutum and thinning of tegmen tympani (a-e), features characteristic of cholesteatoma.
MRI with DWI shows characteristic diffusion restriction, distinguishing them from other lesions. Non-EPI DWI in coronal is extremely useful in detecting small cholesteatoma and in distinguishing cholesteatoma from inflammatory changes3. Fig 8: Cholesteatoma.
CT (a,b.c) and MR images (d,e,f) shows postoperative changes of the left temporal bone. The mastoidectomy defect is filled with soft tissue mass, with small area of high intensity on non-EPI DWI (e) and DWI-b1000 (f) which is suggestive for residual cholesteatoma.
Cholesterol Granuloma
Cholesterol granulomas, often located in the petrous apex or mastoid air cells, arise from hemorrhage and entrapment of blood products within non-ventilated spaces. Characteristically, they appear hyperintense on both T1- and T2-weighted MRI images (due to chronic blood breakdown products) and typically show minimal or no enhancement4.
Fig 9: Cholesterol granuloma.
MRI imaging shows a right petrous apex lesion with non-aggressive bony expansion on CT (a), hyperintensity on T2 (b) and FLAIR (c), and high T1 signal (d) due to cholesterol, consistent with a cholesterol granuloma.
Most are asymptomatic and do not require intervention unless they expand to compromise adjacent structures or cause hearing loss.Schwannoma
Facial nerve and vestibular schwannomas follow the course of cranial nerves VII and VIII, often causing progressive facial nerve palsy or hearing loss. Features include canal widening on CT and homogeneously enhancing lesions on MRI5.
Fig 10: Facial nerve Schwannoma.
CT (a,b,c) and MRI (d.e,f) images show benign, smooth cystic enlargement of the facial nerve course on the right, consistent with a cystic facial nerve Schwannoma.
Paraganglioma (Glomus Tumors)
Glomus jugulare (jugular foramen) and glomus tympanicum (middle ear) are highly vascular tumors. They frequently present with pulsatile tinnitus and/or conductive hearing loss. On CT, look for an enlarged jugular foramen and “moth-eaten” permeative bone erosions.
Fig 11: Paraganglioma.
CT images demonstrate a well-defined, strongly early enhancing, highly vascular mass centered around the right internal jugular vein (d,e,f), showing "moth-eaten" lytic bone destruction of the jugular foramen (a, b, c). Note the parotid space extension of the lesion.
MRI classically demonstrates a “salt-and-pepper” appearance due to high vascular flow voids, and strong enhancement. They can be locally aggressive, warranting surgical or endovascular treatment to prevent complications. Fig 12: Paraganglioma.
MRI images of the same patient as Figure 11 show the right jugular paraganglioma with low T1 signal (a, b) and high signal with characteristic "salt-and-pepper" appearance from flow voids on T2-weighted images (c). The lesion shows some mild diffusion facilitation (d) with avid contrast enhancement (e, f).
Fig 13: Paraganglioma.
Imaging demonstrates a mass at the left jugular foramen with characteristic "salt-and-pepper" appearance on T2-weighted MRI (a), low T1 signal (b), avid enhancement (c, d), restricted diffusion on DWI (e), and prominent vascular supply on angiography (f), features consistent with jugular paraganglioma.
Petrous Apicitis
Petrous apicitis, or petrositis, is an inflammatory process affecting the petrous apex—often secondary to chronic otitis media or mastoiditis. Patients may present with deep ear pain, persistent discharge, or even cranial nerve VI palsy (Gradenigo’s syndrome). On CT, there may be sclerosis or lytic changes in the petrous apex; MRI can show enhanced inflammatory changes or abscess formation. Prompt antibiotic therapy and possible surgical drainage are crucial to prevent complications.
Fig 14: Petrous apicitis.
There are features of petrous apex inflammation with bony erosion on CT (a), T1 hypointensity (b), T2 hyperintensity (c), restricted diffusion on DWI (d, e), and peripheral post-contrast enhancement (f), consistent with petrous apicitis abscess formation.
Fibrous Dysplasia
A benign fibro-osseous disorder, fibrous dysplasia replaces normal bone with fibrous tissue. On CT, it displays a characteristic “ground-glass” appearance and may cause painless bony expansion. MRI helps assess any soft-tissue involvement. Treatment is typically conservative unless there is functional or cosmetic impairment.
Fig 15: Fibrous Dysplasia.
CT image shows “ground glass” expansile lesions of the left viscerocranium characteristic of fibrous dysplasia.
Meningeoma
Meningiomas originate from meningothelial cells and can involve the petrous apex, internal auditory canal, or dura of the middle cranial fossa. MRI typically shows a vividly enhancing, dural-based mass with a “dural tail”.
Fig 16: Petroclival menigeoma.
MR images with gadolinium show petroclival meningioma on the right with strong contrast enhancement. Note the infiltration of the Meckel cave on the right.
“Don’t Touch” Lesions
Petrous Apex Effusion
Fluid accumulation in the petrous apex, often incidental due to chronic inflammation, sinus disease, or obstructed air cells, appears as T2 hyperintensity without enhancement on MRI, and usually doesn’t require treatment.
Fig 17: Petrous apex effusion.
MRI images of a right sided petrous apex lesion with T2 hyperintensity (a, b, c), low DWI (d) and high ADC signal (e), and lack of post-contrast enhancement (f), consistent with non-infectious petrous apex effusion.
Petrous apex cephalocele
A cystic lesion resulting from herniation of meninges into the petrous apex. Imaging typically shows a well-defined lesion which follows CSF signal, with no restricted diffusion or enhancement, and is often connected to the CSF space.
Fig 18: Petrous apex cephalocele.
MRI images show a T2 hyperintense lesion in the right petrous apex in continuation with the Meckel cave (a-c, f), which suppresses on FLAIR (d) and doesn’t enhance on postcontrast T1 (e), often associated with empty sella (f).