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    Home > Active Ingredient News > Study of Nervous System > MRI performance of cerebral hematoma (detailed illustration)

    MRI performance of cerebral hematoma (detailed illustration)

    • Last Update: 2022-10-25
    • Source: Internet
    • Author: User
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    The pathological evolution of hematoma after cerebral hemorrhage is: erythrocyte suspension - hemoconcentration - blood clot formation and contraction - erythrolysis - low-protein hematoma
    .
    The evolution of hemoglobin in hematoma is: oxygenated hemoglobin (HBO2)-deoxyhemoglobin (DHB)-methemoglobin (MHB)-hemosiderin (H-S), which may overlap.

    According to the pathology of cerebral hematoma and the change of hemoglobin, the MR signal of cerebral hematoma is:

    1.
    In the hyperacute phase (< 24 hours), the hematoma is mainly composed of HBO2 in intact red blood cells, which can be divided into three stages on MR:

    (1) In stage I (0-3 hours), the hematoma showed low signal on T1-weighted image and high signal
    on T2-weighted image.

    (2) In stage II (3-12 hours), the hematoma showed a slightly higher signal on the T1-weighted image and a high signal on the T2-weighted image; Mild cerebral edema
    develops.

    (3) In stage III (6-24 hours), the hematoma can be equal signal on T1 and T2 weighted images, and moderate cerebral edema
    appears at this time.

    2.
    In the acute phase (2-7 days), HBO2 in the hematoma gradually evolves
    to DHB.

    (1) In stage I (2-3 days), HBO2 in intact red blood cells has evolved into DHB
    .
    The hematoma is equal or slightly less intense on the T1-weighted image and typically low-signal on the T2-weighted image, with severe cerebral edema
    .

    (2) Stage II (3-4 days), hematoma except DHB, has been converted into intracellular MBH, showing typical high intensity on T1-weighted images and typical lowest black signals on T2-weighted images, with severe cerebral edema
    in this stage.

    (3) Stage III (5-7 days), this stage is characterized by the beginning of lysis of red blood cells, the hematoma is still typically high on the T1-weighted image, and the low signal is still on the T2-weighted image, (but not as black as stage II.
    ), and the cerebral edema is reduced to moderate.

    3.
    Subacute phase (8-30 days).

    (1) In stage I (8-15 days), the hematoma is already surrounded by free diluted MHB, and the central part is still unevolved DHB, which is most characteristic in the T1-weighted image
    .
    Surrounded by a high-signal thick ring, with DHB low-signal in the center, a slightly low-signal thick ring around the T2-weighted image, and a lower-signal DHB in the center, cerebral edema changes from moderate to mild
    .

    (2) In stage II (16-30 days), DHB in the center of the hematoma was gradually replaced by free diluted MHB, and the high signal was gradually completed in all imaging sequences, with T1-weighted image being the most obvious, T2-weighted image evolution becoming slower, hemosiderin black lines visible around the hematoma, and cerebral edema from mild to disappear
    .

    4.
    Chronic phase (1-2 months).

    The hematoma, consisting of free diluted MHB surrounded by hemosiderin and a deposition ring, and a high-signal hematoma surrounded by a black low-signal ring, is the MR feature of chronic intracerebral hematomas, most clearly
    developed on T2-weighted images.

    5.
    Residual cavity (late February to several years after bleeding).

    (1) Stage I pointed out that from the end of February to the end of April after blood, the hematoma was mainly composed of low protein cystic fluid with cyst change and liquefaction, and MR showed long T1 and T2 signals
    unique to liquid.
    Low signal near cerebrospinal fluid on T1-weighted images and near cerebrospinal fluid on T2-weighted images
    .

    (2) Phase II pointed out that 5 to 1 year after blood, the water in the cyst fluid was absorbed, leaving only the free diluted MHB, which showed a cord-like high signal in all imaging sequences, and the hemosiderin deposited around the narrow residual cavity was low in
    all imaging sequences.

    (3) Stage III pointed out that more than one year after blood, MHB almost completely disappeared, high-signal MHB in the center of the residual cavity disappeared, and only hemosiderin low signal remained, which showed low signal
    on T2-weighted images.

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