Acute epidural hematomas are often associated with skull fractures and lacerations of the dural vessels, most often meningeal arteries and veins but occasionally a dural sinus. Two-thirds of epidural hematomas are in the temporo-parietal region and they usually have a biconvex or lentiform configuration. Epidurals are limited by the firmer attachment of the dura at the suture margins, but they may cross the midline, especially with superior sagittal sinus lacerations, and they also can bridge the supra- and infratentorial compartments with tears along the torcula and transverse sinuses.

      Subdural hematomas, both acute and chronic, are most often caused by bleeding from torn bridging dural veins. Subdural hematomas are less frequently associated with skull fractures, but more frequently associated with parenchymal brain damage. The subdural space is a more freely communicating space and the hematomas form a crescentic shaped layer over the brain surface. Subdural hematomas readily cross suture lines but do not cross the midline. Instead, they extend along the dura of the falx into the interhemispheric fissure and onto the tentorium, which epidurals cannot do. Both epidural and subdural hemorrhages occur within the confined space of the bony calvarium and compress the adjacent brain, often requiring emergency evacuation.

      Chronic subdural hematomas are usually related to a slower venous bleed without accompanying cerebral parenchymal injury. A thick,vascular dural membrane forms that can be a source for repeated episodes of hemorrhage. These collections are more often biconvex, rather than the crescentic shape of acute subdural hematomas. The injury leading to a chronic subdural can be relatively minor and may have occurred weeks before presentation. Patients often present with disturbances of mentation and consciousness rather than focal or lateralizing signs. An iatrogenic cause is overshunting or too rapid decompression of chronic hydrocephalus.

      Subdural hygromas or effusions consist of collections of CSF in the subdural spaces, presumably due to a traumatic arachnoid tear or they may also develop following ventricular shunting. They may accumulate slowly during the first few days following head trauma, especially in the pediatric population.


      Multiple studies have demonstrated improved visualization of extra-axial hemorrhage with MR compared to CT, largely related to the high conspicuity of hyperintense subacute hemorrhage (methemoglobin) on T1-weighted images and the multiplanar capabilities of MR. Coronal images are very helpful for identifying subtemporal collections and hemorrhage adjacent to the tentorium cerebelli. Chronic subdural hematomas are often isointense with gray matter on T1-weighted images, probably due to dilution and partial resorption or breakdown of free methemoglobin. High T1 signal within what otherwise appears to be a chronic subdural hematoma suggests rebleeding. Hemosiderin is rarely seen in subdural hematomas without repeated episodes of bleeding, due to either low macrophage activity or removal of hemosiderin that has formed. The presence of membranous strands coursing through an extra-axial collection is additional evidence for a chronic subdural hematoma. The thick subdural membranes will also enhance following contrast infusion. Endnote  

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