As the blood accumulated in the epidural space is confined within suture lines, accumulation of additional blood will cause bulging in this space, and thus resulting in a typical "biconvex" appearance on CT scans. EDH can be due to arterial or venous rupture depending on the locations. Arterial injuries results in more rapidly growing hematoma when compared to venous injuries. At the pterion region, middle meningeal artery is most commonly affected. When fracture is crossing areas where dural venous sinuses resides, venous hemorrhage can occur such as falx cerebri, tentorium cerebelli, and vertex (where superior sagittal sinus resides). Anterior temporal EDH is usually caused by sphenoparietal sinus. Such EDH is limited and does not require surgery because its extension is confined within sphenosquamosal suture and orbital fissure. In 20 to 50% of epidural hemorrhage cases, there is a lucid interval where a person regained consciousness after being knocked unconscious and then followed by deterioration of consciousness after that.When the epidural hematoma is large enough, it will cause mass effect on contralateral brain which lead to midline, subfalcine (below the falx cerebri), and trans-tentorial (crossing tentorium cerebelli) herniations. This phenomenon can cause the subject to lose consciousness and eventually death. Therefore, large EDH requires emergent surgical clot evacuation. Embolisation of middle meningeal artery is performed if the hemorrhage is medium or small. Subdural hemorrhage
Subdural hemorrhage (SDH) results from tearing of the bridging veins in the subdural space between the dura and arachnoid mater.
SAH in CAA usually occurs in those who age more than 60 years, temporary motor and sensory deficits, and intracranial bleed in white matter adjacent to cerebral cortex. Basal ganglia, posterior fossa, and brainstem are spared. Boston criteria is used to determine the likelihood of a cerebral hemorrhage due to CAA. Definitive diagnosis of CAA is by performing brain biopsyCT scan may show hyperdense intra-axial hemorrhage in the subcortical region. Diffuse white matter hypodensities in both cerebral hemispheres may represents microangiopathic changes. On MRI these lesions will be presented as blooming artifact on gradient echo and susceptibility weighted imaging. Hemorrhagic conversion of ishemic infarction
43% of those with infarcted brain tissue will develop hemorrhagic conversion. Risk of hemorrhagic is further increased with recanalisation of veins or arteries. Several types of hemorrhages can occur such as petechial hemorrhages around the infarcted margin (HI1), confluent petechial hemorrhages within the infarcted tissue (HI2), hematoma occupying less than 30% of the infarcted tissue (PH1), hematoma involving greater than 30% of infarcted tissue with small mass effect (PH2), and hematoma involving greater than 30% of the infarcted tissue with significant mass effect. However, only PH2 is clinically significant. Those who has infarction should be monitored frequently with CT brains to access hemorrhagic conversions or worsening vasogenic oedema that may require neurosurgical decompression. Dual energy CT scan maybe useful to differentiate the high densities caused by reperfusion hemorrhage (bleeding after endovascular stroke treatment) and high density due to iodinated contrast administered during cerebral angiography.