Timeline diagram of MRI and CT characteristics of intracerebral hemorrhage

Timeline of CT density and MRI signal intensity characteristics of intracranial (intraparenchymal) hemorrhage.

Note: The time course displayed here is not derived from experimental data, but rather represents the typical values given for intraparenchymal hemorrhages in the literature. The time course may differ substantially for very big or very small hemorrhages and does not fit the changes in subarachnoid or subdural hematomas.

Hyperacute intraparenchymal hemorrhage (within the first hours of the hemorrhage):

• T1w heterogenous lesion, clot mostly isointense or slightly hypointense to surrounding brain tissue.
• T2w heterogenous lesion, clot center is mostly isointense or (slightly) hyperintense to surrounding brain tissue (Oxy-Hb). Clot periphery shows hypointense rim (early Desoxy-Hb).
• There might be early perifocal vasogenic edema.
• Explanation: Hyperacute hemorrhages often present as heterogenous lesions. There is a clot forming with focally increasing hematocrit and decreasing extracellular free water, other parts of the hematoma show more serum parts or mostly fibrin components. Most of the hemoglobin is in Oxy-Hb state (weakly diamagnetic) and found intracellular in the clot's erythrocytes. In T2w the clot is isointense or shows (slightly) hyperintense portions (Oxy-Hb effect) as well as slightly hyperintense portions reflecting plasma released from the clot formation (plasma swirl). In T2w there is a hypointense periphery to the clot due to beginning Desoxy-Hb formation. There is rapid desoxygenation of the blood at the hematoma - brain tissue - interface. Desoxy-Hb formation is progressing towards the center (this is not to be confused with the really black rim in later hemorrhage stages due to hemosiderin and other blood products with thousandfold stronger susceptibility effect than Desoxy-Hb. If you have a susceptibility weighted image (SWI / T2*) weighted image there might already be a pretty dark rim in the lesion periphery). Especially the SWI / T2* image helps confirm the currect diagnosis of hemorrhage in the hyperacute setting by exaggerating the magnetic susceptibility effects. T1w shows isointense clot and slightly hypointense plasma portions. 

Acute intraparenchymal hemorrhage (1 to 2 days):

• T1w signal intensity of the lesion center remains intermediate-to-low (depending on clot formation).
• T2w signal intensity of the lesion center drops in comparison to surrounding brain tissue (Desoxy-Hb effect). This depends greatly on hemorrhage size. There might be sedimentation.
• Increasing perifocal vasogenic edema.
• Explanation: There is more and more Desoxy-Hb as the clot's erythrocytes are being desoxygenated progressing from the periphery to the center. Desoxy-Hb is paramagnetic and thus produces magnetic susceptibility effects leading to a signal loss in T2w.

Early subacute intraparenchymal hemorrhage (2 to 7 days):

• T1w signal intensity of the core lesion gradually increases, progressing from the outside to the lesion core (Met-Hb effect).
• T2w signal intensity of the lesion center stays low (Desoxy-Hb and Met-Hb effect, Met-Hb is compartmented intracellularly). Depending on hemorrhage size there might be sedimentation
• Perifocal edema.
• Explanation: Formation of Met-Hb at the lesion border, which is stronger paramagnetic than Desoxy-Hb was. We see T1 time shortening (effect on bound water close to Met-Hb molecules). There still is signal loss in T2w due to intracellularly concentrated Met-Hb and resulting local magnetic susceptibility effects.

Late subacute intraparenchymal hemorrhage​ (7 to 14-28 days):

• T1w high signal intensity of quite some part of the lesion periphery or of the complete lesion depending on lesion size (Met-Hb effect).
• T2w signal slowly increases (decompartmentalization of Met-Hb reducing susceptibility, loss of Desoxy-Hb).
• Perifocal edema decreases.
• Black rim in T2w surrounding the lesion (ferritin/hemosiderin)
• Explanation: As erythrocytes break down in the late first week, there is now increasing amounts of extracellular Met-Hb and decreasing amounts of concentrated Met-Hb. We see T1 time shortening like in early subacute hemorrhage (effect on bound water close to Met-Hb molecules), but now we see decreasing T2 signal loss too due to a reduction in local magnetic susceptibility effects by decompartmenization of Met-Hb, which is now freely dispersed in the hematoma cavity. There is a black rim in T2w because of accumulating ferritin/hemosiderin.

Chronic intraparenchymal hemorrhage (>14-28 days):

• T1w low signal intensity of the lesion center/cavity.
• T2w high signal intensity of the lesion center/cavity (water effect)
• Perifocal edema disappears.
• Black rim in T2w surrounding the lesion cavity (ferritin/hemosiderin).
• Explanation: In the lesion periphery hemosiderin and ferritin, superparamagnetic substances with resulting high magnetic susceptibility effetcs, are accumulated in macrophages resulting in the surrounding dark rim. If there is a remaining lesion center it is a cavity containing a fluid consisting of water, protein and extracellular hemoglobin breakdown products (hemichromes, which are diamagnetic and thus show no paramagnetic effects) resulting in a cystic appearance.