Central nervous system disorders

V./3.2.: Radiological aspects of ischemic cerebral infarcts

V./3.2.1.: Introduction

The goal of early diagnosis is to exclude the bleeding, which can be detected safely using CT. Differentiation of ischemic and haemorrhagic ictus is important, because their therapies differ basically. If we excluded the bleeding, the neurologist expert starts the thrombolysis based on the acute neurological deficit and after the deliberation of the patient’s status. Thrombolysis might be - regarding its technique - general or local, which can be performed by the radiologist.

V./3.2.2.: Temporal radiological change of ischemic lesions

(N.B: The classification of acute-chronic ischemic infarct is varying according to different „schools”.)

V./3.2.2.1.: Hyperacute phase (in 12 hours)

CT image might be normal in 50-60% of cases. Hperdens artery sign (so-called Gács-sign) occurs in 25-50% of the cases, which means the hyperdensity of intraluminal thrombus in the artery compared to the streaming blood. Intraarterial hyperdensity most often occurs in the main branch of the middle cerebral artery (M1, M2 part of MCA), sometimes in smaller branches as well, also in case of basilar artery thrombosis. Blurring of lentiform nucleus might be an early sign of MCA-territorial lesions.

Contrast enhanced CT performed in hyperacute phase might have a differential diagnostical value in the differentiation of tumor and abscess. Contrast medium gets out into the extracellular space as a sign of blood-brain barrier (BBB) damage, but it is not visible, because the amount of contrast medium is not enough for visualization due to the the low, reduced regional cerebral bloodflow (rCBF – see it below too!). CT angiography (CTA, CT-angio) demonstrates the whole perfusion blood volume of the brain with „single slab” quantitative CT-perfusion technique. On the level of the clinically suspected territory (cerebral bloodflow [CBF – see it below too!] and mean transit time), these CT techniques evoke MR imaging, and do not cause any time delay, respectively.

The vascular occlusion related filling defect can be visualized on CTA images well, perfusion measurement is also possible by this time, which indicates the territory of hypoperfusion obviously.

Extent of the infarct can be diagnosed early by the detection of the restricted diffusion using diffusion weighted MR technique (DWI – diffusion weighed imaging). The ordinary spin echo T1 and T2 sequences cannot detect the infarct in the early phase, only if it became defined only, as the sign of irreversible damage. Diffuse calcification of arterial walls and high hematocrit levels, which increase the density of streaming blood in the vessels significantly, may cause difficulties in the early diagnosis on CT.

V./3.2.2.2.: Acute phase – between 12-24 hours

In case of middle cerebral artery occlusion basal ganglia become hypodense, border of cortex-medulla gets blurry in the insula, and the sulci narrow. Using MR DWI technique, high signal appears very early in the diffusion restricted areas, even when other imaging modalities do not detect these areas (due to the cytotoxic edema). If our goal is to detect the functionally endangered, but yet structurally intact areas around the surely later necrotising center, we can assess it with comparison of perfusion technique (PWI – demonstrates reduced blood perfusion/-flow; mismatch, tissue at risk). Its assessment is often performed using CT with fusion of CT and MR images (N.B.: people think that this assessment is fusty nowadays).

V./3.2.2.3.: Subacute phase – between days #1-3

The mass effect increases, which can be perceived well if the infarct has a large extension: sulci will be compressed, cortex-medulla border gets blurry, hypodensity develops mainly in the white matter. At this time hemorrhagic transformation may occur in the grey matter (cortex, basal ganglia). Important to note that it is not generated by the antithrombotic therapy, because hemorrhagic transformation can occur without it. MR is more sensitive to detect the even small hemorrhages (petechial bleeding) than CT, since this test is rarely performed in this case, frequency of their occurance is unknown, but it seems that their prevalences increase. Supposedly the reperfusion, which develops from the necrotised cerebral tissue, might be in the background.

V./3.2.2.4. Subacute phase – between days #4-7

Edema and mass effect persists several days later, hypodensity darkens, peripheral enhancement is well recognisable on CT following contrast administration. Important to know this phenomenon because it might cause differential diagnostical difficulties in case of contrast enhanced scans after an ischemic infarct (even incidentally). However, marginal girland-like enhancement may occur for appr. 6-8 weeks after the ictus, due to the penetration of blood-brain barrier, which is fed by luxury perfusion.

V./3.2.2.5.: Subacute phase – on weeks #1-8.

Contrast enhancement persists henceforward, mass effect is still obtained which slowly starts to decrease. (Transient) calcification may occur in children. The contrast enhancement lasts for 2-5 weeks in subacute phase (88-93%). Its causes: capillary proliferation (luxury perfusion) + BBB damage, collateral circulation, which takes until the termination of gliosis. It can be better seen in cortex than in the medulla. Attention! Contrast enhancement is able to alter the ischemic area to an isodense area, thus unenhanced scans are necessary as well!

Flow void (on unenhanced and contrast enhanced scans) is visible in the referred vessel on MR scan at earliest, and vessel enhancement is apparent, respectively (due to slow flow); this phenomenon may arise in minutes and last for weeks. Cerebral swelling (narrowing of the sulci) is visible already in 2 hours because of the intracellular (cytotoxic) edema on T1 weighted images. Signal intensity (SI) may increase on T2 scans in 2-4 hours, but it will be surely positive only 24 hours later.

Extracellular (vasogenic) edema indicates decreased signal intensity on T1 scans. Meningeal enhancement may occur 1-3 days later.

Predictive value of the enhancement:

• - if it is early (<3 days) and its extension exceeds the extent of high signal intensity on T2 scans, and there is a minimal or reversible neurological deficit which usually resolves in 1-2 days;

• - if it is late (1-2 weeks) and the extension of high signal intensity area on T2 scans has equal extension than the enhancement or exceeds that, fixated neurologic deficit, infarct is expected. However, these are only very weak diagnostical MR signs in contrast to the very strong evidence based DWI, in which the signal intensity is high because of the restricted diffusion.

V./3.2.2.6.: Chronic phase (months, years)

Hypodensity decreases increasingly (CT), reaching the hypodensity of the liquor. The enhancement ceases, the lesion demarcates sharply and cystic encephalomalacia gets formed on its place which leads to a volume reduction of the cerebral parenchyma (calcification may occur in peripheral areas). The unilateral ventricle dilates „onto it”. In this case, MR scan demonstrates the sign of free fluid (T2 high signal) such as on DW images on which the sign looks like that in a cyst, because the diffusion is not restricted.

V./3.2.3.: Diffusion MR imaging in stroke

If Brown-movement of molecules is unhampered (water, liquor), their diffusion is fast, SI decreases in the affected area. Diffusion is restricted in directed, transversal directions in the cerebral tissue, viz. the vertical orientation of fibres and the limiting effect of membranes sets a limit to this phenomenon. Cytotoxic edema (intracellular edema, cell expansion, narrowing of interstitium) causes also restricted diffusion also in the infarct, thus SI increases in the infarcerated area. Later, the diffusion increases with the formation of vasogenic edema, reaching the level of normal cerebral tissue. Moreover, diffusional moving possibilities of fluids increase again in this type of edema. Encephalomalacia (cystic encephalomalacia): after the development of the chronic infarct, diffusion becomes almost such free as in the liquor.

Differential diagnostics of the age of infarct with diffusion technique:

• - acute phase – high SI (restricted diffusion);

• - subacute phase – moderate SI, isointense, maybe slightly decreased,

• - chronic phase – weak or almost disappeared signal (free diffusion).

Following clarification of circumstances and collecting relevant diagnostic informations, immediate agressive therapy is needed to protect the damageable cerebral areas and for reperfundation as well.

V./3.2.4.: Perfusion MR/CT studies

This study detects the transit of intravenously administered bolus in the cerebral tissue. There is no perfusion in the centre of the infarct, and decreased perfusion is visible in the ischemic penumbra. The ischemic penumbra can be defined by the comparison of perfusion and diffusion images. If the extension of both of these images does not match, this state is a „mismatch”. With this method the possibility of resulution might be predicted.