The causes of meningiomas are not well understood. Most cases are sporadic, appearing randomly, while some are familial. Persons who have undergone radiation, especially to the scalp, are more at risk for developing meningiomas, as are those who have had a brain injury. Atomic bomb survivors from Hiroshima had a higher than typical frequency of developing meningiomas, with the incidence increasing the closer that they were to the site of the explosion. Dental x-rays are correlated with an increased risk of meningioma, in particular for people who had frequent dental x-rays in the past, when the x-ray dose of a dental x-ray was higher than in the present.

Having excess body fat increases the risk.

A 2012 review found that mobile telephone use was unrelated to meningioma.

People with neurofibromatosis type 2 (NF-2) have a 50% chance of developing one or more meningiomas.

Ninety-two percent of meningiomas are benign. Eight percent are either atypical or malignant.

Many individuals have meningiomas, but remain asymptomatic, so the meningiomas are discovered during an autopsy. One to two percent of all autopsies reveal meningiomas that were unknown to the individuals during their lifetime, since there were never any symptoms. In the 1970s, tumors causing symptoms were discovered in 2 out of 100,000 people, while tumors discovered without causing symptoms occurred in 5.7 out of 100,000, for a total incidence of 7.7/100,000. With the advent of modern sophisticated imaging systems such as CT scans, the discovery of asymptomatic meningiomas has tripled.

Meningiomas are more likely to appear in women than men, though when they appear in men, they are more likely to be malignant. Meningiomas may appear at any age, but most commonly are noticed in men and women age 50 or older, with meningiomas becoming more likely with age. They have been observed in all cultures, Western and Eastern, in roughly the same statistical frequency as other possible brain tumors.

Epidemiological studies are required to determine risk factors. Aside from exposure to vinyl chloride or ionizing radiation, there are no known environmental factors associated with brain tumors. Mutations and deletions of so-called tumor suppressor genes, such as P53, are thought to be the cause of some forms of brain tumor. Inherited conditions, such as Von Hippel–Lindau disease, multiple endocrine neoplasia, and neurofibromatosis type 2 carry a high risk for the development of brain tumors. People with celiac disease have a slightly increased risk of developing brain tumors.

Although studies have not shown any link between cell phone or mobile phone radiation and the occurrence of brain tumors, the World Health Organization has classified mobile phone radiation on the IARC scale into Group 2B – possibly carcinogenic. Discounting claims that current cell phone usage may cause brain cancer, modern, third-generation (3G) phones emit, on average, about 1% of the energy emitted by the GSM (2G) phones that were in use when epidemiological studies that observed a slight increase in the risk for glioma – a malignant type of brain cancer – among heavy users of wireless and cordless telephones were conducted.

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.

Despite the personality and behavior changes that occur in people with brain tumors, little research on such changes has been done. A person's personality may be altered due to the tumor damaging lobes of the brain. Since the frontal, temporal, and parietal lobes control inhibition, emotions, mood, judgement, reasoning, and behavior, a primary or secondary tumor in that region can cause inappropriate social behavior, temper tantrums, laughing at things which merit no laughter, and even psychological symptoms such as depression and anxiety.

Personality changes can have damaging effects such as unemployment, unstable relationships, and a lack of control.

In most cases, the cause of acoustic neuromas is unknown. The only statistically significant risk factor for developing an acoustic neuroma is having a rare genetic condition called neurofibromatosis type 2 (NF2). There are no confirmed environmental risk factors for acoustic neuroma. There are conflicting studies on the association between acoustic neuromas and cellular phone use and repeated exposure to loud noise. In 2011, an arm of the World Health Organization released a statement listing cell phone use as a low grade cancer risk. The Acoustic Neuroma Association recommends that cell phone users use a hands-free device.

Meningiomas are significantly more common in women than in men; they are most common in middle-aged women. Two predisposing factors associated with meningiomas for which at least some evidence exists are exposure to ionizing radiation (cancer treatment of brain tumors) and hormone replacement therapy.

Central neurocytoma, abbreviated CNC, is an extremely rare, ordinarily benign intraventricular brain tumour that typically forms from the neuronal cells of the septum pellucidum. The majority of central neurocytomas grow inwards into the ventricular system forming interventricular neurocytomas. This leads to two primary symptoms of CNCs, blurred vision and increased intracranial pressure. Treatment for a central neurocytoma typically involves surgical removal, with an approximate 1 in 5 chance of recurrence. Central neurocytomas are classified as a grade II tumor under the World Health Organization's classification of tumors of the nervous system.

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.

About 3 per 100,000 people develop the disease a year. It most often begins around 64 years of age and occurs more commonly in males than females. It is the second most common central nervous system cancer after meningioma.

The term glioblastoma multiforme was introduced in 1926 by Percival Bailey and Harvey Cushing, based on the idea that the tumor originates from primitive precursors of glial cells (glioblasts), and the highly variable appearance due to the presence of necrosis, hemorrhage and cysts (multiform).

The cerebellopontine angle is the anatomic space between the cerebellum and the pons filled with cerebrospinal fluid. This is a common site for the growth of acoustic neuromas or schwannomas. A distinct neurologic syndrome of deficits occurs due to the anatomic proximity of the cerebellopontine angle to specific cranial nerves. Indications include unilateral hearing loss (85%), speech impediments, disequilibrium, tremors or other loss of motor control.

Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Lifestyle diseases including hypertension, smoking, excessive alcoholism, and obesity are associated with the development of brain aneurysms. Cocaine use has also been associated with the development of intracranial aneurysms.

Other acquired associations with intracranial aneurysms include head trauma and infections.

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.

Malignant meningioma is a rare, fast-growing tumor that forms in one of the inner layers of the meninges (thin layers of tissue that cover and protect the brain and spinal cord). Malignant meningioma often spreads to other areas of the body.

The World Health Organization classification system defines both grade II and grade III meningiomas as malignant. Historically, histological subtypes have also been used in classification including:

- clear cell (WHO grade II),

- chordoid (WHO grade II),

- rhabdoid (WHO grade III), and

- papillary (WHO grade III)

Benign or low grade meningiomas (WHO grade I) include meningothelial, fibrous, transitional, psammomatous, angiomatous, microcystic, secretory, lymphoplasmacyte-rich, and metaplastic.

Coarctation of the aorta is also a known risk factor, as is arteriovenous malformation. Genetic conditions associated with connective tissue disease may also be associated with the development of aneurysms. This includes:

- autosomal dominant polycystic kidney disease,

- neurofibromatosis type I,

- Marfan syndrome,

- multiple endocrine neoplasia type I,

- pseudoxanthoma elasticum,

- hereditary hemorrhagic telangiectasia and

- Ehlers-Danlos syndrome types II and IV.

Specific genes have also had reported association with the development of intracranial aneurysms, including perlecan, elastin, collagen type 1 A2, endothelial nitric oxide synthase, endothelin receptor A and cyclin dependent kinase inhibitor. Mutations in interleukin 6 may be protective. . Recently, several genetic loci have been identified as relevant to the development of intracranial aneurysms. These include 1p34-36, 2p14-15, 7q11, 11q25, and 19q13.1-13.3.

A hemangiopericytoma (HPC) is a type of soft tissue sarcoma that originates in the pericytes in the walls of capillaries. When inside the nervous system, although not strictly a meningioma tumor, it is a meningeal tumor with a special aggressive behavior. It was first characterized in 1942.

Hemangiopericytoma located in the cerebral cavity is an aggressive tumor of the Mesenchyme with oval nuclei with scant cytoplasm. "There is dense intercellular reticulin staining. Tumor cells can be fibroblastic, myxoid, or pericytic. These tumors, in contrast to meningiomas, do not stain with epithelial membrane antigen. They have a grade 2 or 3 biological behavior, and need to be distinguished from benign meningiomas because of their high rate of recurrence (68.2%) and metastases (Maier et al. 1992; Kleihues et al. 1993 )."

Because hearing loss in those with NF-2 almost always occurs after acquisition of verbal language skills, patients do not always integrate well into the Deaf culture and are more likely to resort to auditory assistive technology.

The most sophisticated of these devices is the cochlear implant, which can sometimes restore a high level of auditory function even when natural hearing is totally lost. However, the amount of destruction to the cochlear nerve caused by the typical NF2 schwannoma often precludes the use of such an implant. In these cases, an auditory brainstem implant (ABI) can restore a primitive level of hearing, which, when supplemented by lip reading, can restore a functional understanding of spoken language.

The clinical spectrum of the condition is broad. In other words, people with NF II may develop a wide range of distinct problems.

1. Acoustic nerve: 90% of the patients show bilateral acoustic schwannomas on magnetic resonance imaging (MRI).

2. Other cranial nerves and meninges: About 50% of patients develop tumours in other cranial nerves or meningiomas.

3. Spinal cord: About 50% of the patients develop spinal lesions. Only 40% of the spinal lesions are symptomatic. The spinal tumours in NF II are separated in two groups. Intramedullary lesions are located within the spinal tissue and usually belong to the so-called spinal astrocytomas or ependymomas. The extramedullary lesions are located within the small space between the surface of the spinal cord and the bony wall of the spinal canal. These tumours belong to the schwannomas and meningiomas.

4. Skin: If children show neurofibromas, a diagnostic procedure should be performed to decide which form of neurofibromatosis causes the alterations.

5. Eyes: Studies on patients with NF II show that more than 90% of the affected persons suffer eye lesions. The most common alteration in NF II is the juvenile subcapsular cataract (opacity of the lens) in young people.

"Presenting symptoms" (initial concern that brings a patient to a doctor) of a lesion of the nervus vestibulocochlearis due to a tumour in the region of the cerebello-pontine angle are the following: hearing loss (98%), tinnitus (70%), dysequilibrium (67%), headache (32%), facial numbness and weakness (29% and 10% respectively).

"Clinical signs" (alterations that are not regarded by the patient and that can be detected by the doctor in a clinical examination) of the lesion in discussion are: abnormal corneal reflex (33%), nystagmus (26%), facial hypesthesia (26%).

Evaluation (study of the patient with technical methods) shows the enlargement of the porus acousticus internus in the CT scan, enhancing tumours in the region of the cerebello-pontine angle in gadolinium-enhanced MRI scans, hearing loss in audiometric studies and perhaps pathological findings in electronystagmography. Some times there are elevated levels of protein in liquor study.

In NF II, acoustic neuromas usually affect young people, whereas in sporadic forms of acoustic neuromas, the appearance of the tumour is limited to the elderly.

There are two forms of the NF II:

- The "Wishart-Phenotype" is characterized by multiple cerebral and spinal lesions in patients younger than 20 years and with rapid progression of the tumours.

- Patients that develop single central tumours with slow progression after age of 20 are thought to have the "Feiling-Gardner-Phenotype".

70% of patients with carotid arterial dissection are between the ages of 35 and 50, with a mean age of 47 years.

Most individuals come to clinical attention during the 5th decade, although the age range is broad (20 to 80 years). There is an equal gender distribution.

Cortical pseudolaminar necrosis, also known as cortical laminar necrosis and simply laminar necrosis, is the (uncontrolled) death of cells in the (cerebral) cortex of the brain in a band-like pattern, with a relative preservation of cells immediately adjacent to the meninges.

It is seen in the context of cerebral hypoxic-ischemic insults, i.e. strokes.

It is a disorder related to excessive neuronal proliferation and hamartomatous overgrowth affecting the cortical formation. The excessive proliferation is postulated to occur early and to possibly continue beyond the normal proliferative period. Epidermal growth factor is thought to play an important role in the excessive proliferation and the pathogenesis of HME.

Foroozen divides the causes of chiasmal syndromes into intrinsic and extrinsic causes. Intrinsic implies thickening of the chiasm itself and extrinsic implies compression by another structure. Other less common causes of chiasmal syndrome are metabolic, toxic, traumatic or infectious in nature.

Intrinsic etiologies include gliomas and multiple sclerosis. Gliomas of the optic chiasm are usually derived from astrocytes. These tumors are slow growing and more often found children. However, they have a worse prognosis, especially if they have extended into the hypothalamus. They are frequently associated with neurofibromatosis type 1 (NF-1). Their treatment involves the resection of the optic nerve. The supposed artifactual nature of Wilbrand's knee has implications for the degree of resection that can be obtained, namely by cutting the optic nerve immediately at the junction with the chiasm without fear of potentially resulting visual field deficits.

The vast majority of chiasmal syndromes are compressive. Ruben et al. describe several compressive etiologies, which are important to understand if they are to be successfully managed. The usual suspects are pituitary adenomas, craniopharyngiomas, and meningiomas.

Pituitary tumors are the most common cause of chiasmal syndromes. Visual field defects may be one of the first signs of non-functional pituitary tumor. These are much less frequent than functional adenomas. Systemic hormonal aberrations such as Cushing’s syndrome, galactorrhea and acromegaly usually predate the compressive signs. Pituitary tumors often encroach upon the middle chiasm from below. Pituitary apoplexy is one of the few acute chiasmal syndromes. It can lead to sudden visual loss as the hemorrhagic adenoma rapidly enlarges.

The embryonic remnants of Rathke’s pouch may undergo neoplastic change called a craniopharyngioma. These tumors may develop at any time but two age groups are most at risk. One peak occurs during the first twenty years of life and the other occurs between fifty and seventy years of age. Craniopharyngiomas generally approach the optic chiasm from behind and above. Extension of craniopharyngiomas into the third ventricle may cause hydrocephalus.

Meningiomas can develop from the arachnoid layer. Tuberculum sellae and sphenoid planum meningiomas usually compress the optic chiasm from below. If the meningioma arises from the diaphragma sellae the posterior chiasm is damaged. Medial sphenoid ridge types can push on the chiasm from the side. Olfactory groove subfrontal types can reach the chiasm from above. Meningiomas are also associated with neurofibromatosis type 1. Women are more prone to develop meningiomas.

Once considered uncommon, spontaneous carotid artery dissection is an increasingly recognised cause of stroke that preferentially affects the middle-aged.

The incidence of spontaneous carotid artery dissection is low, and incidence rates for internal carotid artery dissection have been reported to be 2.6 to 2.9 per 100,000.

Observational studies and case reports published since the early 1980s show that patients with spontaneous internal carotid artery dissection may also have a history of stroke in their family and/or hereditary connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndrome, autosomal dominant polycystic kidney disease, pseudoxanthoma elasticum, fibromuscular dysplasia, and osteogenesis imperfecta type I. IgG4-related disease involving the carotid artery has also been observed as a cause.

However, although an association with connective tissue disorders does exist, most people with spontaneous arterial dissections do not have associated connective tissue disorders. Also, the reports on the prevalence of hereditary connective tissue diseases in people with spontaneous dissections are highly variable, ranging from 0% to 0.6% in one study to 5% to 18% in another study.

Internal carotid artery dissection can also be associated with an elongated styloid process (known as Eagle syndrome when the elongated styloid process causes symptoms).