Acute stroke

We will discuss the following topics:

The purpose of imaging tests in patients with acute stroke is to:

In this way, we can select those patients
who are likely to receive thrombolysis.

Early signs of CT cerebral ischemia

60% of infarct foci can be displayed by CT within 3~6 hours, and almost all of them are visible
within 24 hours.

In the early stage of cerebral ischemia, cytotoxic edema
due to the failure of ion pumps.

Brain water content increased by 1%, and CT attenuation decreased by 2.
5Hu
.

Figure below The density of brain tissue decreases, and the realm of gray and white matter is blurred
.

CT low density is highly specific for irreversible ischemic brain injury if it is detected
within the first 6 hours.

Patients who developed stroke symptoms and developed a low density of CT within the first 6 hours were shown to have a larger infarct volume, more severe symptoms, a more unfavorable clinical course, and even a higher risk of
bleeding.

So whenever you see a low density of stroke patients, it means bad news
.

The absence of low density on CT is a good sign
.

The bean nucleus is vague and is an important sign of
infarction.

It is seen in middle cerebral artery infarction and is one of the
earliest and most common signs.

Island belt sign

Refers to the low density and swelling
of the insula.

This is a very indicative and occult early CT sign of middle cerebral artery infarction
.

This area is very sensitive to ischemia because it is the region furthest from collateral blood flow
.

MCA dense sign

This is the result of a clot or emboli in
MCA.
Figure below MCA dense sign, CTA can be seen MCA occlusion
.

Hemorrhagic infarction

15% of MCA infarctions are initially hemorrhagic
.

Bleeding is most easily detected by CT, but gradient echo MR sequences or SWI are also sensitive
.

CTA and CT perfusion

Start by looking at the image below, and then try to detect anomalies
.

The situation is very delicate, with some low density
in the right insula.

It is suggestive of infarction, but sometimes it may be leukoencephalopathy in elderly patients, and it is very difficult to
identify.

The following figure shows CTA to identify the right MCA embolization
.

CT perfusion
diffuses by CT and MR, and we can diagnose infarction, but we cannot rule out large ischemic semi-dark zones (tissues at risk).


Through perfusion studies, we are told which area is at risk
.

About 26% of patients require perfusion studies to get a correct diagnosis
.

With a good team, CT, CTP, and CTA can complete the examination in 15 minutes and subsequently provide comprehensive diagnostic information
.

In the figure below, non-contrast CT scan excludes bleeding and CTP is performed, showing perfusion defects
.

This was followed by a CTA and observation
of the left internal carotid artery.

MRI imaging

PD/T2WI and FLAIR infarcts are hyperintensive, but they may be negative
within 2 to 4 hours of onset.

The figure below T2WI and FLAIR shows hyperintensity
in the middle cerebral artery supply area.

Note the involvement
of the legiform nucleus and insula.

DWI is the most sensitive sequence
for stroke imaging.

DWI is sensitive
to Brownian motion limits of extracellular water caused by cytotoxic edema.

Under normal circumstances, water hydrons have the ability
to spread outside the cell.

The high signal on DWI shows that the ability of water hydrons to diffuse outside the cell is limited
.

Start by looking at the image below, and then try to detect anomalies
.

Signs are subtle, with the left frontal region less dense, swollen and absent
sulci compared to the contralateral side.

Now continue with the DWI image of this patient, the infarction is clear
.

When we compare the results of T2WI and DWI in time, we will notice the following:

This happens between
10-15 days for DWI camouflage
.

The cases in the figure below show normal DWI
.

On T2WI, there may be some subtle hyper-intensity
in the right occipital lobe in the vascular area of the posterior cerebral artery.

T1WI after Gd manifests as gyrus enhancement, suggesting infarction
.

It is thought that everything that is bright on DWI is necrotic tissue
.

However, there are now some studies that suggest that some of these may be potentially reversible damage
.

If the DWI images in the acute phase are compared with the T2WI images in the chronic phase, it is found that the affected brain volume in the DWI is larger than the final infarct area
.

MR perfusion is comparable
to perfusion CT.

Areas of abnormal perfusion may be dead tissue or tissue
at risk.

Combining diffusion and perfusion images helps us define tissues at risk, the ischemic semi-dark zone
.

In the image below, we first have a diffusion image that represents an irreversible area of change (necrotic tissue).


There is a large area of low perfusion in
the middle.

Diffusion-perfusion mismatches are indicated in blue, which is at-risk but not completely necrotic tissue that may be salvaged
with treatment.

The picture below shows a patient
with sudden onset of neurological symptoms.
MR is
performed 1 hour after the onset of symptoms.

T2 was not abnormal, although on DWI there was a large area of limited
spread in the right MCA supply area.

Note the involvement of the
basal ganglia area.

There is a perfectly matched perfusion image, so this patient should not receive any form of thrombolytic therapy
.

Shown below is another MCA infarction
.
It has a low density on CT, and the DWI matches perfusion and is not suitable for thrombolysis
.

Another example in the figure below shows the DWI and ADC plots
.

Now we can see that there is a serious mismatch
.

Almost the entire left cerebral hemisphere is at risk due to hypoperfusion
.

This patient is an ideal candidate for
treatment.

Provincial medical case, 38 years old, sudden neurological symptoms, emergency CT and CTA/P, left frontal parietal temporal lobe saw patchy hypoperfusion area, MTT, TTP, Tmax increased in a large area, CBF decreased in a large range, CBV small pieces were slightly reduced, and there was a mismatch
in the abnormal perfusion area at the corresponding level.
Consider cerebral infarction (stage III).

Subsequently, thrombectomy is involved