It can cross the suture lines, but not across dural reflections such as falx cerebri or tentorium cerebelli. Therefore, subdural hematoma always limited to one side of the brain. Density of SDH reduces as it progresses from acute to chronic forms. However, areas with low density may not represent chronic SDH entirely as unclotted blood products that are due to active bleed can also give low density appearance on CT scans especially those with coagulopathy. Those with SDH that have same density with brain parenchyma may represent acute bleed such as those with anemia, arachnoid tear, and the mixing of hemorrhage and CSF. SDH usually have high or mixed densities during first two days of trauma, followed by isodensity at 11 days after trauma, and hypodensity after 14 days of trauma. Membranes with granulation tissue can rupture within SDH, and give high density appearance on CT scan. Over a prolonged period of time, calcifications can form. SDH can be treated with burr hole drainage, craniotomy or port system placement for blood clot evacuation, or middle meningeal artery embolisation.Subdural hematoma maybe less acute than epidural hematoma due to slower blood accumulation, but it still has the potential to cause brain herniation that may require surgical evacuation. Clinical features depend on the site of injury and severity of injury. Patients may have a history of loss of consciousness but they recover and do not relapse. Clinical onset occurs over hours.
These cases warrants investigations to look for aneurysms that can cause such bleeding. Non-traumatic
Hypertensive bleed
Intracranial bleed in hypertensive subjects usually occurs at 50 to 60 years of life with 30 to 50% chance of death. Such hemorrhages are typically located in the basal ganglia, cerebellum, or occipital lobes. Other location such as bleed within the cerebral cortex and intracranial bleed in people younger than 50 years should prompt further investigations on other causes of bleed such as brain tumour or cerebral arteriovenous malformation. The bleed can be very small without any significant effect on surrounding brain or large hemorrhage that exerts mass effecct on adjacent brain. Follow up CT scan is recommended. Those with extension of bleed into the ventricular system, expansion of bleeding, or increasing cerebral oedema on CT scan gives poorer prognosis. CT angiography (CTA) of brain can be performed to investigate the source of bleeding. An image during the delayed phase of the CTA may be taken to look for pooling of contrast that signifies active bleeding (known as "Spot sign"). Presence of "Spot sign" signifies poor clinical outcome for the subject. Cerebral amyloid angiopathy
Cerebral amyloid angiopathy (CAA) is the deposition of Amyloid beta peptide protein within the brain. Accumulation of such peptide proteins within the walls of the arteries can cause weakening of the walls and causes microhemorrhages, SAH within the cerebral sulci or large cerebral intraparenchymal bleed. SAH in CAA can be differentiated from vasculitis by its presentations.