I. Overview of meningioma
Meningiomas are derivatives that originate from the meninges and meningeal spaces. They may arise from dural fibroblasts and soft meningeal cells, but most arise from arachnoid cells and can occur anywhere that contains an arachnoid component, such as intracerebroventricular meningiomas arising from the choroid plexus tissue within the brain.
The occurrence of meningiomas may be associated with certain internal environmental changes and genetic variants and is not due to a single factor. It may be associated with factors such as cranial trauma, radiation exposure, viral infections, and combined bilateral auditory neuromas. The common feature of these pathological factors is that they have the potential to mutate cell chromosomes or to increase the rate of cell division.
Clinical manifestations of meningioma
Many asymptomatic meningiomas are incidental, mostly benign, slow-growing, and clearly bounded by brain tissue; only a very small percentage (about 1.7%) are malignant. 50% are located in the parsagittal sinus, the convex surface of the brain, and the pars falciformis, followed by the pterygoid crest, saddle node, olfactory groove, pontocerebellar horn and cerebellar curtain, etc. Those growing in the ventricles are rare and can also be seen in the epidural space. Other sites are occasionally seen. The incidence of meningioma is 19.2% of intracranial tumors, ranking 2nd, with a female:male ratio of 2:1.
Meningioma is a slow-growing intracranial occupying lesion that causes corresponding neurological symptoms and signs due to compression of brain tissues and structures adjacent to the tumor, which is directly related to the tumor growth site and growth rate. The most common signs and symptoms of meningioma are headache and seizures, which are often the first symptoms. Depending on the location of the tumor, visual field, smell or hearing impairment and limb movement disorders may also occur. Because most meningiomas grow slowly, the course of the disease is long, with some reports suggesting that early symptoms of meningioma can take an average of 2.5 years, and in a few patients, up to 6 years.
Most patients complain of headache, but there is no correlation between the site of the headache and the location of the tumor. In older patients, seizures are particularly common as the first symptom. 50% of meningioma patients have seizures, and limited seizures are the most common symptom of paraganglioma of the middle sagittal sinus. grand mal seizures are common in frontal, temporal, and occipital lobe meningiomas, and in children, they often manifest as increased intracranial pressure.
With the increasing popularity of CT examinations, many patients have only mild headaches, even by chance for the discovery of meningioma by CT scan. Because of the slow growth of the tumor, it often grows very large while the clinical symptoms are not yet severe. Sometimes the patient has severe fundus optic papillary edema or even secondary optic nerve atrophy, while the headache is not severe and there is no vomiting. It is worth noting that when the tumor in the dumb area grows very large and the brain tissue can no longer compensate for it, the patient only shows the manifestation of increased intracranial pressure, and the condition will deteriorate suddenly, and even brain herniation and death will occur in a short period of time.
Diagnosis of meningioma
(1) Morphology, i.e. the shape and location of the tumor and its occupational effect.
(2) The density of tumor in CT and the signal intensity of MRI, and its performance after enhancement.
1.CT cranial scan:
The advantage of CT is that it can clearly show the calcification and bony changes (hyperplasia or destruction) of the tumor. A typical meningioma, in an unenhanced CT scan, shows an isolated isointense or high-density occupying lesion. Its density is uniform and consistent with well-defined margins, and calcifications are visible within the tumor. Enhancement reveals marked enhancement of the tumor, although a portion of the tumor does not appear vascular-rich on cerebral angiography.
This is because the contrast agent enters the brain tissue directly from the capillaries surrounding the meningioma and there is no blood-brain barrier between the two. Approximately 15% of meningiomas are associated with atypical necrosis, cystic degeneration, or intratumoral hemorrhage. Brain edema around the tumor is helpful in determining the growth rate of the tumor. In slow-growing tumors, edema may be mild or even absent, and edema around meningiomas that are rich in blood vessels is more extensive. Occasionally, meningioma is combined with large edema around it, which needs to be distinguished from malignant meningioma or metastatic brain cancer.
2.Magnetic resonance scan ( MRI ).
MRI generally shows equal or slightly longer T1 and T2 signals. 60% of the tumors have equal signal with gray matter on T1 image, and 30% have low signal below gray matter. On T2 image, 50% are isosignal or high signal, 40% are moderate high signal, and may be mixed signal. The tumor is well-defined, round or round-like, and most of the edges have a low-signal band in an arc or ring shape, which is the residual subarachnoid space (cerebrospinal fluid).
The parenchymal part of the tumor shows homogeneous and obvious enhancement by venous enhancement. Dural enhancement at the base of the tumor may result in a characteristic sign, the “dural tail”, which is more characteristic of meningioma, but not unique to meningioma. The advantage of MRI is that it can clearly show the relationship between the tumor and the surrounding soft tissue. The disappearance of the subarachnoid interface between the meningioma and the brain indicates that the tumor is growing aggressively, making total surgical resection more difficult.
MRI of meningiomas in the skull base, saddle area and pterygoid crest, or meningiomas with extracranial collaterals, has a clearer image than CT. MRI is also superior to CT in showing the proximity of the tumor to important blood vessels.
It is best to perform both CT and MRI on the same patient to obtain a more correct qualitative diagnosis. This is because meningiomas have similar presentation and characteristics in both images, and because MRI without enhancement can render 10% of meningiomas undiagnosed. Some meningiomas are not detected by MRI: a small asymptomatic meningiomas without combined edema and occupying effects, especially near the top; b multiple meningiomas that tend to miss small tumors; and c recurrent meningiomas. With contrast injection, the above disadvantages can be overcome.
(3) Other findings, such as skull involvement, calcification, and vasodilatation by compression.
IV. Treatment of meningioma
1.Surgical treatment.
Meningioma is a tumor outside the brain parenchyma, 92% of which are benign. Therefore, total surgical resection of the tumor is the preferred method, and in order to achieve the purpose of radical surgery, in principle, complete resection of the tumor and its adherent dura mater and skull should be pursued.
Grading of surgical resection of meningioma.
Grade IV: partial resection of tumor; Grade V: only craniotomy and decompression, and either biopsy or no biopsy of tumor.
2.Radiation therapy.
Benign meningioma has excellent effect of total resection, but because of its growth location, about 17-50% of meningioma cannot be completely resected. In addition, there are a few malignant meningiomas that cannot be fully resected. In recent years, due to the improvement of radiosurgery equipment and the efficacy of a large number of cases, radiation therapy is considered beneficial, especially for meningiomas in special areas, such as the cavernous sinus and slope, and for those who still have residual tumors after surgery, and gamma knife is the treatment of choice for meningiomas in the cavernous sinus area. Malignant meningioma and vascular ependymal meningioma are sensitive to radiotherapy and the effect is certain. While the effectiveness of radiotherapy for general benign tumors still has different opinions.
3.Hormone therapy.
Hormone receptor antagonists are used to treat these tumors. Mifepristone (mifeprinstoneRU486), a progesterone receptor antagonist, is used as an anti-meningioma drug, which can inhibit the growth of meningioma cells in vitro.
4. Gene therapy: It is still in the exploratory stage, and its effectiveness has not been confirmed.
V. Efficacy and recurrence of meningioma
Most meningiomas are benign and have good prognosis if they can be cured. Because they are extramedullary tumors, most patients have good quality of survival after surgery and can resume work and normal life, but those located in the medial pterygoid crest, cavernous sinus, slope and other surgically difficult areas have poor prognosis, high surgical mortality, many postoperative sequelae and poor quality of survival. In addition, the recurrence rate after meningioma surgery is often between 13% and 40%, so even patients with Simpson grade I surgery still have a high recurrence rate after 10D20 years of follow-up, and therefore patients should have regular imaging examinations after surgery.
Most meningiomas can be cured by total surgical resection, and even those that are not can be put into remission for a longer period of time. Some meningiomas are prone to recurrence, with recurrence rates ranging from 9% to 32% even in those who have achieved grade I or II surgical resection. There are two reasons for recurrence, one is local invasion of the tumor. The second is the presence of more or less residual tumor cells near the primary focus. The literature reports that benign meningiomas take 5-10 years to recur, while tumors that grow locally invasive may recur in less than a year.
The first choice in the management of recurrent meningiomas remains surgical resection. Depending on the patient’s signs and symptoms and CT analysis, the decision to reoperate may be made. The risk of reoperation depends not only on the age of the patient, but also on the general status of the patient and the location of the tumor. Secondary surgery is not always curative. However, radiation therapy is effective for meningiomas that have not been fully resected and for inoperable recurrent meningiomas.
What kind of meningioma can be treated without surgery?
Generally speaking, if the diagnosis is correct, the meningioma is less than 3 cm in diameter, and there are no symptoms caused by meningioma, it can be observed dynamically and not operated for the time being. In the beginning, MRI is often repeated 2-3 months after the last examination, and if there is no change, observation is continued. Subsequently, the review is repeated six months after the last MRI, and if there is still no significant increase in meningioma, the review interval can be set at one year.
If the tumor grows faster, or if the meningioma becomes symptomatic, surgery will be required. During the observation period, if signs of tumor progression such as significantly enlarged meningioma or enlarged peritumor edema and corresponding symptoms are found, surgery should be scheduled as soon as possible. Special sites such as meningioma of the saddle node and meningioma of the pontocerebellar horn may have symptoms such as loss of vision and visual field defects, and the tumor may be 1-2 cm or even a few millimeters in diameter.
For those who need surgery but the patient is too old to tolerate surgery, or the tumor is in a special location and the risk of surgery is too great for the patient to accept, gamma knife treatment can be considered. How to deal with specific cases involves many issues to be decided by doctors with extensive clinical experience.
Seven, the concept of minimally invasive in the treatment of meningioma
In recent years, the concept of minimally invasive surgery has taken off in all specialties of surgery, and the impact is quite far-reaching. The current general concept of minimally invasive is the application of small incisions and lumpectomy. It goes without saying that this is also the main goal of minimally invasive in neurosurgery. However, the neurosurgical community has always had the concept of reducing unnecessary intraoperative brain injury as an important part of minimally invasive surgery, and minimal brain injury has always been the ultimate goal of minimally invasive surgery.
The functional giant meningioma has always been a challenge for neurosurgery. Due to factors such as huge tumor, rich blood supply, and adjacent non-injurable important blood vessels, there are cases of surgical damage to adjacent important functional structures resulting in severe disability or even death of patients. For surgery of giant meningiomas in functional areas, implementing the concept of minimally invasive and minimally invasive can significantly improve the outcome.
First, precise positioning, whether preoperative CT or intraoperative navigation, aims to reasonably determine the extent of surgical exposure from the incision delineation stage, i.e., adequate and avoiding excessive; second, anesthesia cooperation, adequate preoperative and intraoperative communication with the anesthesiologist, and reasonable intraoperative use of dehydration, hyperventilation, and blood pressure control at appropriate times can help reduce intraoperative strain and intraoperative bleeding; and third. Minimize persistent brain strain.
In the past, when we did large meningioma surgery, we often took the whole block resection approach to reduce bleeding, but the block resection and intratumoral resection to reduce the tumor body can effectively reduce the strain on the surrounding brain tissue when separating the peri-tumor, which can be well achieved with the help of advanced surgical instruments (e.g. Ellman radiofrequency knife); finally, the peri-tumor arachnoid interface should be carefully distinguished under the microscope to protect important blood vessels. Special attention should be paid to the protection of the reflux veins.