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The lysis of the erythrocytes would also occur. Within the next few hours of the stroke, a peri-haematoma oedema and ischemia would develop and increase the space-occupying effect (Chakrabarty and Shivane, 2008). Within the next 2-3 weeks, the ischemia would manifest as brown discoloration. On the microscopic level, haemosiderin would form and phagocytosis by the macrophages would also occur. Astrocytes hypertrophy and new blood vessels would be seen at the margin of the haematoma (Chakrabarty and Shivane, 2008). In the next few months, a friable brown clot would become apparent and there would be an organization of the haematoma through phagocytosis of the blood and necrosis in the macrophages. From such point until the next few years, there would be a cavity which would contain blood-stained fluid in the area where the ischemia shall have occurred. The blood would also continually be resorbed (Chakrabarty and Shivane, 2008). The MRI seeks to establish the presence of blood in brain haemorrhages. It also seeks to localize the various haemorrhages, to determine if it is extra-axial, to distinguish subarachnoid haemorrhages, subdural hematoma, and to determine the presence of epidural hematoma. In case it is intra-axial, the goal is to establish the specific neuroanatomic site and to establish the age of the haemorrhage, including its cause. As the haemorrhage would age, changes in the haemoglobin would become apparent; and the different forms of oxyhemoglobin, deooxyhemoglobin, and methemoglobin before the red blood cells are then broken down into the ferritin and the hemosiderin (Atlas and Thulburn, 2002). In the hyperacute phase or in the first 24 hours of the incident, oxyhemoglobin intracellular is apparent. In the acute phase or within the first three days, deoxyhemoglobin, still intracellular is seen (Ashtekar, 2011). In the first three days or in the early subacute phase, methemoglobin in the intracellular location becomes evident. In the next seven days or during the late subacute phase, methemoglobin extracellular manifests and finally, in the chronic phase or after 14 days, ferritin and hemosiderin, extracellular becomes apparent (Ashtekar, 2011). Where there is an infarct in the brain, bleeding often follows. Haemorrhage caused by infarction may be seen with cytotoxic oedema which matches an arterial quality in the bleeding. However, such connection may be hard to assess when early significant bleeding impacts on the underlying infarct (Ashtekar, 2011). As soon as the bleeding occurs, blood is introduced into the subarachnoid space. In cases where pressure is great, the brain parenchyma is usually dissected and filled. Vascular malformations, very much like arteriovenous malformations or AVMs, arteriovenous dural fistulae, and cavernous malformations are apparent in the MRIs for brain haemorrhages (Ashtekar, 2011). On the MRI, the AVM would often be seen as a tightly packed complex honeycomb with various flow voids which translates to high-impact signal loss. Increased signal intensity may be caused by slow or high flow thrombosis (Ashtekar, 2011). Cavernous hemangiomas usually manifest as popcorn-like shapes with well-defined cores of mixed signal intensity caused by haemorrhage in different stages (Ashtekar, 20 ...Show more
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Summary

Brain MRI 1. Review the relevant properties of blood, and the changing MRI appearance of haemorrhage in the brain over time. Within a few seconds of an ischemic stroke, microscopically, changes are already seen with the rupture of the blood vessel wall. Within a few minutes from the initial rupture, a haematoma forms and appears as bright red acute haemorrhage and on a microscopic level there is an extravasation of the blood (Chakrabarty and Shivane, 2008)…
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