Ischemic brain injury resulting from an insufficient blood supply to the brain, is one of the leading causes of secondary brain damage after head trauma. Vascular injury usually causes death shortly after an injury. Although it is a diffuse type of brain injury itself, diffuse vascular injury is generally more likely to be caused by focal than diffuse injury. Swelling, commonly seen after TBI, can lead to dangerous increases in intracranial pressure. Though swelling itself is a diffuse type of injury, it can result from either focal or diffuse injury. See also
Focal neurologic deficit

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pointed out that IDH1 and IDH2 mutant cells produce an excess metabolic intermediate, 2-hydroxyglutarate, which binds to catalytic sites in key enzymes that are important in altering histone and DNA promoter methylation. Thus, mutations in IDH1 and IDH2 generate a "DNA CpG island methylator phenotype or CIMP" that causes promoter hypermethylation and concomitant silencing of tumor suppressor genes such as DNA repair genes MGMT and ERCC1. On the other hand, Cohen et al. and Molenaar et al. pointed out that mutations in IDH1 or IDH2 can cause increased oxidative stress. Increased oxidative damage to DNA could be mutagenic. This is supported by an increased number of DNA double-strand breaks in IDH1-mutated glioma cells. Thus, IDH1 or IDH2 mutations act as driver mutations in glioma carcinogenesis, though it is not clear by which role they are primarily acting. A study, involving 51 patients with brain gliomas who had two or more biopsies over time, showed that mutation in the IDH1 gene occurred prior to the occurrence of a p53 mutation or a 1p/19q loss of heterozygosity, indicating that an IDH1 mutation is an early driver mutation. Pathophysiology
High-grade gliomas are highly vascular tumors and have a tendency to infiltrate diffusely. They have extensive areas of necrosis and hypoxia. Often, tumor growth causes a breakdown of the blood–brain barrier in the vicinity of the tumor.