Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 8  |  Issue : 6  |  Page : 751-759  

Magnetic resonance imaging of cerebellopontine angle lesions


Department of Radiodiagnosis, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, Maharashtra, India

Date of Web Publication19-Nov-2015

Correspondence Address:
Pratiksha Yadav
Department of Radiodiagnosis, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.169917

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  Abstract 

Background: Cerebellopontine angle (CPA) tumors are usually benign, and they are divided into extra-axial, intra-axial, extradural, and petrous axis tumors. CPA pathologies can be asymptomatic or it may present with vertigo, tinnitus, or unilateral hearing loss depending upon the site of tumor origin and displacement of the neurovascular structure. Aim and Objectives: To evaluate the role of magnetic resonance imaging (MRI) aided with contrast-enhanced MRI as an imaging modality for diagnosis of CPA lesions. Materials and Methods: Analysis of 36 patients of CPA lesions over a period of 2 years was done. MRI was performed on Siemens 1.5 Tesla MAGNETOM Avanto Machine. Conclusion: There are spectrums of pathologies, which can present with these symptoms, which includes tumors, vascular malformations, and vascular loop compressing vestibulocochlear nerve or mastoid pathology so it is important to investigate the patient by MRI. Contrast-enhanced MRI is the most sensitive investigation in the evaluation of the CPA lesions, its characteristic, and its extent.

Keywords: Arachnoid, cerebellopontine angle, epidermoid, mastoid, meningioma, schwannoma, tinnitus, vestibulocochlear vertigo


How to cite this article:
Yadav P, Jantre M, Thakkar D. Magnetic resonance imaging of cerebellopontine angle lesions. Med J DY Patil Univ 2015;8:751-9

How to cite this URL:
Yadav P, Jantre M, Thakkar D. Magnetic resonance imaging of cerebellopontine angle lesions. Med J DY Patil Univ [serial online] 2015 [cited 2019 Dec 14];8:751-9. Available from: http://www.mjdrdypu.org/text.asp?2015/8/6/751/169917


  Introduction Top


Lesions of the cerebellopontine angle (CPA) comprise 10% of all intracranial tumors. [1],[2] Most common extra-axial tumors of CPA are vestibular schwannomas, which constitutes the about 70-80% of all CPA lesions. The next in order are: Meningiomas (5-12%) and epidermoid cysts (2-6%). [1],[2],[3] The other lesions include arachnoid cysts, facial nerve schwnnomas. A glomus jugulare tumor may spread into the CP region from the temporal bone. Other vascular tumors, such as hemangiomas and hemangioblastomas, may occur primarily within this area. Intra-axial tumors of CPAs are an astrocytoma, medulloblastoma, ependymoma, and metastasis. Various embryonic tumors, including dermoid tumors, teratomas, and chordomas, may develop in the CPA. Malignant tumors of the CPA are quite rare, but chondrosarcomas, malignant choroid plexus papillomas, and metastatic tumors have been encountered.

CPA tumors, although uniform in location, are diverse pathologically and present clinically depending upon the site of tumor origin and displacement of the neurovascular structures. The tumors can derive from many anatomical structures, including primary origin from internal auditory meatus, ponto-cerebellar cistern, and the lateral recess of the fourth ventricle, temporal bone, brain stem, or cerebellar nervous tissue. [4],[5],[6] Clinical presentation of the CPA tumors is variable and it depends upon the size and location of the tumor. It can be asymptomatic in early stage or it can give vertigo, tinnitus, or hearing loss. Vascular compression of the vestibulochoclear nerve also causes vertigo and tinnitus. Large CPA lesions may compress the pons, the ipsilateral cerebellar hemisphere, the trigeminal nerve anteriorly and superiorly, and the IX, X, and XI nerves posteriorly. Computerized tomography (CT) and magnetic resonance imaging (MRI) are the primary modalities for diagnosis of cerebellopotine lesions. MRI is considered superior in differentiating the different types of CPA masses. Knowledge of typical signal characteristics and more specific features such as a hemispheric or ice-cream cone shape, adjacent hyperostosis, a dural tail, extension into one or more skull base foramina, and enlargement of the internal auditory canal (IAC) helps in limiting the differentials considered. Recent advanced MRI techniques that include diffusion-weighted imaging (DWI), MR spectroscopy, and MR perfusion can help provide a more specific diagnosis.


  Materials and Methods Top


In our study, we analyzed 36 patients of CPA masses, which had come in our hospital and they were detected CPA pathologies on MRI. All MRI were performed on SIEMENS 1.5 Tesla MAGNETOM Avanto Machine. The size of the bore was 60 cm and overall length of the system was 160 cm. The MRI system used zero helium boils off technology. T2-weighted image (T2WI) axial, sagittal and coronal planes, T1-weighted image (T1WI) axial and sagittal plane, and constructive interference in steady state (CISS) axial images were taken, postgadolinium T1WI in axial, coronal and sagittal plane were also obtained whenever needed.


  Results Top


Most common extra-axial tumors of CPA are acoustic schwannomas; second most frequent CPA tumors are meningiomas. Epidermoid cyst and arachnoid cysts are less common CPA tumors. Intra-axial tumors at CPAs are ependymoma, astrocytoma, medulloblastoma, or metastasis. In our study, there were 11 cases of schwannoma, 5 cases of meningiomas, 4 cases of arachnoid cyst, 3 cases of epidermoid cyst, 2 cases of ependymoma, 2 cases of astrocytoma, and 1 case of medulloblastoma. There were 3 cases of metastasis. One case of mastoid hypersinus and 4 cases of vasculonervous conflicts were observed.



Normal anatomy of cereabellopontine angle

The CPA is the space bound by the cerebellum, pons, and temporal bone. The space is bound anteriorly by the posterior surface of the temporal bone and posteriorly by the anterior surface of the cerebellum. The inferior olive and the superior boundary form the medial boundary by the inferior border of the pons and cerebellar peduncle. The cerebellar tonsil forms the inferior border [7] [Figure 1]. It contains the short intracranial courses of the fifth, seventh, and eighth cranial nerves. The seventh and eighth cranial nerves course superiorly and laterally toward the IAC within this space. Superiorly, the fifth nerve is visible, with the ninth, tenth, and eleventh nerves located inferiorly. The seventh and eighth nerves are encased in the glial tissue throughout their intracranial course Schwann cells surround these nerves beginning in the IAC, near the porus. The Glial-Schwann junction is also known as Obersteiner-Redlich zone. The vestibular ganglion (Scarpa's ganglion) is located near the mid portion of the IAC. [7] The division of the eighth nerve into vestibular and cochlear segments occurs in the subarachnoid space or in the medial segment of the IAC. Vestibular segment divides into superior and inferior vestibular nerves, which occupy the posterior half of the IAC.
Figure 1: Normal anatomy. Axial magnetic resonance imaging constructive interference in steady state image showing normal anatomy of the cerebellopontine angle arrow (a) is showing internal auditory canal, anterior is VII nerve (b), posterior is VIII nerve (c). P = Pons, mcp = Middle cerebellar peduncle, CH = Cerebellar hemisphere

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  Discussion Top


Vestibular schwannoma

Schwannoma is a benign (World Health Organization [WHO] Grade I) encapsulated tumor that arise from the Schwann cells of the nerve sheaths of cranial and spinal nerves. [8] It accounts for 5-10% of primary intracranial neoplasms and for nearly 30% of intraspinal tumors. [9],[10] Vestibular schwannomas represent 80-85% of the CPA tumors. [3] Intracranial schwannomas occur in all the age groups, but the peak incidence is in the fourth to seventh decades of life. [2],[3] There is a distinct sex predilection with a female-to-male ratio of 2:1. [9],[10]

Most common site of schwannoma is Scarpa's ganglion where the highest concentration of schwann cells.

The symptom of vestibular schwannomas depends upon the size and location of the tumor. The growth rate of schwannoma is variable, but usually it is slow, 1-2 mm/year. When it is in the intracanalicular stage it may present as a unilateral sensorineural hearing loss, tinnitus, or vertigo [Figure 2]a. In cisternal stage, it worsens the hearing loss, tinnitus, disequilibrium, and possible headache [Figure 2]b. When tumor progresses further, it compresses the brainstem and trigeminal symptoms may also develop [Figure 2]c. Further progress of the tumor causes pressure on the fourth ventricle with obstructive hydrocephalus, facial weakness, headache, vision loss, or diplopia may occur [Figure 2]d.
Figure 2: Stages of schwannoma: Magnetic resonance imaging axial constructive interference in steady state images depicting the progression of the schwannoma. (a) Intracanalicular schwannoma of the stage a when it present with hearing loss, vertigo, or tinnitus. (b) Tumor in cisternal space, symptoms get worsen and disequlibrium and headache may occur. (c) Depicting the next stage of the schwannoma which is compressing the pons and trigeminal symptoms and disequilibrium may occur. (d) Further progression of tumor, which is compressing the VI ventricle and worsening of the above symptoms occur with obstructive hydrocephalus of the lateral and III ventricles

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Bilateral vestibular schwannomas strongly suggest the presence of neurofibromatosis type 2 (NF-2), a neurocutaneous disorder associated with a mutation on the long arm of chromosome 22. [11] The occurrence of bilateral vestibular schwannomas is almost considered the pathognomonic of this disorder, which has also been termed multiple inherited schwannomas, meningiomas, and ependymomas. [12] Such patients typically present clinically in the second and third decades of life, much earlier than those with the sporadic intracranial schwannoma. [9]

MRI is the very good modality to detected small tumors, especially within the IAC, because of the lack of bone-induced artifact and the multidimensional capability of this modality. The transition zone between the central (oligodendroglial) and peripheral (Schwann cell) portions of the eighth (vestibulocochlear) nerve, the presumed site of the origin of schwannomas of this nerve, occurs within the canal. Tumors <5 mm in diameter can be reliably identified on CISS images, appearing as homogeneously mildly hypo- or iso-intense (to adjacent brain) ovoid or tubular intracanalicular masses [Figure 3]a, hypointense on T1WI with intense homogeneous contrast-enhancement [6],[10],[13],[14] [Figure 3]c and d. On T2W sequences, they appear mildly to markedly hyperintense and may be obscured by the similarity in signal intensity to that of the surrounding cerebrospinal fluid (CSF) [Figure 3]b.
Figure 3: Schwannoma presented with hearing loss, tinnitus, and headache (a) Constructive interference in steady state axial image and (b) T2-weighted imaging showing right sided intracanalicular and cerebellopontine angle tumor compressing the pons. (c) It is hypointense on T1-weighted imaging and showing (d) intense homogeneous enhancement of the tumor.Tumor is encasing the VII and VIII nerves

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In larger tumors, intratumoral degenerative changes may result in an increase in heterogeneity of signal. On axial images, the tumor often has a comma-like shape with a globular cisternal mass medially and a short tapered fusiform extension laterally into the IAC. Homogeneous contrast-enhancement is seen in the most of the cases. [6],[13],[14] Compression and displacement of the adjacent cerebellar hemisphere, pons, or medulla may occur as the tumor enlarges.

The differential diagnosis is meningioma and epidermoid tumor. [6],[13],[14] Meningioma involving the dura of the posterior margin of the petrous temporal bone can project posteriorly into the CPA and simulate a vestibular schwannoma. Such lesions represent the about 10% of CPA masses. [6] Although meningiomas are typically denser on CT, these two neoplasms may have identical signal intensity characteristics on MRI. However, meningiomas are usually situated eccentric to the IAC and form a more obtuse angle with the petrous ridge than schwannomas. [14] Extension of meningioma into the IAC is uncommon but not unknown, [15] and rarely schwannoma may simulate the appearance of a dural tail on postcontrast images. [16]

Meningioma

Meningiomas are solid, well-circumscribed, and slow-growing tumors that are composed of neoplastic meningothelial cells originating from the arachnoid layer of the meninges with a broad attachment to the adjacent dura. Meningiomas account for about 30% of all primary brain tumors with annual incidence off about 4.5/100,000 individuals. [17]

Meningiomas are second most frequent CPA tumor, which constitutes 10-15% cases. [18] They occur with a peak incidence in the fifth through seventh decades of life. [19] Meningiomas occur preponderantly in females, with a female-to-male ratio of at least 2:1. [18] However, meningiomas associated with hereditary tumor syndromes such as NF-2 generally occur in younger patients and do not demonstrate any gender predilection. [19]

The WHO classifies meningiomas into the following three grades: Benign (Grade I), atypical (Grade II), and anaplastic or malignant (Grade III). The grading has been done on the basis of histological markers, which include the presence and number of mitotic figures, overall cellularity, nuclear to cytoplasmic ratio, nuclear prominence, and the presence of necrosis. [20] Though the majority of meningiomas are benign Grade I tumors, 23-24% of the tumors are atypical (Grade II) and 1-3% are found to be anaplastic (Grade III) under the new WHO classification system. [21],[22]

Common sites are in the frontal and parietal convexities and the parasagittal region (in close association with the falx cerebri); tumors in these locations constitute about 50% of all intracranial meningiomas. Meningiomas arising in relation to the sphenoid wings, olfactory grooves, sylvian fissures, and parasellar regions represent about 35%. [19] Less than 10% arise below the level of the tentorium, mainly from the meninges overlying the clivus and petrous pyramid. Multiple meningiomas are commonly associated with NF-2. Invasion of the dura and encasement or invasion of the nearby dural venous sinuses is common. [19] On CT, meningiomas appear hyperdense, approximately 20% show calcification and after the intravenous administration of contrast medium, meningiomas typically show homogeneous contrast-enhancement (increase of 40-50 HU or more). [23]

On noncontrast MRI, the majority of meningiomas have a homogeneous appearance similar to that seen on CT, it show typical broad base at the meningeal origin and hemispheric shape on the opposite side. On T1WIs, they appear iso- to hypo-intense to the adjacent cerebral cortex. On T2WIs, about 50% are mildly hyperintense relative to adjacent gray matter and 50% are isointense to the cortex [23] [Figure 4]a. It is hypointense on CISS sequence obliterating the vestibulocochlear nerve [Figure 4]b). A minority of meningiomas may appear heterogeneous in a signal pattern on both T1- and T2WIs because of the presence of intratumoral lipoblastic or cystic changes calcifications, or prominent vessels. [23] Meningiomas show homogenous enhancement on postcontrast T1WI [Figure 4]c and d. Indistinct irregular tumor margins, a mushroom-like extension of opacified tumor well away from the main ovoid tumor mass, and prominent venous drainage centrally from the tumor are CT and MRI signs that may suggest an aggressive anaplastic or malignant meningioma invading the brain. [24]
Figure 4: Meningioma is causing sensorineural hearing loss. (a) STIR axial image show a well-defi ned broad based hyperintense lesion in left cerebellopontine angle, (b) which are obliterating the course of left VII and VIII nerves. Postcontrast T1-weighted imaging (c) axial and (sagittal) images showing intense homogenous post contrast enhancement

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MRI enables more accurate localization and evaluation of these tumors. The interface between the inner margin of the extra cerebral tumor mass and the invaginated or displaced cortex can be recognized on MRI from the presence of a cleft of CSF or the interposition of the vascular flow voids of the displaced arteries and veins on the pial surface of the brain. [23] Furthermore, invasion of adjacent brain by meningiomas arising from the tentorium, the falx, and the dura of the lateral wall of the cavernous sinus can be recognized as a breech in the hypointense dural rim at the tumor margin. [25] Finally, arterial encasement and partial dural venous sinus invasion are more readily and accurately depicted by the contrast between the flow void and the tumor tissue. [23]

A thickened tapered extension of the contrast-enhancing dura is commonly identified at the margins of the tumor. This dural tail may indicate the presence of tumor infiltration or may be due to a proliferative dural reaction. [26],[27] Because a major prognostic factor in the recurrence of meningiomas after surgery is the extent of tumor resection, the careful assessment must be made of pre- and post-operative contrast MR images for the presence of a dural tail. [19]

MR spectroscopy provides additional information to narrow down the differential diagnosis of tumors by neuroimaging is difficult. Cho reflects membrane turnover, correlates with malignancy in astrocytic tumors, and forms high peaks in meningioma. The most common proton spectrum found in meningiomas is a high Cho peak with low or absent NAA and creatine and variable amounts of lactate. A high ratio of alanine to creatine has been found in meningiomas because of the high alanine and low creatine content, and this is a relatively specific finding for meningioma. Alanine is seen as doublet centered at 1.47 ppm and inverts on the long-TE sequence. [28]

Arachnoid cysts

Arachnoid cysts are benign, congenital, intra arachnoidal space-occupying lesions representing 1% of all intracranial masses. [29] They have clear CSF as its contents and do not communicate with the ventricular system. [30]

Most arachnoid cysts are supratentorial in location. 50-60% are found in the middle cranial fossa. Other locations include the suprasellar cistern and posterior fossa (10%), where they occur most commonly in the CPA cistern. Less common locations are within the interhemispheric fissure; over the cerebral convexity; or in the choroidal fissure, cisterna magna, quadrigeminal cistern, and the vermian fissures. [30],[31]

There are several theories to their origin. They may be secondary to "splitting" or a diverticulum of the developing arachnoid. A newer concept for the middle fossa arachnoid cyst is the failure of temporal embryonic meninges to merge as the sylvian fissure forms. These two layers remain separate, forming duplicate arachnoid. Other mechanisms might include active fluid secretion by the cyst wall, slow distention by CSF pulsations, or one-way ball-valve flow of CSF. [32] The cause has also been attributed to trauma, mastoiditis, meningitis, and subarachnoid hemorrhage. [31] Arachnoid cysts are usually asymptomatic it can give symptoms when they enlarge resulting the mass effect. Large arachnoid cyst at CPA can compress the vestibulocochlear nerve and present with tinnitus or hearing loss, when it compress pons can present vertigo.

MRI is the diagnostic technique of choice as it can demonstrate the exact location, extent, and the relationship of the arachnoid cyst to the adjacent brain or spinal cord. On MRI, arachnoid cysts appear as well-defined nonenhancing intracranial masses that follow CSF intensity on all sequences [Figure 5]a and b. Arachnoid cysts and epidermoid cysts may have similar characteristics on T1W and T2WIs, and shows no enhancement with gadolinium. However, arachnoid cysts follow CSF signals on all sequences in particular, on the fluid-attenuated inversion recovery sequence-unlike epidermoid cysts. DWIs allow easier differentiation as epidemoid cysts show restricted diffusion. Phase contrast imaging can be employed not only to determine if the cyst communicates with the subarachnoid space, but also to identify the location of this communication. Determination of whether the arachnoid cyst is communicating to the CSF spaces is important in the preoperative evaluation. [33] There are CSF flow patterns specific to each entity and PC MRI may help in differentiating, communicating, and noncommunicating arachnoid cysts. [34] The size of arachnoid cysts varies from small and incidental to a large space-occupying lesion with the extensive compression of the underlying brain.
Figure 5: Arachnoid cyst. T2-weighted imaging (a) and constructive interference in steady state (b) axial magnetic resonance imaging images showing a well-defi ned cerebrospinal fl uid signal intensity lesion at left cerebellopontine angle compressing the VII and VIII nerves

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Epidermoid cysts

Epidermoid cysts are congenital intradural lesions arising from the inclusion of ectodermal epithelial elements during neural tube closure. [35] They are the third most common CPA masses after acoustic schwannomas and meningiomas. The CPA is the most common site of the occurrence of intracranial epidermoid tumors, accounting for 5% of tumors in this region. [36] They comprise 1% of all intracranial tumors. The most common locations include the brainstem, pituitary gland, and in the posterior fossa along the cerebellum and brainstem.

Epidermoid cysts typically show undulating margins and model their shape to conform to the cerebropontine angle. The cyst has a tendency to insinuate itself around the nerves and blood vessels in the cerebropontine angle and engulf cranial nerves and vessels. Margins are usually scalloped or irregular. They usually do not enhance with gadolinium and do not bleed.

On CT scans, epidermoid lesions have decreased attenuation. They usually have the same attenuation as that of CSF; this makes their differentiation from arachnoid cysts difficult on CT scans, but they can be easily differentiated by MRI. On T1WIs, these lesions are generally slightly hyper- or iso-intense relative to the gray matter. More specifically, the T1W signal intensity tends to vary with the lipid content, with the signal intensity being increased in lesions with a high lipid content. [37] The lesions are usually isointense relative to CSF on T2WIs, but they may be slightly hyperintense [Figure 6]a. Compression of the vestibulocochlear nerve seen on CISS image [Figure 6]c. Diffusion MR imaging sequence is the most important sequence in differentiating epidemoid and arachnoid cysts. Epidermoid cyst show restricted diffusion on DWI [37] [Figure 6]d. It does not enhance on postcontrast T1WI [Figure 6]b.
Figure 6: Epidermoid cyst. Axial T2-weighted imaging (a) showed an irregular hyperintense lesion occupying the right cerebellopontine angle and internal auditory canal. It is hypointense on T2-weighted imaging and (b) hypointense on T1 weighted image (c) on constructive interference in steady state axial image, it showed involving the course of right vestibulocochlear nerves (d) it showed restriction on diffusionweighted imaging

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Vascular lesions

Such as vertebrobasilar dolichoectasia (elongation and dilatation of vertebral and basilar artery), vascular loops, and aneurysms accounts for 2-5% of CPA masses. They may cause compressive symptoms of cranial nerves. Vascular loop caused by tortuous anterior inferior cerebellar artery may cause acoustic nerve symptoms such as vertigo and pulsatile tinnitus [Figure 7]. Micro vascular compression of a vestibulocochlear nerve in the CPA usually caused by a tortuous anterior inferior cerebellar artery or posterior inferior cerebellar artery or their branches. [38] Venous causes include idiopathic intracranial hypertension, jugular bulb variants, and dural venous thrombosis. [39] MRI with CISS images can demonstrate the vascular loop adjacent to the vestibulocochlear or facial nerve [Figure 8]. Microvascular decompression surgery has been used to treat the cases. [40]
Figure 7: Vascular loop causing pulsatile tinnitus axial constructive interference in steady state image showed a linear structure corresponding to left anterior inferior cerebellar artery, which loops around left VII and VIII nerves at cerebellopontine angle

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Figure 8: Dilated sigmoid sinus and inferior petrosal sinus causing tinnitus. (a) Dilated sigmoid sinus at right cerebellopontine angle on T1 weighted axial image. (b) On post contrast T1 weighted axial image showing compression of vestibulocochlear nerve due to dilated sigmoid sinus

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Intra-axial tumors

Intra-axial tumors at CPA include medulloblastoma, ependymoma, hemangioblastoma, and metastasis. Medulloblastoma is a brain tumor of neuroepithelial origin, which represents 15-30% of a pediatric brain tumor and <1% of adult brain tumor. [41] These are hypointense on T1WI and hyperintense on T2WI [Figure 9]a, it give intense postcontrast enhancement medulloblastoma [Figure 9]b can involve CPA in the extreme case of foraminal extension usually in exophytic cerebellar mass. Ependymomas represent 3-9% of neuroepithelial neoplasm and, 6-12% of all pediatric tumors. [42] The majority of intracranial ependymomas located in the posterior fossa, which arise from the floor of the fourth ventricle. Ependymomas are iso- or hypo-intense on T1WI and hyperintense on T2WI with the specks of calcification and hemorrhage are commonly seen. It shows heterogeneous postcontrast enhancement. Ependymomas represent 3-9% of neuroepithelial neoplasm and, 6-12 % of all pediatric tumors. [42] The majority of intracranial ependymomas located in the posterior fossa, which arise from the floor of the fourth ventricle. Ependymomas are iso- or hypo-intense on T1WI and hyperintense on T2WI with the specks of calcification and hemorrhage are commonly seen. It shows heterogeneous postcontrast enhancement.
Figure 9: Medulloblastoma. A well-defi ned mass seen involving the posterior fossa and fourth ventricle it is extending till left cerebellopontine angle and compressing left VII and VII nerves. (a) It is hyperintense on T2-Weighted imaging and (b) show peripheral rim enhancement on post contrast T1 weighted image

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Mastoid pneumoceles or hypersinus

Pneumoceles are uncommon and defined as enlarged aerated paranasal sinuses or air cells with focal or diffuse thinning of the bony walls. Hypersinus is the enlarged sinus without expansion of the surrounding bony wall. [43] Pneumosinus dilatans also used as a descriptive term of the dialated paranasal sinus regardless of the cause. Pneumoceles are reported to affect the mastoid air cells and paranasal sinuses. [43],[44] It may be asymptomatic or present with a headache or vertigo. In our case, the patient presented with tinnitus and conductive hearing loss by compromising the lumen of the external auditory canal [Figure 10]a-c. Our patient had no history of trauma, infection or previous surgery. Pneumocele may be developmental, postinflammatory, or posttraumatic. Treatment of pneumocele is decompression surgery.
Figure 10: Mastoid pneumocele on the left side is causing tinnitus. Axial T2-weighted imaging (a) and coronal T2-weighted imaging (c) showing dilatation of left mastoid air cells, which are causing mass effect on left cerebellar hemisphere reaching up to the left cerebellopontine angle. Computerized tomography axial image in bone window (b) showing expansion of mastoid air cells with expansion of bony walls

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  Conclusion Top


CPA tumor mostly present with vertigo or tinnitus, however, sometimes it is incidental findings. A very good knowledge of the radiological anatomy and pursuit of correct MRI protocol is necessary to diagnose the CPA mass lesions, vasculo-nervous conflicts and secondary involvement of the CPA.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]


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