Radiographic signs of intracerebral hemorrhage

Cerebral haemorrhage

Radiographic signs

(1) CT performance

1.
Acute phase (including hyperacute phase and acute phase)

(1) Typical performance: high-density foci in the brain that are round, circular linear or irregular, with CT values between 50~80Hu
.
Hematomas can break into the ventricles or subarachnoid space, and break into the ventricles to form a ventricular cast.

Perifocial edema is mild, and hematoma may have a mass effect
.
In the acute phase, there is generally no need for enhancement, and even if enhancement is performed, the lesion is not strengthened
.

(2) Atypical manifestations: hematoma is of equal density, which is seen in patients with coagulation abnormalities, platelet insufficiency, decreased hemoglobin, excessive fibrinolytic reaction, hemolytic reaction, blood clot non-contraction, hemorrhagic diathesis, etc.
; the presence of fluid levels in blood clots (erythrocyte deposition sign), mainly due to coagulation abnormalities; The density of hematomas is generally reduced and seen in fluid level, which is seen in patients on thrombolytic therapy; Perifocal edema is very pronounced and can be seen in patients with
hemorrhage after cerebral infarction.

2.
Subacute stage: the density of hematoma gradually decreases and is of equal density
.
The following signs may be present:

(1) Signs of ice melting: the hematoma is absorbed around the periphery, and the center is still a high-density area
.

(2) The mass effect and perifocial edema are gradually reduced
.

(3) Some patients have hydrocephalus
.

(4) Enhanced scanning, the lesion shows annular or fusiform strengthening, such as the central part of the bleeding is not absorbed, can be "target"
.

3.
Chronic stage: the lesion is round, round-like or fissured with low density
.

(2) MR performance

MRI has unique advantages in showing bleeding, determining the timing and cause of bleeding, and MRI signals can reflect the evolution of
oxyhemoglobin (ob→), deoxyhemoglobin (DHB), methemoglob→in (MHB), methemoglobin (MHB), → hemosiderin.

Changes in sequence signals such as MR T1 and T2 are closely related to iron metabolism;

The paramagnetic effect of iron is related to the oxygenation state of hemoglobin and the integrity of red blood cell membranes;

1.
Hyperacute stage: In the initial stage, the hematoma content is similar to blood and is a protein solution
.
When imaging with medium and high magnetic field machine, it is an equal signal on T1; When imaging with a low magnetic field machine, it may be a high signal in T1, which may be related
to the fact that the low magnetic field machine is more sensitive to the action of proteins.
Because oxyhemoglobin has an antimagnetic effect, resulting in a shortening of T2, the hematoma appears equisignal, uneven, or hyperintense
on T2.
Perifocal edema may occur 3 hours after bleeding, and the mass effect is mild, unless the hematoma is large
.

2.
Acute phase: red blood cell membrane integrity, deoxyhemoglobin caused by local magnetic field unevenness, due to magnetic sensitivity effect accelerates proton out of phase, can significantly shorten the T2 value, but the effect on T1 value is small, hematoma on T1 slightly lower or equal signal, on T2 low signal
.
Vasogenic edema appears around the foci, and the mass effect is obvious
.

3.
Subacute phase

(1) Subacute early stage: methemoglobin in red blood cells causes T1 and T2 to be shortened, the center of the hematoma is still equi-signaled on T1, and the peripheral is hyperintensive, and the hypersignal gradually expands to the center; Low signal
on proton-weighted and T2.

(2) Subacute late stage: hematoma hemolysis appears, methemoglobin is deposited outside the cell, T1 is shortened, and T2 is prolonged
.
Hematoma in

Both T1 and T2 showed high intensity, perifocial edema, and the mass effect gradually decreased
.

4.
Chronic phase

(1) Early chronic stage: hematomas are highly intensed
in both T1 and T2.
Hemosiderin rings around the lesion cause T2 to be shortened, equisignaling on T1 and low on
T2.
Edema and mass effect disappear.

(2) Late chronic stage: typical cases form cyst-like T1 low signal, T2 high signal foci, but low signal hemosiderin rings
can still be seen around.

In conclusion, MRI findings are closely
related to the age of the hematoma.

Guide

The specific causes of intracranial hemorrhage are diverse, and neuroimaging plays an important role
in the diagnosis and treatment.
This article lists typical imaging data for common causes of intracranial hemorrhage to help you better understand intracranial hemorrhage
.
Without further ado, let's look at the picture
together.

Traumatic intracranial hemorrhage

Traumatic subarachnoid hemorrhage

Figure 1

Epidural hematoma Figure 2

Subdural hematoma Figure 3

In order to see the lesion clearly, some adjustments
were made to the window width of the CT.
Compared with the subdural window (Figures C, D), lesions are less pronounced
on the standard brain window (Figures A, B).
Hemorrhagic contusion of the right anterior temporal lobe and subarachnoid hemorrhage covering the sulci (triangular arrow) are seen, and arcuate subdural hematoma foci (long tail arrow)
are seen under the bony plate.

Figure 4

In this case, a brain herniation
was caused by a large subdural hematoma.
Non-contrast CT shows a large subdural hematoma on the left (long tail arrow), loss of compression on the basal cistern (Figure A, triangular arrow), infrasickle herniation of the brain (Figure B, C, triangular arrow), and left cerebellar notch hernia (Figure C, dotted arrow).

Hemorrhagic parenchymal contusion

Figure 5

This figure shows the evolution of hemorrhagic parenchymal contusion over time
.
Figure A~C shows the examination performed when receiving the patient, and Figure D~F shows the review after 2 hours
.
Multiple small hemorrhages
may be seen in the left orbitofrontal lobe and left anterior temporal lobe.
In subsequent imaging, bleeding from contusion expanded
.

Brain microhemorrhage Figure 6

This patient underwent CT and MRI to evaluate for hemorrhagic parenchymal contusion
.
The GRE (panel B) and SWI (panel C) sequences on MRI show hemorrhagic contusions (long-tailed arrows) more pronounced
than non-contrast CT (panel A).
In addition, GRE and SWI sequences can show cerebral microhemorrhages (triangular arrows)
in the white matter of the brain.

Parenchymal hemorrhage caused by hypertension

Figure 7

This hypertensive patient with cerebral hemorrhage has typical "punctate signs"
.

Figure A: Non-contrast CT shows massive intracerebral hemorrhage (long tail arrow)
in the right basal ganglia region.

Figure B: The arterial phase of CTA scan shows punctate high-density opacities (long tail arrows), known as "punctate signs"
.
According to the definition of "punctate signs", punctate strengthening is a high-density foci
where the edges of the hematoma are not connected to the blood vessels.

Figure C: CTA scan delay period shows a high-density shadow (long tail arrow)
in the same location as Figure B in active bleeding foci.

Parenchymal hemorrhage caused by cerebral amyloid angiopathy

Figure 8

In this case, non-contrast CT scan (Figure A), MRI GRE (Figure B), and SWI (Figure C) sequences show in-brain bleeding (long tail arrow)
in the right temporal and occipital lobes.
This bleeding typically manifests itself as lobar hemorrhage, which is not limited to the area supplying the arteries
.
This patient was eventually diagnosed with cerebral amyloid angiopathy
.

Figure 9

This figure shows a sequence of MRI examinations in two patients with cerebral amyloid angiopathy
.

Figures A and B: In the FLAIR sequence of the MRI of this patient, the entire white matter region of the brain showed a diffuse hypersignal abnormality, that is, a microangiopathy secondary to amyloid-β peptide deposition in the arterial wall (Figure A, long-tail arrow).

In addition, cortical hemorrhages (Figure B, long tail arrows) and microbleed foci (Figure B, triangular arrows) show abnormally low signals
.

Fig.
C and D: In the imaging examination of the second patient, the white matter abnormality is not as significant as the previous case (Fig.
C, long-tail arrow), but there are still several microbleed foci (Fig.
D, triangular arrow).

Intracranial aneurysm Figure 12

Patients have a ruptured aneurysm of the anterior communicating artery, leading to subarachnoid hemorrhage
.

Figure A: Non-contrast CT showing extensive high-density opacities in the basal cistern, confirming the diagnosis
of subarachnoid hemorrhage.

Figure B: CTA showing a cystic aneurysm (long tail arrow)
at the anterior communicating artery complex.

Figure C: After 3D reconstruction, the aneurysm of the anterior communicating artery is clearly visible (long tail arrow).

Cerebrovascular malformations

Figure 13

In this case, imaging in a pediatric patient with intraparenchymal hemorrhage
due to rupture of cerebellar arteriovenous malformation.

Fig.
A: Non-contrast CT scan shows high-density opacities in the right frontal lobe, suggesting intraparenchymal hemorrhage (long tail arrow).

Figure B: MIP image of CTA showing vascular tangles (long tail arrows)
visible along the anterior edge of the bleeding foci.

Figure C: DSA examination confirms the presence of an arteriovenous malformation (long tail arrow) and shows a small early draining cortical vein shadow (triangular arrow).

Dural-arteriovenous fistula

Figure 14

This example is an intraparenchymal hemorrhage
secondary to a dural arteriovenous fistula rupture.

Fig.
A: Non-contrast CT scan shows high-density opacities in the right temporal lobe, suggesting intracerebral parenchymal hemorrhage (long tail arrow).

Figure B: CTA shows that the edge of the bleeding area is covered with a cortical vein (long tail arrow).

Fig.
C: After injection of contrast from the right external carotid artery, the contrast of the right sphenoid parietal sinus is not clear in the arterial phase (long tail arrow
.

Figure D: DSA delayed period with further retrograde filling
of the right sphenopatopial sinus (long tail arrow) and cortical vein (triangular arrow) contrast agent.
This cortical vein corresponds to the vein shown on the
CTA.
Figure 15

In women with hypercoagulable states, intracerebral parenchymal hemorrhage is secondary to superior sagittal sinus thrombosis
.

Non-contrast CT scan showed multiple foci of intraparenchymal hemorrhage (Fig.
A), and MRI (Fig.
B~D) further showed low-signal hemorrhage foci of the brain parenchyma, and the lesion was accompanied by peripheral high-intensity edema
.
In Figures C and D, the filling defect (triangular arrow) in the superior sagittal sinus is thrombosis, the cause of
intracranial hemorrhage in the patient.
A filling defect extending into the right anterior cortical vein is also seen in Figure D
.

Vasculitis or vascular lesions

Figure 16

In middle-aged women, the main symptom is headache, which is later confirmed to be subarachnoid hemorrhage
secondary to cerebral arterial vasculitis.

Figure A: FLAIR imaging by MRI shows abnormally high signal (long tail arrow)
within the right margin sulcus.

Figure B: The GRE sequence further confirms the abnormally low signal in the sulci as subarachnoid hemorrhage (long tail arrow).

Figures C and D: DSA show small bead-like changes in the M4 segment of the right middle cerebral artery (long tail arrow) and distal right anterior cerebral artery (not shown), consistent with
vasculitis.

Fungal aneurysm

Figure 17

In this case, subarachnoid hemorrhage
secondary to rupture of a fungal aneurysm of the right middle cerebral artery.

Fig.
A~C: The FLAIR sequence and GRE sequence of MRI confirmed subarachnoid hemorrhage (Fig.
A, B), and the enhanced scan showed a circular strengthening area of the left anterior central sulcus along the blood vessel, that is, a fungal aneurysm
.

Fig.
D~F: DSA shows a lobulated fungal aneurysm
located in the left anterior central artery.
This fungal aneurysm shows best
in a lateral magnification view.