An X-ray computed tomography (CT) or magnetic resonance imaging (MRI) scan is necessary to characterize the anatomy of this tumor as to size, location, and its heter/homogeneity. However, final diagnosis of this tumor, like most tumors, relies on histopathologic examination (biopsy examination).

The majority of patients can be expected to be cured of their disease and become long-term survivors of central neurocytoma. As with any other type of tumor, there is a chance for recurrence. The chance of recurrence is approximately 20%. Some factors that predict tumor recurrence and death due to progressive states of disease are high proliferative indices, early disease recurrence, and disseminated disease with or without the spread of disease through the cerebral spinal fluid. Long-term follow up examinations are essential for the evaluation of the outcomes that each treatment brings about. It is also essential to identify possible recurrence of CN. It is recommended that a cranial MRI is performed between every 6–12 months.

If resected, the surgeon will remove as much of this tumor as possible, without disturbing eloquent regions of the brain (speech/motor cortex) and other critical brain structure. Thereafter, treatment may include chemotherapy and radiation therapy of doses and types ranging based upon the patient's needs. Subsequent MRI examination are often necessary to monitor the resection cavity.

The diagnosis is based on tissue, e.g. a biopsy. Histologically subependymomas consistent of microcystic spaces and bland appearing cells without appreciable nuclear atypia or mitoses. The nuclei tend to form clusters.

Definitive treatment for ganglioglioma requires gross total surgical resection, and a good prognosis is generally expected when this is achieved. However, indistinct tumor margins and the desire to preserve normal spinal cord tissue, motor and sensory function may preclude complete resection of tumor. According to a series by Lang et al., reviewing several patients with resected spinal cord ganglioglioma, the 5- and 10-year survival rates after total resection were 89% and 83%, respectively. In that study, patients with spinal cord ganglioglioma had a 3.5-fold higher relative risk of tumor recurrence compared to patients with supratentorial ganglioglioma. It has been recognized that postoperative results correlate closely with preoperative neurological status as well as the ability to achieve complete resection.

With the exception of WHO grade III anaplastic ganglioglioma, radiation therapy is generally regarded to have no role in the treatment of ganglioglioma. In fact, radiation therapy may induce malignant transformation of a recurrent ganglioglioma several years later. Adjuvant chemotherapy is also typically reserved for anaplastic ganglioglioma, but has been used anecdotally in partially resected low grade spinal cord gangliogliomas which show evidence of disease progression.

Surgical excision of the central neurocytoma is the primary consensus among practicing physicians. The surgeons perform a craniotomy to remove the tumor. The ability to remove the tumor and to what extent it is removed is dependent upon the location of the tumor and surgeon experience and preference. The extent of the disease plays a large part in determining how effective the surgery will be. The main goal of a complete surgical resection, of the tumor, can also be hindered by the adherence of the tumor to adjoining structures or hemorrhages. If there is a recurrence of the central neurocytoma, surgery is again the most notable treatment.

The histopathologic grading of oligodendrogliomas is controversial. Currently the most commonly used grading schema is based on year 2007 World Health Organization (WHO) guidelines. An updated classification is in progress. Oligodendrogliomas are generally dichotomized into grade II (low grade) and grade III (high grade) tumors. The designation of grade III oligodendroglioma (high grade) generally subsumes the previous diagnoses of anaplastic or malignant oligodendroglioma.

Unfortunately, the WHO guidelines include subjective criteria in differentiating grade II and grade III tumors including the appreciation of "significant" hypercellularity and pleomorphism in the higher grade lesion. In addition, the presence of low mitotic activity, vascular proliferation and necrosis, including pseudopallisading necrosis are insufficient by themselves to elevate the grade of these tumors. This leads to inevitable interobserver variability in diagnosis by pathologists. The ultimate responsibility for making treatment decisions and interpretation of these diagnoses lies with the oncologist in consultation with the patient and their family.

It has been proposed that WHO guidelines should contain a category for grade IV oligodendrogliomas which essentially appear to be glial neoplasms with overwhelming features of glioblastoma multiforme (GBM) arising from known lower grade oligodendrogliomas or GBM with a significant proportion of oligodendroglial differentiation. The diagnostic utility of this latter category is uncertain as these tumors may behave either like glioblastoma or grade III oligodendrogliomas. As such, this is an exceptionally unusual diagnosis.

The updated WHO guidelines published in 2007 recommends classifying such tumors for the time being as 'glioblastoma with oligodendroglioma component'. It remains to be established whether or not these tumors carry a better prognosis than standard glioblastomas.

Like most tumors in the brain, astroblastoma can be treated through surgery and various forms of therapy. Many publications within the last decade have suggested a noticeable improvement in success rate of patients. With the advancement of cutting-edge technology and novel approaches in stem cells, patients are hopeful that they be happy and healthy through old age.

The following factors influence an oncologist's specific treatment plan:

1. Patient's overall medical history

2. Localization and grade severity of the tumor

3. Age and tolerance to certain medications, procedures, and treatment

4. Predicted progress of recovery

5. Final anticipated outcome of treatment

Because of the rarity of these tumors, there is still a lot of unknown information. There are many case studies that have been reported on patients who have been diagnosed with this specific type of tumor. Most of the above information comes from the findings resulting from case studies.

Since Papillary Tumors of the Pineal Region were first described in 2003, there have been seventy cases published in the English literature. Since there is such a small number of cases that have been reported, the treatment guidelines have not been established. A larger number of cases that contain a longer clinical follow-up are needed to optimize the management of patients with this rare disease.

Even though there is a general consensus on the morphology and the immunohistochemical characteristics that is required for the diagnosis, the histological grading criteria have yet to be fully defined and its biological behavior appears to be variable. This specific type of tumor appears to have a high potential for local recurrence with a high tumor bed recurrence rate during the five years after the initial surgery. This suggests the need for a tumor bed boost radiotherapy after surgical resection.

As stated above, the specific treatment guidelines have not yet been established, however, gross total resection of the tumor has been the only clinical factor associated overall and progression-free survival. The value of radiotherapy as well as chemotherapy on disease progression will need to be investigated in future trials. With this information, it will provide important insight into long-term management and may further our understanding of the histologic features of this tumor.

Computed Tomography (CT) is generally not a recommended modality for diagnosis and evaluation of spinal cord tumors. Evaluation with Magnetic Resonance (MR) most commonly demonstrates a circumscribed solid or mixed solid and cystic mass spanning a long segment of the cord with hypointense T1 signal and hyperintense T2 signal in the solid component. Enhancement patterns are highly variable, ranging from minimal to marked, and may be solid, rim, or nodular. Adjacent cord edema and syringomyelia and peritumoral cysts may be present in addition to reactive scoliosis.

It is nearly impossible to differentiate ganglioglioma from other more common intramedullary neoplasms based on imaging alone. Astrocytoma and ependymoma are more familiar intramedullary tumors which share many similar features to ganglioglioma, including T2 hyperintensity, enhancement, tumoral cysts, and cord edema. Poorly defined margins may be more suggestive of astrocytoma, while a central location in the spinal cord, hemorrhage, and hemosiderin staining are often seen with ependymoma. Hemangioblastoma and paraganglioma are less usual intramedullary tumors, but since they are more frequently encountered than ganglioglioma, they should also be included in the differential diagnosis.

Although often described as benign, a teratoma does have malignant potential. In a UK study of 351 infants and children diagnosed with "benign" teratoma reported 227 with MT, 124 with IT. Five years after surgery, event-free survival was 92.2% and 85.9%, respectively, and overall survival was 99% and 95.1%. A similar study in Italy reported on 183 infants and children diagnosed with teratoma. At 10 years after surgery, event free and overall survival were 90.4% and 98%, respectively.

Depending on which tissue(s) it contains, a teratoma may secrete a variety of chemicals with systemic effects. Some teratomas secrete the "pregnancy hormone" human chorionic gonadotropin (βhCG), which can be used in clinical practice to monitor the successful treatment or relapse in patients with a known HCG-secreting teratoma. This hormone is not recommended as a diagnostic marker, because most teratomas do not secrete it. Some teratomas secrete thyroxine, in some cases to such a degree that it can lead to clinical hyperthyroidism in the patient. Of special concern is the secretion of alpha-fetoprotein (AFP); under some circumstances AFP can be used as a diagnostic marker specific for the presence of yolk sac cells within the teratoma. These cells can develop into a frankly malignant tumor known as yolk sac tumor or endodermal sinus tumor.

Adequate follow-up requires close observation, involving repeated physical examination, scanning (ultrasound, MRI, or CT), and measurement of AFP and/or βhCG.

Extraspinal ependymoma, usually considered to be a glioma (a type of non-germ cell tumor), may be an unusual form of mature teratoma.

Medical imaging plays a central role in the diagnosis of brain tumors. Early imaging methods – invasive and sometimes dangerous – such as pneumoencephalography and cerebral angiography have been abandoned in favor of non-invasive, high-resolution techniques, especially magnetic resonance imaging (MRI) and computed tomography (CT) scans. Neoplasms will often show as differently colored masses (also referred to as processes) in CT or MRI results.

- Benign brain tumors often show up as hypodense (darker than brain tissue) mass lesions on CT scans. On MRI, they appear either hypodense or isointense (same intensity as brain tissue) on T1-weighted scans, or hyperintense (brighter than brain tissue) on T2-weighted MRI, although the appearance is variable.

- Contrast agent uptake, sometimes in characteristic patterns, can be demonstrated on either CT or MRI scans in most malignant primary and metastatic brain tumors.

- Pressure areas where the brain tissue has been compressed by a tumor also appear hyperintense on T2-weighted scans and might indicate the presence a diffuse neoplasm due to an unclear outline. Swelling around the tumor known as "peritumoral edema" can also show a similar result.

This is because these tumors disrupt the normal functioning of the BBB and lead to an increase in its permeability. However, it is not possible to diagnose high- versus low-grade gliomas based on enhancement pattern alone.

The definitive diagnosis of brain tumor can only be confirmed by histological examination of tumor tissue samples obtained either by means of brain biopsy or open surgery. The histological examination is essential for determining the appropriate treatment and the correct prognosis. This examination, performed by a pathologist, typically has three stages: interoperative examination of fresh tissue, preliminary microscopic examination of prepared tissues, and follow-up examination of prepared tissues after immunohistochemical staining or genetic analysis.

The likelihood of low-grade astroblastoma returning after surgery is highly improbable, but some patients have exhibited recurrence. Patients with low-grade lesions can remain asymptomatic after surgery and show recurrence 1–2 years in follow-up sessions. However, since residual tissue size is a large determinant for profiling recurrence, it is almost never the case that a low-grade astroblastoma continues to appear in size and strength after the second resection. Usually, patients are not recommended for resection at all and are simply directed towards other therapeutic techniques. Most children can continue to lead productive, healthy lives after a low-grade astroblastoma is treated.

Papillary tumors of pineal region are extremely rare, constituting 0.4-1% of all central nervous system tumors. These tumors most commonly occur in adults with the mean age being 31.5. There have been cases reported for people between the ages 5 to 66 years. There is a slight predominance of females who have these tumors.

Ependymomas make up about 5% of adult intracranial gliomas and up to 10% of childhood tumors of the central nervous system (CNS). Their occurrence seems to peak at age 5 years and then again at age 35. They develop from cells that line both the hollow cavities of the brain and the canal containing the spinal cord, but they usually arise from the floor of the fourth ventricle, situated in the lower back portion of the brain, where they may produce headache, nausea and vomiting by obstructing the flow of cerebrospinal fluid. This obstruction may also cause hydrocephalus. They may also arise in the spinal cord, conus medullaris and supratentorial locations. Other symptoms can include (but are not limited to): loss of appetite, difficulty sleeping, temporary inability to distinguish colors, uncontrollable twitching, seeing vertical or horizontal lines when in bright light, and temporary memory loss. It should be remembered that these symptoms also are prevalent in many other illnesses not associated with ependymoma.

About 10% of ependymomas are benign myxopapillary ependymoma (MPE). MPE is a localized and slow-growing low-grade tumor, which originates almost exclusively from the lumbosacral nervous tissue of young patients. On the other hand, it is the most common tumor of the lumbosacral canal comprising about 90% of all tumoral lesions in this region.

Although some ependymomas are of a more anaplastic and malignant type, most of them are not anaplastic. Well-differentiated ependymomas are usually treated with surgery. For other ependymomas, total surgical removal is the preferred treatment in addition to radiation therapy. The malignant (anaplastic) varieties of this tumor, malignant ependymoma and the ependymoblastoma, are treated similarly to medulloblastoma but the prognosis is much less favorable. Malignant ependymomas may be treated with a combination of radiation therapy and chemotherapy. Ependymoblastomas, which occur in infants and children younger than 5 years of age, may spread through the cerebrospinal fluid and usually require radiation therapy. The subependymoma, a variant of the ependymoma, is apt to arise in the fourth ventricle but may occur in the septum pellucidum and the cervical spinal cord. It usually affects people over 40 years of age and more often affects men than women.

Extraspinal ependymoma (EEP), also known as extradural ependymoma, may be an unusual form of teratoma or may be confused with a sacrococcygeal teratoma.

The 5-year disease-free survival for age >5 years is 50-60%. Another report found a similar 5-year survival at about 65% with 51% progression-free survival. The 10-year disease-free survival is 40-50%. Younger ages showed lower 5 and 10-year survival rates. A 2006 study that observed 133 patients found 31 (23.3%) had a recurrence of the disease within a five-year period.

Oligodendrogliomas cannot currently be differentiated from other brain lesions solely by their clinical or radiographic appearance. As such, a brain biopsy is the only method of definitive diagnosis. Oligodendrogliomas recapitulate the appearance of the normal resident oligodendroglia of the brain. (Their name derives from the Greek roots 'oligo' meaning " few" and 'dendro' meaning "trees".) They are generally composed of cells with small to slightly enlarged round nuclei with dark, compact nuclei and a small amount of eosinophilic cytoplasm. They are often referred to as "fried egg" cells due to their histologic appearance. They appear as a monotonous population of mildly enlarged round cells infiltrating normal brain parenchyma and producing vague nodules. Although the tumor may appear to be vaguely circumscribed, it is by definition a diffusely infiltrating tumor.

Classically they tend to have a vasculature of finely branching capillaries that may take on a "chicken wire" appearance. When invading grey matter structures such as cortex, the neoplastic oligodendrocytes tend to cluster around neurons exhibiting a phenomenon referred to as "perineuronal satellitosis". Oligodendrogliomas may invade preferentially around vessels or under the pial surface of the brain.

Oligodendrogliomas must be differentiated from the more common astrocytoma. Non-classical variants and combined tumors of both oligodendroglioma and astrocytoma differentiation are seen, making this distinction controversial between different neuropathology groups. In the US, in general, neuropathologists trained on the West Coast are more liberal in the diagnosis of oligodendrogliomas than either East Coast or Midwest trained neuropathologists who render the diagnosis of oligodendroglioma for only classic variants. Molecular diagnostics may make this differentiation obsolete in the future.

Other glial and glioneuronal tumors with which they are often confused due to their monotonous round cell appearance include pilocytic astrocytoma, central neurocytoma, the so-called dysembryoplastic neuroepithelial tumor, or occasionally ependymoma.

Anaplastic astrocytoma, Astrocytoma, Central neurocytoma, Choroid plexus carcinoma, Choroid plexus papilloma, Choroid plexus tumor, Dysembryoplastic neuroepithelial tumour, Ependymal tumor, Fibrillary astrocytoma, Giant-cell glioblastoma, Glioblastoma multiforme, Gliomatosis cerebri, Gliosarcoma, Hemangiopericytoma, Medulloblastoma, Medulloepithelioma, Meningeal carcinomatosis, Neuroblastoma, Neurocytoma, Oligoastrocytoma, Oligodendroglioma, Optic nerve sheath meningioma, Pediatric ependymoma, Pilocytic astrocytoma, Pinealoblastoma, Pineocytoma, Pleomorphic anaplastic neuroblastoma, Pleomorphic xanthoastrocytoma, Primary central nervous system lymphoma, Sphenoid wing meningioma, Subependymal giant cell astrocytoma, Subependymoma, Trilateral retinoblastoma.

Use of telomerase inhibitors such as Imetelstat seem to have very low toxicity compared to other chemotherapy. The only known side effect of most telomerase inhibitors is dose-induced neutropenia. Neuropsychological deficits can result from resection, chemotherapy, and radiation, as well as endocrinopathies. Additionally, an increase in gastrointestinal complications has been observed in survivors of pediatric cancers.

A subependymoma is a type of brain tumor; specifically, it is a rare form of ependymal tumor.

The prognosis for a subependymoma is better than for most ependymal tumors, and is considered a grade I tumor in the World Health Organization (WHO) classification.

They are classically found within the fourth ventricle, typically have a well demarcated interface to normal tissue and do not usually extend into the brain parenchyma, like ependymomas often do.

Based on a survey of >800, surgical removal of the entire involved kidney plus the peri-renal fat appeared curative for the majority of all types of mesoblastic nephroma; the patient overall survival rate was 94%. Of the 4% of non-survivors, half were due to surgical or chemotherapeutic treatments. Another 4% of these patients suffered relapses, primarily in the local area of surgery rare cases of relapse due to lung or bone metastasis.. About 60% of these recurrent cases had a complete remission following further treatment. Recurrent disease was treated with a second surgery, radiation, and/or chemotherapy that often vincristine and actinomycin treatment. Removal of the entire afflicted kidney plus the peri-renal fat appears critical to avoiding local recurrences. In general, patients who were older than 3 months of age at diagnosis or had the cellular form of the disease, stage III disease, or involvement of renal lymph nodes had a higher recurrence rate. Among patients with these risk factors, only those with lymph node involvement are recommended for further therapy.

It has been suggested that mesoblastic nephroma patients with lymph node involvement or recurrent disease might benefit by adding the ALK inhibitor, crizotinib, or a tyrosine kinase inhibitor, either larotrectinib or entrectinib, to surgical, radiation, and/or chemotherapy treatment regimens. These drugs inhibit NTRK3's tyrosine kinase activity. Crizotinib has proven useful in treating certain cases of acute lymphoblastic leukemia that are associated with the "ETV6-NTRK3" fusion gene while larotrectinib and entrectinib have been useful in treating various cancers (e.g. a metastatic sarcoma, papillary thyroid cancer, non-small-cell lung carcinoma, gastrointestinal stromal tumor, mammary analog secretory carcinoma, and colorectal cancer) that are driven by mutated, overly active tyrosine kinases. Relevant to this issue, a 16-month-old girl with infantile fibrosarcoma harboring the "ETV6–NTRK3" fusion gene was successfully trated with larotrectinib. The success of these drugs, howwever, will likely depend on the relative malignancy-promoting roles of ETV6-NTRK3 protein's tyrosine kinase activity, the lose of ETV6-related transcription activity accompanying formation of ETV6-NTRK3 protein, and the various trisomy chromosomes that populate mesoblastic nephroma.

Cystic nephromas are diagnosed by biopsy or excision. It is important to correctly diagnose them as, radiologically, they may mimic the appearance of a renal cell carcinoma that is cystic.

Ependymoma is a tumor that arises from the ependyma, a tissue of the central nervous system. Usually, in pediatric cases the location is intracranial, while in adults it is spinal. The common location of intracranial ependymoma is the fourth ventricle. Rarely, ependymoma can occur in the pelvic cavity.

Syringomyelia can be caused by an ependymoma.

Ependymomas are also seen with neurofibromatosis type II.

Diagnosis of mesoblastic nephroma and its particular type (i.e. classic, mixed, or cellular) is made by histological examination of tissues obtained at surgery. Besides its histological appearance, various features of this disease aid in making a differential diagnosis that distinguish it from the following childhood neoplasms:

- Wilm's tumor is the most common childhood kidney neoplasm, representing some 85% of cases. Unlike mesoblastic nephroma, 3 years of age. Bilateral kidney tumors, concurrent birth defects, and/or metastatic disease at presentation favor a diagnosis of Wilm's tumor.

- congenital infantile sarcoma is a rare aggressive sarcoma typically presenting in the lower extremities, head, or neck of infants during their first year of life. The histology, association with the "ETV6-NRTK3" fusion gene along with certain chromosome trisomies, and the distribution of markers for cell type (i.e. cyclin D1 and Beta-catenin) within this tumor are the same as those found in cellular mesoblastic nephroma. Mesoblastic nephroma and congenital infantile sarcoma appear to be the same diseases with mesoblastic lymphoma originating in the kidney and congenital infantile sarcoma originating in non-renal tissues.

- Rhabdoid tumor, which accounts for 5-510% of childhood kidney neoplasms, occurs predominantly in children from 1 to 2 years of age. Unlike mesoblastic nephroma, rhabdoid tumors may present with tumors in other tissues including in ~13% of cases, the brain. Rhabdoid tumors have a distinctive histology and abnormalities (i.e. loss of heterozygosity, single nucleotide polymorphism, and deletions) in chromosome 22.

- Clear cell sarcoma of the kidney, which is responsible for 5-10% of childhood pediatric tumors, occurs predominantly in children from 2 to 3 years of age. Unlike meoblastic nephorma, clear cell sarcoma of the kidney presents with metastasis, particularly to bone, in 5-6% of cases; it histology is diverse and has been mistaken for mesoblastic nephroma. One chromosomal translocations t,(10;17)(q22;p13), has been repeatedly reported to be associated with clear cell sarcoma of the kidney.

- Infantile myofibromatosis is a fibrous tumor of infancy and childhood most commonly presenting during the first 2 years of life as a single subcutaneous nodule of the head and neck region or less commonly as multiple lesions of skin, muscle, bone, and in ~33% of these latter cases, visceral organs. All of these lesions have an excellent prognosis and can regress spontaneously except for those in which there is visceral involvement where the prognosis is poor. While infantile myofibromatosis and classic mesoblastic nephroma have been suggested to be the same diseases because of their very similar histology, studies on the distribution of cell-type markers (i.e. cyclin D1 and Beta-catenin) indicate that they have different cellular origins.