What Is the Ependyma?

Subependymoma is a benign slow-growing benign tumor that is rarely seen. It was first discovered and described by Scheinker in 1945. Later, the authors successively reported it, and found that some cases of subventricular ependymal tumors have a family history, and they believe that there may be genetic factors in their pathogenesis. Other authors believe that subventricular ependymal tumors are a type of hamartoma caused by local abnormalities of the ependyma, and there may be long-term chronic ependymal inflammation leading to healthy search of the ependymal or subependymal glia. Observation of the ultrastructure of subependymal ependymal tumors caused by cell proliferation indicates that the tumor cells may be derived from subependymal cells that have the dual differentiation ability to ependymal cells or stellate cells.

Ependymal tumor

Ependymal tumors originate from central nervous system tumors of the ventricle cells of the ventricle and the central canal of the spinal cord or white matter ependymal cells in the brain. More men than women, more common in children and youth. Disease description: Ependymal tumors originate from central nervous system tumors of the ventricle cells of the ventricle and the central canal of the spinal cord or white matter ependymal cells in the brain. Gliomas account for 18.2%, more men than women, more common in children and young people, about 75% are under the curtain, only 25% on the curtain. Most tumors are located in the ventricle, and a small number of tumors are in brain tissue.

Overview of Ependymoma Diseases

Subependymoma is a benign slow-growing benign tumor that is rarely seen. It was first discovered and described by Scheinker in 1945. Later, the authors successively reported it, and found that some cases of subventricular ependymal tumors have a family history, and they believe that there may be genetic factors in their pathogenesis. Other authors believe that subventricular ependymal tumors are a type of hamartoma caused by local abnormalities of the ependyma, and there may be long-term chronic ependymal inflammation leading to healthy search of the ependymal or subependymal glia. Observation of the ultrastructure of subependymal ependymal tumors caused by cell proliferation indicates that the tumor cells may be derived from subependymal cells that have the dual differentiation ability to ependymal cells or stellate cells.

Epitubular tumor symptoms and signs

Different types of ependymoma

The manifestations of different types of tumors are longer in patients with subventricular ependymoma, with an average of 10-14 months. Submental ependymal tumors are mainly manifested as paroxysmal nausea, vomiting (60% -80%), and headache (60% -70%). Later, unstable walking (30% -60%), dizziness (13%), and Speech disorders (10%). The signs were mainly cerebellar ataxia (70%), optic disc edema (72%), neurological disorders (20% -36%), and abnormal tendon reflexes (23%). The most common symptom of fourth ventricular ependymal tumor is abnormal gait. Symptoms of supraventricular ependymoma are mainly headache, vomiting, drowsiness, anorexia, and diplopia (67% to 100%), and seizures (25% to 40%). Ventricular meningiomas located in the cerebellar pontine angle may have tinnitus, deafness, and neurological symptoms in the posterior group. Children under the age of 2 have special symptoms, mainly irritability, drowsiness, loss of appetite, increased head circumference, full forefoot, stiff neck, stunted growth, and weight loss.
Ependymal tumor
Due to the rapid growth of tumors, the disease of anaplastic ependymal tumors is short, and the symptoms of cranial hypertension are obvious. About 40% of patients with subependymal ependymal tumors have symptoms. Symptoms often occur in tumors located in the clear septum, Monro's foramen, aqueduct, fourth ventricle, and spinal cord. Patients mainly presented with headache, blurred vision, unstable walking, memory loss, neurological symptoms, nystagmus, dizziness, nausea, and vomiting. 88% of patients have hydrocephalus.

Different parts of ependyma

The manifestations of tumors in different parts Due to the different tumor sites, the clinical symptoms of patients with ependymal tumors are very different. Nausea, vomiting, and headaches are relatively non-specific, and they are the most common clinical symptoms above and below the scene. Generally speaking, posterior cranial foci tumors show symptoms of increased intracranial pressure (vomiting and headache) and are also accompanied by gait instability. Oncology tumors often show local motor dysfunction, visual impairment and epilepsy, and symptoms of epilepsy It accounts for 25% of children with supraventricular ependymoma, and neck pain and stiffness are also common symptoms of posterior cranial alveolar ependymoma, which may be related to tumor invasion of the cervical nerve root. Optic disc edema is the most common sign in children with ependymoma in any part. Other signs vary according to the location of the tumor. Nystagmus, meningeal signs, and poor ranging are most common in posterior fossa lesions. Hemiplegia and tendon reflexes Hyperthyroidism and abnormal visual field are the most common signs of tumors on the screen. Ataxia is seen in both on-screen and under-screen lesions.
Before the diagnosis is confirmed, the duration of symptoms ranges from 1.5 to 36 months. The duration of disease in most children lasts about 12 months. The length of the disease varies according to the location and grade of the tumor. The average course of oncology tumors is 7 months (2 weeks to 3 years), and the average course of posterior cranial alveolar tunica tumors is 9 months (2 weeks to 2 years). Generally speaking, benign lesions are more common than malignant lesions. Longer course, symptoms of posterior alveolar meningiomas that invade surrounding structures take 5.4 months, while tumors that do not invade generally take 11 months to show symptoms; calcified supraventricular meningiomas are better than none Symptoms of calcified tumors have a longer duration, but there is no significant difference in the duration of symptoms in patients with and without calcification in posterior cranial alveolar meningiomas.

Ependymoma

Ependymoma of fourth ventricle

Because the tumor is located in the ventricle of the brain, it is easy to block the cerebrospinal fluid circulation, and symptoms of increased intracranial pressure often occur early. When the tumor compresses the nucleus of the cerebellum at the bottom of the fourth ventricle or the cerebellar feet laterally, it can clinically cause cerebral nerve damage and cerebellar symptoms.
Symptoms of increased intracranial pressure: It is characterized by intermittent and related to changes in head position. In the late stage, the head is often forced, and the head is mostly forward or lateral flexion. As posture changes can stimulate the nerve nucleus at the bottom of the fourth ventricle, especially the vagus nerve and vestibular nerve nucleus, manifested as severe headache, dizziness, vomiting, pulse, breathing changes, sudden loss of consciousness and recovery due to the affected abductor nucleus Vision and nystagmus are called Brun sign. Due to tumor activity, the cerebrospinal fluid circulation can be blocked due to sudden blockage of the mesopores or aqueducts, which can cause an episodic increase in intracranial pressure. This phenomenon usually occurs when the body position changes suddenly. Severe intracranial pressure can cause cerebellar crisis.
Symptoms of brainstem and neurological damage: There are fewer symptoms of brainstem. When tumors are oppressed or infiltrated to the bottom of the fourth ventricle, symptoms of pontine and medulla nucleus involvement may occur. Most of them occur after the intracranial pressure increases. There are also neurological symptoms as the first symptoms. The appearance, involvement process and extent of neurological damage symptoms are closely related to the location and extension of tumors. The tumor in the upper part of the fourth ventricle mostly affects the nerve cores of the , , , and iliac crests. The growth along the midline affects the medial longitudinal bundle. Eyeballs can appear to be paralyzed to the affected side, and eye movement can also be skewed and twisted. The fourth ventricle The tumors in the lower part mainly affect the nucleus of , , , and phrenic nerves. The first symptoms are often vomiting and hiccups, followed by dysphagia, hoarseness, and visceral symptoms caused by vagus nerve stimulation, and sometimes even sphincter muscles. Dysfunction and dyspnea; tumors that originate in the crypt of the fourth ventricle, often develop into the cerebellar horn of the ipsilateral pontine, and are mainly affected by , , and phrenic nerves, which are mainly manifested as facial sensory disorders, hearing and Vestibular hypofunction and dizziness. When the brainstem long conduction tract is involved, it is mostly caused by tumor or chronic occipital foramen hernia compression on the brainstem, which may have weak limbs, low or disappeared tendon reflexes, and pathological reflexes are often bilateral. Ventricular meningiomas in the four ventricles often pass down the foramen magnum and develop into the upper cervical spinal cord, which can reach the neck level of 2-3 at least, sometimes around the upper cervical spinal cord, showing neck pain and stiffness. Cerebral palsy.
Cerebellar symptoms: Cerebellar symptoms are generally mild. They are caused by tumor growth along the lateral or dorsal side that affects the cerebellar feet or ventral cerebellum. They are characterized by walking instability, nystagmus is often seen, and some patients show ataxia and muscle strength. Diminish.

Ventriculoventricular tumor

The lateral ventricular ventricular meningioma originates from the lateral ventricle wall. It is more common in the lateral ventricle frontal angle and body. The tumor grows slowly and can grow large and fill the entire lateral ventricle. A small number of tumors can be drilled through the interventricular fora The symptoms of intraventricular and lateral ventricle tumors are as follows:
Symptoms of increased intracranial pressure: Because the tumor grows slowly, the symptoms are not obvious before it causes cerebrospinal fluid circulation disturbance. Because the tumor has a certain degree of activity in the ventricle, it can produce paroxysmal headache and vomiting with changes in body position, which are sometimes light and heavy, and difficult to be detected. Patients often keep the head in a certain position (that is, forced head position). When the volume of the tumor increases enough to cause cerebrospinal fluid circulation to be blocked, a series of symptoms such as persistent headache, vomiting, and optic disc edema increase, such as increased intracranial pressure. A sudden increase in intracranial pressure can cause coma or death. Pediatric patients may have an enlarged skull and decreased vision due to chronic intracranial pressure.
Ependymal tumor
Local symptoms of tumors: In the early stage, tumors have less compression on brain tissue, and local symptoms are not obvious. When tumors grow larger, especially when they invade the thalamus, inner capsule and basal ganglia, or when tumors invade the brain parenchyma, Hemiparesis, hemiplegia, and central facial paralysis. Epilepsy caused by tumors is rare for authors.

Ependymoma of third ventricle

Meningiomas of the third ventricle are extremely rare, and the tumors are mostly located in the posterior part of the third ventricle. Due to the narrow space of the third ventricle, it is very easy to block the cerebrospinal fluid circulation and cause obstructive hydrocephalus. Early intracranial pressure increased and showed progressive increase. Sometimes due to the tumor's flap-like obstruction of the interventricular foramen and the upper aqueduct, symptoms such as paroxysmal headache and vomiting may occur, and may be accompanied by low fever. Optic nerve compression symptoms and pituitary and hypothalamus symptoms can be seen in the front of the third ventricle. Those who are located behind the third ventricle may develop symptoms such as supraoptic dyskinesia.

Intraventricular ependymoma

Some ependymal tumors do not grow on the ventricle and are located in the brain parenchyma. The tissue source is ectopic ependymal cells of the embryo, or tumors originating from the ventricular wall may grow into the brain parenchyma. Those on the scene are more common in the frontal and parietal lobe. Tumors are often located in the deep part of the brain near the ventricle and are also exposed on the surface of the brain. The clinical manifestations are similar to the symptoms of occupying parts of the brain. They are common in younger children. More difficult.

Etiology of ependymal tumor disease

Ependymal tumors are mostly located in the ventricle, and the main body of a few tumors is located in brain tissue. Posterior cranial alveolar meningiomas mainly occur in the depressions of the parietal, base, and lateral walls of the fourth ventricle. Most of the tumors in the fourth ventricle originate from the medulla oblongata. The growth of the tumor can occupy the fourth ventricle and cause obstructive hydrocephalus. Sometimes the tumor can extend through the middle hole to the large occipital cistern. A few can compress or even surround the medulla oblongata or project into the spinal canal to compress the upper cervical spinal cord. Some tumors originate from the fourth ventricle parietal, occupying the cerebellar hemisphere or vermiform, occasionally tumors occur in the bridge cerebellar horn. Supraventricular tumors are more common in the lateral ventricle and can originate in various parts of the lateral ventricle, often infiltrating into the brain parenchyma. Occurred in the third ventricle are rare, those located in the front can extend to the bilateral ventricles through the interventricular foramen. Suprameningioventricular tumors are thought to originate from the ventricle epithelium of the lateral ventricle or triple ventricle. The tumor can be either completely in the ventricle, part of the ventricle, or part of the ventricle. However, tumors may also occur anywhere in the cerebral hemisphere and are completely located outside the brain. The tumor originates from the ependymal cell ridge, which may be the result of deformities when the neural tube is folded. Such tumors are more common in the frontal and temporal lobes. , Parietal lobe and third ventricle.

Clinical manifestations of ependyma

Tumors located in the fourth ventricle are prone to block the cerebrospinal fluid circulation and produce early symptoms of intracranial hypertension. Most often, headache is the first symptom, accompanied by vomiting, dizziness, and forced head position. When the tumor enlarges and involves the cerebellar vermicomb or hemisphere, symptoms such as impaired balance, walking instability, and ataxia may occur. When the tumor compresses the brainstem or cranial nerve, a corresponding cranial nerve disorder may occur. Supracranial tumors of cranial hypertension appear later, and the course of the disease can be as long as 4-5 years.

Imaging findings of ependyma

CT CT findings of ependyma

Plain scan tumors are cauliflower-like, dense or mixed-density masses.
When the tumor is located in the fourth ventricle, the remaining ventricle is generally visible around the tumor; it is a band-shaped or crescent-shaped positive cerebrospinal fluid density zone. The tumor on the screen often occurs around the ventricle, and is mostly located in the parietal and occipital lobe.
20% of the tumors were calcified, showing single or multiple spots.
Tumors often have cystic changes; enhanced scans show moderate intensification.
Ependymal tumor
Obstructive hydrocephalus can occur.
When subventricular metastasis occurs, focal density increased block shadows or strip density increased shadows can be seen around the lateral ventricle.

MRI MRI features of ependyma

Most patients have epilepsy as the first symptom, and the majority are middle-aged and elderly. Among the 19 cases in this group, 11 cases are over 40 years old, accounting for 58% of the total.
Tumors are usually close to the lateral ventricle and often occur at the junction of the temporomandibular occipital junction. In this group, 63% of the tumors appear in this area, which is close to the reports in the literature.
The tumor has a high probability of calcification and cystic changes. This group exceeds 80%. Although there is a gap between 50% and 60% reported in the literature, it indicates that calcification and cystic changes are common.
The parenchymal part of the tumor is often significantly enhanced, while the cysts and calcification are not enhanced.
Edema around the tumor is generally mild.
In short, because of the richer information displayed on MRI, parenchymal ventricular aneurysm, the imaging changes have certain characteristics, and the diagnostic coincidence rate is higher than that of CT. However, the diagnosis needs to be related to intracranial astrocyte tumor, To distinguish oligodendroglioma, glioblastoma, and giant single lymphoma, in order to make a more accurate diagnosis from the perspective of imaging.
Astrogliomas have important value in the identification of the following 3 points on the scene:
The solid part of the tumor has stripe or punctate calcification, and the ependymoma should be considered. Astrocyte calcification is rare.
The edema around the ventricular ependymoma is mild or non-edema, and astrocyte tumors are often accompanied by more obvious edema.
(3) The age of onset of ependymal tumors is more common in adolescents, and the age of clinical onset of astrocyte tumors is more common in 40-50 years old.
Oligodendroglioma is not significantly more intensive than ependymal tumor. Glioblastomas mostly occur in people over 50 years of age. The tumors progress rapidly, and they often expand along the white matter bundles. They extend to the bilateral cerebral hemispheres by corpus callosum, anterior and posterior joints, and gliomas have more bleeding. . Giant solitary lymphoma is generally non-calcified, and the MR signal is more homogeneous, which is usually homogeneous and significantly enhanced, while the ependymal tumor is heterogeneous and irregularly enhanced.
In summary, MRI can clearly show the lesions of ependymal tumors, and its MRI manifestations are characteristic, which is of great value for the diagnosis and differential diagnosis of ependymal tumors.

Epidemiopathoma

The study found that more than 50% of the ependymal tumors have lost the chromosome 22 fragment, but the gene sequence on the missing fragment has not been identified. Other studies have shown that monkey vacuolar virus (SV40) is closely related to ependymal tumors. SV40 can express "T antigen" (Tag) in infected cells. Tag can interact with human DNA polymerase alpha to stimulate viral DNA replication and inhibit the function of p53 protein. Bergsagel et al. Found in 11 cases of ependymal tumors that 10 of the tumor cells contained SV40 gene-related sequences and confirmed the expression of Tag. Pathological manifestations of tumors:
The ventricular ependymoma is mostly located in the ventricle, and a small part can be located in the brain parenchyma and the pontine cerebellum. The tumor was red, lobulated, brittle in texture, generally rich in blood supply, and clear in borders. The supraventricular ventricle tumor base is broad grayish red and sometimes cystic. The morphology of ependymal tumors under light microscope is not completely consistent, the cells proliferate moderately, the nucleus is large, round or elliptical, mitotic figures are rare, and there may be calcification or necrosis. The section of the tumor under low magnification looks like "leopard skin", which is one of the diagnostic signs of ependymal tumor. There are two structural characteristics of high-power ependymoma: one is a "palisade-like" structure formed by tumor cells arranged in the direction of the protrusion toward the tumor vessel wall, called a "false rosette" nodule, and its central blood vessel The surrounding area is a non-nucleated area composed of long, glial fiber-containing cell protrusions, and the periphery is tightly surrounded by tumor cell nuclei. This structure as a whole is smaller and less common than "false roses", but has diagnostic value for ependymal tumors. The "real chamber tubule rose" structure is formed by a small number of uniformly shaped polygonal tumor cells arranged radially, and a lumen is formed in the center. Immunohistochemical staining showed that GFAP, vimentin, and fibronectin were positive.
Ependymal tumor
Interstitial ependymal tumors account for 45% to 47% and 15% to 17% of the supra- and sub-occipital ependymal cell tumors, respectively, also known as malignant ependymal tumors. Microscopically, tumor cells had obvious proliferation, diverse morphology, atypical nuclei, abundant chromatin in the nuclei, and more common divisions. The tumor loses the arrangement structure of the epithelial cells of the ependymal membrane, the intrastromal arrangement of the tumor is disordered, the blood vessel proliferation is obvious, and necrosis can occur. Anaplastic ependymal tumors are prone to the dissemination and implantation of tumor cells and cerebrospinal fluid. The incidence rate is 8.4%, and the tumors behind the scenes are as high as 13% -15.7%.
Subventricular ependymal ependymal tumors are mostly located in the ventricular system with clear boundaries. In addition to those located in the ventricle, they can grow in the transparent septum, aqueducts, and central spinal cord. Tumors often have a vascular pedicle connected to the brainstem or ventricle wall. Light microscopy showed tumor cell edema, which contained a dense fibrous matrix and glial fibers. The nuclei of tumor cells are oval in shape, with chromatin distributed in spots, and there are few mitotic figures. Some tumors may have calcification or cystic changes. No astrocytic cells were found in the subventricular ependymal tumor, which could be distinguished from the subcellular ependymal giant cell astroma.

Epitubular tumor diagnosis

Epitubular tumor diagnosis

Diagnosis: According to clinical manifestations and auxiliary examinations, diagnosis can usually be made.
Laboratory examination: Most patients have increased lumbar puncture pressure, especially when subtumoral tumors are associated with hydrocephalus. About half of the patients have increased CSF protein, and about 1/5 of the patients have increased CSF cells. Because tumor cells often shed in the cerebrospinal fluid, microscopic examination of the cerebrospinal fluid requires attention and identification of white blood cells.

Auxiliary examination

Other auxiliary examinations: CT and MRI of the skull have diagnostic value for ependymal tumors. The tumor showed a slightly high-density shadow with clear borders on the plain CT scan, which was mixed with low density. High-density calcification is often present in tumors, and calcification and cystic changes are more common in subtumor tumors than in subtumor tumors. Some of the tumors are located in the parenchyma of the brain, and the surrounding brain tissue shows a mild to moderate edema band. On MRI, T1 weighting is low and equal signal shadow, and proton weighting and T2 weighting are high signal. After injection of the enhancer, the tumor showed moderate to obvious enhancement, some of which were irregularly enhanced. Anaplastic ependymal tumors are significantly enhanced on CT and MRI. Tumor MRI shows low signal T1W, high signals on T2W and proton-weighted images, and the signal within the tumor is uneven, with necrotic cysts. Subventricular ependymal tumors appear on the CT as well-defined low-density tumor shadows in the ventricle. On MRI, the tumor showed T1W as a low signal, and T2W and proton weighting showed a high signal shadow. About half of the tumors have non-uniform signals and are caused by calcification or cystic changes. After injection of the enhancer, some tumors may be unevenly strengthened.

Epimental tumor treatment plan

Total surgical resection of tumor is the first choice for treatment of ependymal tumors. Ventricular ependymal tumors can be drained before surgery to reduce intracranial pressure. Surgical mortality of supraventricular epidural tumors has decreased to 0% -2%, while mortality of sub-occult tumors has been 0% -13%. For patients who cannot undergo a total tumor resection, radiation therapy should be performed after surgery. Although there is no uniform understanding of postoperative radiotherapy for ependymal tumors, most authors still recommend a radiation dose of 50-55Gy. Because most of the tumor beds recur in situ, it is not necessary to prevent the cerebral spinal cord from prophylaxis. Adult patients have no significant effect on postoperative chemotherapy, but chemotherapy is still an important adjuvant therapy for patients with relapse or young children who are not suitable for radiotherapy. Commonly used chemotherapeutic drugs are carmustine, lomustine, etoposide (etoposide), cyclophosphamide and cisplatin. Chemotherapy for infants under 3 years of age can be started 2-4 weeks after surgery, and the next course of treatment can be started after 4 weeks of rest. Surgery for anaplastic angioplasty is still the main measure of treatment, postoperative radiotherapy is necessary, radiotherapy should be early, the dose should be larger, 55-60Gy. Prophylactic cerebrospinal radiotherapy is also required. Chemotherapy is one of the methods of adjuvant therapy to control tumor growth in the short term. Surgery is the main measure to eradicate subventricular ependymoma. With the application of microneurosurgical technology, the surgical mortality rate is almost zero. Because the subependymal epidural tumor grows expansively and has a clear boundary, most tumors can be completely resected. For those with deep tumor growth sites and difficult to achieve complete tumor resection, subtotal resection can also achieve good therapeutic effects. Radiotherapy is generally not routinely used. However, for patients with pleomorphic changes in the nucleus of the tumor, or patients with mixed ependymoma-subventricular ependymoma, radiotherapy is recommended. Epimental tumors have a higher recurrence rate, and the prognosis of posterior fossa tumors in children is poor. Almost all cases have recurred at different times after surgery. Epimental tumors are prone to intraspinal dissemination and implantation. There are studies and statistics on 436 cases of epimental tumors of all age groups, with 11% of them being implanted. Intraventricular ependymoma is more common in the spinal canal than on the screen. The incidence of ependymoma was significantly higher than that of ependymoma. Extracranial metastases of intracranial ependymal tumors are rare and only reported in individual cases. Clinical reports on disseminated implants often underestimate the true rate of this phenomenon, as spinal cord imaging is not routinely performed in the vast majority of cases. Analysis of clinical data of patients with spinal implantation and metastasis of posterior cranial alveolar tumors showed that the incidence of disseminated implantation was 6%, while the combined incidence of 21 series reported was 15%.
Ependymal tumor
The incidence of subarachnoid implantation and dissemination varies according to the location of the tumor. The rate of intraspinal dissemination and implantation of supraventricular ependymoma is 8%, while the incidence of posterior cranial alveolar tumour implantation is 15 %. Different tumor pathological grades also have significant differences in metastatic dissemination. About 20% of high-grade ependymal tumors have intraspinal dissemination and implantation, while the proportion of low-grade tumors has 9%. In general, high-grade ependymal tumors are more likely to have intra-vertebral implants than lower-grade tumors. In addition, sub-occipital ependymal tumors have a higher rate of dissemination and metastasis than superficial tumors. The possibility of pia matereal metastases directly affects the determination of the scope of radiotherapy. Although the spread of cerebrospinal fluid detected at autopsy is relatively common, neuroimaging examinations performed before radiotherapy show that except for young children, the rate of tumor spread Very low. The Children's Tumor Investigation Group reported that 43 cases of ventricular meningioma had no positive myelography findings or spinal canal MRI findings before radiotherapy, and most patients with pial meningeal metastases had concurrent recurrence of the primary site.

Epitubular tumor complications

If surgical treatment is performed, the following complications may occur:
Intracranial hemorrhage or hematoma is not carefully related to hemostasis during the operation. With the improvement of surgical skills, this complication has rarely occurred. The wound is carefully stopped to stop bleeding and repeated irrigation before the cranial closure can reduce or avoid intracranial hemorrhage after surgery.
Cerebral edema and postoperative high intracranial pressure can use dehydration drugs to reduce intracranial pressure, and glucocorticoids can reduce cerebral edema.
The loss of phrenic nerve function is related to the important functional areas and structures of the injury during the operation. Avoid the injury as much as possible during the operation and treat it symptomatically.

Prognosis and prevention of ependyma

Prognosis

Prognosis: Factors affecting the prognosis of ependymoma include the location of the tumor, the type of histology, the rate of recurrence, and age, among which the first two play a decisive role. Recurrence in the domestic data was within 20 months on average. The 5-year survival rate of ebroblastoma is only 15%. Another potentially important prognostic factor is the degree of surgical resection. Survival rates in the near-total resection group have significantly improved. 50% to 60% of patients with total tumor resection have no tumor recurrence within 5 years, compared with 21% of patients with subtotal resection. Postoperative radiation dose above 45Gy can effectively control tumor growth. The five-year survival rates for on- and under-tumor tumors were 35% and 59%, respectively. Older patients with subventricular ependymoma have a slightly better prognosis. The average survival time for patients under 10 years is 2 years, while the average survival time for patients over 15 years is 4.3 to 6.0 years. Malignant changes can occur after recurrence. Malignant ependymal tumors in children recur quickly. The average recurrence period is 18 months, and the prognosis is poor. Invasion of the brainstem based on neuroimaging and signs of neurological damage to the brain is also closely related to poor prognosis. Anaplastic ependymal tumors have a poor prognosis, a high recurrence rate, about 68%, and are easily spread along the cerebrospinal fluid. The 5-year survival rate is 25% -40% lower than that of ependymoma. Patients with subventricular ependymal tumors generally have a good prognosis, with rare recurrence or cerebrospinal fluid dissemination.

Prevention of ependymal tumor

Prevention: No special.

Epidemiology

The total incidence of ependymoma and malignant ependymoma accounts for 2% -9% of intracranial tumors and 10% to 18.2% of neuroepithelial tumors. There are more men than women, and the ratio of men to women is 1.9: 1. It is more common in children and young people. The incidence rate is higher in children. The peak age of onset is 5 to 15 years, accounting for 6.1% to 12.7% of children's intracranial tumors, and 8.0% to 20.9% of all neuroepithelial tumors. The age of children with fourth ventriculoventricular aneurysm is younger than that of children with other parts of ventricular aneurysm. The overall male to female ratio is 1: 1. Generally, three-quarters of the tumors are located under the curtain and one-fourth are located on the curtain, accounting for the vast majority of children. Looking back at the reports of several groups of tubal ependymal tumors, out of 455 such tumors, 151 (33%) were on the screen and 304 (67%) were under the screen. A study of ependymoma in children shows that malignant ependymoma is more on the veil (81%: 19%), while low-level ependymoma is more common in the posterior cranial fossa (61%). : 39%). Subventricular ependymal tumors account for 0.2% -0.7% of intracranial tumors and 0.4% in autopsies. Onset around the age of 40, more common in men. About 1/3 of the tumors are located on the screen, 2% are located on the cervical spinal cord, and the remaining nearly 2/3 are located below the screen.

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