I. General evolution pattern of MRI signal of intracerebral hematoma
Intracerebral hematoma can be generally divided into hyperacute phase, acute phase, early subacute phase, middle subacute phase, late subacute phase, and chronic phase.
(A) Hyperacute phase (this phase is rare in clinical practice and can be ignored from memory)
It is the immediate stage of bleeding, when the leaked blood has not yet clotted. In fact, this phase lasts only a few minutes to tens of minutes and is rarely encountered clinically. The uncoagulated blood in the hyperacute phase exhibits the long T1 and long T2 characteristics of the blood, and therefore appears as a slightly low signal on T1WI and a high signal on T2WI.
(II) Acute phase
It is usually within 2 days after bleeding. In this phase, the cell membrane of erythrocytes remains intact and the intracellular oxygenated hemoglobin releases oxygen to become deoxyhemoglobin. The paramagnetic effect of deoxyhemoglobin causes local magnetic field inhomogeneity and accelerates proton out-of-phase, so the hematoma T2 value is significantly shortened and shows low signal on T2WI or T2*WI. The intracellular deoxyhemoglobin has less influence on the T1 value, so the signal change of the hematoma in this stage is not obvious on T1WI, and it often shows slightly low signal or isosignal.
(C) Subacute early stage
It is usually from day 3 to day 5 after bleeding. The cell membrane of erythrocytes remains intact during this period, and intracellular methemoglobin begins to appear, so this period is also called the intracellular phase of methemoglobin. The appearance of intracellular methemoglobin generally develops gradually from the periphery of the hematoma to the center. Because of the strong paramagnetic properties of intracellular anhemoglobin, the T1 value of the hematoma is shortened, and therefore the hematoma gradually develops high signal from the periphery to the center on T1WI. The hematoma at this stage does not show high signal on T2WI, and generally remains low signal.
(iv) Subacute middle stage
It is usually from day 6 to day 10 after bleeding. The cell membrane of erythrocytes starts to rupture during this period, and nor-ferric hemoglobin overflows into the extracellular phase, so this period is also called the nor-ferric hemoglobin extracellular phase. The rupture of erythrocytes also generally progresses from the periphery of the hematoma to the center. The hematoma in this stage still shows high signal on T1WI and gradually spreads from the periphery to the center of the hematoma on T2WI.
(V) Late subacute stage
It is usually 10 days to 3 weeks after bleeding. At this stage, the erythrocytes are completely disintegrated and the hematoma is predominantly filled with ortho-hemoglobin, but macrophages in the periphery of the hematoma engulf the hemoglobin and form iron-containing hemoglobin. The intracellular iron-containing hemoglobin is significantly paramagnetic and will cause local magnetic field inhomogeneity. Therefore, the hematoma in this stage is high signal on T1WI and T2WI, but a low signal ring appears around the hematoma on T2WI.
(VI) Chronic phase
This is usually after 3 weeks or several months of bleeding. The hematoma is gradually resorbed or liquefied, and there are obvious deposits of iron-containing heme in the macrophages around the lesion. Therefore, the hematoma gradually evolves into a liquefied foci in this stage, with low signal on T1WI and high signal on T2WI; the surrounding iron-containing hemoglobin shows a low signal ring on T2WI and equal signal or slightly high signal on T1WI.
Second, a few notes on the hemorrhage MRI signal
What was introduced earlier is the typical pattern of MRI signal evolution of intracerebral hematoma, and the signal changes of intracerebral hemorrhage in some cases in clinical work may not be consistent with it, and the possible reasons are.
(1) individual differences.
(2) the difficulty in determining the exact time of hemorrhage, and
(3) recurrent hemorrhage in the lesion.
(4) differences in the size of the lesions, (5) differences in the size of the lesions, and
(5) the MRI signal evolution of the hematoma can vary at different field intensities.
Different physicians may have different opinions on whether CT or MRI should be used for intracerebral hemorrhage. It is generally believed that the MRI presentation of hematomas is complex and the early presentation of hemorrhage is atypical, so CT examination may be preferred for cases with a clinical diagnosis of acute intracerebral hemorrhage. For subacute or chronic hematomas, MRI examination is more sensitive than CT, and the judgment of the cause of hemorrhage is better than CT, and MRI can be preferred.
All of the above results are complicated, and we are all extremely confused, so it is simple to summarize them, see roughly as follows.
Within 7 days of hemorrhage: T1WI: equal signal T2WI: slightly low signal
Bleeding 1 to 4 weeks: T1WI, T2WI: both high signal
After 1 month of hemorrhage: T1WI: low signal T2WI: high signal in the center and low signal in the periphery
Within one week of hemorrhage, MRI is less accurate than CT.