An X-ray computed tomography (CT) or magnetic resonance imaging (MRI) scan is necessary to characterize the extent of these tumors (size, location, consistency). CT will usually show distortion of third and lateral ventricles with displacement of anterior and middle cerebral arteries. Histologic analysis is necessary for grading diagnosis.

In the first stage of diagnosis the doctor will take a history of symptoms and perform a basic neurological exam, including an eye exam and tests of vision, balance, coordination and mental status. The doctor will then require a computerized tomography (CT) scan and magnetic resonance imaging (MRI) of the patient's brain. During a CT scan, x rays of the patient's brain are taken from many different directions. These are then combined by a computer, producing a cross-sectional image of the brain. For an MRI, the patient relaxes in a tunnel-like instrument while the brain is subjected to changes of magnetic field. An image is produced based on the behavior of the brain's water molecules in response to the magnetic fields. A special dye may be injected into a vein before these scans to provide contrast and make tumors easier to identify.

If a tumor is found, it will be necessary for a neurosurgeon to perform a biopsy on it. This simply involves the removal of a small amount of tumor tissue, which is then sent to a neuropathologist for examination and grading. The biopsy may take place before surgical removal of the tumor or the sample may be taken during surgery. Grading of the tumor sample is a method of classification that helps the doctor to determine the severity of the astrocytoma and to decide on the best treatment options. The neuropathologist grades the tumor by looking for atypical cells, the growth of new blood vessels, and for indicators of cell division called mitotic figures.

There are no precise guidelines because the exact cause of astrocytoma is not known.

It is recommended that children with TSC be screened for SEGA with neuroimaging every 1–3 years.

Usually—depending on the interview of the patient and after a clinical exam which includes a neurological exam, and an ophthalmological exam—a CT scan and or MRI scan will be performed. A special dye may be injected into a vein before these scans to provide contrast and make tumors easier to identify. The neoplasm will be clearly visible.

If a tumor is found, it will be necessary for a neurosurgeon to perform a biopsy of it. This simply involves the removal of a small amount of tumorous tissue, which is then sent to a (neuro)pathologist for examination and staging. The biopsy may take place before surgical removal of the tumor or the sample may be taken during surgery.

Diagnosis is made by imaging with a contrast-enhanced MRI or CT scan of the brain.

PXA is diagnosed through a combination of diagnostic processes:

- Initially, a doctor will interview the patient and do a clinical exam, which will include a neurological examination.

- A CT scan of the brain, and/or an MRI scan of the brain and spine, will be performed. A special dye may be injected into a vein before these scans to provide contrast and make tumors easier to see.

- For children experiencing seizures, an EEG might be part of the diagnostic process (the goal being to record the brain's electrical activity in order to identify and localize seizure activity).

- Finally, a biopsy of the tumor, taken through a needle during a simple surgical procedure, helps to confirm the diagnosis.

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 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.

The risk of meningioma can be reduced by maintaining a normal body weight, and by avoiding unnecessary dental x-rays.

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.

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.

Microscopically, an astrocytoma is a mass that looks well-circumscribed and has a large cyst. The neoplasm may also be solid.

Under the microscope, the tumor is seen to be composed of bipolar cells with long "hairlike" GFAP-positive processes, giving the designation "pilocytic" (that is, made up of cells that look like fibers when viewed under a microscope). Some pilocytic astrocytomas may be more fibrillary and dense in composition. There is often presence of Rosenthal fibers, eosinophilic granular bodies and microcysts. Myxoid foci and oligodendroglioma-like cells may also be present, though non-specific. Long-standing lesions may show hemosiderin-laden macrophages and calcifications.

With treatment, pleomorphic xanthoastrocytomas are associated with a high rate of cure.

- Grade II pleomorphic xanthoastrocytomas are known to progress towards grade II tumors, which are more likely to recur after surgical removal.

- Grade III anaplastic pleomorphic xanthoastrocytomas may evolve and show signs of anaplasia, according to evidence in the medical literature.

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

Observation with close imaging follow-up may be used in select cases if a meningioma is small and asymptomatic. In a retrospective study on 43 patients, 63% of patients were found to have no growth on follow-up, and the 37% found to have growth at an average of 4 mm / year. In this study, younger patients were found to have tumors that were more likely to have grown on repeat imaging; thus are poorer candidates for observation. In another study, clinical outcomes were compared for 213 patients undergoing surgery vs. 351 patients under watchful observation. Only 6% of the conservatively treated patients developed symptoms later, while among the surgically treated patients, 5.6% developed persistent morbid condition, and 9.4% developed surgery-related morbid condition.

Observation is not recommended in tumors already causing symptoms. Furthermore, close follow-up with imaging is required with an observation strategy to rule out an enlarging tumor.

Medulloblastomas affect just under two people per million per year, and affect children 10 times more than adults. Medulloblastoma is the second-most frequent brain tumor in children after pilocytic astrocytoma and the most common malignant brain tumor in children, comprising 14.5% of newly diagnosed cases. In adults, medulloblastoma is rare, comprising fewer than 2% of CNS malignancies.

The rate of new cases of childhood medulloblastoma is higher in males (62%) than females (38%), a feature which is not seen in adults. Medulloblastoma and other PNET`s are more prevalent in younger children than older children. About 40% of medulloblastoma patients are diagnosed before the age of five, 31% are between the ages of 5 and 9, 18.3% are between the ages of 10 and 14, and 12.7% are between the ages of 15 and 19.

The prognosis for gliomatosis cerebri is generally poor. Surgery is not practical considering the extent of the disease, standard chemotherapy (nitrosourea) has been unsuccessful, and while brain irradiation can stabilize or improve neurologic function in some patients, its impact on survival has yet to be proven.

In 2014, Weill Cornell Brain and Spine Center launched an international registry for Gliomatosis Cerebri, where tissue samples can be stored for genomic study.

The cumulative relative survival rate for all age groups and histology follow-up was 60%, 52%, and 47% at 5 years, 10 years, and 20 years, respectively. Patients diagnosed with a medulloblastoma or PNET are 50 times more likely to die than a matched member of the general population.

The most recent population-based (SEER) 5-year relative survival rates are 69% overall, but 72% in children (1–9 years) and 67% in adults (20+ years). The 20-year survival rate is 51% in children. Children and adults have different survival profiles, with adults faring worse than children only after the fourth year after diagnosis (after controlling for increased background mortality). Before the fourth year, survival probabilities are nearly identical. Longterm sequelae of standard treatment include hypothalamic-pituitary and thyroid dysfunction and intellectual impairment. The hormonal and intellectual deficits created by these therapies causes significant impairment of the survivors.

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.

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.

For low-grade tumors, the prognosis is somewhat more optimistic. Patients diagnosed with a low-grade glioma are 17 times as likely to die as matched patients in the general population.

The age-standardized 10-year relative survival rate was 47%. One study reported that low-grade oligodendroglioma patients have a median survival of 11.6 years; another reported a median survival of 16.7 years.

Surviving the symptoms of high-grade astroblastoma is not life-threatening, but a significant portion of patients die due to repeated recurrence of tumors as they continue to grow and spread. Unlike conventional low-grade tumors, high-grade tumors associate a plethora of factors when they metastasize to other areas of the body. Therefore, complications frequently occur after surgery is performed since an oncologist cannot efficiently control the tumor in a suitable time-frame. Cases in literature confirm that high-grade patients face up to five or six resection surgeries and "still" experience symptoms post-operatively. The dual-action of chemotherapy and radiotherapy can slow down recurrence when gross total resection is performed multiple times, but there is no guarantee that the tumor will ever be in remission.

Gliomas are rarely curable. The prognosis for patients with high-grade gliomas is generally poor, and is especially so for older patients. Of 10,000 Americans diagnosed each year with malignant gliomas, about half are alive one year after diagnosis, and 25% after two years. Those with anaplastic astrocytoma survive about three years. Glioblastoma multiforme has a worse prognosis with less than a 12-month average survival after diagnosis, though this has extended to 14 months with more recent treatments.

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.

Before the advent of MRI, diagnosis was generally not established until autopsy. Even with MRI, however, diagnosis is difficult. Typically, gliomatosis cerebri appears as a diffuse, poorly circumscribed, infiltrating non-enhancing lesion that is hyperintense on T2-weighted images and expands the cerebral white matter. It is difficult to distinguish from highly infiltrative anaplastic astrocytoma or GBM.