Classification of PAL:

Developmental Lesions:

• Cholesterol granulomas: they are among the most common PAL; the suggested cause is that aggressive pneumatization of the petrous apex leads to exposure of bone marrow, whose hemorrhages lead to foreign-body reaction, subsequent cyst formation (filled with viscous brown fluid, granulation tissue, and cholesterol crystals) and bone remodeling and expansion. They are usually hyperintense on both T1- and T2-weighted images and will remain hyperintense after fat suppression. After contrast administration, there may be subtle peripheral enhancement secondary to inflammatory response but no central [4,5]. (Figures 4-7).

• Cholesteatoma: classified as congenital (more common in apex, arising from aberrant ectoderm trapped during embryogenesis) or acquired. At CT they cause variable degrees of bone destruction. MR findigns are: intermediate to low signal intensity on T1-weighted images, high signal intensity on T2-weighted/FLAIR and restricted diffusion (often). Enhancement is not usually seen after contrast material administration, but a thin rim may be present [3-5]. (Figure 8).

• Petrous Apex Mucoceles: caused by post-inflammatory obstruction of a pneumatized petrous apex air cell. They typically have low to intermediate signal intensity on T1W and high signal on T2-weighted images [6]. (Figure 9).

• Petrous Apex Cephalocele: they are one of the most common findings in petrous apex; represents protrusion of arachnoid or dura mater into the petrous apex.  They are smoothly marginated and have the same signal intensity characteristics as cerebrospinal fluid (CSF) [7,8]. (Figures 10-12).

Inflammatory Lesions

• Petrous Apicitis: infectious process caused by medial extension of acute otitis media into a pneumatized petrous apex. Subsequent obstruction of drainage from the petrous apex to the middle ear may result in formation of a purulent abscess. Acute febrile illness and symptoms of the classic Gradenigo triad (ear pain, palsy of the sixth cranial nerve, and facial pain) may be present. Complications include meningitis, cranial nerve involvement (trigeminal ganglion and abducens nerve lie close to the petrous apex), cerebral abscess formation, bone erosion and venous sinus thrombosis [3,9,10]. (Figures 13-15).

• Petrous Apex Osteomyelitis: caused by direct medial extension of necrotizing otitis externa or by retrograde spread of thrombophlebitis along the venous plexus of the petrous carotid canal. Patients typically complain of severe, deep ear pain that is out of proportion to the physical findings. Pseudomonas is the most common causative organism. CT may show either bony erosions or sclerosis. MR imaging determines the extent of the disease demonstrating the replacement of the fatty bone marrow by the infectious process and the surrounding soft tissue and intracranial involvement [2,3,11]. (Figure 16).

• Wegener Granulomatosis: necrotizing vascular disorder, commonly seen in the sinonasal region but may affect middle ear and mastoid. In the later stage, granuloma depicts as soft-tissue mass at CT, hypointensity on both T2- and T1-weighted MR sequences, with variable degrees of contrast enhancement [12].

Benign Tumors

• Meningioma: those located in Petroclival and cerebellopontine angle usually involve the petrous apex. Petroclival meningiomas originate from the medial aspect of the petrous apex and course over its wall. Cerebellopontine angle meningiomas arise from the dura mater along the posterior surface of the petrous apex and can extend into the IAC. Meningiomas appear as dural-based masses that are typically slightly hyperattenuating to brain tissue on CT images, iso- to hypointense on T1-weighted images, and iso- to hyperintense on T2-weighted images. They usually enhance avidly after contrast administration [3,4,13]. (Figure 17).

• Schwannoma: usually originate from the fifth, seventh, or eighth cranial nerves. A rare type of petrous apex schwannoma is the primary intraosseous schwannoma which is found in the petrous carotid canal and is thought to arise from the deep petrosal nerve of the periarterial carotid plexus. At MR imaging, they generally appear as well-circumscribed, smoothly expansile masses that are iso- to hypointense on T1-weighted images and hyperintense on T2-weighted images, with enhancement on gadolinium-enhanced images. Occasionally, intracranial schwannomas may be cystic and contain fluid levels. Schwannomas of the eighth cranial nerve may fill the IAC and  enlarge the porus acusticus [3]. (Figure 18).

• Paraganglioma: They arise from paraganglia in the adventitia of the jugular bulb, the superior ganglion of the Xth nerve, or along the Jacobsen and Arnold nerves. Most of them are benign but locally aggressive, but some of them degenerate. They may invade the petrous apex via preformed air cell tracts from their sites of origin in the jugular foramen or middle ear.  Large paragangliomas may have a characteristic salt-and-pepper appearance on T1-weighted images. The hypointense “pepper” represents high-velocity flow voids of feeding arterial branches in the tumor (also evident on T2-weighted images), while the less commonly seen hyperintense “salt” represents underlying foci of hemorrhage. These tumors usually enhance intensely after contrast material administration, and may associate show typical moth-eaten or permeative bone changes [3,14,15]. (Figures 19-21).

• Condroma: usually arise at the junction of the petrosphenoidal, petroclival, and spheno-occipital synchondroses [3].

Malignant Tumors

• Chondrosarcoma: malignant cartilaginous tumors typically originate at the petroclival and petrosphenoidal synchondroses. At MR imaging, the lesions have low to intermediate signal intensity on T1-weighted images and high signal intensity on T2-weighted images relative to that of brain tissue. Signal heterogeneity can be seen and may be due in part to the presence of mineralized chondroid matrix. They demostrate variable degrees of enhancement after contrast material administration [3]. (Figure 22).

• Metastasis: The petrous apex is the most common site of metastasic disease within the temporal bone; the most frequently reported primary neoplasms are lung, prostate and breast cancers. Treatment is primarily palliative [17].

• Nasopharyngeal Carcinoma: occasionally spreads to the petrous apex by direct extension; infiltration into the IAC may occur, leading to compression of the eighth cranial nerve and symptoms of vertigo, sensorineural hearing loss, or tinnitus. It demonstrates intermediate to high signal intensity (usually greater than that of muscle) on T2-weighted images, low signal intensity on T1-weighted images, and moderate enhancement on contrast-enhanced images [3]. (Figures 23-24).

• Others: Lymphoma, Rhabdomyosarcoma, Langerhans Cell Histiocytosis…

Vascular Lesions

• Petrous Carotid Aneurysm: Most petrous ICA aneurysms are large and fusiform, and CT shows expansion of the carotid canal in the anterior petrous apex. Endovascular or surgical interventions are considered for symptomatic patients. (Figure 25).

• Intraosseous Dural Arteriovenous Fistula: the vascular nidus is situated within bone [3,18].

Osseous Dysplasias

• Fibrous Dysplasia: CT is usually diagnostic and shows characteristic ground-glass internal matrix.

• Paget Disease: show osteolytic, mixed, and sclerotic areas, depending on the phase of the disease.

• Osteopetrosis type 2: autosomal-dominant, also known as Albers-Schönberg disease, onset occurs in adolescence/adulthood. Radiographically, the hallmark is diffuse increased density within the medullary portion of calvarial and skull base and petrous apices with relative sparing of the cortices (CT) with diffuse low signal on axial T2-weighted MR images [3,14,19]. (Figure 26).

Normal Variants

• Petrous Apex Pneumatization: may be asymmetric in up to 10% of patients. (Figures 27-28).

• Petrous Apex Effusion: can develop within pneumatized petrous apex cells and can occasionally mimic masses; lack of bone remodeling and preservation of bone septa helps to rule out mucocele [3,4,14]. (Figure 29).