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KEY FACTS

Terminology
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction
- Stroke, brain attack = descriptive terms, not diagnosis
Imaging
- Major artery (territorial) infarct - Generally wedge-shaped; both gray matter (GM) and white matter (WM) involved
- Embolic infarcts - Often focal/small, at GM-WM interface
- NECT - Hyperdense vessel = clot (dense MCA sign) - Loss of GM-WM distinction in first 3 hours (50-70%) - Insular ribbon sign: GM-WM interface lost - "Disappearing" basal ganglia sign - Calcified embolus - Do not miss this (high risk of recurrent stroke)
- CTA: Excellent for large vessel occlusions (LVOs)
- pCT: CBF/CBV "mismatch" estimates penumbra - Beware ghost infarct core! - May exclude patients who would benefit from endovascular treatment
- MR - Parenchymal ± intraarterial FLAIR hyperintensity - ↑ intensity on DWI with corresponding ↓ on ADC - ↓ CBF, variable ↓ CBV on MR perfusion
Top Differential Diagnoses
- Hyperdense vessel mimics (normal; polycythemia)
- Parenchymal hypodensity (many nonvascular causes)
Pathology
- Severely ischemic core - CBF < (6-8 cm³)/(100 g/min)
- Peripheral penumbra - CBF between (10-20 cm³)/(100 g/min)
Clinical Issues
- 2nd most common cause of death worldwide
- Most common cause of morbidity in USA
- Thrombectomy = treatment of choice for LVOs

TERMINOLOGY

Synonyms
- Stroke and brain attack - Not diagnosis; terms for sudden onset of neurologic deficit
Definitions
- Interrupted blood flow to brain resulting in cerebral ischemia/infarction

IMAGING

General Features

Best diagnostic clue

- High signal on DWI + low signal on ADC = reduced diffusivity
- ↓ cerebral blood flow (CBF), variable cerebral blood volume (CBV) on CT perfusion (pCT) or MR perfusion (pMR)

Location

- Vascular territory or at border zones (watershed)

Size

- Dependent on degree of compromise and collateral circulation

Morphology

- Large vessel occlusion (LVO)
        - Conforms to arterial territory [most common = middle cerebral artery (MCA)]
        - Generally wedge-shaped, involves both gray matter (GM) and white matter (WM)
- Embolic infarcts (often focal, at GM-WM interface)
- Watershed infarcts (border zone between perforating, cortical arteries)

CT Findings

NECT

- Hyperdense vessel (high specificity, low sensitivity)
        - Represents acute thrombus in cerebral vessel(s)
        - Hyperdense M1 MCA in 35-50%
        - Dot sign: Occluded MCA branches in sylvian fissure (16-17%)
- Loss of GM-WM distinction in first 3 hours (50-70%)
        - Obscuration of deep gray nuclei
                  - "Disappearing" basal ganglia
        - Loss of cortical "ribbon"
- Parenchymal hypodensity
        - **A**lberta **S**troke **P**rogram **E**arly **C**omputed **T**omographic **S**core (ASPECTS)
                  - Numerical calculation (1 point subtracted for each affected area)
                  - Can be automatically generated with artificial intelligence (AI)
- Gyral swelling, sulcal effacement appears between 12-24 hours
- "Hemorrhagic transformation" in 15-45%
        - Delayed onset (24-48 hours) most typical
        - Can be gross (parenchymal) or petechial
- Calcified embolus (1-2%)
        - Round/ovoid hyperdensity in vessel lumen or sulcus
        - Calcific valvular disease > cervical atrioventricular septal defect (ASVD) as source
        - High risk for recurrent strokes

CECT

- Enhancing cortical vessels = slow flow or collateralization
- Absent vessels = occlusion
- Cortical/gyral enhancement after 48-72 hours

CTA: Identify LVOs, dissections, stenoses, status of collaterals
pCT - Shows CBF, CBV, TTP, or MTT - AI programs provide rapid, easy-to-read, real-time views of brain perfusion - Select stroke patients with LVOs for thrombectomy - Ischemic core = volume of area with > 70% ↓ in CBF (rCBF < 0.3) - Often overestimates initial infarct core → ghost infarct core (GIC) - GIC = initial core - final infarct > 10 mL - Common in patients imaged in early time window with fast, complete reperfusion (TICI2b) - pCT CBF may exclude patients who would benefit from endovascular treatment!

MR Findings

T1WI

- Early cortical swelling and hypointensity, loss of GM-WM borders

T2WI

- Cortical swelling, hyperintensity develops by 12-24 hours
- May normalize 2-3 weeks post ictus (MR "fogging")

FLAIR

- Parenchymal hyperintensity appears while other sequences normal
- Intraarterial hyperintensity = sign of major vessel occlusion or slow flow
        - **Absence** of FLAIR intravascular hyperintensity associated with future lack of recanalization

T2* GRE

- Arterial blooming (thrombosed vessel) ± parenchymal hemorrhage
- May see susceptibility from calcified embolus

DWI

- Hyperintense (cytotoxic edema)
        - Improves hyperacute stroke detection to 95%
        - Usually correlates to "infarct core" (final infarct size); some diffusion abnormalities reversible (TIA, migraine)
        - Restriction typically lasts 7-10 days
                  - Can persist up to 2 months post ictus
- Corresponding low signal on ADC maps
        - May normalize after tissue reperfusion
        - After 10 days hyper- or isointensity on ADC map (T2 shine-through)
                  - May mimic diffusion restriction on DWI
- DTI
        - DTI with at least 6 directions can calculate DTI trace, ADC maps
        - More sensitive for small ischemic foci, emboli, distal cortical strokes
- Distinguish cytotoxic from vasogenic edema in complicated cases

PWI

- Dynamic contrast bolus or arterial spin-labeled techniques
        - Maximum slope gives rCBF, rCBV
        - Deconvolution gives absolute values
- Bolus-tracking T2* gadolinium perfusion imaging (PWI) with CBV map
        - ↓ perfusion; 75% larger than DWI abnormality
        - DWI/PWI "mismatch": Penumbra or "at-risk" tissue

T1WI C+

- Variable enhancement patterns evolve over time
        - Hyperacute: Intravascular enhancement (stasis from slow antegrade or retrograde collateral flow)
        - Acute: Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days)
        - Subacute: Parenchymal enhancement (appears after 24-48 hours, can persist for weeks/months)

MRA: Major vessel occlusions, stenoses, status of collaterals
MRS: ↑ lactate, ↓ NAA

Angiographic Findings
- DSA - Only used if thrombectomy is considered - Vessel occlusion (cut-off, tapered "rat tail," clot with "tram-track") or stenosis - ± slow antegrade flow, assess retrograde collateral flow - "Bare area" of non- or underperfused brain in late arterial/capillary phases

Imaging Recommendations

Protocol advice

- Initial NECT (exclude hemorrhage/stroke mimic)
- CTA + pCT
- ± MR with fast DWI, FLAIR, T2* GRE
        - ± MRA, PWI
- DSA if thrombectomy is option (selected patients up to 24 hours)

DIFFERENTIAL DIAGNOSIS

Hyperdense Vessel Mimics
- Intraarterial blood is always slightly hyperdense to normal brain!
- High hematocrit (polycythemia)
- Microcalcification in vessel wall
- Diffuse cerebral edema makes vessels appear relatively hyperdense
Parenchymal Hypodensity (Nonvascular Causes)
- Infiltrating neoplasm (e.g., astrocytoma)
- Cerebral contusion
- Inflammation (cerebritis, encephalitis)
- Evolving encephalomalacia
- Dural venous thrombosis with parenchymal venous congestion and edema
- Seizure

PATHOLOGY

General Features

Etiology

- Many causes (thrombotic vs. embolic, dissection, vasculitis, hypoperfusion)
- Early: Critical disturbance in CBF
        - Severely ischemic core has CBF < (6-8 cm³)/(100 g/min) [normal ~ (60 cm³)/(100 g/min)]
        - Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
        - Bulk of final infarct → cytotoxic edema, cell death
- Later: Evolution from ischemia to infarction depends on many factors (e.g., hyperglycemia influences "destiny" of ischemic brain tissue)
- Ischemic penumbra CBF between (10-20 cm³)/(100 g/min)
        - Theoretically salvageable tissue

Associated abnormalities

- Cardiac disease, prothrombotic states
- Additional stroke risk factors: C-reactive protein, homocysteine

Gross Pathologic & Surgical Features
- Acute thrombosis of major vessel
- Pale, swollen brain; GM-WM boundaries blurred
Microscopic Features
- After 4 hours: Eosinophilic neurons with pyknotic nuclei
- 15-24 hours: Neutrophils invade, necrotic nuclei look like "eosinophilic ghosts"
- 2-3 days: Blood-derived phagocytes
- 1 week: Reactive astrocytosis, ↑ capillary density
- End result: Fluid-filled cavity lined by astrocytes

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- Focal acute neurologic deficit
- Paresis, aphasia, ↓ mental status

Demographics

Age

- Any age; most common in older adults
- Consider underlying disease (sickle cell, moyamoya, neurofibromatosis type 1, cardiac, drugs) in children, young adults

Sex
```
- No sex predilection
```

Epidemiology

- 2nd most common cause of death worldwide
- Most common cause of morbidity in USA

Natural History & Prognosis
- Clinical diagnosis inaccurate in 15-20% of strokes
- ~ 50% of patients with LVO, thrombectomy achieve functional independence
- Prognosis poor if ASPECTS ≤ 5
- Malignant MCA infarct (coma, death) - Up to 10% of all stroke patients (↑ risk with large infarct volumes) - ↑ inflammasome activation → proinflammatory cytokines; fatal brain swelling with ↑ ICP
Treatment
- "Time is brain" - IV thrombolysis = ~ 10% successful/sufficient recanalization - IV rTPA window < 3 hours if thrombectomy not available - Thrombolysis in cerebral infarction (TICI scale) = reperfusion grade - Grade ≥ 2B is "successful" reperfusion; 2C = near-perfect reperfusion - TICI 3 = best functional outcome - Now procedure of choice with LVO = mechanical thrombectomy - Stent retriever better outcome than aspiration only - ± new devices to ↓ distal embolization
- Patient selection most important factor in outcome - AHA/ASA guidelines: Age ≥ 18 years, ASPECTS/NIHSS score ≥ 6 - Symptom onset < 6 hours - No parenchymal hematoma on CT - DAWN, DEFUSE 3 trials have broadened window - Some advocate treating "almost anyone" (ASPECTS = 0-5) - Up to 24 hours in some cases - Even failed/incomplete recanalization shows ↓ likelihood for very poor outcome, not generally harmful

DIAGNOSTIC CHECKLIST

Consider
- Rarely, ischemia or seizure may mimic tumor or encephalitis

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References

Selected References

Images

Selected Images

Coronal graphic illustrates left M1 occlusion. Proximal occlusion affects the entire middle cerebral artery (MCA) territory, including the basal ganglia (perfused by lenticulostriate arteries ). Acute ischemia is often identified by subtle loss of the gray matter-white matter interfaces with blurring of the basal ganglia and an insular ribbon sign on the initial CT.

Axial NECT in a 46-year-old man shows a very "dense" left MCA compared to the normal minimally hyperdense right MCA .

Graphic shows anatomic regions for calculating the ASPECTS score. M1-M2 represent the MCA cortex with each area allotted 1 point. The insular cortex (I), lentiform nuclei (L), caudate head (C), and internal capsule (IC) are scored with 1 point each.

More cephalad graphic shows the superior 3 MCA territories. The ASPECTS score is calculated by subtracting 1 point for each affected area from 10 (normal total score).

Axial NECT in a 47-year-old woman with sudden onset of right hemiparesis shows hypodensity in the left lateral basal ganglia, insula, and parietal lobe. The total ASPECTS score was 6.

MIP of the CTA in the same patient shows an abrupt cut-off of the proximal M1 MCA segment.

Axial CT perfusion with cerebral blood volume (CBV) shows reduced CBV in the left temporal and parietal lobes, as well as the lateral basal ganglia, external capsule, and insula.

Axial cerebral blood flow (CBF) map shows a more extensive area of reduced perfusion, suggesting there is a significant penumbra of brain that is ischemic but not infarcted. CBF in the left basal ganglia and thalamus is also reduced, suggesting the proximal M1 occlusion has also compromised the deep gray nuclei.

Automated CT perfusion in the same case shows CBF < 30% = 68 mL, volume of brain with Tmax > 6.0 seconds = 108 mL, and mismatch volume (penumbra) of 40 mL.

(L) Pretreatment AP view of the left internal carotid artery (ICA) DSA in the same case shows the proximal MCA occlusion . (R) Following stent-retriever thrombectomy, the clot has been removed and the M1 MCA appears nearly normal. Blood flow to the distal MCA is mostly restored.

Axial T1WI MRs show the 2 vascular watershed zones (WSZs). Blue depicts the cortical (external) WSZs between the major territorial arteries [anterior cerebral artery (ACA), MCA, posterior cerebral artery (PCA)]. The yellow depicts the subcortical (internal or deep) WSZs between perforating arteries and major territorial arteries.

Axial FLAIR MR in a 48-year-old woman with TIAs shows white matter hyperintensities aligned front to back just above the level of the lateral ventricles.

Axial DWI MR in the same patient shows acute lacunar infarcts in almost a "string of pearls" configuration.

Axial ADC confirms the deep white matter lesions exhibit acutely restricted diffusion.

2D TOF MRA of the left ICA in the same patient shows a "flow gap" at the junction of the cavernous and supraclinoid segments, indicating a high-grade stenosis.

2D TOF MRA of the right ICA in the same patient shows a high-grade stenosis of the right supraclinoid ICA just before the origin of the PCA. The critical stenoses in both ICAs resulted in the deep WSZ infarcts.

Axial NECT in a 65-year-old man with TIAs and a history of mitral valve replacement was initially read as normal. However, this image shows a calcified cerebral embolus in the right sylvian fissure.

More cephalad NECT in the same patient shows a 2nd calcified embolus . A 3rd embolus was present in the interhemispheric fissure (not shown). Calcified cerebral emboli carry ~ 50% risk of repeated strokes. Cardiac sources are most common followed by calcified ASVD plaques at carotid bifurcation.

Axial NECT for a brain attack patient in the ER with sudden-onset aphasia is normal.

Axial CT perfusion in the same patient was obtained immediately following the NECT. The CBV appears grossly normal.

Axial CBF map in the same patient shows markedly reduced perfusion in the inferior division of the left MCA .

TTD in the same patient shows severely reduced TTD, consistent with acute ischemia without infarction. IV TPA was administered and the symptoms resolved.

Additional Images

Axial NECT in a 60-year-old woman admitted for rapid stroke evaluation shows hypodensity in the right posterior frontal lobe . The right MCA appears slightly hyperdense.

Axial CTA in the same patient shows an abrupt cut-off of contrast in the right MCA just distal to its origin from the ICA.

Axial T2 GRE MR in the same patient shows striking blooming from a right M1/proximal M2 thrombus.*

Axial FLAIR MR in the same patient shows edematous right posterior frontal gyri as well as hyperintensity in the ipsilateral insula , caudate head, and putamen .

Axial DWI MR confirms acute infarction in the territories of the lateral lenticulostriate arteries and superior division of the right MCA.

Axial NECT in an 89-year-old man who had several visits to the ER for several falls (to "rule out subdural hematoma") shows a calcified cerebral embolus in a right hemisphere sulcus.

Sagittal reformatted NECT in the same patient shows the location in the right superior temporal sulcus . The patient was subsequently shown to have calcific mitral valve disease. Calcified cerebral emboli carry a high risk of repeated stroke.

Axial FLAIR MR shows intravascular signal beginning near the genu.

More cephalad FLAIR MR in the same patient shows gyral hyperintensity and intravascular signal in the M2 (insular) MCA segments .

Axial NECT in a 35-year-old man shows a dense left MCA , indicating acute thrombus involving the entire MCA from its origin to its bifurcation.

More cephalad NECT shows the basal ganglia are effaced and the gray matter-white matter interfaces in the insula, left posterior frontal lobe, and opercula are poorly defined.

The left basal ganglia are edematous and have "disappeared" as they are now nearly the same density as the surrounding white matter. The gray matter-white matter interfaces in the posterior temporal and anterior parietal lobes are effaced.

More cephalad NECT shows loss of sulci and gray matter-white matter differentiation in the left parietal lobe. Because of his poor ASPECTS score (2, being generous) he was not considered a good candidate for thrombectomy despite his relatively young age.

Axial FLAIR MR scan obtained 3 hours later in the same patient shows hyperintensity in the left basal ganglia, insula, and the entirety of the left cerebral hemisphere supplied by the MCA.

Axial DWI MR in the same patient shows restricted diffusion in the complete left MCA territory.

Axial NECT at 6 hours in the same patient shows thrombus in the horizontal MCA as well as hypodensity in the left frontal and anterior temporal lobes . The suprasellar cistern is normal and there is as yet no evidence for descending transtentorial herniation.

Axial NECT through the basal ganglia and insula shows extensive hypodensity in the entire left MCA territory . Mass effect is developing with compression of the left frontal horn .

More cephalad NECT in the same patient at 6 hours following ictus shows the wedge-shaped hypodensity involves the complete left frontal and parietal opercula. The massive edema developing in the entire left MCA territory makes this a so-called "malignant" MCA infarct.

Twelve hours after admission, the same patient became unresponsive. His left pupil was dilated and he was rushed to the operating room where an emergent craniectomy was performed. Postoperative NECT at 20 hours shows hypodensity throughout the left MCA territory. Note the brain bulging out through the craniectomy defect.

More cephalad NECT in the same patient shows the completed total MCA territory infarct.

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KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Pathology

Clinical Issues

TERMINOLOGY

Synonyms

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Size

Morphology

CT Findings

NECT

CECT

MR Findings

T1WI

T2WI

FLAIR

T2* GRE

DWI

PWI

T1WI C+

Angiographic Findings

Imaging Recommendations

Protocol advice

DIFFERENTIAL DIAGNOSIS

Hyperdense Vessel Mimics

Parenchymal Hypodensity (Nonvascular Causes)

PATHOLOGY

General Features

Etiology

Associated abnormalities

Gross Pathologic & Surgical Features

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Demographics

Age

Sex

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Consider

References

Selected References

Images

Selected Images

Additional Images

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