Acute cerebral infarct is an emergency neurological condition in which ischemic necrosis develops in the corresponding vascular territory due to occlusion of a brain artery. It most commonly occurs in the middle cerebral artery (MCA) territory. Cytotoxic edema develops within minutes, and diffusion restriction on DWI is the earliest imaging finding (positive within minutes of symptom onset). DWI-FLAIR mismatch (DWI positive, FLAIR negative) is used to estimate acute infarct timing (<4.5 hours) and is critically important for thrombolytic therapy decisions. Stroke subtypes (atherosclerotic, cardioembolic, lacunar, watershed) show different imaging patterns and require different treatment strategies.
Age Range
50-90
Peak Age
70
Gender
Male predominant
Prevalence
Very Common
In acute cerebral infarct, occlusion of a brain artery (thrombotic or embolic) halts perfusion of downstream tissue and initiates the ischemic cascade. Within minutes, ATP production ceases, Na+/K+-ATPase pumps fail, and sodium/water influx into cells occurs (cytotoxic edema). This cell swelling narrows the extracellular space and restricts Brownian motion of water molecules; this is visualized as diffusion restriction on DWI (bright signal) and low signal on ADC maps. Within the first 4-6 hours, the blood-brain barrier is still intact and no signal change appears on FLAIR/T2, producing DWI-FLAIR mismatch — this timing window is critical for thrombolytic therapy. Over hours to days, vasogenic edema is added (blood-brain barrier breakdown), FLAIR/T2 hyperintensity becomes prominent, and mass effect increases. On perfusion imaging, diffusion-perfusion mismatch (DWI lesion < perfusion defect) represents salvageable penumbra tissue and is used for endovascular therapy decisions.
The combination of hyperintense signal on DWI with corresponding hypointense signal on ADC map in a vascular territory distribution is the signature finding of acute ischemic infarct. This finding reflects cytotoxic edema and becomes positive within minutes of symptom onset, making it the earliest and most sensitive imaging finding for acute stroke diagnosis.
On DWI (Diffusion Weighted Imaging) sequences, hyperintense signal (bright) is observed in a vascular territory distribution. This finding becomes positive within minutes of symptom onset and is the most sensitive (88-100%) and earliest imaging finding for acute ischemic stroke diagnosis. Diffusion restriction occurs due to cytotoxic edema causing water influx into cells and narrowing of extracellular space. The lesion boundary corresponds to vascular distribution (MCA, ACA, PCA territories or watershed zones).
Report Sentence
Diffusion restriction is observed on DWI sequences in a [vascular territory] distribution, confirmed by corresponding low signal on ADC maps. Findings are consistent with acute ischemic infarct.
DWI-FLAIR mismatch: diffusion restriction is positive on DWI while no signal change is yet visible on FLAIR sequences in the same region. This mismatch indicates that acute infarct age is approximately <4.5 hours and is known as the 'tissue clock.' FLAIR becoming positive (hyperintensity) becomes visible after 4.5-6 hours in the vascular territory and reflects vasogenic edema development. DWI-FLAIR mismatch is critically important in wake-up stroke patients where symptom onset time is unknown for thrombolytic therapy decision-making.
Report Sentence
While diffusion restriction is observed on DWI in a [vascular territory] distribution, no signal change has yet been detected on FLAIR sequences in the same region (DWI-FLAIR mismatch positive). This finding suggests infarct age of approximately less than 4.5 hours.
Early findings of acute infarct on non-contrast CT: insular cortical ribbon sign (loss of insular ribbon — obscuration of gray-white matter differentiation of insular cortex), lentiform nucleus hypodensity, sulcal effacement (due to local edema), dense vessel sign (hyperdense thrombus in occluded artery — especially 'hyperdense MCA sign'). These findings may be visible 1-3 hours after symptom onset but CT is much less sensitive than DWI (40-60% vs 88-100%). ASPECTS (Alberta Stroke Program Early CT Score) is used for systematic assessment of early ischemic changes.
Report Sentence
Early ischemic changes are observed on non-contrast CT in a [vascular territory] distribution: [insular ribbon loss/lentiform nucleus hypodensity/sulcal effacement]. ASPECTS score: [score]/10. [Hyperdense MCA sign is identified/not identified].
On T2-weighted sequences, hyperintense signal is observed in the acute infarct area in a vascular territory distribution. This finding is related to vasogenic edema development and usually becomes apparent 6-12 hours after symptom onset (later than DWI). Mass effect (sulcal effacement, ventricular compression) may accompany. In the subacute period (3-7 days), T2 hyperintensity reaches maximum level. In the chronic period (weeks-months), it remains hyperintense as gliotic scar and encephalomalacia but mass effect resolves and ex-vacuo dilation develops.
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Hyperintense signal change is observed on T2-weighted sequences in a [vascular territory] distribution with [accompanying mass effect/sulcal effacement].
On perfusion MR imaging (DSC or ASL), perfusion defect on MTT (Mean Transit Time) and Tmax maps is larger than the diffusion restriction area on DWI. This difference is called 'diffusion-perfusion mismatch' and represents salvageable penumbra tissue. Tmax >6 seconds threshold is the most commonly used parameter for defining penumbra (DEFUSE/EXTEND trials). On CBV maps, low perfusion is seen in the infarct core and preserved or mildly increased perfusion in the penumbra (autoregulation). This mismatch is critically important for endovascular thrombectomy decisions (6-24 hour window).
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On perfusion MR imaging, a perfusion defect (Tmax >6s) significantly larger than the diffusion restriction area on DWI is observed, with diffusion-perfusion mismatch suggesting the presence of salvageable penumbra tissue. Estimated penumbra volume: [volume] mL.
On SWI sequences, hypointense signal (susceptibility vessel sign) is observed in the occluded artery due to thrombus — the MR equivalent of the dense vessel sign on CT and more sensitive. Additionally, prominent deep medullary veins ('brush sign') may be seen in the acute infarct area — this finding reflects increased oxygen extraction in surrounding tissue and helps distinguish the infarct core from penumbra. If hemorrhagic transformation is present, microbleeds are detected early on SWI.
Report Sentence
On SWI sequences, susceptibility vessel sign is observed along the [artery] course, consistent with arterial occlusion. [Brush sign/hemorrhagic transformation finding is identified/not identified].
On CT angiography, cessation of contrast passage (cutoff sign) is observed in the occluded artery. MCA M1 or ICA terminal occlusion is the most commonly imaged pattern. Collateral circulation status (leptomeningeal collaterals) is critical for prognosis and treatment decisions — good collateral filling indicates penumbra preservation. When evaluated together with CT perfusion, infarct core (low CBV) and penumbra (prolonged MTT, preserved CBV) maps are generated. Tandem lesions (extracranial ICA + intracranial) are evaluated on CT angiography.
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On CT angiography, occlusion (cutoff sign) is observed at the [artery — segment] level. Leptomeningeal collateral filling is assessed as [good/moderate/poor]. [On CT perfusion, infarct core: [volume] mL, penumbra: [volume] mL].
On MR spectroscopy (MRS), a lactate peak (doublet at 1.33 ppm) is observed in the acute infarct area — indicating anaerobic glycolysis. N-acetylaspartate (NAA, 2.02 ppm) decreases — reflecting neuronal damage/loss. Choline/creatine ratio is usually normal (unlike tumors). When evaluated together with DWI, the lactate peak reveals the metabolic status of ischemic tissue. In the penumbra zone, lactate increase with partial preservation of NAA may indicate viable but ischemic tissue.
Report Sentence
On MR spectroscopy, lactate peak at 1.33 ppm and NAA peak decrease are observed in the infarct area, consistent with ischemic metabolic changes.
Criteria
Large territorial infarct due to stenosis or occlusion of a major cerebral artery (ICA, MCA M1, basilar). Proximal artery stenosis or occlusion on CT/MR angiography. Usually involves both cortical and subcortical areas. Atherosclerotic risk factors (hypertension, diabetes, hyperlipidemia, smoking) are present.
Distinct Features
Large, wedge-shaped lesion conforming to vascular territory. Both cortex and white matter are involved. High risk of hemorrhagic transformation (especially after reperfusion). Dense vessel sign/susceptibility vessel sign may be present early.
Criteria
Embolic infarct occurring in the presence of a cardiac source (atrial fibrillation, endocarditis, mural thrombus, PFO). Usually sudden onset, may involve multiple vascular territories. High rate of hemorrhagic transformation (up to 70%). Early reperfusion may be seen due to embolus fragmentation.
Distinct Features
Simultaneous lesions in multiple vascular territories, cortical-predominant distribution (emboli lodge in cortical branches), early hemorrhagic transformation, extensive edema. Multiple scattered diffusion restriction foci may be seen on DWI.
Criteria
Infarct <15 mm due to small penetrating artery occlusion. Most commonly seen in basal ganglia, thalamus, pons, internal capsule, and corona radiata. Hypertension and diabetes are the most important risk factors (lipohyalinosis). Typical clinical syndromes: pure motor, pure sensory, ataxic hemiparesis, dysarthria-clumsy hand.
Distinct Features
Small (<15mm), round/oval, deep-seated lesion. Small bright focus on DWI. No large vessel occlusion or cortical involvement. In the chronic period, lacunar cavity forms (CSF intensity).
Criteria
Infarct occurring in the border zone between two major cerebral arterial territories. Associated with systemic hypotension or proximal artery stenosis. Internal (deep) watershed: adjacent to lateral ventricle, between cortical and deep perfusion zones. External (superficial) watershed: ACA-MCA or MCA-PCA border zone.
Distinct Features
Typical pattern: multiple small infarcts in parasagittal/parasuprasylvian alignment in external watershed ('string of pearls'), linear lesion in deep white matter near ventricle in internal watershed. Does not conform to classic territorial distribution. May be bilateral. Hemodynamic cause (cardiac surgery, shock, severe carotid stenosis).
Distinguishing Feature
Brain abscess shows diffusion restriction on DWI (purulent content with high viscosity) but the distribution does not conform to a vascular territory, it enhances in a round/oval ring pattern, and surrounding edema is more prominent. Diffusion restriction within the abscess cavity is homogeneous whereas infarct distribution conforms to vascular anatomy. Abscess shows amino acid and succinate peaks on MRS that are not seen in infarct.
Distinguishing Feature
Glioblastoma shows irregular ring enhancement and distribution not conforming to vascular territory. It may show diffusion restriction in cellular areas on DWI but the distribution is tumoral, not vascular. Perfusion shows increased CBV (neovascularization) but MTT may be shortened unlike early infarct. MRS shows elevated choline/creatine ratio (cellular proliferation), while choline is usually normal in acute infarct. In the subacute period, infarct may show enhancement but not as massive and irregular as glioblastoma.
Distinguishing Feature
Primary CNS lymphoma has periventricular or deep gray nuclei localization, enhances homogeneously and avidly, and shows prominent diffusion restriction on DWI. However, the distribution does not conform to a vascular territory and is usually a single or few lesions. Perfusion shows CBV increase milder than AVM and different from infarct. Dramatic shrinkage with steroid therapy ('ghost tumor') aids diagnosis and is not seen in infarct. MRS may show elevated lipid peak.
Distinguishing Feature
Toxoplasmosis creates multiple ring-enhancing lesions in immunosuppressed patients and may show central diffusion restriction on DWI. However, the distribution does not conform to a vascular territory, typically locates in basal ganglia and corticomedullary junction, shows ring enhancement, and has prominent surrounding edema. Response to empirical therapy (shrinkage in 2-3 weeks) aids diagnosis. Serology may be positive.
Urgency
emergencyManagement
Akut inme protokolu — 'time is brain'. iv-tPA (alteplaz) <4.5 saat icerisinde (DWI-FLAIR mismatch ile uzatilabilir), mekanik trombektomi <24 saat icerisinde (genis damar tikanikligi + uygun penumbra). Destek tedavisi, antikoagulasyon (kardiyoembolik), antiagregan (aterosklerotik), risk faktoru kontrolu.Biopsy
Not NeededFollow-up
24-48 saat kontrol BT (hemorajik transformasyon), 3-7 gun kontrol MR (infarkt hacmi). Uzun donem: 3-6 ay MR, etiyolojiye yonelik tedavi, sekonder koruma.Acute cerebral infarct is a neurological emergency — 'time is brain'. Approximately 1.9 million neurons are lost every minute. IV thrombolytic therapy (alteplase) must be administered within <4.5 hours of symptom onset; DWI-FLAIR mismatch can extend the time window in stroke with unknown onset. In large vessel occlusion, mechanical thrombectomy can be performed between 6-24 hours (with appropriate penumbra per DAWN/DEFUSE criteria). Imaging directly determines emergency treatment decisions: CT (hemorrhage exclusion), CT angiography (occlusion detection), DWI (infarct confirmation), perfusion (penumbra assessment). Etiology investigation (cardiac, large vessel, small vessel, rare causes) determines the secondary prevention strategy.
Acute cerebral infarct is a neurological emergency. IV tPA (alteplase) can be administered within 4.5 hours and mechanical thrombectomy for large vessel occlusions within 24 hours. DWI-FLAIR mismatch and perfusion imaging guide treatment decisions. Hemorrhagic transformation is the most important complication after thrombolysis.