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Cerebral amyloid angiopathy may cause intraparenchymal hemorrhage even in patients without elevated blood pressure. Unlike hypertension, cerebral amyloid angiopathy does not typically affect blood vessels to deep brain structures. Instead, it is most commonly associated with hemorrhage of small vessels in the cerebral cortex. [2]
Yellow softening is the third type of cerebral softening. As its name implies, the affected softened areas of the brain have a yellow appearance. This yellow appearance is due to atherosclerotic plaque build-up in interior brain arteries coupled with yellow lymph around the choroid plexus, which occurs in specific instances of brain trauma. [2]
The breakdown of the tight endothelial junctions that make up the blood–brain barrier causes extravasation of fluid, ions, and plasma proteins, such as albumin, into the brain parenchyma. [18] Accumulation of extracellular fluid increases brain volume and then intracranial pressure causing the symptoms of cerebral edema. [1]
Cerebritis is the inflammation of the cerebrum, which performs a number of important functions, such as memory and speech.It is also defined as a purulent nonencapsulated parenchymal infection of the brain which is characterized by nonspecific features on CT scans (ill-defined low density area with peripheral enhancement) and cannot reliably be distinguished from neoplasms.
Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.
Trauma is the most common cause of intracranial hemorrhage. It can cause epidural hemorrhage, subdural hemorrhage, and subarachnoid hemorrhage. Other condition such as hemorrhagic parenchymal contusion and cerebral microhemorrhages can also be caused by trauma. [3]
They were the first to identify and describe the symptoms and causes of this syndrome. In their original description, they reported findings from autopsies that showed spinal cord necrosis and multiple tortuous and thickened blood vessels on the surface of the spinal cord. This condition was later called necrotizing myelopathy. [3]
Brain herniation is associated with hyperventilation, extensor rigidity, pupillary asymmetry, pyramidal signs, coma and death. [10] Hemorrhage into the basal ganglia or thalamus causes contralateral hemiplegia due to damage to the internal capsule. [7] Other possible symptoms include gaze palsies or hemisensory loss. [7]