Oligodendroglioma

Introduction to oligodendroglioma Oligodendroglioma originates from oligodendrocytes, which account for 5%-10% of gliomas and 1.3%-4.4% of intracranial tumors. Most oligodendrogliomas occur in adults with a peak age of 50 to 60 years. The Department of Neuropathology, Dsseldort University, Germany, reported an average age of 42.6 years for 64 patients with WHO class II oligodendroglioma. About 6% of oligodendrogliomas occur in infants and children, and the average age of onset tumors at surgery is 10 years old, 7.5 years under the curtain. The incidence rate of males is higher than that of females, and the ratio of male to female is 1.1 to 3:1 to 2. Tumors occur in the cerebral cortex and cerebral hemisphere, and about 50% to 65% of tumors occur in the forehead. Other parts are eucalyptus > parietal lobe > occipital lobe. Oligodendrogliomas of the cerebellum, brainstem, spinal cord, and primary pia mater have also been reported. Tumors often grow slowly and have no envelope, but they have clear boundaries with normal brain tissue, mainly with expansive growth and slow growth. The incidence of calcification is high, ranging from 50% to 80%. Bleeding and cystic changes are rare. basic knowledge The proportion of illness: 0.001% - 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: nausea and vomiting

Causes of oligodendroglioma

Although oligodendroglioma and oligodendroglioma are among the most common central nervous system tumors in rats caused by chemical carcinogens such as ethylnitrosourea and methylnitrosourea, There is no convincing evidence that these substances are carcinogenic in the development of human gliomas. Individual oligodendroglioma cases have a history of previous radiotherapy, but these reports account for only a small percentage of all oligodendroglioma cases. The SV40 viral sequence was recently reported in 3/12 oligodendrogliomas. In addition, 2/12 cases of oligodendroglioma were positive for BK and JC viruses.

However, other authors did not detect any JC viral sequences in primary oligodendrogliomas and astrocytomas. Thus, the role of the virus in human oligodendrocyte tumors is still unclear.

[Organic origin]

The oligodendroglioma nomenclature is mainly based on histopathological changes, and the morphology of the tumor cells resembles normal oligodendrocytes, but there is limited evidence of whether this cell origin is true. It is not known whether oligodendroglioma originates from mature oligodendrocytes or tumorous transformation of mature glial precursor cells. Experimental studies suggest that one of the sources of oligodendrocytes in the development of rodent central nervous system tissue is biphasic precursor cells (O2-A precursors), which can differentiate into oligodendrocytes or Type 2 astrocytes. Oligodendrogliomas and oligodendrogliomas are derived from common precursor cells, tumor transformations of human precursor cells that are very similar to rodent O-2A precursors. This hypothesis has not been confirmed.

Oligodendroglioma prevention 1. Maintain an optimistic and happy mood. Long-term mental stress, anxiety, irritability, pessimism and other emotions will make the balance of the cerebral cortex excitatory and inhibition process imbalance, so you need to maintain a happy mood. 2, life restraint pay attention to rest, work and rest, life orderly, maintain an optimistic, positive, upward attitude towards life has a great help to prevent disease. Do the regularity of tea and rice, live daily, not overworked, open-minded, and develop good habits.

Oligodendroglioma complications Complications, nausea and vomiting

Nausea and vomiting, low-grade gliomas have a better prognosis than high-grade gliomas, with an average survival of 5-10 years, and 10-year survivors account for 5%-50%, of which 50%-75% The patient eventually died of the disease.

Symptoms of oligodendroglioma Common symptoms Intracranial hypertension Motor dysfunction Sensory disorder Visual impairment Optic papilledema Vomiting Epilepsy and epileptic seizures

Occurs in 35-40 years old. The common first symptom is focal epilepsy, and local neurological dysfunction depends on the lesion. Intracranial hypertension often occurs in the late stage, and mental symptoms can also occur.

Similar to astrocytoma, and closely related to the tumor site and its growth characteristics. Common symptoms are epilepsy, which is found in 52 to 79% of patients, the highest incidence of epilepsy in glioma, and often the first symptom of this tumor. Those who have been mistaken for primary epilepsy and have been delayed for many years are not discovered until symptoms of increased intracranial pressure occur. Hemiplegia and partial sensory disturbances are found in about one-third of patients, mainly caused by tumor invasion movements and sensory centers. Psychiatric symptoms are also common, mostly due to impregnation of the frontal lobe. Increased intracranial pressure appeared later, in addition to headache, vomiting, visual acuity and papilledema accounted for about 1/3. Others may have corresponding lesion symptoms depending on the tumor site.

Examination of oligodendroglioma

1, CT performance:

1 is a slightly dense mixed mass with clear edges; the cystic zone is low density.

2 There is calcification in the tumor, which is strip, spotted or large and irregular, and the curved strip calcification is characteristic.

3 peritumoral edema is light, and the occupancy effect is light.

4 enhanced scan shows that the tumor is mild to moderately enhanced, but it may not be strengthened; atypical cases may show low density of cortex, similar to brain infarction.

2, MR performance:

1 Most tumor contours are visible and edema is mild.

2 T1 weighting and T2 weighting in the tumor can be seen as irregular low signal (caused by calcification).

3 Most tumors are patchy and unevenly enhanced.

4 malignant edema and enhancement are obvious, and it is difficult to distinguish from grade III and IV astrocytomas.

3, the giant inspection

The oligodendroglioma has a clearer border, soft texture, and grayish pink. If the tumor is extensively mucoid, it can be jelly-like. Tumors are often located in the cerebral cortex and white matter, showing pial infiltration. Calcification is common, especially around the tumor and near the cerebral cortex. Cystic changes and intratumoral hemorrhage are also seen.

4. Histopathology

The oligodendroglioma cells are of medium density, round and uniform in size. In paraffin sections, the cytoplasm is swollen and translucent (honeycomb). Other features include microcalcification, mucus/cystic changes, and dense branched capillary networks. Significant nuclear atypia and rare schizophrenia can still diagnose WHO class II oligodendroglioma, but markedly active mitosis, microvascular proliferation, or significant necrosis indicates tumor progression to metamorphic WHO class III oligodendroglioma.

Cellular oligodendroglioma is a medium-density, single-form glioma. Although some small specimens only show scattered oligodendroglioma cells, they can be diagnosed by typical nuclear and brain parenchymal invasive growth. . High-density cell nodules with clearer boundaries are often seen in some well-differentiated tumor tissues. The tumor cells are round in shape and uniform in size, slightly larger than normal oligodendrocytes, and have deep chromatin. The mitosis is lacking or less. In conventional formaldehyde-fixed, paraffin-embedded tissues, tumor cells are denatured due to acute swelling, the cell membrane is clear, the cytoplasm is translucent, and the nucleus is located in the center, producing a typical honeycomb-like characteristic. Although this is an artificial phenomenon, it is very useful for diagnosis. help. This artifact is seen in smear or frozen sections, but disappears in the fast-fixed paraffin sections after freezing.

Some oligodendrogliomas contain small obese cells that are cytoplasmic, nuclear-biased, and GFAP-positive, and are called small obese cells or micro-obese cells (see below). GFAP-negative sign-like cells are seen in some rare cases. In some rare cases, large sign-like cells (inhibited cell-like oligodendroglioma) can be seen. Some oligodendrogliomas contain eosinophilic granule cells. Oligodendrogliomas show a typical dense chicken-claw-like branched capillary network. In some cases, the capillary interstitial divides the tumor into lobular. Tumors are prone to bleeding.

An important histological feature of calcified oligodendroglioma is microcalcification, sometimes associated with blood vessels, in tumors, or in tumor-infiltrating brain tissue, but this is not unique to oligodendroglioma. . Although neuroimaging shows clear calcification, it is not necessarily seen in tissue sections of incomplete tumor specimens. Extracellular mucus deposition and/or microcapsule formation are common.

Growth mode oligodendrogliomas grow slowly in the cerebral cortex and white matter. Tumor cells in the cortex form secondary structures, such as satellite phenomena around neurons, which surround the blood vessels and under the pia mater. Focal pia mater infiltration can cause significant fibrous tissue responses. Rare growth mode is that the tumor cells are arranged in parallel, the elongated nucleus forms a palisade-like structure, and occasionally a pseudo-purple group around the blood vessels. These growth modes exist only in some tumors.

5, immunohistochemistry

There are currently no specific and sensitive antibodies to human oligodendrocytes. Oligodenomas co-express s-100 protein, carbohydrate epitope, anti-lue-7 (HNK1, cD57) and enolase with other neuroectodermal tumors. GFAP not only reacts with intratumoral reactive astrocytes, but also with neoplastic oligodendrocytes, such as small obese cells and glial fibrillar oligodendrocytes. GFAP present in small obese cells and glial fibrillar oligodendrocytes has been identified by ultrastructural studies. Some studies suggest that these cells are transitions between astrocytes and oligodendrocytes, which are transitional cell phases during oligodendrocyte development. Small obese cells and/or glial fibrillar oligodendrocytes are not associated with prognosis. Oligodendrogliomas express a wave protein but are negative for keratin. Some keratin antibodies such as AEl/AE3 can cross-react with other intermediate filaments, including GFAP, and therefore have a false positive response. Some differentiated antibodies expressed in normal oligodendrocytes in vivo and in vitro have been identified, including basic myelin protein (MBP), proteolipid protein (PLP), myelin-associated glycoprotein (MAG), galactolipids such as Galactocerebroside (GC) and sulfuric acid milk; some gangliosides and enzymes such as carbonic anhydrase C, 2,3 cyclic nucleoside-3 phosphatase (CNP), glycerol-3-phosphatase dehydrogenase and Lactate dehydrogenase (LDH). However, none of them has been used as a marker for the diagnosis of oligodendroglioma. Some of them are not expressed in tumors (such as MBP), some are expressed only in a few cases (such as MAG, GC, PLP and CNP), or their expression is not limited to oligodendroglioma (such as carbonic anhydrase) C).

Diagnosis and differentiation of oligodendroglioma

Diagnostic points

Oligodendroglioma, according to its slow growth, high incidence of epilepsy and high rate of calcification, and more common lesions in the frontal lobe and psychiatric symptoms, can be initially diagnosed clinically, but often with other gliomas, especially It is difficult to identify with astrocytoma, and it needs to be examined by tissue to get correct identification. CT brain scan, MRI and other X-ray examinations can determine the location and extent of the lesion.

1 cell glioma: rare, occurs in children and young people, 80% occur in the age of 30, the incidence of less glioma is deep.

2 low grade astrocytoma: the position is often deep, the tumor density is low, the calcification is less punctate or patchy, and some patients have heavier peritumoral edema.

3 meningioma: the base adjacent to the meninges or skull plate, with the skull at an obtuse angle, the local skull may have proliferative changes, intratumoral calcification is mostly sand-like; enhanced scan showed obvious tumor enhancement.

4 vascular malformations: CT can be shown as high density, but calcification is relatively rare and small in scope, often without a mass effect.

Differential diagnosis

Differential diagnosis of oligodendroglioma includes central glial and neuronal tumors, such as clear cell ependymoma, central neuroblastoma, and embryonic dysplastic neuroepithelial neoplasia (DNT). All of these tumors, like oligodendrogliomas, have histological features of oligodendrocyte-like cells (OLC) with uniform cell size, nuclear roundness, and cytoplasmic transparency. These cells can be distinguished under an electron microscope. Immunohistochemical staining of nerve-specific markers of synaptophysin is helpful in distinguishing between central neuroblastoma and oligodendroglioma, but the positive result of judging synaptophysin should be carefully considered due to oligodendroglioma The gray matter is diffusely infiltrated, and the residual nerve fibers are colored, which is mistaken for tumor coloration. Several recent studies have reported that typical oligodendrogliomas can be stained by neuromarkers, including synaptophysin and neurofilament proteins. This focal immune response is not as strong and diffuse as a neurological tumor, so it has nothing to do with prognosis.

The identification of oligodendroglioma and clear cell meningioma is not difficult. The PAS staining of clear cell meningiomas is positive, and the immunohistochemical staining of epithelial membrane antigen (EMA) is positive. Interstitial oligodendroglioma is sometimes very similar to metastatic (clear cell) cancer. Unlike oligodendroglioma, metastatic carcinoma is bordered with surrounding brain tissue and immunohistochemically stained for epithelial markers such as keratin and EMA. .

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