Primary glioblastoma multiforme accounts for the vast majority of cases (60%) in adults older than 50 years Secondary

glioblastoma multiformes (40%) typically develop in younger patients (< 45 y) through malignant progression from a low-grade astrocytoma (WHO grade II) LOH on chromosome arm 10q is the most frequent gene alteration for both primary and secondary glioblastomas; it occurs in 60-90% of cases. The p53 gene appears to be deleted or altered in approximately 25-40% of all glioblastoma multiformes, more commonly in secondary glioblastoma multiformes. Overexpression or activation mutations in EGFR gene are more common in primary glioblastoma, with mutations appearing in 40-50% of these tumors Glioblastoma multiformes occur most often in the subcortical white matter of the cerebral hemispheres Tumor infiltration often extends into the adjacent cortex or the basal ganglia. When a tumor in the frontal cortex spreads across the corpus callosum into the contralateral hemisphere, it creates the appearance of a bilateral symmetric lesion, hence the term butterfly glioma

The most common presentation of patients with glioblastomas is a slowly progressive neurologic deficit, usually motor weakness. However, the most common symptom experienced by patients is headache. Alternatively, patients may present with generalized symptoms of increased intracranial pressure (ICP), including headaches, nausea and vomiting, and cognitive impairment. Seizures are another common presenting symptom

On CT scans, glioblastomas usually appear as irregularly shaped hypodense lesions with a peripheral ringlike zone of contrast enhancement and a penumbra of cerebral edema. MR spectroscopy demonstrates an increase in the choline-to-creatine peak ratio, an increased lactate peak, and decreased N- acetylaspartate (NAA) peak in areas with glioblastomas. Tumor metabolite conc measurement below

Glioblastoma multiformes are composed of poorly differentiated, often pleomorphic astrocytic cells with marked nuclear atypia and brisk mitotic activity. Necrosis is an essential diagnostic feature, and prominent microvascular proliferation is common. Macroscopically, glioblastomas are poorly delineated, with peripheral grayish tumor cells, central yellowish necrosis from myelin breakdown, and multiple areas of old and recent hemorrhages. Most glioblastomas of the cerebral hemispheres are clearly intraparenchymal with an epicenter in the white matter, but some extend superficially and contact the leptomeninges and dura glial fibrillary acidic protein (GFAP) remains the most valuable marker for neoplastic astrocytes

The most common site of occurrence of juvenile pilocytic astrocytoma is the cerebellum.[1] These tumors are usually discrete, indolent lesions associated with cyst formation. The cysts may be unilocular or multilocular, with an associated tumor nodule. The most common presenting symptoms are associated with increased intracranial pressure resulting from mass effect or hydrocephalus. Symptoms may include headache, nausea, vomiting, irritability, ataxia, and visual complaints, depending on the site of occurrence
well-circumscribed lesion with an associated macrocyst. The nodular portion of the lesion usually demonstrates homogeneous contrast enhancement. Calcification is present in 10% of juvenile pilocytic astrocytomas. Other low-grade gliomas are typically hypoattenuating or hypointense, poorly defined, nonenhancing lesions on CT and MRI scans. Macroscopically, 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[5]). There is often presence of Rosenthal fibers,[6] eosinophilic granular bodies and microcysts Histopathology of Rosenthal-fibres. H&E staining showing these elongated eosinophilic structures in a case of pilocytic astrocytoma Meningiomas in specific locations may give rise to the stereotyped symptoms

Location Parasagittal Subfrontal

Symptoms Monoparesis of the contralateral leg Change in mentation, apathy or disinhibited behavior, urinary incontinence Olfactory groove Anosmia with possible ipsilateral optic atrophy and contralateral papilledema (this triad termed Kennedy-Foster syndrome) Cavernous sinus Multiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased vision and diplopia with associated facial numbness Occipital lobe Contralateral hemianopsia Cerebellopontine Decreased hearing with possible facial weakness and facial numbness angle Spinal cord Localized spinal pain, Brown-Sequard (hemispinal cord) syndrome Optic nerve Exophthalmos, monocular loss of vision or blindness, ipsilateral dilated pupil that does not react to direct light stimulation but might contract on consensual light stimulation; often, monocular optic nerve swelling with optociliary shunt vessels Sphenoid wing Seizures; multiple cranial nerve palsies if the superior orbital fissure involved Tentorial May protrude within supratentorial and infratentorial compartments, producing symptoms by compressing specific structures within these 2 compartments[4] Foramen Paraparesis, sphincteric troubles, tongue atrophy associated with magnum fasciculation The best-characterized and most common genetic alteration is the loss of the NF2 gene (NF2) on chromosome 22q[7] . NF2 encodes a tumor suppressor known as merlin (or schwannomin) The role of inflammation (eg, posttraumatic insult) resulting in the upregulation of COX-2 has been investigated in the tumorogenesis of meningiomas Meningiomas are usually globular, well-demarcated neoplasms. They have a wide dural attachment and become invaginated into the underlying brain without invading it. Their cut surface is either translucent pale or homogeneously reddish brown The 3 most common histologic subtypes of meningiomas are the meningothelial (syncytial), transitional, and fibroblastic meningiomas.

Meningothelial meningiomas reveal densely packed cells that are arranged in sheets with no clearly discernible cytoplasmic borders. Although not prominent, whorls are present (calcified whorls are termed psammoma bodies). Nuclei show intranuclear vacuoles. Fibroblastic (fibrous) meningiomas reveal sheets of interlacing spindle cells. The intercellular stroma is composed of reticulin and collagen. The transitional variety reveals features common to both the meningothelial and fibroblastic varieties; others include angiomatous, microcystic, secretory, clear cell, choroid, lymphoplasmacyte-rich, papillary, and metaplastic variants
positive for epithelial membrane antigen (EMA) in 80% of cases. They stain negative for anti-Leu 7 antibodies (positive in schwannomas) and for glial fibrillary acidic protein (GFAP).

The tumor is usually gray, well-circumscribed, and takes on the form of space it occupies. They are usually dome-shaped, with the base lying on the dura. Histologically, the cells are relatively uniform, with a tendency to encircle one another, forming whorls and psammoma bodies (laminated calcific concretions).[8] They have a tendency to calcify and are highly vascularized.
Histologically, ependymomas are characterized by ependymal pseudorosettes with glial fibrillary acidic protein (GFAP)positive processes tapering toward blood vessels but the presence of perivascular pseudorosettes or true rosettes establishes the diagnosis Ependymomas are composed of cells with regular, round to oval nuclei. There is a variably dense fibrillary background. Tumor cells may form gland-like round or elongated structures that resemble the embryologic ependymal canal, with long, delicate processes extending into the lumen; more frequently present are perivascular pseudorosettes in which tumor cells are arranged around vessels with an intervening zone consisting of thin ependymal processes directed toward the wall of the vessel Patients with medulloblastoma most commonly have symptoms related to increased intracranial pressure (as a consequence of hydrocephalus). medulloblastoma appears as a pinkish-gray mass usually arising from the cerebellar vermis in children. Cysts, areas of necrosis, or calcification are rare. On microscopic examination, cells are small and poorly differentiated, with scant cytoplasm and little stroma (see the image below). A high mitotic index is common. Classic Homer-Wright rosettes can be seen in one fifth of cases. Elongated cells surrounding eosinophilic circular zones devoid of lamina and blood vessels form these pseudorosettes

Grossly, oligodendrogliomas appear as well defined, solid, and pinkish grey, frequently with areas of calcification and sometimes with areas

of necrosis and cystic degeneration. Intratumoral hemorrhage may be present and in some patients may be massive and responsible for sudden death.

Microscopic
Oligodendrogliomas are distinctive, consisting of homogeneous, compact, rounded cells with distinct borders and clear cytoplasm surrounding a dense central nucleus, giving them a "fried egg" appearance