Intracranial Hemorrhage Evaluation with MRI


Hyperacute hemorrhage

Freshly extravasated erythrocytes from the arterial blood contain fully oxygenated hemoglobin with unpaired electrons. Hence, oxygenated blood is diamagnetic. In the absence of a paramagnetic component, no proton-electron dipole-dipole interaction occurs, and no paramagnetic relaxation enhancement is observed. Therefore, the bulk of the hyperacute hematoma appears identical to most brain lesions on MRI.
Hyperacute hemorrhage appears slightly hypointense or isointense relative to the brain on T1-weighted images and slightly hyperintense to the brain on T2-weighted images. T2-weighted MRI images may show a thin, irregular rim of marked hypointensity; this is attributed to rapid deoxygenation at the blood-brain interface. This hypointensity is marked on T2-weighted gradient-echo images. Such lesions do not enhance after the administration of a gadolinium-based contrast agent. On diffusion MRI, the lesion demonstrates restricted diffusion compared with normal brain parenchyma.

Acute hemorrhage

The acute phase begins after a few hours and is characterized by the formation of deoxyhemoglobin. This process first occurs in the periphery and then affects the center. The iron atom in deoxyhemoglobin has 5 unpaired electrons; hence, it is paramagnetic. The magnetic susceptibility of deoxyhemoglobin is different for intracellular and extracellular locations. Acute hematoma contains intracellular deoxyhemoglobin and appears markedly hypointense on T2-weighted MRI images. At high-field strengths, T2-weighted images—and especially gradient-echo images—depict marked hypointensity.
During the acute phase, the clot retracts, increasing the hematocrit and surrounding edema, which appears as a hyperintense perilesional rim on T2-weighted MRI. The increased hematocrit causes a parallel increase in T1 and T2 relaxation times.
With an acute hematoma, T1-weighted images show isointensity or slight hypointensity. This appearance is observed because the 3-dimensional structure of deoxyhemoglobin blocks the access of water protons to iron atoms and thus prevents the magnetic dipole-dipole interaction. Hence, the T1 relaxation time is not shortened. A thin hyperintense rim is sometimes seen in the periphery; this is caused by early oxidation of deoxyhemoglobin to methemoglobin.

Early subacute hemorrhage

The early subacute phase begins after 2-7 days. An inflammatory cell response can be observed in the surrounding tissues. Macrophages invade the boundary of the hematoma to clear extravasated material and damaged tissue. When low oxygen tension continues, the amount of reducing substances declines. This change causes a failure in RBC metabolism, and iron atoms are oxidized to the ferric state. The result is the formation of methemoglobin and, thus, exposure of the iron atoms to water protons. This pattern decreases the T1 relaxation time and leads to marked hyperintensity on T1-weighted MRI.
A susceptibility effect is present because the RBC membrane remains intact. Hence, continued hypointensity is observed on T2-weighted images.

Late subacute hemorrhage

Over several days to weeks, the energy status of the RBC declines, causing a loss of cellular integrity, and the cells lyse. This event marks the beginning of the late subacute phase. As the loss of RBC integrity removes the paramagnetic aggregation responsible for susceptibility-induced T2 relaxation, T2 shortening disappears.
Methemoglobin freely diffuses in the hematoma cavity in a locally homogeneous magnetic field. This pattern lengthens T2 and, hence, increases the signal intensity on T2-weighted imaging. Extracellular methemoglobin further enhances T1 relaxation, which manifests as high signal intensity on T1-weighted images.

Chronic hemorrhage

Over months, the hematoma enters the chronic phase. As methemoglobin is broken down into small degradation products, its shortening effects are lost. The degree of hyperintensity on T1- and T2-weighted images lessens as the concentration of methemoglobin decreases with protein breakdown.
The center of the hematoma may evolve into a fluid-filled cavity with signal intensity characteristics identical to those of CSF. In addition, the walls of the cavity may collapse, leaving a thin slit.
As proteins are degraded, iron atoms that are liberated from the heme molecule are scavenged by macrophages and converted into ferritin, which can be recycled. In most cases, the degree of iron deposition overwhelms the recycling capacity, and the excess is locally concentrated into hemosiderin molecules. The iron in hemosiderin does not have access to water protons and, therefore, exerts only a susceptibility effect without notable dipole-dipole interactions. These processes lead to marked hypointensity seen at the rim of the hematoma on T2-weighted MRIs. This appearance may persist indefinitely.
  • Hyperacute hemorrhage (see the following image)Axial MR images show a hyperacute hematoma in the Axial MR images show a hyperacute hematoma in the right external capsule and insular cortex in a known hypertensive patient. Axial T1-weighted image (T1W) shows isointense to hypointense lesion in the right temporoparietal region that is hyperintense on T2-weighted (T2W) imaging and with susceptibility appearing as low signal intensity due to blood on gradient-echo (GRE) images. A small rim of vasogenic edema surrounds the hematoma
  • Acute hemorrhage (see the following image)
    MR images show an acute hematoma in the left frontMR images show an acute hematoma in the left frontal region. Axial T1-weighted (T1W) and T2-weighted (T2W) images show hypointensity due to the hematoma. A small rim of vasogenic edema surrounds the hematoma seen on T2W imaging. Courtesy Dr Nikhil Unune, MBBS, DMRD, consultant radiologist, Satara, Maharashtra, India.
  • Early subacute hemorrhage (see the following image)
    MR images show early subacute hematoma in the leftMR images show early subacute hematoma in the left occipital region. The lesion is seen as hyperintensity on T1WI and hypointense on T2WI with marked susceptibility due to hematoma on gradient-echo (GRE) imaging. The intraventricular hematoma also is well visualized as low signal on GRE imaging.
  • Late subacute hemorrhage (see the following image)
    MR images show late subacute hemorrhage in both thMR images show late subacute hemorrhage in both thalamic regions in a patient with known cerebral malaria. T1-weighted, T2-weighted, and gradient-echo (GRE) images all show a hyperintense hematoma. Both T2W and GRE images show a hypointense rim due to hemosiderin.
  • Chronic hemorrhage (see the following image)
    MR imaging shows a late subacute to chronic hematoMR imaging shows a late subacute to chronic hematoma as a space-occupying lesion in the right posterior fossa. The hematoma shows a large medial subacute component and a small lateral chronic component. The chronic component (arrow) is hypointense on both T1-weighted and T2-weighted imaging. This hypointensity is enhanced due to the blooming effect of blood on the gradient-echo (GRE) image.


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