Detailed explanation of cerebrovascular blood supply distribution and MRI manifestations of common cerebrovascular diseases

First, the cerebral artery blood supply area

The ICA supply area :P posterior inferior cerebellar artery (PICA, blue) is located in the posterior occipital part of the cerebellar and is in balance with the anterior inferior cerebellar artery (AICA) supply area (purple) located on the side
.
The larger the PICA supply area, the smaller the AICA supply area, and vice versa
.

Supracerebellar artery (SCA, gray): The SCA supply area is located on the surface of the supracerebellar and cerebellar enchantery
.

Vertebral and basilar artery branches: These branches supply the medulla oblongata (light blue) and pons (green).

Anterior choroidal artery (AchA, blue): AChA The blood supply area includes part of the hippocampus, the hindlimb of the internal capsule, and extends upward to the lateral region
of the central part of the lateral ventricle.

Lsoriae artery (LSA): lateral LSA (orange) is a deep perforated artery of the middle cerebral artery (MCA), supplying most of the basal ganglia; Medial LSA (dark red) originates from the anterior cerebral artery, usually segment A1.

The Heubner artery is the largest medial bean-striae artery that supplies the anteromedial caudate nucleus and the anterior inferior part of the
internal capsule.

Anterior cerebral artery (ACA, red): ACA supplies the medial surface of the frontal and parietal lobes, the corpus callosum, the basal ganglia, and the anterior part of the
internal capsule.

Middle cerebral artery (MCA, yellow): The cortical branches of the middle cerebral artery supply the sides of the hemisphere, except for the medial prefrontal and parietal lobes (anterior cerebral artery) and the lower temporal lobe (posterior cerebral artery).

The posterior cerebral artery (PCA, green) extends :P 1 segment from the beginning of the PCA to the posterior communicating artery, forming the Willis ring
.
The thalamic perforation artery originates at the P1 segment and supplies blood
to the midbrain and thalamus.
The cortical branches of PCA supply the temporal lobe, the medial and lower sides of the occipital lobe, the visual cortex, and the pressure of
the corpus callosum.

Second, the basal ganglia blood supply area

Detailed distribution of vascular supply in the basal ganglia

Red: medial bean artery; Yellow: lateral bean artery; Blue: anterior choroidal artery; Green: Posterior cerebral perforator artery (P1 segment)

Third, the posterior inferior cerebellar artery blood supply area

CT on the left shows that the low-density area of the left cerebellum is the area of infarction of the left posterior inferior cerebellar artery (PICA), caused by vertebral artery dissection (blue arrow).

Unilateral PICA supply infarction with a medial boundary at the midline is clear and sharp because the superior vermicular branch is sagittal and does not cross the midline
.
In the late infarction, the boundaries are blurred
.

In the early stages, edema can cross the midline, making diagnosis difficult
.
Infarctions at the pontine level are usually paramedian with well-defined boundaries because the branching sagittal position of the basal ganglia is out of shape rather than crossing the midline
.
Bilateral infarctions are rarely observed because survival time is too short in these patients, but small bilateral infarctions are sometimes seen
.

4.
Superior cerebellar artery blood supply area

Cerebellar infarction in the SCA supply area and brainstem infarction in the PCA supply area, note that the midline is also clearly bounded

5.
Anterior cerebral artery blood supply area

Anterior cerebral artery (ACA):

Segment A1: from the beginning to the anterior communicating artery, the medial bean artery (the caudate nucleus head and the lower part of the forelimb of the internal capsule) is emitted;

Segment A2: bifurcation from anterior communicating artery to pericallosum and marginal artery;

Segment A3: major branches (medial frontal lobe, superior medial parietal lobe, anterior corpus callosum).

6.
Anterior choroidal artery supply area

Anterior choroidal artery (AChA) infarction:

The anterior choroidal artery generally originates in the internal carotid artery, but can also originate from the posterior communicating artery and the terminal bifurcation of the internal carotid artery and the beginning segment of the middle cerebral artery
.
It provides blood supply to the hindlimbs of the internal capsule, globus pallidus, caudate nucleus caudal, lateral part of the geniculate body, optic tract, parahippocampal gyrus, amygdala, hippocampus, etc.
, and rarely involves the entire area in AChA infarction, and the hindlimbs of the internal capsule also receive blood supply
from the lateral bean striated artery.
The main features of its anatomy are that the stroke is relatively long, the lumen is relatively thin, and the blockage
of blood vessels is easy to occur due to the lack of collateral circulation.
If there is an anterior choroidal artery blockage, vascular dissection, aneurysm, it can cause clinical symptoms
such as contralateral hemiplegia, contralateral hemisensory impairment, hemianopia, temporal lobe epilepsy.

7.
Middle cerebral artery blood supply area

MCA infarction, lateral bean artery area also affected (orange arrow)

MCA includes cortical and deep perforators (lateral leguette arteries).

8.
Bean-striae arterial blood supply area

1.
Medial bean artery

It is a branch
of the A1 segment of the anterior cerebral artery.

Supply the anterior lower part of the basal nucleus
.

It also supplies the internal capsule forelimb together with the Huebner recurrent artery, which is also a branch of
the anterior cerebral artery.

2.
Lateral bean artery

It is a branch
of the M1 segment at the level of the middle cerebral artery.

Supply of the caudate nucleus head and caudate nucleus, as well as most of
the globus pallidus and putamen.

It is also involved in the supply of the forelimb and hindlimb parts of the inner capsule

CT and T2W gradient echo images: hemorrhagic infarction confined to the lateral legume artery

Infarction in the left MCA supply area with extensive gyrus intensification (hyperperfusion), which may sometimes be confused with tumor enhancement

9.
Posterior cerebral artery blood supply area

Left occipital visual cortex infarction

infarction in the left PCA supply area, note the absence of the gray/white matter demarcation in the left occipital lobe region

Deep or proximal embolism of PCA causes ischemia in the thalamus and/or midbrain and cortex;

Superficial or distal embolism of PCA affects only cortical structures;

Only about 5% of ischemic strokes involve PCA or its branches
.

10.
Abnormalities in cerebral artery blood supply area

Selective arterial spin labeling allows visualization of perfusion zones of each artery, which plays an important role in certain cerebrovascular diseases such as acute stroke, aortic occlusion disease and arteriovenous malformations, and can provide valuable hemodynamic information
.

Left and right internal carotid artery and vertebrobasilar perfusion area

Left lacunar infarction with normal cerebral perfusion

Patients with left-sided watershed infarction, left frontal cortical infarction (arrowhead), note that the left frontal lobe is supplied by the right internal carotid artery, and there is a variation in cerebral perfusion

For multiple cerebral infarction, note that the left occipital lobe infarction (arrow) is also in the perfusion area of the left internal carotid artery, and the vertebral artery is not involved in the blood supply

11.
Watershed infarction area

Celebral watershed infarction refers to infarction caused by localized ischemia in the adjacent 2 or 3 cerebral artery supply areas or basal ganglia deep through the arterial blood supply, and its incidence accounts for 10%
of ischemic cerebrovascular disease 。 Traditionally, watershed cerebral infarction is mainly divided into cortical watershed infarction (CWI) and internal watershed infarction (IWI),
while both cortical and subcortical watershed infarction are mixed.

The cortical type can be divided into precortical type (AWI) and posterior cortical type (PWI).

The former is an infarction between ACA and MCA, and the latter is an infarction between MCA and PCA
.

Subcortical watershed infarction (IWI) is an infarct of the marginal zone between the deep and superficial perforating arteries of the brain, which can be divided into: partial IWI (P-IWI, single or beaded infarct in the center of the semi-oval) and continuous IWI (C-IWI, that is, the transventricle band infarction).

Clinical features:

Compared with focal cerebral infarction, patients with watershed cerebral infarction generally have a history of transient ischemic attack (TIA), and IWI has a higher proportion of middle cerebral artery or internal carotid artery stenosis or occlusion, which is more likely to manifest as rose-shaped infarction, and CWI patients are more likely to have small cortical infarction
.
The clinical manifestations of watershed cerebral infarction depend on the location and extent of
the infarction.

(1) The clinical manifestations of the precortical type are central hemiplegia and hemisensory impairment dominated by the upper limbs, which may be accompanied by frontal lobe symptoms, and the dominant hemisphere involvement is manifested as cortical motor aphasia
.

(2) The retrocortical type is most common with hemianopia, and there may be cortical sensory impairment, hemiparesis, etc.
, transcortical sensory aphasia when the dominant hemisphere is involved, and body image disorder
in the non-dominant hemisphere.

(3) The subcortical type can involve the basal nucleus, internal capsule and lateral ventricular body, mainly hemiplegia and hemisensory impairment
.

(4) The cerebellar type is mostly manifested as mild ataxia and consciousness impairment
.

(This part is from: Dinghu Images, author: Fu Xiu)

12.
Lacunar cerebral infarction

Lacunar infarcts are small infarcts
deep in the brain (basal ganglia, thalamus, white matter) and brainstem.
Lacunar infarction is caused
by occlusion of a single deep perforated artery.
Accounts for 25%
of ischemic strokes.
Atherosclerosis is the most common cause of lacunar infarction, followed by emboli.

25% of patients with clinically and radiographically diagnosed lacunar infarction are likely to be cardiogenic
.

PRES is short for
reversible posterior encephalopathy syndrome.
It is also known as reversible posterior leukoencephalopathy (RPLS) and has many causes of PRES, including high blood pressure, eclampsia and pre-eclampsia, immunosuppressive drugs such as cyclosporine, etc
.
This mechanism is not fully understood, but is thought to be associated with hyperperfusion states, disruption of the blood-brain barrier, and possible spillage of fluid containing large molecules, leading to cortical or subcortical oedema
.

Typical imaging findings of PRES are high-intensity FLAIR in the parietal-occipital cortex and subcortical white matter and can occur anywhere in the whole brain, but relatively infrequently the brainstem, basal ganglia, and cerebellum are affected
.

The figure above shows that the back of the brain and basal ganglia are involved;

After 4 days in this patient, most of the abnormal signals disappeared

13.
Cerebral vein drainage area

The distribution of cerebral venous drainage is slightly more variable than the distribution of arterial blood supply, and the above figure is a rough drainage map

cortical veins (red) merge into the superior sagittal sinus; The sphenoidal sinus (yellow) joins the cavernous sinus; Internal cerebral vein (blue); Labbe vein (green)

Cerebral vein thrombosis is caused by occlusion of the sinuses and/or cortical veins, usually resulting in complete occlusion further by partial thrombosis
or external compression.
Dehydration, pregnancy, hypercoagulable states, and adjacent infections (eg, mastoiditis) are predisposing factors
.
Cerebral vein thrombosis has no specific manifestations, is difficult to diagnose, and often presents as a hemorrhagic infarction in the atypical arterial supply area
.
Imaging tests play an important role
in its diagnosis.

The left transverse sinus is not shown on MRV images, possibly due to developmental abnormalities or occlusion; However, the left transverse sinus is clearly visible on the T1WI image, so the transverse sinus of the MRV image is not visible due to
occlusion.

In the same patient as above, the left transverse sinus is clearly visible on T1WI image (blue arrow), CT shows high-density thrombosis in the left transverse sinus (yellow arrow), and FLAIR shows left temporal lobe venous infarction

Deep cerebral vein thrombosis presents clinically with severe diencephalic dysfunction such as coma, eye movements, and pupillary reflex disorders, and usually has a poor
prognosis.
Mild symptoms with reduced levels of unconsciousness or brainstem symptoms may be misdiagnosed
.
Deep vein thrombosis should be suspected in young women with lesions located in bilateral basal
ganglia or thalamus.

Patients with cerebral deep vein thrombosis, bilateral basal ganglia infarction

In the same patient as above, the intracerebral vein, straight sinus, and right transverse sinus flow empty signal disappeared (blue arrow); Absent right transverse sinus signal of MRV (yellow arrow)

14.
MRI manifestations of common cerebrovascular diseases

1.
Ischemic stroke

Etiology: atherosclerosis

Embolism (arterial thrombosis, cardioembolus shedding, fat droplets, amniotic fluid)

vasculitis

Venous thrombosis

Classification: ischaemic , hemorrhagic, lacunar

Pathological: cytotoxic edema

Angiogenic edema

Necrosis of brain tissue (softening of infarct foci, glial hyperplasia may occur peripherally)

The site of onset corresponds to the arterial vascular distribution

Cerebral artery blood supply distribution map:

Mastering the distribution area of arterial blood supply is conducive to distinguishing
cerebral infarction from inflammatory lesions, demyelinating lesions in the brain, and neoplastic lesions.

Watershed infarction:

Watershed infarction is infarction in the arterial junction area, which is mainly divided into cortical type and subcortical type
.
The cortical type mainly occurs in the frontal lobe and occipital parietal lobe, and is mostly triangular, wedge-shaped or fan-shaped, with the tip pointing to the lateral ventricle; The subcortical type is infarct in the area where the deep perforating artery meets the artery of the cerebral cortex, and is mostly manifested as band-like and beaded changes
.

Imaging findings of cerebral infarction:

by stages

Hyperacute phase (<6h): negative CT and MRI examination, DWI showed obvious hyperintensity (cytotoxic edema, reduction of extracellular space, limited movement and diffusion of water molecules);

Acute phase (6~72h): CT showed low density area, MRI showed long T1 and long T2 abnormal signals, DWI showed obvious high signal;

Subacute stage (72h~10d): CT shows triangular or wedge-shaped low-density areas involving gray and white matter at the same time, MRI can be accompanied by bleeding, DWI is obviously high intensity, the mass effect is significant, and the enhanced scanning can be seen in dot-like strengthening;

Chronic phase (>11d): encephalomalacia, cerebral atrophy;

Episodic left limb weakness for 3 hours (hyperacute phase of cerebral infarction)

T1WI and T2WI showed no obvious abnormalities, T2-Flair showed slightly higher signal in the right basal ganglia area, slightly higher signal in the corresponding area of DWI, and slightly lower signal in ADC, indicating that diffusion was limited, and there was no obvious gross pathological change, so it was consistent with imaging changes
in cerebral infarction in the hyperacute stage.

Right limb weakness for 9 hours (acute phase of cerebral infarction)

DWI basal ganglia area can see obvious high signal, corresponding ADC phase presents low signal, T2WI has shown high signal changes, and there is a mild mass effect, adjacent lateral ventricles have mild compression, so in line with acute stage cerebral infarction imaging changes
.

In addition, an abnormal signal can also be seen in the pressure of the right corpus callosum, the T2 phase shows the center high signal, similar to the cerebrospinal fluid signal, the edge is slightly higher signal, DWI shows the center low signal, the edge is slightly higher signal, then whether the edge high signal is really diffusion limited, but combined with the ADC phase, there is no corresponding low signal change, which is the colloidal hyperplasia
formed at the edge after the formation of the brain softening foci.

Subacute phase of cerebral infarction

In the left occipital lobe and temporal lobe T2 phase, patchy and plaque-like abnormalities can be seen slightly higher signal, adjacent sulci narrowing, brain gyrus swelling, T1 is slightly lower signal, DWI is patchy and plaque-like high intensity, and the corresponding ADC value decreases, which is consistent with the imaging changes
of cerebral infarction in the subacute stage.

The subacute phase of cerebral infarction is often not easy to distinguish between the acute phase, and the general imaging report combines the two, because clinical thrombolytic therapy has a certain timeliness, if the patient's image changes are in line with the hyperacute phase infarction, it needs to be listed separately, and the patients who meet the conditions for thrombolysis need to provide corresponding treatment methods
in time.

The same patient, with enhanced scanning, showed abnormal enhancement of the left occipital lobe and temporal lobe in the gyrus or strips, as mentioned above, in the subacute stage of cerebral infarction, enhancement and enhancement can appear; This scattered strip enhancement along the brain gyrus is different from neoplastic lesions, which often have parenchymal masses
.

Chronic phase of cerebral infarction

This is a patient with a chronic stage of cerebral infarction, the left basal ganglia area has formed infarct softening foci, adjacent to the cerebral sulci widening, brain parenchyma atrophic changes, left lateral ventricular traction, slightly enlarged, T2 is obviously high-intensive, T1 is obviously low-signal, DWI is obviously not limited
.
At the same time, the patient's image can see that the left side of the brain foot is smaller than the opposite side, which is consistent with the changes
in Waller's degeneration.

Hemorrhagic cerebral infarction

In T2W1, it can be seen that the right temporal occipital lobe is slightly higher in the form of sheets, the corresponding brain parenchyma is swollen, the sulci is narrowed, the DWI is obviously diffuse limited, T1WI is mainly slightly lower signal, and the dotted or slightly higher signal along the brain gyrus can be seen inside, indicating a small amount of red blood cell exudation, consistent with the image changes
of hemorrhagic cerebral infarction.
It appears within 1 week of the onset of acute cerebral infarction, or when collateral vessels are established in 1~2 weeks
.

Cortical necrosis

This is also a patient after cerebral infarction, the right temporal occipital lobe T2WI sees a large sheet slightly higher signal, no obvious narrowing of the sulci, no obvious gyrus swelling, indicating that there is no obvious mass effect, the corresponding DWI is not limited, the ADC value is increased, indicating that the lesion time is longer, and the swelling of brain tissue has subsided
.

T1 shows multiple linear, gyrus-like slightly higher signals in the cortex, which is different from hemorrhagic cerebral infarction, and the time does not occur in the acute infarction stage, and the site is in the cortex, not in the center of the
lesion.
Cortical layered necrosis occurs 2 weeks after infarction, especially in 1~2 months, and rarely can last up to 1 and a half years, T2WI is equal and low intensity, and there is no hemosiderin deposition-like signal change
.
It is mainly involved in gray matter, because gray matter is sensitive to hypoxia and sugar deficiency, and is prone to neuronal damage
.
For patients with infarction and T1 hyperintensity changes, multiple sequence judgments need to be integrated to avoid missed diagnosis and misdiagnosis
.

Watershed infarction

The upper row of images is infarction at the junction of the anterior cerebral artery and the middle cerebral artery, and the lower row image is infarction in the junction area of the middle cerebral artery and the posterior cerebral artery.
Red arrows in the frontal lobes of the upper row of images indicate cortical infarction, triangular or wedge-shaped, with the tip pointing towards the lateral ventricle; A red box indicates a subcortical infarction with banded or beaded changes, and the vasocular flow of the right internal carotid artery disappears, suggesting vascular occlusion (indicated by a blue arrow).

Glial hyperplasia of cerebral infarction

Oval abnormal signals were visible next to the right ventricle, T2WI showed obvious high signal, consistent with cerebrospinal fluid signal, T1WI low signal, DWI was not limited, the edge was ring-shaped high signal, and the ADC value was not low, indicating the formation of softening foci and marginal glial hyperplasia
after cerebral infarction.

T2 permeability effect

T2WI in the right basal ganglia area can be seen softening foci similar to cerebrospinal fluid signal, T1WI is low signal, colloidal hyperplasia changes with slightly higher signal can be seen at its edges, and DWI is obviously high signal, corresponding to ADC value is not low, indicating that DWI high signal is not really limited in dispersion, but caused by
T2 transmission effect.

Percheron arterial infarction

Pathogenesis: caused by occlusion of an aortic artery (Percheron artery) from the P1 segment of one posterior cerebral artery, which branches to supply the bilateral thalamus;

Etiology: cerebral small vessel disease, heart disease, aortic disease, etc.
;

Typical clinical manifestations: triad of impaired consciousness, vertical fixation paralysis, memory deficit;

Imaging findings: bilateral thalamus, midbrain long T1 long T2 signal, midbrain "V" sign

Schematic diagram of Percheron arteries

Bilateral thalamic symmetric diffusion is limited, midbrain "V" sign, Percheron arterial infarction is rare, but through typical clinical manifestations and typical imaging findings, diagnosis is not difficult
.

Venous cerebral infarction

MR manifestations are associated with secondary brain parenchymal changes caused by intradural sinus thrombosis and obstruction of venous return; Cerebral parenchymal changes include edema (usually vasogenic edema), hemorrhagic foci; The site of bleeding is often located at the junction of the gray and white matter of the brain; DWI performance varies; Inconsistent
with arterial vascular distribution.

Cerebral venous drainage map

The drainage area of the red part of the cortical vein is mainly the frontal lobe, frontopatoparietal lobe, cortex, and subcortex, and will eventually drain into the superior sagittal sinus; The yellow part is dominated by the frontotemporal junction area and the tempooccipital junction area, and finally drains into the cavernous sinus; The green part is the Labbe vein drainage area, mainly the tempooccipital part, which is drained into the transverse sinus; The blue part of the deep white matter and gray matter area of the brain is the drainage area of the internal cerebral vein, and finally drains into the Galen vein system
.

Venous cerebral infarction

The left temporal occipital lobe is obviously swollen, a large patchy abnormal signal can be seen, T2WI is a high signal, T1WI is a slightly lower signal, and a strip of slightly higher signal shadow can be seen inside, indicating that there is hemorrhage, as mentioned above, in the subacute stage of arterial cerebral infarction can also be combined with cerebral hemorrhage, but DWI should be obviously limited diffusion, and the patient's DWI diffusion is not limited; Suggests not arterial infarction
.

In the same patient, the left transverse sinus and sigmoid sinus vascular flow void shadow disappeared, manifested as hyperintensity, combined with MRV showed that the left internal jugular vein, transverse sinus, and sigmoid sinus were not developed, and venous sinus thrombosis was diagnosed with venous cerebral infarction
.

Arterial versus venous cerebral infarction

2.
Hemorrhagic stroke

Etiology: hypertension, aneurysm, vascular malformation, brain tumor;

Common sites: internal capsule-basal ganglia, thalamus, followed by cerebellum, brainstem, subarachnoid space;

Pathological stage: acute phase (within 1 week)

Absorption period (2nd week ~ 2 months)

Cystic period (> February)

Imaging staging: schematic diagram of changes in each stage of MRI hemorrhage

Chronic phase -- hematoma shrinkage + loss of peripheral edema + perifocial hemosiderin deposition

Long T1, long T2, liquid signal + black ring

Subarachnoid hemorrhage

The intracranial blood vessels rupture and blood enters the subarachnoid space

Etiology: aneurysm rupture is the most common, hypertension, vascular malformation, trauma, etc.
;

Male, 70 years old, unconscious for 1h

High-density hemorrhage foci were seen in anterior longitudinal fissure, bilateral lateral fissure, bilateral ventricle and triventricle, and the amount of bleeding was large.

In the same patient, T2WI can see slightly higher signal shadow of anterior longitudinal fissure, T1WI and other signals, similar to white matter signal, DWI is also equivalent signals, consistent with imaging changes in the acute phase of cerebral hemorrhage; Pay attention to the observation that a nodular or capsular abnormally low signal shadow can be seen in the red box of T2WI, which is close to the vascular flow void shadow, combined with the patient's CT showing a large number of subarachnoid space, considering the rupture and bleeding of the anterior communication aneurysm;

In the same patient, with MRA, an aneurysm can be seen in the anterior communicating artery area;

Arteriovenous malformations (AVMs)

AVM is composed of malformed vascular masses that communicate directly between cerebral arteries and veins and structural disorders between the two;

Often onset at the age of 20~40;

The incidence of middle cerebral artery system is high, followed by the anterior cerebral artery, involving the cerebral cortex (50%);

AVM complicated by cerebral hemorrhage incidence incidence 40~78%;

Typical radiographic findings: supplying artery, central tumor nest, coarse drainage vein;

Male, 28 years old, sudden headache with body convulsions for 3 days

An abnormal signal cluster can be seen in the right frontal lobe, the center is dominated by low signal, and a high-intensity edema band can be seen at the edge, note that the posterior edge of the lesion can be seen tortuous vascular flow void shadow performance; In combination with MRA, it can be seen that the right middle cerebral artery extends towards the lesion, which is closely related to the lesion (indicated by the red arrow), and in combination with MRV, a vein can be seen extending from the lesion area and draining to the superior sagittal sinus (indicated by the blue arrow); Has the typical imaging findings
of supplying arteries, aneurysm nests, draining veins, and AVM.

Cavernous hemangioma

Lesion characteristics: cavernous abnormal vascular mass composed of many thin-walled blood vessels, sporadic and genetic;

Accounting for 5%~16% of all vascular malformations;

Mostly occurs in 20~50 years old, more common in women;

64%~80% occur in the cerebellar enchantrum, mainly under the cortex;

20%~36% occur under the cerebellar curtain, and the brainstem and cerebellar vermis are more common;

Pathological manifestations: a large number of irregular reticular space, a single layer of blood vessel wall, lack of muscle layer and elastic layer, thrombus inside, no brain tissue in between;

Recurrent bleeding, calcification, hemosiderin deposition, gradual increase of the lesion;

Clinical manifestations: asymptomatic, bleeding, epilepsy

Image features:

CT 30%~50% is not displayed, can be manifested as < 3cm isodensity nodules, common calcification;

MRI popcorn-like, mulberry-like mass, central signal mixing, peripheral low-signal ring, common fluid level of subacute bleeding, small lesions manifested as punctate hypointensity, no enhancement or mild enhancement on enhanced scanning;

Female, 29 years old (cavernous hemangioma, supratentorial hemangioma)

An abnormal nodular shadow was visible in the left frontal lobe, with a mixed signal of high and low in the center of the T2WI lesion, a low-signal ring at the edge (hemosiderin deposition), a slightly lower signal in T1WI, and a low signal in DWI

Male, 46 years old, dizziness for 1 week (cavernous hemangioma, subcurtain)

The lesion is in the left cerebellum, and the remaining imaging characteristics are basically the same as above

Female, 51 years old, intermittent headache and dizziness for 1 month (lateral ventricular cavernous hemangioma, rare)

The patient was hospitalized with a cerebral hemorrhage 2 years ago, and the CT at that time was shown below

A type of round high-density hemorrhage can be seen in the posterior corner of the left ventricle, with relatively clear boundaries, and symptomatic treatment is given according to cerebral hemorrhage;

Symptoms have been intermittent for 2 years

This CT is shown below

The high-density foci of the lateral ventricle are enlarged before, and there is low-density edema adjacent to the brain parenchyma, and the high and low density of the lesion center can be clearly seen at individual levels;

The left ventricular triangle is enlarged, there is a mass lesion, T2WI shows mixed signals, low signal is slightly visible at the edge, and the boundary between the adjacent ventricular wall and brain parenchyma is relatively clear, and there is a certain degree of compression edema adjacent brain parenchyma;

T1WI showed that the lesion boundary was clear, mainly slightly lower signal, and a little slightly higher signal (bleeding foci) was visible inside;

DWI is a mixed signal of high and low

The lesions on the enhanced scan showed obvious uneven enhancement, and there was no obvious abnormal enhancement in the adjacent brain parenchyma

T2WI signal is mixed, repeated bleeding, occurs in the lateral ventricular triangle, where cavernous hemangiomas are less common and need to be differentiated
from other tumors (such as: ependymoma, meningioma, choroid plexus papilloma, etc.
).

Final pathological diagnosis: lateral ventricular cavernous hemangioma