Stroke

Stroke is among the important causes of mortality and morbidity in modern societies. Stroke is the 3rd most common cause of death in the USA after cardiovascular deaths and all cancers. When all cancers are not considered as a single disease, but separately, stroke ranks second. The morbidity due to stroke is around 75% on average, and it causes significant losses in the society and in the life of the individual.

Since death in brain cells is irreversible, it is not possible to reanimate neurons after death with current treatments. The aim of treatment can be summarized as preventing the death of new neurons and reducing complications.

Another important aspect in stroke is to remember that prevention is more effective and cheaper than treatment. Preventable risk factors for stroke are hypertension, smoking and atherosclerosis. Early treatment of hypercholesterolemia-causing factors and timely intervention to existing atheroma plaques should be strategic goals.

The aim of treatment in stroke is not to restore dead neurons, but to prevent new neuron death and to keep stroke complications under control.

If we classify stroke events according to the cause, 80%
1.Ischemic (Atherosclerotic or embolic)
2.Hemorrhagic
3. Hypoxic
4.Hyperfusion
We can evaluate it as 5.ve Venous.

The purposes of imaging in stroke can be divided into primary imaging and secondary imaging.

Purpose of primary imaging
1. Evaluate my parenchyma.
To detect the presence and absence of infarct.
In case of infarct
Calculate the size of the infarct area in cm3 or ml.
To identify which regions in the brain anatomy the infarct affects
To determine which vascular structures the infarct coincides with the irrigation area.
To detect the presence and absence of bleeding
To rule out other lesion types that may be the cause of the acute neurological picture.
2. Evaluate stenosis and obstruction in vascular structures
Extracranial vascular structures
Intracranial vascular structures
3. Evaluation of perfusion.
4. To evaluate the presence of penumbra.

Purpose of follow-up or secondary imaging
1. Monitoring the development of the primary disease
Monitoring whether the infarct area is enlarged
Monitoring for new embolisms and infarcts
2. Monitoring the complications of the primary disease
Edema and herniation
hemorrhagic transformation
3. Monitoring response to treatment
4. To follow up treatment complications.

We can evaluate ischemic strokes according to the vascular areas involved.

1.MCA
2.ACA
3.PCA
4. Vertebrobasilar
5.Unilateral ICA
6. Lentriculostriate
7. Lacunar
8.Global
9.Watershed

The imaging modalities that can be used in stroke can be summarized as MR, CT and Doppler.

Non-contrast CT sensitivity in ischemic stroke is around 16%. This figure rises to 50% in strokes involving large areas. The specificity of CT is around 96%.

The sensitivity of general MR sequences in ischemic stroke is around 83%. MR specificity has been reported as 98%.

The sensitivity of diffusion + ADC sequences, which is the gold standard in ischemic stroke, is between 90-100%, and the specificity is between 90-100%. Diffusion + ADC is also the first positive imaging modality.

In hemorrhagic stroke, CT sensitivity and specificity are 90% and 100%, MR sensitivity and specificity are 80% and 100%.

Perfusion examination on CT can be performed on a limited number of sections. It is easier to apply compared to MR and more difficult to interpret because of the low SNR. Perfusion examination in MR can be performed on a wider area, it is more difficult to apply and easier to interpret.

Doppler is not a method that can be used to visualize the intracranial area, but can only be used to evaluate the proximal ICA. It can be used to rule out ICA pathologies when CT and MR are not available.

Computed Tomography

Despite its low sensitivity, CT is still used in the initial evaluation of stroke cases in many centers because it is accessible and inexpensive. CT takes a short time and can be used to rule out bleeding.

At <3 hours, 2-20% of occluded vascular structure “bright vein” finding can be observed on CT. In order to distinguish the occluded segment from an atherosclerotic vascular structure, it is necessary to examine the bone window and see if the lesion is symmetrical.

CT at < 3 hours can be used to detect cervical and intracranial vascular structures with interrupted angiocirculation.

If a suspicious area is considered at < 3 hours, CT perfusion examination may be considered in this area.

in 3-6 hours
Hyperdense artery sign persists. In addition:
Flattening (deletion) of sulci
Disappearance of white matter gray matter contour
Deletion of the lentiform nucleus
Disappearance of the insular strip

The results can be followed.

in 8-24 hours

The infarct area begins to appear hypodense.

1-7 days (Peak 2-4 days)

Mass effect and herniation can be observed.

The mass effect decreases in 2-3 weeks.
In 2-3 weeks, 80% of infarcts begin to enhance contrast. The reason for this is the absence of the blood brain barrier in newly formed vascular structures.

1-3 months

Encephalomalastic changes begin to appear. These
Hypodense sometimes cavitation areas in CSF density
cortical atrophy and
They may appear as exvacuo dilatation in adjacent ventricles due to negative mass effect.

For the evaluation of penumbra in CT, the difference between the mean transit time (MTT) and cerebral blood volume (CBV) can be calculated during contrast medium passage.

MR examination in stroke.

Diffusion and ADC map, cervical and cranial MRA, T2*GRE and perfusion studies should be used in addition to general sequences in MRI examination in stroke.

Diffusion +ADC provides information specific to ischemic stroke. Provides information about cervical and cranial MRA vascular patency. T2*GRE helps to rule out bleeding. Perfusion evaluation is used to determine the hypoperfused area and to calculate the penumbra.

Diffusion + ADC

Unlike somatic cells, brain cells do not have energy and oxygen stores. Therefore, they are heavily dependent on the supply of nutrients and O2.

ATP in the cell is depleted shortly after the blood flow is cut off. The Na+/K+ pump in the cell wall does not work. As a result, the extracellular fluid enters the cell. This phenomenon is called cytotoxic edema.

With two gradient pulses placed on either side of the 180o pulse in MR, protons whose positions have changed with diffusion movement during this period can be detected. The passage of significant amount of fluid from the extracellular space to the intracellular space leads to restriction of diffusion. Since more signals are obtained in the diffusion sequence from the displaced protons, the cytotoxic edema area leads to a brighter appearance on diffusion images.

It is known that diffusion images are affected by T2 value and some other parameters. This is called T2 shine through. ADC map is prepared to eliminate the effect of T2 and other parameters. In areas where diffusion is really restricted, ADC images are displayed in dark. When diffusion and ADC are evaluated together, the highest sensitivity and specificity values ​​are obtained in radiology. 90-100% and 90-100%.

The diffusion increase and ADC effect begin within the first 5 minutes and continue until the fifth day. From the 5th day, membrane destruction begins in the cells, so the restriction on fluid diffusion is lifted. This process is called pseudonormalization or pseudoeversal. With pseudonormalization, diffusion images return normally within 1-4 weeks.

The findings in T1 in MRI are similar to the findings in CT.

In the first 3 hours, the appearance of signal void may disappear in the affected main vascular structures.

after 2-3 hours

Flattening in sulci,
Blurring of white matter-grey matter boundaries.
Disappearance of the insular strip
Absence of the lentiform nucleus

after 18-24 hours

Hypointense areas should be expected in T1.

on T2 and FLAIR

Absence of flow-void in clogged arteries is an early finding.

The signal in the tissue begins to increase in 2-3 hours. Signal increase within 24 hours is observed in 100% of patients. Signal intensity reaches its maximum in 2-4 days.

Contrast retention, mass effect, and negative mass effect periods due to encephalomalacia, which occur with the development of infarct in MRI, are similar to CT.

T2*GRE

It is applied to view the bleeding area. Bleeding area is monitored in bright appearance.

Flow-void vascular structures can be observed as low or high signal areas.

SWI is another sequence that can show bleeding.

MRI Angio

It is performed to examine the patency of vascular structures. Examination is done separately for ICA and vertebrobasilar system and intracranial vascular structures.

While diffusion sequences show us the areas where irreversible neuroal death occurs, they do not provide information about the tissues that contribute to the symptoms or not due to hypoperfusion. To reach this information, sequences that give information about perfusion are needed. The most common method for this is to examine the paramagnetic effect created during the passage of the contrast agent with bolus-tracking. Many separate parameters such as CBV, MTT, initial peak, maximum peak can be evaluated from the contrast transition. The sensitivity of the mean transition time and the FX rate are high. The sensitivity of the CBV parameter is low and the YN rate is high.

Comparison of DWI and PWI domains can show 4 patterns.

DWI < PWI = Penumbra
DWI = PWI = no penumbra
DWI > PWI = Reperfusion occurs
DWI (-), PWI (+) = Ischemia, infarct (-)

Permeability:

One of the factors leading to reperfusion bleeding is thought to be increased vascular permeability.

Some other risk factors are:

1. The size of the original (Core) infarct area
2.HT
3. Former foci of microbleeding shown on SWI
4.Coagulopathy

In contrast, there is no contrast staining in these areas since there is no contrast transition to the irrigation area of ​​the occluded vessel. Observation of the staining pattern in contrast-enhanced examination 2 hours after reperfusion is provided is considered as a risk factor for vascular damage and reperfusion bleeding.

Xanthine metabolism is thought to play a role in reperfusion injury. A significant portion of ATP may have been converted to Xanthine 60 minutes after cytotoxic edema. In the case of reperfusion, after O2 is supplied, Xanthin Oxidase oxidizes Xanthine, while oxidant metabolites such as Peroxynitrite and Nitric Oxide, which can cause oxidative damage, are formed as a by-product.

Therapeutic hypothermia is applied to many stroke patients to reduce reperfusion injury. In this process, the body core temperature is reduced by 32o with different methods.

Another method claimed to reduce reperfusion injury is to use the tissue plasminogen activator called Desmoteplase obtained from vampire bat saliva (Desmodus rotundus) during thrombolysis. Although desmoteplase is claimed to be less neurotoxic than alteplase, phase3 trials have not been completed.

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