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 standard work-up for AT/RT includes:

- Magnetic resonance imaging (MRI) of the brain and spine

- Lumbar puncture to look for M1 disease

- Computed tomography (CT) of chest and abdomen to check for a tumor

- Bone marrow aspiration to check for bone tumors. Sometimes the physician will perform a stem cell transplant

- Bone marrow biopsy

- Bone scan

The initial diagnosis of a tumor is made with a radiographic study (MRI or CT-). If CT was performed first, an MRI is usually performed as the images are often more detailed and may reveal previously undetected metastatic tumors in other locations of the brain. In addition, an MRI of the spine is usually performed. The AT/RT tumor often spreads to the spine. AT/RT is difficult to diagnose only from radiographic study; usually, a pathologist must perform a cytological or genetic analysis.

Examination of the cerebrospinal fluid is important (CSF), as one-third of patients will have intracranial dissemination with involvement of the CSF. Large tumor cells, eccentricity of the nuclei, and prominent nucleoli are consistent findings. Usually only a minority of AT/RT biopsies have rhabdoid cells, making diagnosis more difficult. Increasingly it is recommended that a genetic analysis be performed on the brain tumor, especially to find if a deletion in the INI1/hSNF5 gene is involved (appears to account for over 80% of the cases). The correct diagnosis of the tumor is critical to any protocol. Studies have shown that 8% to over 50% of AT/RT tumors are diagnosed incorrectly.

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

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.

Neuroimaging, such as MRI, is the main diagnostic tool for brain stem gliomas. In very rare cases, surgery and biopsy are performed.

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.

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.

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.

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.

The primary diagnosis is made with a computed tomography scan (CT scan). On a scan, hemangioblastoma shows as a well-defined, low attenuation region in the posterior fossa with an enhancing nodule on the wall. Sometimes multiple lesions are present.

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.

Cytogenetics is the study of a tumor’s genetic make-up. Fluorescent "in situ" hybridization may be able to help locate a mutation or abnormality that may be allowing tumor growth. This technique has been shown to be useful in identifying some tumors and distinguishing two histologically similar tumors from each other (such as AT/RTs and PNETs). In particular, medulloblastmas/PNETs may possibly be differentiated cytogenetically from AT/RTs, as chromosomal deletions of 17p are relatively common with medulloblastoma and abnormalities of 22q11.2 are not seen. However, chromosomal 22 deletions are very comomon in AT/RTs.

In importance of the "hSNF5/INI1" gene located on chromosomal band 22q11.2 is highlighted, as the mutation’s presence is sufficient to change the diagnosis from a medulloblastoma or PNET to the more aggressive AT/RT classification. However, this mutation is not present in 100% of cases. Therefore, if the mutation is not present in an otherwise classic AT/RT immunohistochemical and morphologic pattern then the diagnosis remains an AT/RT.

Treatment typically consists of radiotherapy and steroids for palliation of symptoms. Radiotherapy may result in minimally extended survival time. Prognosis is very poor, with only 37% of treated patients surviving one year or more. Topotecan has been studied in the treatment of brainstem glioma, otherwise, chemotherapy is probably ineffective, though further study is needed.

Brainstem glioma is an aggressive and dangerous cancer. Without treatment, the life expectancy is typically a few months from the time of diagnosis. With appropriate treatment, 37% survive more than one year, 20% survive 2 years. and 13% survive 3 years.This is not for all brainstem glioma, this statistic reflects DIPG. There are other brainstem gliomas.

It is very difficult to treat glioblastoma due to several complicating factors:

- The tumor cells are very resistant to conventional therapies.

- The brain is susceptible to damage due to conventional therapy.

- The brain has a very limited capacity to repair itself.

- Many drugs cannot cross the blood–brain barrier to act on the tumor.

Treatment of primary brain tumors and brain metastases consists of both symptomatic

and palliative therapies.

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.

A 2014 investigation made a screening of various drugs for anti-glioblastoma activity and identified 22 drugs with potent anti-glioblastoma activity, including the combination of irinotecan and statins.

The standard treatment for DIPG is 6 weeks of radiation therapy, which often dramatically improves symptoms. However, symptoms usually recur after 6 to 9 months and progress rapidly.

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.

Urine catecholamine level can be elevated in pre-clinical neuroblastoma. Screening asymptomatic infants at three weeks, six months, and one year has been performed in Japan, Canada, Austria and Germany since the 1980s. Japan began screening six-month-olds for neuroblastoma via analysis of the levels of homovanillic acid and vanilmandelic acid in 1984. Screening was halted in 2004 after studies in Canada and Germany showed no reduction in deaths due to neuroblastoma, but rather caused an increase in diagnoses that would have disappeared without treatment, subjecting those infants to unnecessary surgery and chemotherapy.

Surgery to attempt tumour removal is usually not possible or advisable for DIPG. By nature, these tumours invade diffusely throughout the brain stem, growing between normal nerve cells. Aggressive surgery would cause severe damage to neural structures vital for arm and leg movement, eye movement, swallowing, breathing, and even consciousness.

A neurosurgically performed brain-stem biopsy for immunotyping of diffuse intrinsic pontine glioma has served a limited recent role in experimental clinical studies and treatment trials. This however is not the current standard of care as it presents considerable risk given the biopsy location, and thus is appropriately performed in the context of participation in an ongoing clinical treatment trial.

Pontine biopsy is in no way a therapeutic or curative surgery, and the risks (potentially catastrophic and fatal) are only outweighed when the diagnosis is uncertain (extremely unusual) or the patient is enrolled in an approved clinical trial.

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.

An MRI is better than a CT scan when a brainstem tumor is in the differential diagnosis.

The outcome for hemangioblastoma is very good, if surgical extraction of the tumor can be achieved; excision is possible in most cases and permanent neurologic deficit is uncommon and can be avoided altogether if the tumor is diagnosed and treated early. Persons with VHL syndrome have a bleaker prognosis than those who have sporadic tumors since those with VHL syndrome usually have more than one lesion.

Magnetic resonance imaging (MRI) and computed tomography (CT) brain scans can be used to identify these tumors.