[Overview] 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 cranial trauma, radiation exposure, viral infection, and the combination of bilateral auditory neuromas. The common feature of these pathological factors is their potential to mutate cell chromosomes or to increase the rate of cell division. It is commonly believed that cell division in arachnoid cells is slow, and the above factors accelerate the rate of cell division, which may be the important early stage leading to cell degeneration.
In recent years, developments in molecular biology have led to some success in the study of the etiology of meningiomas. Many studies have shown that in many tumors, changes in the DNA structure of a certain chromosome have been confirmed by the school. High or low doses of radiation, as well as many viruses, can alter the DNA structure.
Similarly, specific genetic changes are combined in patients with bilateral auditory neuromas. It is clear that there are many abnormal internal environmental and genetic factors in meningioma patients, all of which play a role in altering the chromosomal structure of the human body. Molecular cell biology studies confirm that the chromosomes of meningiomas are abnormal. The most common abnormality is the lack of a gene fragment on the 22 pairs of chromosomes. Since each individual chromosome contains thousands of genes, the absence of DNA within a chromosome would result in the loss of an extremely large amount of genetic information. With many studies, it can be speculated that all meningiomas may be double chromosome pairs lacking one or several genes.
These large changes in karyotype can occur in one of the 22 pairs of chromosomes that appear small on the conventional karyotype. Therefore, the key to clarifying the molecular biochemistry of meningiomas is to develop techniques that can confirm very small changes in human chromosomes. Once meningiomas are identified in 22 pairs of chromosomal genes lacking a pull, the selection of an experimental approach and gene therapy for meningeal skulls will become possible.
[Pathology]
Meningiomas are spherical in growth and have a clear border with brain tissue. The tumor profile is a dense gray or dark red tissue, sometimes containing sand granules within the tumor. Intratumoral necrosis is seen in malignant meningiomas. Meningiomas can sometimes thicken or thin the adjacent skull by invasion. Tumors can range in size from 1 cm in diameter to more than 10 cm in diameter and can be spherical, conical, flat, or dumbbell-shaped.
The common meningiomas are of the following types.
1)Endothelial type
2) Fibroblastic
3) Vascular
4) sand type
5) Mixed or migratory type
6)malignant meningioma
7)Meningeal sarcoma
[Clinical manifestations]
1)Meningioma is a benign tumor with slow growth and long course. FzrRchmg et al. observed 17 cases of meningioma up to 21 months and found that the average annual growth volume of tumor was 3.6%, and the growth rate of male 2 cases was l 8% and 21%.
2) Focal symptoms, because the tumor is swelling growth, patients often have headache and canker sores as the first symptoms. Depending on the location of the tumor, visual acuity, visual field, smell or hearing disorder and limb movement disorder can also occur. In elderly patients, epileptic seizures are especially common as the first symptom.
3) The symptoms of increased intracranial pressure are mostly not obvious, especially in elderly patients. With the increasing popularity of cT examinations, many patients have only mild headache, or even incidental finding of meningioma by CT scan. Because of the slow growth of the tumor, the tumor often grows very large while the clinical symptoms are not yet severe. Sometimes the patient’s fundus optic papillary edema is already severe and even secondary optic nerve atrophy occurs, 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 suddenly deteriorate and even develop brain herniation in a short period of time.
4) Effects of meningeal cripples on cranial bone: Meningioma near the cranial bone can often cause changes in bone quality. This can be manifested as thinning of the bone plate under pressure, or destruction of the bone plate, or even erosion through the bone plate to the subcapsular cavity membrane, with localized elevation of the scalp. The endosteal plate can also be thickened. The thickened skull may contain tumor tissue.
[Auxiliary examination]
CT performance: Before the appearance of cT, the diagnosis of meningioma could be confirmed based on the patient’s clinical presentation, supplemented by cranial plain film and cerebral angiography. cT has greatly improved the localization and qualitative diagnosis of meningioma. A typical meningioma presents as an isolated isointense or hyperintense occupying lesion on an unenhanced CT scan. Its density is uniform and consistent with well-defined margins, and calcifications are visible within the tumor. Enhancement reveals significant tumor enhancement, although a portion of the tumor is not shown to be vascular-rich on cerebral angiography.
This is due to the absence of a blood-brain barrier between the two, as the proportion of meningiomas is directed from the capillaries surrounding the meningioma into the brain tissue. Approximately 15% of meningiomas are associated with atypical necrosis, cystic changes, or intratumoral hemorrhage. In observing meningiomas on CT, it is important to note the relationship of the tumor to adjacent tissues such as the skull, cerebellar curtain, and sagittal sinus, so coronal and lateral reconstructions are sometimes important. Brain edema around the tumor is helpful to determine the growth rate of the tumor. In slow-growing tumors, edema may be mild or even absent, while edema around vascular-rich meningiomas tends to be more extensive.
Occasionally, meningioma is surrounded by a large combined edema, which needs to be differentiated from malignant meningioma or metastatic brain cancer. The cause of peripheral edema in meningioma is not well understood and may be related to disruption of the normal blood-brain barrier in patients with meningioma and the secretion of certain substances from meningioma tissue. Recently, it has been suggested that the water around the meningioma on the curtain is related to the prostaglandin level of the tumor or the effect of tumor progesterone receptor release.
(5) Magnetic resonance imaging: It is best to perform a comparative analysis of CT and MRI on the same patient. This is because the meningeal smoke is not detected in both types of tumors. This is because meningeal smoke has similar manifestations and features in both images, and MRI without enhancement can render 10% of meningiomas undiagnosed. Some meningeal cancers are not detected by MRI: 1) small asymptomatic meningiomas without combined edema and occupying effects, especially near the top, 2) multiple meningiomas in which small tumors are easily missed, and 3) recurrent meningiomas. These disadvantages can be overcome with the injection of (Gaddo1inium, DTPA) contrast agent.
[Treatment and Prognosis]
As with other intracranial tumors. Surgical resection of meningioma is an effective treatment for meningioma. With the development of microsurgical techniques. With the development of microsurgical techniques, surgical instruments such as bipolar electrocoagulation, ultrasonic aspirators, and lasers have been improved and popularized, the surgical results of meningiomas have been improved, allowing most patients to be cured. Meningioma has a good prognosis and most patients can be cured.