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.

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.

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.

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.

Most of the brain is separated from the blood by the blood-brain barrier (BBB), which exerts a restrictive control as to which substances are allowed to pass. Therefore, many tracers that reach tumors in the body very easily would only reach brain tumors once there is a disruption of the BBB. Thus the disruption of the BBB, which can be detected by MRI and CT, is regarded as the main diagnostic indicator for malignant gliomas, meningiomas, and brain metastases.

Although there is no specific or singular clinical symptom or sign for any brain tumors, the presence of a combination of symptoms and the lack of corresponding clinical indications of infections or other causes can be an indicator to redirect diagnostic investigation towards the possibility of an intracranial neoplasm. Brain tumors have similar characteristics and obstacles when it comes to diagnosis and therapy with tumors located elsewhere in the body. However, they create specific issues that follow closely to the properties of the organ they are in.

The diagnosis will often start by taking a medical history noting medical antecedents, and current symptoms. Clinical and laboratory investigations will serve to exclude infections as the cause of the symptoms. Examinations in this stage may include the eyes, otolaryngological (or ENT) and electrophysiological exams. The use of electroencephalography (EEG) often plays a role in the diagnosis of brain tumors.

Swelling or obstruction of the passage of cerebrospinal fluid (CSF) from the brain may cause (early) signs of increased intracranial pressure which translates clinically into headaches, vomiting, or an altered state of consciousness, and in children changes to the diameter of the skull and bulging of the fontanelles. More complex symptoms such as endocrine dysfunctions should alarm doctors not to exclude brain tumors.

A bilateral temporal visual field defect (due to compression of the optic chiasm) or dilation of the pupil, and the occurrence of either slowly evolving or the sudden onset of focal neurologic symptoms, such as cognitive and behavioral impairment (including impaired judgment, memory loss, lack of recognition, spatial orientation disorders), or emotional changes, hemiparesis, hypoesthesia, aphasia, ataxia, visual field impairment, impaired sense of smell, impaired hearing, facial paralysis, double vision, or more severe symptoms such as tremors, paralysis on one side of the body hemiplegia, or (epileptic) seizures in a patient with a negative history for epilepsy, should raise the possibility of a brain tumor.

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.

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.

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.

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 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.

Several different types of magnetic resonance imaging (MRI) may be employed in diagnosis: MRI without contrast, Gd contrast enhanced T1-weighted MRI (GdT1W) or T2-weighted enhanced MRI (T2W or T2*W). Non-contrast enhanced MRI is considerably less expensive than any of the contrast enhanced MRI scans. The gold standard in diagnosis is GdT1W MRI.

The reliability of non-contrast enhanced MRI is highly dependent on the sequence of scans, and the experience of the operator.

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.

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.

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.

The auditory brainstem response (ABR) test gives information about the inner ear (cochlea) and nerve pathways for hearing via ongoing electrical activity in the brain measured by electrodes placed on the scalp. Five different waves (I to V) are measured for each ear. Each waveform represents specific anatomical points along the auditory neural pathway. Delays of one side relative to the other suggest a lesion in cranial nerve VIII between the ear and brainstem or in the brainstem itself. The most reliable indicator for acoustic neuromas from the ABR is the interaural latency differences in wave V: the latency in the impaired ear is prolonged. Different studies have indicated the sensitivity of ABR for detection of acoustic neuromas 1cm or larger to be between 90 and 95%. Sensitivity for neuromas smaller than 1cm are 63-77%. A newer technology, stacked ABR, may have sensitivity as high as 95% with specificity 88% for smaller tumors. ABR is considerably more cost effective, but MRI provides more information.

Stapedius reflex (SR) and caloric vestibular response (CVR) are non-invasive otologic tests for auditory neural function. These are not primary diagnostics for CPA neuromas, and are usually used in conjunction

with ABR.

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.

Treatment of choroid plexus carcinoma depends on the location and severity of the tumor. Possible interventions include inserting shunts, surgical resection, radiotherapy, and chemotherapy. Inserting a shunt could help to drain the CSF and relieve pressure on the brain. The best outcomes occur when total resection of the tumor is combined with adjuvant chemotherapy and radiotherapy. In the event of subtotal resection or widespread leptomeningeal disease, craniospinal irradiation is often used.

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.

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.

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.

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.

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.

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.