Petrous Apex Lesions
Ann Marie Visosky, M.D.
March 9, 2006

Regarding the anatomy of the petrous apex, it is a very difficult region in the temporal bone to access. Detailed descriptions have been published explaining the anatomy of the petrous apex for surgical benefits. Briefly, the petrous apex fits between the clivus anteromedially and the otic capsule posterolaterally. The anterior surface forms the middle fossa, and the anterior tip is where the internal carotid artery passes as it enters the cavernous sinus. Most divide the petrous apex into an anterior and posterior portion, with the anterior being the larger of the two. It lies medial to the cochlea and is the most frequent region involved into disease processes. The region often contains bone and is mucosally lined pneumatized cells. At the posterior portion of the petrous apex is the smaller of the two and lies between the semicircular canals and the IAC. It is mostly composed of solid bone of otic capsule origin and, in some people, it also contains pneumatized cells.

Due to the vast number of vital structures that pass near the petrous apex, diseases or lesions in this area can result in certain symptomatology; but they can go undetected for long periods of time due to vague symptoms as well. These can include headaches that are usually retroorbital or vertex due to traction of the dura on the middle fossa. Eustachian tube dysfunction can lead to conductive hearing loss. There can be vertigo, hearing loss, and facial paralysis due to involvement of the otic capsule or the IAC. Sensory disturbances or facial pain can result from involvement of cranial nerve V due to compression and/or irritation of the gasserian ganglion. Cranial neuropathies of the anterior involvement can be at the VI cranial nerve as well as occasionally the III or the IV, and the posterior involvement can affect IX through XII.

Overall, the lesions of the petrous apex are quite rare and the differential, as shown here, is quite long. What I will focus on today is the inflammatory and infective lesions of the petrous apex. Due to the emphasis on time, I will not go over the neoplasm except to say that those listed meningiomas are the most common. In the osteodystrophy category, there are multiple osseous conditions that can involve the petrous apex, all being part of larger disease processes that can include Paget disease, fibrodysplasia, and osteopetrosis. Petrous carotid aneurysms are also quite rare, and the symptoms can depend on what direction the aneurysm expands. I will briefly touch upon arachnoid cysts and normal variants later in the talk.

With today’s advancements in imaging technology, the petrous apex lesions are more easily diagnosed; and better management plans can be cultivated preoperatively. There are CT and MRI findings that are characteristic of certain petrous apex lesions and, today, MRI and CT imaging are used in conjunction with each other in the diagnosis and surgical planning of petrous apex lesions. We will be reviewing these throughout the talk. In reviewing the incidence of petrous apex lesions, Muckle and colleagues out of the House Institute looked at their experience over a two-decade period with petrous apex lesions, and this included 66 patients overall. They found no difference in the male to female ratio. The average age of the patients was approximately 40 years, and they had a mean period of symptoms of about 9 months. Their mean follow-up was 27 months.

This first table depicts the prevalence of petrous apex lesions found in their study. Cystic lesions were the most common with cholesterol granulomas being by far the most common. While they acknowledge that meningiomas are the most common of the solid tumors, they did not include that in their study, as they said that they are usually secondarily involved in the area. The second table illustrates the most common presenting symptoms that their patients reported: hearing loss, dizziness, headache, and tinnitus being the most common. On the imaging studies, those lesions that extended beyond the confines of the petrous apex were found 43% of the time to involve the carotid canal, 28% of the time to involve the clivus, and 19% to involve the middle cranial fossa.

Regarding cholesterol granulomas, the term describes the foreign body giant cell reaction to cholesterol with associated fibrosis, vascular proliferation, hemosiderin-laden macrophages, and round cells. They can be found throughout the temporal bone and usually are seen in conjunction with serous otitis media, chronic otitis media, with or without cholesteatoma, seen in prior otologic surgery or local trauma. Past terms for these lesions have included epidermoid cysts, which really is an improper term as really there is no squamous and epithelial lining, mucosal cysts, or giant cholesterol cysts. They were first reported in the mastoid and middle ear in the later part of the 19th century, but petrous apex cholesterol granuloma was not recognized as a distinct entity until the late 1980s.

Regarding the pathology, we see cholesterol crystals surrounded by multinucleated foreign body giant cells embedded in this fibrous granulation tissue with histiocytes, roundcell infiltration, macrophages, and many capillaries. On imaging, as seen in our case presentation, there is a smoothly marginated expansile mass that is not enhancing and isodense with the brain and, on MRI, there is classic finding of hyperintensity on T 1 and T 2 images with no change with gadolinium.

Jackler and Cho in 2003 wrote a paper on a new theory to explain the development of cholesterol granulomas of the petrous apex. The classic theory that they term the obstruction-vacuum theory was developed from observations from tympanomastoid cholesterol granulomas. This classic theory has been that of inadequate ventilation. You have poor ventilation interfaced with drainage in a usually pneumatized space that leads to negative pressure, reabsorption of air, mucosal edema, hemorrhage, and ultimately a cholesterol granuloma forms. The cholesterol is generated by the catabolism of hemoglobin and by local tissue breakdown. Bone destruction is believed to result from this pressure necrosis. Jackler and Choreport that the classic hypothesis does not adequately explain the occurrence of petrous apex cholesterol granulomas because first hypoventilation is the underlying trigger. If it is the underlying trigger, then why do not we see these in patients with longstanding Eustachian tube dysfunction, and also troubling is that they usually form in very well pneumatized petrous apices that are indicating freedom of disease.

Their new theory is that of exposed bone marrow. They hypothesized that it is aggressive pneumatization that creates bony defects into the bone marrow spaces. Then you get coaptation of marrow, and mucosa create proclivity to hemorrhage, and this hemorrhage is triggered, and clot obstructs the apical outflow tract. This leads to breakdown of the blood, the foreign body reaction leading to a sterile inflammatory reaction, and cyst expansion, and bone erosion. This illustration, from their paper, illustrates the interface of the marrow and the cells leading to hemorrhage. They looked at radiographic findings of 13 ears of patients with cholesterol granulomas and compared it to 31 ears of patients that had well pneumatized petrous apices, but no granulomas; and 6 of the 13 had incomplete partition between the clivus and the petroclival region, but histologic studies are yet to follow. Whatever the pathophysiology of this entity is, and perhaps it is multifactorial, the treatment is surgical drainage with marsupialization of the cyst with the goal, as I said, of drainage and permanent aeration. Total excision is not necessary. Recurrent rates have been reported anywhere from 12% to 60%.

We will go now to petrous apex cholesteatomas. Most agree on the classification of petrous apex cholesteatomas as congenital or acquired. The congenital cholesteatomas are thought to arise from a squamous epithelial rest that are in the normal pneumatized bone, and acquired cholesteatoma is caused by hypoventilation of the middle ear with resultant retraction of the tympanic membrane. Deep penetration into the petrous apex is relatively rare, but can occur through a variety of routes, usually being the supralabyrinthine or subcochlear. Both forms usually involve the anterior portion of the petrous apex. On pathology, both the congenital and the acquired cholesteatomas are identical. They are keratin-filled, epithelial-lined cysts that demonstrate linear growth patterns characteristic of ordinary skin.

Regarding the imaging characteristics on CT scan, we see smoothly marginated expansile lesions with no enhancement with contrast. You cannot differentiate between a congenital cholesteatoma and a cholesterol granuloma on CT scan, but a well pneumatized contralateral petrous apex lesion is highly suggestive of a cholesterol granuloma. As with cholesteatomas in other areas of the temporal bone, we see an MRI nonenhancing lesion with low intensity on T 1 and we see high intensity on T 2 .

Switching to effusions and mucoceles, obstruction of a highly pneumatized petrous apex can lead to effusion formation. With the persistence of effusion, septations of the apex break down and a mucocele can form. They can expand and cause symptoms similar to a cholesterol granuloma. Radiographically, they do appear like cholesterol granuloma with CT imaging revealing nonenhancing, homogeneous, sharply marginated lesions that, unlike cholesterol granulomas, are isodense with CSF fluid. An effusion alone will show soft tissue density without the breakdown of septations. Now on MRI, we have hypointensity on T 1 images. Retained mucus will show a hyperintense lesion on T 2.

Next, we will switch to infectious causes; and I would like to talk a bit about petrous apicitis, as we did have a Grand Rounds last year on skull base osteomyelitis. In the pre-antibiotic era, suppuration of the petrous apex was a common and often fatal sequelae of middle ear and mastoid disease. With the advent of antibiotics, suppurative petrous apicitis rarely results in intracranial complications. In 1988, Goldstein and colleagues reported that approximately 2 out of 100,000 children with acute otitis media end up developing acute petrous apicitis. Now, it is a rare, but life-threatening condition and, with improved antibiotics, it has led to a decrease in its incidence. As I mentioned, it is a complication of otitis media. The potential complications include labyrinthitis, meningitis, and intracranial abscess. It can lead to a retropharyngeal abscess, venous sinus thrombosis, carotid artery involvement, and cranial neuropathies.

The clinical symptoms that are notable include pain. With posterior petrous apex involvement, the pain is usually occipital, parietal, or temporal. With anterior involvement, patients usually complain of frontal or retroorbital pain. Other symptoms include facial nerve involvement, vertigo, fevers, and as mentioned in advanced cases, meningitis and other severe complications.

On CT scan, we see an expansile lesion with possible irregular margins in the pneumatized petrous apex and, on MRI, a hypointensity on T 1 and hyperintensity on T 2. This is an example of a patient with petrous apicitis with a T 1 MRI with fat saturation and gadolinium demonstrates enhancement of the petrous apex and the clivus and on T 2 .

In 1907, Gradenigo described this triad of symptoms of acute suppurative otitis media, retroorbital pain, and diplopia due to abducens nerve palsy. This is caused by compression and edema of cranial nerve VI as it passes through Dorello's canal made up by the petroclinoid ligament. The case series that were done in the 1930s and 1940s show that it is actually somewhat rare to have all three symptoms, and we should not rely on that in making the diagnosis.

Now, the treatment of petrous apicitis has had a complex history over the last century. In the early 1900s, Streit drained a petrous tip abscess through a middle cranial fossa craniotomy and Gradenigo drained abscesses of the petrous tip by radical mastoidectomy and labyrinthectomy. In 1926, Sears had a more conservative view and advocated for paracentesis and to reserve mastoidectomy and labyrinthectomy only for recalcitrant cases but, in the pre-antibiotic era, such treatment frequently was inadequate; and many of the surgical procedures, which form our current basis of approaches, were formed.

In 1931, Eagleton described several approaches which included through the middle fossa, posterior fossa, as well as labyrinthectomy. He, after opening the sublabyrinthine, subcochlear, subarcuate, pericarotid, and sinodural angle, said that this unlocked the petrous pyramid and was able to drain the petrous apex or petrous apicitis.

In 1933, Ramadier and Lempert, in 1937, described what is termed the classical approach to a petrous apicectomy. In Lempert’s approach, a radical mastoidectomy is performed. The anterior canal wall is removed and so is the mandibular condyle. The bony covering is taken off the internal carotid artery; and the petrous apex is entered through a triangular opening between the cochlea, middle fossa dura, and internal carotid artery.

In 1937, Dearmin advocated for the infralabyrinthine approach; and later, in 1960s and 1970s, House, Hendershot, and Wood all advocated for a middle cranial fossa approach.

Today, treatment of petrous apicitis, since the introduction of antibiotics, really has evolved into a culture-directed antibiotic therapy with myringotomy and PE tube placement and surgery reserved more for those that are showing no improvement or having worsening symptoms. Most common organisms in acute petrous apicitis can be Streptococcus pneumonia, H. flu, and Staphylococcus aureus.

To touch a bit about normal variance, I think it is important just to mention that, with so many people these days getting imaging studies, these diagnoses are coming up more and more. It is estimated that 10% to 15% of anterior petrous apices and 30% of posterior apices are pneumatized and, of those, it is reported that 4% to 6.8% exhibit asymmetric pneumatization. The majority, however, are marrow filled. The high fat content of the bone marrow space in the less pneumatized petrous bone is hyperintense on T 1, hypointense on T 2, but neither will be expansile.

Regarding giant air cells, you can see a distortion of the surrounding structures, and it is usually considered as giant cell if it is greater than 1.5 cm in diameter. On CT, as shown here, you see a large smooth air cell and it can have stellate margins.

Arachnoid cysts are benign pockets of CSF. Very rarely they are found in the petroclival region. They are thought to expand by a noncommunicating cyst continuing to produce CSF or by a communicating cyst but, because of a functional unidirectional valve, permit CSF to enter the cavity.

On CT, we see an erosive and smoothly demarcated area. On MRI, it is hypointense on T 1 and hyperintense on T 2. To tell the difference between a cholesteatoma and an arachnoid cyst, fluid-attenuated inversion recovery imaging, or FLAIR imaging, is used which has a special heavily weighted T 2 image. With this type of imaging, the free water in the arachnoid cyst would actually have low signal intensity and the cholesteatoma high signal intensity.

We will switch now just to discuss some key points on surgical approaches. As I mentioned, most of our approaches have come from methods devised to drain the petrous apex of infection. They all allow access to the petrous apex, but provide varying degrees of exposure and have different associated morbidities. The nature of the lesion and the amount of hearing that the patient has preoperatively help the surgeon to decide which approach in which to access the petrous apex. Sometimes, there has to be a compromise between the optimal access and imaging and hearing preservation. However, all of these approaches do have the goal of preservation of important vascular and nervous structures that lie in close proximity to the petrous apex. The translabyrinthine and transotic approaches allow for direct route, but they do sacrifice serviceable hearing. The infratemporal approach, as described by Fisch, also gives a direct route, but requires anterior displacement of the mandibular condyle as well as mobilization of the zygoma.

The infracochlear approach, as described here in a picture from Dr. Coker’s atlas, allows for hearing preservation and adequate room for drainage, but there can be insufficient room if you have to do aggressive debridement of that area. The middle cranial fossa approach provides drainage of the cyst, but not a way of permanent aeration and can be technically challenging. The transmastoid infralabyrinthine approach, as shown in this picture, also allows for hearing preservation, wide access to the posterior and inferior aspects, but can be limited by a high jugular bulb. As shown here, if this jugular bulb is coming on too high, you will not have nice access. A transsphenoidal approach can be utilized if the lesion abuts the posterior wall of the sphenoid, but it allows limited exposure, and it can be difficult to maintain drainage and is in close proximity to the internal carotid artery.

Let’s return to our case presentation. Our patient underwent a right transmastoid infralabyrinthine approach for marsupialization of the petrous apex cyst. It was shown to have a brown oily fluid. There were crystals and golden-colored debris that emanated from the cyst cavity, consistent with a cholesterol granuloma; and this was confirmed on pathology. I put one of the CT scan images up again, just to note on our patient how highly pneumatized his mastoid cavity was, and that provided good access to the cyst. This is an intraoperative picture. We can see a little bit of change in the hue as we near the cyst wall. Here is his facial nerve, and the posterior canal in here. A postoperative audiogram was obtained in clinic, and that showed preservation of his hearing.

I would like to take a few moments now to introduce an additional procedure called the circumferential petrous apicectomy, which provides an additional means to access the petrous apex in cases of petrous apicitis and skull-based osteomyelitis. The goal being that this procedure is to remove as much the temporal bone as possible while preserving hearing and facial nerve function. It is option in patients who show no improvement on IV antibiotics or whose exam is showing impending complications, and surgery is necessary. You remove bone circumferentially around the pathway that includes the ear canal, tympanic membrane, ossicular chain, and inner ear. This procedure has been performed on five patients by Dr. Oghalai, with modifications to fit each patient’s specific areas of disease. First, as the picture to the left illustrates, the curved incision is used to permit a middle fossa craniotomy as well as a mastoidectomy, which starts by starting 2 cm posterior and inferior to the mastoid tip, and the incision ends at the zygomatic root in the preauricular crease. The skin and the subcutaneous tissue in the deep plane to the temporoparietal fascia are elevated, and then the entire temporalis muscle is elevated out of the temporal fossa and retracted anteriorly. The mastoidectomy is then performed, along with an extended facial recess approach. The facial nerve is skeletonized circumferentially using a fallopian bridge technique, as described by Dr. Jackler, and here you can see the skeletonization of the semicircular canals as well. This technique allows for maximum removal of the bone without having to transpose the facial nerve or remove the ear canal. The mastoid tip air cells are completely removed down to the level of the digastric muscle; and the bone overlying the sigmoid sinus, posterior fossa, and middle fossa dura is thinned and then removed. The infra- and supralabyrinthine air cells are removed down to the level of the jugular bulb and the sinodural angle, respectively. Then, a bone flap is removed in order to perform a middle fossa craniotomy. A malleable retractor is used to support and protect the temporal lobe dura; and bone removal starts in the anterior petrous apex, as seen here, and then you skeletonize the internal auditory canal. The anterior apex cells can be removed to the petrous carotid artery laterally; and bone removal can extend medially to the clivus,with the inferior petrosal sinus marking the inferior limit of removal at the petrous apex. If vascularized tissue is needed to fill the cavity, you can take the temporalis muscle and bisect it vertically. This picture is showing the anterior portion being placed into the petrous apex, and this posterior portion is placed and stitched into the mastoid cavity. This picture illustrates, in grey, all of the bone that can be removed with this type of procedure and the blue showing the external auditory canal, the semicircular canals, and the cochlea all being preserved.

These imaging pictures are of a 14-year-old boy who underwent this procedure. He had been treated by his primary care doctor for otitis media, and symptoms seemed to resolve. Then, six weeks later, he developed all the symptoms consistent with Gradenigo syndrome. This is his preoperative MRI, this is the picture that I showed you earlier, that shows petrous apex and clivus enhancing. This is a preoperative CT scan and his postoperative scan showing all of the bone that had been removed in the mastoid as well as the petrous apex. He ended up going to surgery. He was admitted, cultures were taken of his draining ear, and he was started on antibiotics. He showed no improvement after a week and continued to have his VI nerve palsy, and that was when it was decided he needed to go to the operating room. He received a full six-week course of IV antibiotics and, postoperatively, has done very well with resolution of his VI nerve palsy; and his postoperative audiogram shows normal hearing.

In summary, petrous apex lesions are rare lesions. They can remain silent for prolonged periods of time, as well as they may cause vague symptoms. The petrous apex remains a technically difficult region to reach surgically. Cholesterol granuloma is the most common lesion of the petrous apex, and there are multiple approaches that exist for accessing the petrous apex. Residual hearing, anatomy and the lesion etiology help dictate the approach chosen by the surgeon. For infectious processes of the petrous apex that may be recalcitrant to antibiotic therapy, a circumferential petrosectomy does allow for aggressive bone removal with functional preservation.

Case Presentation:

The patient is a 40 year-old man who experienced one episode of diplopia lasting for a week. He was seen by an ophthalmologist. His ophthamological exam was normal and his blurry vision improved. He also experienced intermittent right frontal headaches. An MRI had been ordered which revealed a right petrous apex lesion. He was referred for further management.

He had no significant past medical history. He denied otalgia, retro-orbital pain, diplopia, hearing loss, vertigo or decrease in facial sensation. His physical exam revealed normal appearing tympanic membranes. There were no middle ear masses seen and no effusions were present. All of his cranial nerves were grossly intact and the remainder of his head and neck exam was also normal.

His imaging studies included an MRI and CT scan. The MRI showed a hyperintense lesion on both T1 and T2 weighted images with extension into the right clivus. The CT scan showed bony destruction of the right petrous apex and portion of the clivus. The lesion was measured as 2.7 x 1.9 x 2.0 cm on imaging. The imaging findings were consistent with a cholesterol granuloma.

His audiogram demonstrated normal hearing in both ears on pure tone averages. His discrimination score was 84% in the right ear and 92% in the left ear. Tympanograms were normal bilaterally.

He underwent a right transmastoid infralabyrinthine approach with marsupialization of the right petrous apex lesion. Brown oily fluid, crystals and golden colored debris emanated from cyst cavity consistent with a cholesterol granuloma. This was confirmed pathology.

Post-operatively the patient has done very well. A post-operative audiogram performed in clinic demonstrated perseveration of his hearing.

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