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

Ganglioneuromas can be diagnosed visually by a CT scan, MRI scan, or an ultrasound of the head, abdomen, or pelvis. Blood and urine tests may be done to determine if the tumor is secreting hormones or other circulating chemicals. A biopsy of the tumor may be required to confirm the diagnosis.

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.

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.

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.

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.

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 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.

Most ganglioneuromas are noncancerous, thus expected outcome is usually good. However, a ganglioneuroma may become cancerous and spread to other areas, or it may regrow after removal.

If the tumor has been present for a long time and has pressed on the spinal cord or caused other symptoms, it may have caused irreversible damage that cannot be corrected with the surgical removal of the tumor. Compression of the spinal cord may result in paralysis, especially if the cause is not detected promptly.

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 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.

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.

It is classified into two types, based on location in the body: peripheral PNET and CNS PNET.

Primitive neuroectodermal tumor (PNET) is a malignant (cancerous) neural crest tumor. It is a rare tumor, usually occurring in children and young adults under 25 years of age. The overall 5 year survival rate is about 53%.

It gets its name because the majority of the cells in the tumor are derived from neuroectoderm, but have not developed and differentiated in the way a normal neuron would, and so the cells appear "primitive".

PNET belongs to the Ewing family of tumors.

DSRCT is frequently misdiagnosed. Adult patients should always be referred to a sarcoma specialist. This is an aggressive, rare, fast spreading tumor and both pediatric and adult patients should be treated at a sarcoma center.

There is no standard protocol for the disease; however, recent journals and studies have reported that some patients respond to high-dose (P6 Protocol) chemotherapy, maintenance chemotherapy, debulking operation, cytoreductive surgery, and radiation therapy. Other treatment options include: hematopoietic stem cell transplantation, intensity-modulated radiation Therapy, radiofrequency ablation, stereotactic body radiation therapy, intraperitoneal hyperthermic chemoperfusion, and clinical trials.

Because this is a rare tumor, not many family physicians or oncologists are familiar with this disease. DSRCT in young patients can be mistaken for other abdominal tumors including rhabdomyosarcoma, neuroblastoma, and mesenteric carcinoid. In older patients DSRCT can resemble lymphoma, peritoneal mesothelioma, and peritoneal carcinomatosis. In males DSRCT may be mistaken for germ cell or testicular cancer while in females DSRCT can be mistaken for Ovarian cancer. DSRCT shares characteristics with other small-round blue cell cancers including Ewing's sarcoma, acute leukemia, small cell mesothelioma, neuroblastoma, primitive neuroectodermal tumor, rhabdomyosarcoma, and Wilms' tumor.

No pathognomonic clinical signs for TSC complex are seen. Many signs are present in individuals who are healthy (although rarely), or who have another disease. In order to meet diagnostic criteria for TSC complex, an individual must either have: 1) Two or more major criteria; or 2) One major criterion along with two or more minor criteria.

In infants, the first clue is often the presence of seizures, delayed development, or white patches on the skin. A full clinical diagnosis involves:

- Taking a personal and family history

- Examining the skin under a Wood's lamp (hypomelanotic macules), the fingers and toes (ungual fibroma), the face (angiofibromas), and the mouth (dental pits and gingival fibromas)

- Cranial imaging with nonenhanced CT or, preferably, MRI (cortical tubers and subependymal nodules)

- Renal ultrasound (angiomyolipoma or cysts)

- An echocardiogram in infants (rhabdomyoma)

- Fundoscopy (retinal nodular hamartomas or achromic patch)

The various signs are then marked against the diagnostic criteria to produce a level of diagnostic certainty:

- Definite – either two major features or one major feature plus two minor features

- Probable – one major plus one minor feature

- Suspect – either one major feature or two or more minor features

Due to the wide variety of mutations leading to TSC, no simple genetic tests are available to identify new cases, nor are any biochemical markers known for the gene defects. However, once a person has been clinically diagnosed, the genetic mutation can usually be found. The search is time-consuming and has a 15% failure rate, which is thought to be due to somatic mosaicism. If successful, this information can be used to identify affected family members, including prenatal diagnosis. , preimplantation diagnosis is not widely available.

The Gold Standard for diagnosis of vestibular schwannoma is without doubt enhanced magnetic resonance imaging (MRI) yet several examinations may arise suspicion of vestibular schwannomas.

Routine auditory tests may reveal a loss of hearing and speech discrimination (the patient may hear sounds in that ear, but cannot comprehend what is being said). Pure tone audiometry should be performed to effectively evaluate hearing in both ears. In some clinics the clinical criteria for follow up testing for AN is a 15 dB differential in thresholds between ears for three consecutive frequencies.

An auditory brainstem response test (a.k.a. ABR) is a much more cost effective screening alternative to MRI for those at low risk of AN. This test provides information on the passage of an electrical impulse along the circuit from the inner ear to the brainstem pathways. An acoustic neuroma can interfere with the passage of this electrical impulse through the hearing nerve at the site of tumor growth in the internal auditory canal, even when hearing is still essentially normal. This implies the possible diagnosis of an acoustic neuroma when the test result is abnormal. An abnormal auditory brainstem response test should be followed by an MRI. The sensitivity of this test is proportional to the tumor size - the smaller the tumor, the more likely is a false negative result; small tumors within the auditory canal will often be missed. However, since these tumors would usually be watched rather than treated, the clinical significance of overlooking them may be negligible.

Advances in scanning and testing have made possible the identification of small acoustic neuromas (those still confined to the internal auditory canal). MRI using as an enhancing contrast material is the preferred diagnostic test for identifying acoustic neuromas. The image formed clearly defines an acoustic neuroma if it is present and this technique can identify tumors measuring down to 5 millimeters in diameter (the scan spacing).

When an MRI is not available or cannot be performed, a computerized tomography scan (CT scan) with contrast is suggested for patients in whom an acoustic neuroma is suspected. The combination of CT scan and audiogram approach the reliability of MRI in making the diagnosis of acoustic neuroma.

With the symptoms above in mind, practitioners would likely look for decreased vision and intraocular masses in making their diagnosis as these have been documented as the most common findings for intraocular schwannomas. Additionally, these tumors are most frequently found in the choroid, at 60%, as compared to the ciliary body (40%) and the iris (11%). Schwannomas generally present themselves as smooth, ovoid masses, lacking pigmentation. However, these tumors can also rarely be colored and lobulated. This overlap can lead to a uveal melanoma diagnosis as these can be characteristics of both.

Diagnosis of tumefactive MS is commonly carried out using magnetic resonance imaging (MRI) and proton MR spectroscopy (H-MRS). Diagnosis is difficult as tumefactive MS may mimic the clinical and MRI characteristics of a glioma or a cerebral abscess. However, as compared to tumors and abscesses, tumefactive lesions have an open-ring enhancement as opposed to a complete ring enhancement. Even with this information, multiple imaging technologies have to be used together with biochemical tests for accurate diagnosis of tumefactive MS.

Tumefactive demyelination is distinguished from tumor by the presence of multiple lesions, absence of cortical involvement, and decrease in lesion size or detection of new lesions on serial imaging

A vestibular schwannoma (VS) is a benign primary intracranial tumor of the myelin-forming cells of the vestibulocochlear nerve (8th cranial nerve). A type of schwannoma, this tumor arises from the Schwann cells responsible for the myelin sheath that helps keep peripheral nerves insulated. Although it is also called an acoustic neuroma, this a misnomer for two reasons. First, the tumor usually arises from the vestibular division of the vestibulocochlear nerve, rather than the cochlear division. Second, it is derived from the Schwann cells of the associated nerve, rather than the actual neurons (neuromas).

Approximately 2,000 to 3,000 cases are diagnosed each year in the United States (6 to 9 per million persons). Comprehensive studies from Denmark published in 2012 showed an annual incidence of 19-23 per million from 2002 to 2008, over the last 30 years the reported incidence have been increasing, until the last decade in which an approximation of the true incidence may have been found. Most recent publications suggest that the incidence of vestibular schwannomas have been rising because of advances in MRI scanning.

Most cases are diagnosed in people between the ages of 30 and 60, and men and women appear to be affected equally. Most vestibular schwannomas occur spontaneously in those without a family history. One confirmed risk factor is a rare genetic mutation called NF2.

The primary symptoms of vestibular schwannoma are unexplained progressive unilateral hearing loss and tinnitus, and vestibular (disequilibrium) symptoms. Treatment of the condition is by surgery or radiation, and often results in substantial or complete hearing loss in the affected ear. Observation (non-treatment) over time also usually results in hearing loss in the affected ear.

The prognosis for individuals with TSC depends on the severity of symptoms, which range from mild skin abnormalities to varying degrees of learning disabilities and epilepsy to severe intellectual disability, uncontrollable seizures, and kidney failure. Those individuals with mild symptoms generally do well and live long, productive lives, while individuals with the more severe form may have serious disabilities. However, with appropriate medical care, most individuals with the disorder can look forward to normal life expectancy.

A study of 30 TSC patients in Egypt found, "...earlier age of seizures commencement (<6 months) is associated with poor seizure outcome and poor intellectual capabilities. Infantile spasms and severely epileptogenic EEG patterns are related to the poor seizure outcome, poor intellectual capabilities and autistic behavior. Higher tubers numbers is associated with poor seizure outcome and autistic behavior. Left-sided tuber burden is associated with poor intellect, while frontal location is more encountered in ASD. So, close follow up for the mental development and early control of seizures are recommended in a trial to reduce the risk factors of poor outcome. Also early diagnosis of autism will allow for earlier treatment and the potential for better outcome for children with TSC."

Leading causes of death include renal disease, brain tumour, lymphangioleiomyomatosis of the lung, and status epilepticus or bronchopneumonia in those with severe mental handicap. Cardiac failure due to rhabdomyomas is a risk in the fetus or neonate, but is rarely a problem subsequently. Kidney complications such as angiomyolipoma and cysts are common, and more frequent in females than males and in "TSC2" than "TSC1". Renal cell carcinoma is uncommon. Lymphangioleiomyomatosis is only a risk for females with angiomyolipomas. In the brain, the subependymal nodules occasionally degenerate to subependymal giant cell astrocytomas. These may block the circulation of cerebrospinal fluid around the brain, leading to hydrocephalus.

Detection of the disease should be followed by genetic counselling. It is also important to realise that though the disease does not have a cure, symptoms can be treated symptomatically. Hence, awareness regarding different organ manifestations of TSC is important.

A study by You et al. was only able to evaluate the 47 documented cases that have been made to date. According to this study, intraocular schwannomas are more prevalent in females as compared to males with a ratio of 3:1. Additionally, individuals are more likely to present with intraocular schwannomas at a younger age than with uveal melanomas, the most common intraocular tumor. According to the participants evaluated in this study, the average age of occurrence was 37 years old, however, it is important to note that the age range documented represented individuals 9–76 years old.

MRI diagnosis is based on lesions that are disseminated in time and space, meaning that there are multiple episodes and consisting of more than one area. There are two kinds of MRI used in the diagnosis of tumefactive MS, T1-weighted imaging and T2-weighted imaging. Using T1-weighted imaging, the lesions are displayed with low signal intensity, meaning that the lesions appear darker than the rest of the brain. Using T2-weighted imaging, the lesions appear with high signal intensity, meaning that the lesions appear white and brighter than the rest of the brain. When T1-weighted imaging is contrast-enhanced through the addition of gadolinium, the open ring enhancement can be viewed as a white ring around the lesion. A more specific MRI, Fluid attenuation inversion recovery (FLAIR) MRI show the signal intensity of the brain. Subjects with tumefactive multiple sclerosis may see a reduction of diffusion of the white matter in the affected area of the brain.

Pathologically, PMG is defined as “an abnormally thick cortex formed by the piling upon each other of many small gyri with a fused surface.” To view these microscopic characteristics, magnetic resonance imaging (MRI) is used. First physicians must distinguish between polymicrogyria and pachygyria. Pachygria leads to the development of broad and flat regions in the cortical area, whereas the effect of PMG is the formation of multiple small gyri. Underneath a computerized tomography (CT scan) scan, these both appear similar in that the cerebral cortex appears thickened. However, MRI with a T1 weighted inversion recovery will illustrate the gray-white junction that is characterized by patients with PMG. An MRI is also usually preferred over the CT scan because it has sub-millimeter resolution. The resolution displays the multiple folds within the cortical area, which is continuous with the neuropathology of an infected patient.