I. What is pterygoid crest meningioma?
Pterygoid crest meningioma accounts for about 13% to 19% of meningiomas and is one of the most common meningiomas at the base of the skull. It can be divided into three subtypes: lateral (large wing), middle (small wing) and medial (bed protrusion) of the pterygoid crest.
What are the manifestations of pterygoid crest meningioma?
1. The incidence of pterygoid meningioma is significantly higher in women than in men.
2. The most common signs and symptoms are headache and epilepsy.
Meningioma of the medial pterygoid crest type grows in the anterior bed process or medial pterygoid crest, and the main symptom is vision loss for many years, which may include monocular vision loss or blindness, visual field loss, monocular pain, ipsilateral optic nerve compression and atrophy, and optic papilledema in the contralateral fundus due to increased intracranial pressure (Foster-Kennedy syndrome); it may invade the cavernous sinus and result in bulbar conjunctival congestion, monocular vision loss, and the first The cavernous sinus may be invaded, resulting in conjunctival congestion, monocular vision loss and paralysis of the third, fourth and sixth pairs of nerves.
4. Meningioma of the medio-lateral pterygoid crest is commonly associated with headache and cranial hypertension, epilepsy, aphasia, contralateral limb weakness, and cone fasciculation; there are often bony warts at the base of the tumor, which may affect the intraorbital volume and cause protrusion of the eye; it may compress the cavernous sinus and cause temporal bulge.
5. Large pterygoid crest meningioma may encircle the internal carotid artery or compress the posterior cerebral artery causing cerebral infarction, and may also manifest as transient ischemic attack.
3. How to diagnose pterygoid meningioma
The possibility of this disease should be thought of for those who have the above-mentioned typical manifestations or have chronic headache, adult epilepsy, mental changes, cranial confined masses, and fundus opisthotonos edema.
1. Cranial radiographs show bone hyperplasia (diffuse bone thickening, radiolucent bone needle-like changes, sclerotic bone hyperplasia), bone destruction (may involve the inner plate, the whole layer or even subcutaneous or submuscular), vascular indentation (a cluster of branching or radiolucent vascular indentation) and tumor calcification (dense snowflake or mass-like calcium spots).
2. Cerebral angiography is characterized by the appearance of tumor staining in the capillary phase or early venous phase. There may also be accelerated circulation, early appearance of draining veins but lack of continuous draining veins, early filling of the feeding arteries, enlargement and tortuous shape of the feeding vessels, and thickening of the blood supply arteries adjacent to the tumor segment.
3. Brain CT shows a homogeneous slightly dense or isodense mass with dotted, stellate or irregular calcification or total calcification of the tumor; round, ovoid or lobulated, with clear borders, connected to the dura mater and/or the inner plate of the skull by a broad base, and there may be localized cranial hyperplasia and destruction; in large cases, there may be peritumoral edema; after enhancement, there is mostly homogeneous enhancement, and 15% of the tumors have high or low density due to intra-tumoral hemorrhage, cystic degeneration or necrosis. In 15% of cases, the enhancement is more homogeneous due to intra-tumor hemorrhage, cystic degeneration or necrosis.
4. Brain MRIT1WI is isosignal or slightly low signal, T2WI is high signal or isosignal; the relationship between the tumor and blood vessels and blood supply can be evaluated according to the flow-void phenomenon; enhancement scans mostly show homogeneous enhancement, and characteristic rat tail or dural tail signs can be seen; postoperative MRI shows dural thickening, which indicates residual tumor or recurrence.
5. Magnetic resonance spectroscopy (MRS) peak acetyl aspartate (NAA) and phosphocreatine/creatine (PCr/Cr) are typical changes of meningioma, and 1HMRS is helpful for tumor grading and recurrence.
6. Positron emission scanning (PET) can be used to evaluate the presence or absence of tumor recurrence and the degree of malignancy.
How to treat pterygoid crest meningioma?
Surgical resection is the main treatment strategy. The frontotemporal approach, centered on the pterygoid point, is often used for craniotomy. The frontotemporal approach is also suitable for meningiomas in all parts of the pterygoid crest. Its advantages include providing the lowest access and separating the tumor in multiple directions, allowing early excision of the hyperplastic skull and blocking the blood supply to the tumor, and controlling the internal carotid artery in the distal and proximal parts of the cavernous sinus when necessary.
1. Lateral pterygoid crest meningioma is mainly supplied by the external carotid artery (such as the middle meningeal artery), and total resection can often be achieved for the middle and lateral meningioma, including the dura mater, skull, orbital roof, and the involved dura mater.
2. Total resection of medial pterygoid crest meningioma is still difficult because it is often adjacent to cavernous sinus, III, IV and VI cerebral nerves, optic nerve, optic cross, pituitary gland and hypothalamus; it is mainly supplied by ophthalmic artery (and anterior sieve artery) and often compresses and encircles the internal carotid artery.