Cerebellopontine Angle Anatomy

The CPA has a triangular shape space located posterior to the pyramid, inferior to the tentorium and lateral to the pons, ventral to cerebellum, and is defined by the CP fissure

The cisternal space of the cerebellopontine angle is defined by the posterior fossa, laterally by the petrous temporal bone, medially by the brainstem and cerebellum and cranial nerves IX, X , XI.

CPA is traversed by crucial structures as limited describes, but to considered:

1. Vestibulocochlear Nerve VIII

2. Facial Nerve VII

3. Anterior Inferior Cerebellar Artery AICA

The initial clinical manifestation depend on the nature and location of the pathological process 

Correctly diagnosing peripheral vestibular disorders is important because they are common and evidence-based treatments improve outcomes

The symptoms usually arise from the cochlear branch lesion, such as irritation of the nerve, and tinnitus become. 

After the hearing loss of the affected side develop neurosensorial progresive and vestibular disturbances. 

This vestibular disturbances represent the usual troublesome, as a tonic desviation in the affecter sider with corrective nystagmus toward the healthy side. 

Gradually balance difficulties, with central compensation help to reduce vestibular symptoms

CPA can cause VII paresis or hemifacial spam.

Acute vertigo is not as frequent  clinical manifestation

As the lesion grows, can affect the cerebellum and predict a neurosensorial symptoms as ataxia, dysmetria and intension tremor by the upward and medial propagation. 

The medial or downward propagation leads the compression of the brainstem wit  pyramidal sympstoms, ipsilateral lession of the VI nerve and afection of the IX, X, XI nerves. 

CT evaluation

 Enlargement of the IAM, remodeling bone findings, variability of the density and cystic components

 Contrast enhancement and heterogenicity of the neural and bony structures.

MRI and sequences

 Depends on the region, or clinical manifestation T1 or T2 is predictable choice of selection for the approach diagnosis.

 Neural or meningeal origin may be predicta ble on the FIESTA or Contrast enhanced T1, or ADC with SWI

Is described the SWIp and SWI or SWAN calcifications on neural lession, the hemorrage is detecrable on GRE or SWI.

 Cisternal and vascular compromise maybe caracterized by FIESTA or CISS sequence 

Is determinant in the detection of the pathologies the use of complementary sequences as 3D or 2D TOFF, even the SPACE sequences to analize vascular origin of the cisternal and pericisternal space compromise.

5-10 % of the intracranial tumors occurs as a cause of the problem.

80% of the CPA tumor are acoustic neuromas from vestibulocochlear nerve VIII

Other become meningiomas, epidermoid and dermoid cysts, and non-acoustic schwannomas.

Vascular causes as CHAVDA types I, II, III may cause defferential diagnosis on tinnitus.

Adjacent tumor to the tentorium, petroclival region, foramen magnum and jugular foramen may cause symptoms related to the CPA syndrome.

Vestibular disorders can simulate lesions of the VII-VIII nerve, vascular lesions of AICA can affect the inner ear and resemble ischemia lesions.

Prolonged hearing loss and vestibulopathy should be considered symptoms of AICA lesions.

In the evaluation of acute vestibular syndrome, MRI should be considered to identify vascular lesions.

. As a vestibular schwannoma the Koos classification scale is used to describe the compromise intra an extra canalicular.

The grade 1 is a intracanalicular tumor, grade 2 with a protrusion into the cerebellopontine cistern and without contact the brainstem. Grade 3 compromise and extension into the cerebellopontine cistern and no desplacement of the brainstem, so the 4 grade is a large and contacting brainstem and nerve displacement.