martedì 4 novembre 2008
Cholesterol granuloma of petrous apex
Figure 1 and Figure 2: Axial and coronal noncontrast CT show non-aggressive expansile lesion of petrous apex. Loss of cortical contiguity with maintenance of a thin rim of cortex in some locations indicates a slowly enlarging benign process.
Figure 3: Axial T1WI MR shows homogeneous high signal with well-defined margins. This lesion expands the petrous apex medially.
Figure 4: Axial T2WI MR reveals homogeneous internal high signal. Note the dark peripheral ring around this lesion consistent with hemosiderin deposition.
Figure 5: High signal on FLAIR.
Figure 6: Coronal T1 weighted image following contrast demonstrates increased signal, without enhancement, consistent with cholesterol granuloma.
Diagnosis: Cholesterol granuloma of petrous apex
Cholesterol granuloma is thought to arise in the mastoid air cells as a result of inadequate ventilation in the setting of otitis media and eustachian tube dysfunction. Hemorrhage in these cells with stasis leads to an inflammatory response with giant cell reaction and bony erosion. Cholesterol granuloma contains brownish fluid with cholesterol crystals. These lesions may be present in the middle ear as well as within the mastoid air cells and petrous apex. Several additional terms are used for these lesions. A cholesterol granuloma at the petrous apex is also called a giant cholesterol cyst. A cholesterol granuloma present in the mastoid is also called a chocolate cyst or blue-dome cyst.
Cholesterol granulomas are bright on all spin-echo sequences, which differentiate them from cholesteatomas. High internal T1 signal is secondary to presence of hemorrhage, blood break-down products, and cholesterol crystals. The primary reason is most likely the presence of paramagnetic intracellular methemoglobin. On T1 post contrast images, the peripheral enhancement may be difficult to appreciate as it is adjacent to an inherent T1 bright lesion. There is no internal enhancement. On T2, there is high internal signal with a peripheral dark hemosiderin ring. Because the lesions are inherently bright on T1, contrast is not very helpful in delineating the diagnosis. MRA is useful for surgical planning, such as assessing for encasement of the petrous ICA. On non contrast CT, the lesions are well defined and smoothly expansile. Faint peripheral enhancement may be present on contrast enhanced CT. CT is useful to evaluate bony destruction and involvement of the adjacent otic capsule and carotid canal. MR is more sensitive than CT for evaluation of recurrence. Increasing T1 signal in the post-operative petrous apex suggests recurrence.
Cholesterol granulomas occur in young to middle-age adults. The most common symptom is sensorineural hearing loss. Other presenting symptoms include tinnitus, hemifacial spasm, facial numbness, trigeminal neuralgia, and abducens palsy.
Cholesterol granulomas have no cyst wall and do not require complete surgical excision. Traditional treatment is drainage with establishment of a permanent ventilation system via a transtemporal approach. Often, silicone tubing is used to stent the drainage system and prevent stenosis. Reported recurrence rate is as high as 60%. The extended middle cranial fossa approach with extradural removal of cholesterol granuloma and obliteration of its cavity has a significant decrease in recurrence rate.
The differential diagnosis of cholesterol granuloma is cholesteatoma. Because they often coexist, confusion in terminology between cholesterol granuloma and cholesteatoma has been noted by many authors. Cholesteatomas are either congenital or acquired and thought to originate from from trapped skin and contains keratin debris, keratinizing squamous epithelium, and fibrous stromal subepithelium. By MRI, cholesteatomas are hypointense or isointense on T1-weighted images and hyperintense on T2 images. It is important to differentiate between cholesterol granuloma and cholesteatoma because of treatment differences. Cholesteatomas, regardless of size, require complete surgical removal.