MRI and CT semiotics of the chronic stage
In the subacute period and during final infarct maturation, CT shows a progressive decrease in tissue density (hypodensity). The margins of the lesion become distinct. In the early stages of maturation, due to blood-brain barrier (BBB) disruption, gyral-pattern contrast enhancement is observed, which can persist for months.
On MRI in T2 and FLAIR sequences, the signal increases (becomes hyperintense) until its characteristics approach those of CSF. Over time, a picture of encephalomalacia develops:
- FLAIR: the center of the area becomes dark (the sequence suppresses signal from free fluid), but a bright rim of gliosis persists peripherally.
- DWI: at later stages, free diffusion is registered (free diffusion) — low signal on DWI and high signal on ADC maps.
- Imaging pitfall: in mature lesions, the T2 "shine through" effect (T2 shine through) is possible, when T2 hyperintensity produces a falsely bright signal on diffusion weighting without true restriction of water molecule motion.
Simultaneously, a loss of brain tissue volume occurs. Neighboring sulci and ventricles expand compensatorily — a phenomenon called ex-vacuo dilatation.
Hemorrhagic transformation and differential diagnosis
During the first two weeks, ischemic but reperfused tissue may become infiltrated with blood. On MRI, traces of such secondary hemorrhage (hemorrhagic transformation) are found in 80% of cases.
The risk is higher with cardioembolic etiology, diabetes mellitus, extensive lesions (especially in the basal ganglia), and following thrombolysis.
- Imaging: On CT, fresh blood appears as an area of increased density (hyperintensity) against the background of the infarction. However, the most sensitive method is MRI using magnetic susceptibility-sensitive sequences (SWI or GRE) — where blood degradation products appear markedly dark (hypointense).
- Differential diagnosis: Hemorrhage must be distinguished from cortical laminar necrosis. The latter yields a gyriform T1 hyperintense signal (gyriform pattern) in the subacute phase, which is associated with an accumulation of lipid-laden macrophages rather than blood degradation.
Secondary consequences and encephalomalacia
In addition to local volume loss, chronic infarctions trigger a cascade of changes in connected anatomical brain structures. The main secondary changes include:
- Wallerian degeneration (Wallerian degeneration): visualized as faint T2 hyperintensity along the course of the ipsilateral corticospinal tract. Often accompanied by asymmetric brainstem atrophy.
- Cerebellar changes: with massive infarctions in the middle cerebral artery (MCA) territory, volume loss of the contralateral cerebellar hemisphere may be observed.
- Pediatric features: the process of encephalomalacia frequently assumes a cystic character, which can cause a paradoxical mass effect.
- Rare outcomes: at very late stages, dystrophic calcification may develop.
Role of extracranial arterial stenoses
About 30% of transient ischemic attacks (TIAs) progress to a full-blown cerebral infarction (the majority within the first few days). The main source of emboli and the cause of hypoperfusion strokes are atherosclerotic plaques at vessel origins and the carotid bifurcation area.
Invasive digital subtraction angiography (DSA) was previously considered the gold standard examination. Today, non-invasive methods are used: ultrasound, CT angiography, and MR angiography (non-contrast TOF or contrast-enhanced CEMRA).
Indications for plaque removal (NASCET, ESCT, and ACST trials):
- Symptomatic stenosis of 70–99%: surgery is strictly indicated; the benefit has been proven.
- Asymptomatic stenosis ≥70%: surgery reduces stroke risk (especially in patients under 75 with low surgical risk).
- Symptomatic stenosis of 50–69%: intervention is discussed, but the benefit is comparable to the risks of the surgery itself.
- Stenosis <50%: surgery is not indicated.
The degree of narrowing is calculated mathematically by comparing the minimum residual lumen with the diameter of the unaffected internal or common carotid artery.
To memorize the diffusion (DWI) dynamics: "Acute — glows (restriction), Subacute — hides (pseudonormalization on days 5–10), Chronic — flows (free diffusion)."
Class and exam questions
How to distinguish an old infarction from an acute one on DWI?
Old lesions show free diffusion: they appear dark on DWI and bright on ADC maps. Acute infarctions, by contrast, glow brightly on DWI due to restricted diffusion.
Why might a lesion be invisible on diffusion MRI in a subacute infarction?
Between days 5 and 10, the pseudonormalization phenomenon occurs. The signal on DWI and ADC maps temporarily returns to normal values, masking small lesions.
What is the difference between NASCET and ESCT stenosis calculations?
The NASCET method compares the narrowest site with the unaffected section of the internal carotid artery distal to the plaque. The ESCT method compares the narrowing with the original true lumen at the level of the carotid bulb.
What else to study on this topic
- Formulas and anatomical landmarks for calculating the degree of carotid stenosis.
- MRI semiotics of cortical laminar necrosis in the subacute phase.
- Principles of visualizing blood degradation products on SWI and GRE sequences.
- Perfusion MRI: assessment of collateral blood flow (CBV) in infarction.
- Paradoxical mass effect in cystic encephalomalacia in children.
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