MRI findings of common cerebrovascular disease

1.

Cause: atherosclerosis

Embolism (arterial thrombosis, cardiogenic embolus shedding, fat droplets, amniotic fluid)

vasculitis

Venous thrombosis

Classification: ischemia, hemorrhagic, lacuncture

Pathology: cytotoxic edema

Angiogenic edema

Necrosis of brain tissue (softening of the infarction foci and possible glial hyperplasia in the periphery)

The site of onset is consistent with the arterial vascular distribution area

Cerebral artery blood supply map:

Mastering the distribution area of arterial blood supply is conducive to distinguishing

Watershed infarction:

Watershed infarction is an infarction in the arterial junction area, which is mainly divided into cortical and subcortical types

Imaging findings of cerebral infarction:

by stages

Hyperacute phase (<6h): CT and MRI test are negative, DWI shows a significant high signal (cytotoxic edema, reduction of extracellular space, limited spread of water molecule movement);

Acute phase (6-72h): CT showed low-density area, MRI showed long T1 long T2 abnormal signal, DWI showed a significantly high signal;

Subacute phase (72h-10d): CT manifestations simultaneously involve triangular or wedge-shaped low-density areas of gray and white matter, MRI can be accompanied by bleeding, DWI shows obvious high signal, significant mass effect, and point-like enhancement of enhanced scanning;

Chronic phase (>11d): brain softening, brain atrophy;

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

T1WI and T2WI showed no obvious abnormalities, T2-Flair showed a slightly elevated signal in the right basal ganglion, a slightly elevated signal in the DWI corresponding region, and a slightly lower ADC signal, indicating that the diffusion was limited and there was no obvious general pathological change, so it was consistent with the imaging changes

Weakness of the right limb for 9 hours (acute stage of cerebral infarction)

The DWI basal ganglion region can see a significant high signal, corresponding to the ADC phase showing a low signal, T2WI has shown a high signal change, and there is a mild mass effect, adjacent lateral ventricles have mild compression, so it is consistent with acute stage cerebral infarction image changes

In addition, the right side of the corpus callosum pressure can also see an abnormal signal, T2 phase shows the central high signal, similar to the cerebrospinal fluid signal, the edge is slightly higher signal, DWI shows the center low signal, the edge slightly high signal, then the edge high signal is really diffuse limited, but combined with the ADC phase, there is no corresponding low signal change, which is the glial 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 T2 phases, patchy and plaque-like abnormalities can be seen with slightly elevated signals, narrowing of adjacent brain sulcus, swelling of the brain gyrus, T1 showing a slightly lower signal, DWI showing patchy, plaque-like high signal, and the corresponding ADC value is reduced, which is consistent with the image changes

The subacute phase of cerebral infarction and the acute phase are often not easy to distinguish, and the general imaging report combines the two, because clinical thrombolytic therapy has a certain timeliness, if the patient's image changes are consistent with the hyperacute stage of infarction, it needs to be listed separately to provide corresponding treatment methods

In the same patient, enhanced scans were done, and abnormal reinforcement of the left occipital lobe and temporal lobes could be seen with gyrus or strips, as mentioned above, enhanced enhancement can occur in the subacute stage of cerebral infarction; This scattered strip of regurgitation, on the other hand, is different from neoplastic lesions, which tend to have substantial masses

Chronic phase of cerebral infarction

This is a patient in the chronic phase of cerebral infarction, the left basal ganglion has formed an infarction softening foci, the adjacent sulcus widens, atrophic changes in the brain parenchyma, left side ventricular traction, slightly enlarged, T2 significantly high signal, T1 significantly low signal, DWI is significantly unlimited

Hemorrhagic cerebral infarction

In T2W1, the right temporal occipital lobe can be seen with a flaky slightly elevated signal, corresponding brain parenchymal swelling, narrowing of the brain sulcus, DWI is significantly diffuse restricted, T1WI is mainly slightly low signal, and its internal visible patch or slightly elevated signal along the brain gyrus indicates that there is a small amount of red blood cell exudation, consistent with the image changes

Layered necrosis of the cortex

This is also a patient after cerebral infarction, the right temporal occipital lobe T2WI sees a large patch of slightly elevated signal, no significant narrowing of the brain sulcus, no obvious gyrus swelling, indicating that there is no obvious mass effect, the corresponding DWI is not restricted, the ADC value is elevated, indicating that the lesion time is long, and the brain tissue swelling has subsided

T1 shows multiple lines, slightly elevated signals of the cerebral gyrus, which differs from hemorrhagic cerebral infarction in that it does not occur during acute infarction and is located in the cortex, not at the center of the

Watershed infarction

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

Cerebral infarction colloidal hyperplasia

Ovoid abnormal signals are visible next to the right side ventricles, T2WI is significantly high signal, consistent with cerebrospinal fluid signals, T1WI low signal, DWI is not restricted, edges are annular high signals, ADC values are not low, suggesting softening foci formation and marginal gliosis

T2 transmittance effect

T2WI in the right basal ganglion region can see a softening foci similar to cerebrospinal fluid signal, T1WI shows a low signal, and the glioproliferative change of slightly higher signal can be seen at the edge, and DWI shows a significantly high signal, corresponding to the ADC value is not low, indicating that the DWI high signal is not really diffusion restricted, but caused by

Percheron arterial infarction

Pathogenesis: caused by occlusion of a main artery (Percheron artery) emitted from the P1 segment of the posterior cerebral artery on one side, which branches supply the bilateral thalamus;

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

Typical clinical manifestations: confusion, vertical gaze paralysis, memory deficit triad;

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

Schematic of the Percheron artery

Bilateral thalamic symmetry diffusion is limited, the midbrain "V" sign, Percheron arterial infarction, although rare, is not difficult
to diagnose with typical clinical and typical imaging findings.

Venous cerebral infarction

MR manifestations are associated with secondary cerebral parenchymal changes due to intradural sinus thrombosis and venous return obstruction; Brain parenchymal changes include edema (usually angiogenic edema), hemorrhagic foci; The site of bleeding is often located at the junction of gray and white matter in the brain; DWI behaves differently; Inconsistent
with arterial vascular distribution.

Distribution of cerebral venous drainage

The drainage area of the red part of the cortical vein, mainly frontal, frontal, cortical, and subcortical, will eventually flow into the superior sagittal sinus; The yellow part is mainly in the frontotemporal junction area and the temporal occipital junction area, and eventually leads into the cavernous sinus; The green part is the Labbe venous drainage area, mainly in the temporal-occipital region, which leads into the transverse sinus; The deep white matter and gray matter areas of the blue part of the brain are the internal venous drainage areas of the brain, which eventually flow into the galen venous line
.

Venous cerebral infarction

The left temporal occipital lobe is significantly swollen, and a large patch of abnormal signals can be seen, T2WI is a high signal, T1WI is a slightly low signal, and a slightly elevated signal shadow of the strip is visible inside, suggesting that there is concomitant bleeding, as mentioned above, in the subacute stage of arterial cerebral infarction, there can also be concomitant cerebral hemorrhage, but DWI should be significantly diffused and limited, 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 shadow disappeared, showing a high signal, combined with MRV can be seen left internal jugular vein, transverse sinus, sigmoid sinus is not developed, the diagnosis of venous sinus thrombosis with venous cerebral infarction
.

Arterial versus venous cerebral infarction

2.
Hemorrhagic stroke

Etiology: hypertension, aneurysms, vascular malformations, brain tumors;

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

Pathological stage: acute phase (within 1 week)

Absorption period (2nd week to 2nd month)

Cystic transformation phase (February >)

Image staging: Schematic diagram of changes in each stage of MRI bleeding

Chronic phase -- hematoma shrinkage + peripheral edema disappearance + perifocal hemosiderin deposition

Long T1, Long T2, liquid signal + black ring

Subarachnoid hemorrhage

Intracranial blood vessels rupture and blood enters the subarachnoid space

Causes: aneurysm rupture is the most common, hypertension, vascular malformations, trauma, etc.
;

Male, 70 years old, unconscious for 1h

High-density hemorrhagic foci can be seen in the anterior longitudinal fissure, bilateral lateral fissure, bilateral ventricle and triventricular ventricles, and the amount of bleeding is large;

In the same patient, T2WI can see the anterior longitudinal fissure slightly elevated signal shadow, T1WI and other signals, similar to the white matter signal, DWI is also an equal signal, consistent with the acute phase of cerebral hemorrhage imaging changes; Note that a nodular or sac-like abnormally low signal shadow can be seen in the red box of T2WI, which is close to the vascular flow air shadow, combined with the patient's CT to show a large number of subarachnoid spaces, considering the rupture and bleeding of the anterior traffic aneurysm;

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

Arteriovenous malformations (AVMs)

AVM consists of deformed vascular masses of direct communication between cerebral arteries and veins and structural disorders between the two;

Usually onset between the ages of 20 and 40;

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

The incidence of AVM complicated by cerebral hemorrhage is 40 to 78%;

Typical imaging findings: blood supply artery, central tumor nest, coarse drainage vein;

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

An abnormal signal cluster can be seen in the right frontal lobe, the center is dominated by low signal, and the edge can be seen with a high-signal edema band, note that the posterior edge of the lesion can see the roundabout vascular flow air shadow performance; In combination with MRA, the right right cerebral artery extends to the lesion and is closely related to the lesion (indicated by the red arrow), in combination with MRV, a vein extends from the visible lesion area and drains to the superior sagittal sinus (indicated by the blue arrow); It has typical imaging findings of blood supply arteries, tumor nests, drainage veins, and AVMs
.

Cavernous hemangioma

Characteristics of the lesion: spongy abnormal blood vessel mass composed of many thin-walled blood vessels, sporadic type, hereditary type;

5% to 16% of all vascular malformations;

It occurs more often in 20 to 50 years old, and is more common in women;

64% to 80% occur on the cerebellar operis, mainly under the cortex;

20% to 36% occur under the cerebellar operis, and the brainstem and cerebellar worms are more common;

Pathological manifestations: a large number of irregular reticular spaces, a single layer of vascular walls, lack of muscle layer and elastic layer, thrombosis inside, no brain tissue in between;

Repeated bleeding, calcification, hemosiderin deposition, and gradual increase in lesions;

Clinical manifestations: asymptomatic, bleeding, epilepsy

Image features:

CT 30% to 50% do not show, can show < 3cm equal density nodules, common calcification;

MRI popcorn-like, mulberry-like mass, mixed central signal, peripheral low signal ring, common fluid level of bleeding in the subacute phase, small lesions with spotted low signal, no reinforcement or mild reinforcement of the enhanced scan;

Female, 29 years old (cavernous hemangioma, supra)

An abnormal nodular shadow is visible in the left frontal lobe, and the center of the T2WI lesion has a mixed signal of high and low, the marginal low signal ring (hemosiderin deposition), the T1WI signal is slightly low, and the DWI signal is low

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

The lesion is in the left cerebellum, and the characteristics of the rest of the image are basically the same as above

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

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

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

Intermittent onset of symptoms over 2 years

The CT is shown in the following figure

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

The left ventricular triangle is enlarged, there is a mass lesion, T2WI shows mixed high and low signals, the margins are slightly visible with low signals, the boundaries of the adjacent ventricular walls and brain parenchymes are relatively clear, and there is a certain amount of compression edema in the adjacent brain parenchymes;

T1WI shows that the lesion boundary is clear, with a slightly lower signal predominantly, and a slightly higher signal (bleeding foci) can be seen internally;

The DWI is a mixed signal of high and low

Contrast scan lesions showed significantly uneven reinforcement, and no significant abnormal enhancement was seen near the brain parenchyma

T2WI signals are mixed, bleeding repeatedly, occur in the lateral ventricular triangle, where cavernous hemangiomas are less common and need to be distinguished from
other tumors (eg, ependymoma, meningioma, choroid plexus papilloma, etc.
).

Final pathological diagnosis: lateral ventricular cavernous hemangioma

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