Ischemic stroke MRI and CT-diagnosis of ischemic stroke

Definition

Ischemic infarction (stroke) is an organic lesion of the Central nervous system caused by an acute violation of cerebral circulation with the development of ischemia of the nervous tissue and the appearance of a heart attack, accompanied by characteristic morphological manifestations on imaging (MRI and CT).

General characteristic

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Figure 1. Diffuse lesion area affecting white matter and cortex, disrupting differentiation, smoothing boundaries. On MRI, ischemic infarction has an increased MR signal for T2, Flair and decreased for T1 (Fig.1). The affected area may have a mass effect, expressed in extensive lesions. On CT, the stroke area has a reduced density relative to the unchanged brain matter (Fig.2), but larger than liquor (~ 25 to 10HU).

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Figure 2.

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Figure 3. In the left temporal lobe there is an area of cytotoxic edema having an increased MR signal on Flair, T2 and a zone of reduced density on CT in the right frontotemporal region (arrows).

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Figure 4. In the left temporal lobe on the IP DWI (diffusion-weighted image) there is a pronounced restriction of diffusion, which creates a picture of sharply increased MR-signal (a characteristic sign of ischemic stroke). On T1 from the specified area there is a slightly noticeable reduced MR signal and a more noticeable increased MR signal on T2 on the MRI in the coronal plane in the left parietal-temporal region.

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Figure 5. On the time-of-Flight ps (TOF = time-of-fly), there is a loss of the MR signal from the right internal carotid artery, due to the lack of blood flow due to thrombosis of this artery (arrows). There is a clearly differentiated reduced density on CT from the stroke area in the right temporal-parietal region in the brain window (arrow).

Phases of the process

  • peracute phase (first 6 hours),
  • acute phase (from 6 hours to 2 days),
  • subacute phase (from 3 days to 2 weeks),
  • chronic phase (outcome and long-term effects - over 2 weeks)

Peracute stage (first 6 hours)

The peracute stage is the time from the onset of symptoms to 6-8 hours.

On MRI in T2, Flair, T1 and normal CT scan changes may not be visible (normal anatomical picture). However, it is possible to observe the first signs on MRI in the form of a barely noticeable increase in the MR signal from the affected area on T2 and Flair. When using the pulse sequence (PS) DWI on MRI with a diffusion coefficient of b=1000, the area of ischemic lesion in the form of cytotoxic edema can be visible from 2.5 hours from the onset of symptoms. 4-5 hours from the clinical manifest of the disease on the DWI (diffusion-weighted image) should be identified confident signs of ischemic lesions, which constitute the so-called "core" of infarction and the area of "ischemic penumbra" (penumbra).

After 6 hours, the PS DWI should confidently give an answer about the presence of ischemic infarction or its absence, but in the case of continued hypotension or hypoglycemia, symptoms may not regress, and ischemia develop a day after the first manifestations. The semiotics of a stroke on conventional PS (T2, T1 and Flair) in the acute phase may be the absence of blood flow through the artery, which looks like an asymmetric MR signal from the main artery (eg, ACI or ACM), which is convincingly visualized using IP TOF (time-of-fly).

Contrast enhancement on MRI in the acute phase is not significant, but in the case of arterial thrombosis, the absence of contrast in the blocked artery is detected. The use of perfusion IP on MRI (including ADSL technology) can detect a decrease in indicators (rCBV, rCBF, MTT) in the area of the heart attack nucleus and some decrease in these indicators in its vicinity (in penumbrae).

In the acute phase there is a set of the first signs on CT:

  • decrease in differentiation of gray and white matter;
  • smoothness of contours of furrows and convolutions;
  • hyperdense thrombus in an artery (most often in ACI or ACM) can be revealed;
  • not sharply expressed asymmetry of brain structures in basal nuclei.

From 4-5 hours, there may be noticeable signs of a decrease in the density of the affected brain structures, especially noticeable when changing the viewport to binary (black and white) mode. With the use of a contrast agent in bolus infusion, depleted blood flow or occlusion of the cerebral artery caused by thrombosis can be detected (the contrast doesn’t go beyond the thrombus). Also, using contrast and perfusion scanning Protocol, it is possible to obtain data on hemodynamics (rCBV, rCBF, MTT), reflecting a decrease in brain matter with differentiation of the nucleus of infarction and penumbra.

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Figure 6. In the early stages of ischemic stroke, CT shows a violation of the distinct differentiation of basal nuclei structures, which isn’t a specific feature, but its sometimes observed (arrows). In this case, a hyperdensic thrombus in the cerebral artery (an area of increased density in the right middle cerebral artery - arrow) can be visualized.

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Figure 7. On MRI in the hyperacute period of ischemia, the usual pulse sequences may have indirect signs or not at all (to demonstrate a normal anatomical picture on T2 and Flair in the presence of symptoms), but on DWI after 3 hours there is an increase in the MP signal due to the restriction of diffusion caused by swelling of nerve cells (cytotoxic edema) and narrowing of intercellular spaces.

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Figure 8. In the early stages of ischemic stroke, in the absence of anatomical changes in the brain substance, blood flow disorders can be detected in the study of MR angiography (however, this is possible only with vessel obstruction - with atherothrombotic or cardioembolic type of infarction!) in the form of absence (or decrease) of the MR signal from the arterial blood current (arrow and dotted line). The maps of the apparent diffusion coefficient (ADC) show a decrease in the MR signal from the affected area into the superacute and acute phases of ischemic stroke (arrows).

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Figure 9. On ordinary SP MRI (T1 and T2), you can also see a blood flow disorder caused by a thrombus or embolus in a large cerebral artery in the form of an asymmetrically lowered (T1) or increased (T2) MR signal-which is characteristic of the lack of blood flow through this artery (in the presented case, this is the internal carotid artery on the left - arrows). So same on gradient echo (GRE, he same T2* or T2-hemo) or on PS SWI (or SWAN) can be to see sharply lowered MR-signal from thrombus in arteries of (arrow).

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Figure 10. On SP T1 has asymmetrically modified MR-signal from the right internal carotid artery (which is not differentialsa - arrow), in contrast to proivopolozhnoe ACI, where there is normal blood circulation in the form of a loss of MR signal (no typical increase in MR signal on T1 from a healthy artery, due to a parallel scanning with respect to the direction of blood flow). On T2 and Flair there is an increase in the MR signal from the thrombosed left internal carotid artery (arrow).

Acute stage (from 6 hours to 2 days)

In the acute phase, all morphological signs of ischemic stroke are revealed. In this phase, there is a death of nerve cells in the nucleus of the infarction and the ischemic penumbra. Thus, thrombolysis in this phase is no longer effective. With the development of cytotoxic edema on MRI, the stroke area looks like a diffuse zone, increased MP signal by T2, Flair and decreased by T1.

In the occluded artery, thrombosis can be detected confidently in the form of an increased MR signal from the vessel at T2, Flair and a reduced one at T1 and T2*. The DWI has a uniformly high MR signal from the affected area, as well as a decrease in the MR signal on the maps of the apparent diffusion coefficient (ADC). On CT in the acute phase, the entire area of the lesion is also well differentiated in the form of a site with the loss of differentiation of individual brain structures with a decrease in its density. Contrast in the acute phase doesn’t detect any pathological areas of contrast accumulation, except for the absence of contrast of the thrombosed vessel in the event that thrombosis persists, and in the case of clot lysis and blood flow recanalization – contrast symmetrically fills the previously affected vessel.

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Figure 11. On CT in the acute phase of ischemic stroke, there is a clearly differentiated hypodens zone affecting gray and white matter, leading to the absence of differences in individual anatomical structures of the brain (arrows). A blood clot in the artery (arrow) is also noticeable.

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Figure 12. On MRI in Flair (Tirm) and T2 modes, a zone of increased MR signal is noted in the area of the brain affected by ischemic stroke (arrows in Fig. 12). In addition, there is a maximum intensity of the MR signal at the DWI from the area of the stroke.

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Figure 13. Ischemic stroke in the left parietal lobe - increased MR signal according to Flair, T2 and DWI.

Subacute stage (3 days-2 weeks)

In the subacute phase is destroyed the blood-brain barrier (BBB) and the appearance of athenaro edema that leads to swelling of the area of ischemic infarction, can increase the mass effect in the case of extensive lesions can cause complications such as herniation of cingulate gyrus under falx (which will lead to compression of the ACA and may cause the expansion of the area of infarction), herniation of the cerebellar tonsils in the foramen Magnum (which can cause hydrocephalus with intracranial hypertension and depression centers of the medulla oblongata).

In large ischemic heart attacks, when there is a lesion of the entire hemisphere of the large brain or the entire cerebellum, palliative neurosurgery techniques can be effective – extensive bone resection trepanation with the removal of part of the bones of the skull vault, so that the developing vasogenic edema does not cause wedging and complications associated with increased intracranial pressure (ICP). The destruction of BBB leads to the accumulation of contrast agent in the area of ischemic stroke (contrast on the so-called "gyral type").

In the case of recanalization of blood flow through the cerebral arteries due to the destroyed BBB, areas of hemorrhagic impregnation and hemorrhage (the"red component" of ischemic infarction) may occur, which on MRI look like a reduced Mr signal on T2, T2*, Flair and increased on T1, and on CT in the form of reticular and focal changes of increased density. In the late periods of the subacute phase, there is a decrease in the MR signal on DWI, which in the case of primary (previously not conducted research) can create difficulties in interpretation (the phenomenon of "pseudonormalization of DWI"), but there is an increase in the MR signal on ADC.

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Figure 14. Sites of hemorrhagic impregnation may appear in the ischemic tissue, which occurs when a blood clot dissolves or the embolus is lysed and appears as fusiform or cloud-like areas of increased density in the ischemic zone on CT (arrows). Joining vasogenic edema can be observed, which leads to an increase in the affected area and can cause wedging (arrow). In the late period of the subacute phase, an attenuation of the MR signal to DWI or its complete regression is noted.

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Figure 15. On MRI, hemorrhagic impregnation is expressed in the appearance of a reduced MR signal, which is clearly detected on the GRE IP (T2 *, SWI, SWAN) - in the basal nuclei on the right. At the same time, at T1, hemorrhagic impregnation looks like a region of an increased MR signal (arrows). When contrasting in this phase, an accumulation of contrast is noted in the ischemically dead nervous tissue, mainly in the cortical region, according to the “chiral” type (arrows).

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Figure 16. Areas of encephalomalacia and emerging cystic-gliotic changes that have an increased MR signal at T2, Flair and retain a high MR signal at DWI from the periphery of these areas.

Chronic stage (more than 2 weeks)

In the chronic phase, reparative and proliferative changes occur, accompanied by regression of vasogenic edema, restoration of BBB (which is reflected in the reduction of contrast until the complete absence of contrast accumulation in the affected area). There is the development of encephalomalacia (softening and lysis of dead tissue), in place of which a liquor cyst is formed (in the case of small strokes or lacunar strokes) or extensive cystic-glious changes. There is a weakening of blood flow or complete thrombosis of the artery in the pool of which there was a heart attack.

With the defeat in semioval centre or with a lesion of the cortex may develop destruction of axonal neurons included pyramidal tract – degeneration Turk-Waller, which is evident in the form of elongated zones of gliosis that follows the course of the pyramidal tract. The high MR signal on DWI is completely regressed, although there may be traces of an increase in MR signal in areas of the brain bordering the zone of cystic-glious changes. The area of cystic-gliotic changes can have the opposite effect to the mass, that is, cause traction (displacement) of brain structures in its direction, which is manifested by the shift of unchanged brain areas (often the opposite side) beyond the midline and the expansion of the ventricular system cavities adjacent to the zone of encephalomalacia and gliosis (which is called ex-vacuo hydrocephalus).

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Figure 17. There is the formation of areas of encephalomalacia-areas of the brain with reduced density (white arrows), adjacent to the zones of cystic-glious changes (areas of complete lysis of brain tissue-yellow arrows). There is also a stretching of the walls of the lateral ventricles, due to the reduction of brain matter and glious tissue (arrows).

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Figure 18. Cystic-gliosis changes (areas of atrophy, lysis of brain tissue and development of reactive proliferative gliosis) in the area of previously deceased ischemic brain tissue having an Mr signal both from unchanged cerebrospinal fluid and an increased Mr signal by T2, Flair from gliosis tissue.

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Figure 19. Cystic-glious changes PS on Flair in sagittal plane. A long (almost lifelong) time in the ischemia area, traces of existing hemorrhages remain in the form of a hemosiderin residue (black arrow). Plot cystic glial transformation with dilation of the lateral ventricle in the surrounding region (black arrows).

Comparative characteristics of CT and MRI (phase of ischemic infarction)

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Figure 20. Comparative morphological characteristics of different phases of ischemic infarction on IP MRI and brain window on CT.

Recurrent Ischemic Stroke

The presence of ischemic stroke in 2-4 times increases the risk of a new stroke in the next six months. Ischemia may occur near a previously existing ischemia zone (in the same vascular basin is a typical feature of atherothrombotic infarcts) or in another area (which is typical for strokes against the background of diabetes, hypotension or arterial hypertension).

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Figure 21. The presence of consequences of ischemic stroke in the form of cystic-gliotic changes in the left frontal lobe is noted (arrows in Fig. 21a). The study was performed for stroke with a diagnosed stroke in the left hemisphere of the cerebellum (asterisk in Fig. 21b). On DWI, there is no change in the MR signal in the left frontal lobe - in the area of cystic-gliotic changes (Fig. 21c), but there is also a pronounced restriction of diffusion in the left hemisphere of the cerebellum - acute ischemic stroke (Fig. 21d).

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Figure 22. After 2 weeks in the same patient (as in Fig.21) there is the appearance of edema and swelling of the medulla in the area of cystic-glious changes in the left frontal lobe-repeated ischemic stroke at the site of cystic-glious changes (arrows in Fig.22A), encephalomalacia in the left hemisphere of the cerebellum-the evolution of ischemic stroke (asterisk in Fig.22b). DWI shows an increase in the MR signal in the left frontal lobe-acute ischemic stroke (Fig.22C), as well as there isn’t a pronounced restriction of diffusion in the left hemisphere of the cerebellum. It’s the late phase of subacute with the outcome in chronic ischemic stroke (Fig.22d).

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Author: radiologist, MD Vlasov Evgeny Aleksandrovich

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