Acute Brain Ischemia/ infarction

Acute Brain Ischemia – infarction

Definition

• Interrupted blood flow to brain resulting in cerebral ischemia/infarction with variable neurologic deficit

• Best diagnostic clue

○ High signal on DWI with corresponding low signal on ADC (reduced diffusivity)

○ Decreased cerebral blood flow (CBF) and cerebral blood volume (CBV) on CT or MR perfusion

• Location

○ ≥ 1 vascular territories or at border-zones ("watershed")

• Size

○ Dependent on degree of compromise and collateral circulation

• Morphology

○ Territorial infarct

– Conforms to arterial territory

– Generally wedge-shaped, both gray matter (GM) and white matter (WM) involved

○ Embolic infarcts (often focal, at GM/WM interface) 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 1st 3 hours (50-70%)

– Obscuration of deep gray nuclei

– Loss of cortical "ribbon"

○ Parenchymal hypodensity

– If > 1/3 MCA territory initially, larger lesion usually develops later

– Temporary transition to isodensity (up to 54%) at 2-3 weeks post ictus (CT "fogging")

○ Gyral swelling, sulcal effacement

appears between12-24 hours

○ "Hemorrhagic transformation" in 15-45%

– Delayed onset (24-48 hours) most typical

– Can be gross (parenchymal) or petechial

○ Calcified embolus

– Round/ovoid hyperdensity in vessel lumen or sulcus

– Source: Heart (calcific valvular disease) > cervical ASVD

– High risk for recurrent strokes

• CECT

○ Enhancing cortical vessels: Slow flow or collateralization acutely

○ Absent vessels: Occlusion

○ Perfusion CT (pCT): Assess ischemic core vs. penumbra; identify patients who benefit most from revascularization

– pCT calculates CBF, CBV, time to peak (TTP); deconvolution can give mean transit time (MTT)

○ Cortical/gyral enhancement after 48-72 hours

• CTA: Identify occlusions, dissections, stenoses, status of collaterals

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 (6 hours post ictus) while other sequences normal

○ Intraarterial FLAIR hyperintensity is early sign of major vessel occlusion or slow flow

• T2* GRE

○ Detection of acute blood products

○ Arterial "blooming" (thrombosed vessel) from clot susceptibility

○ May see susceptibility from Ca++ 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)

– May have reduced sensitivity in brainstem and medulla in first 24 hours

– Restriction typically lasts 7-10 days

□ High signal can persist up to 2 months post ictus

□ After 10 days, T2 effect may predominate over low ADC: T2 "shine-through"

○ Corresponding low signal on ADC maps

– May normalize after tissue reperfusion

– Hyper- or isointensity on ADC map (T2 "shinethrough") may mimic diffusion restriction

○ Distinguish cytotoxic from vasogenic edema in complicated cases

– May be helpful to evaluate new deficits after tumor resection

• PWI

○ Dynamic contrast bolus or arterial spin labeled techniques

– Maximum slope gives relative CBF, CBV

– 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, stenosis, status of collaterals

• MRS: Elevated lactate, decreased NAA

• Conventional MR sequences positive in 70-80%

○ Restricted diffusion improves accuracy to 95%

• Diffusion tensor imaging (DTI)

○ Multidirectional diffusion-weighted images; at least 6 directions can be used to calculate DTI trace and ADC maps

– Higher spatial resolution

○ May be more sensitive for small ischemic foci, emboli, cortical strokes

Angiographic Findings

• Conventional: Vessel occlusion (cut-off, tapered, "tram track")

○ Slow antegrade flow, retrograde collateral flow

• Neurointerventional: IA fibrinolytic therapy for treatment of selected acute nonhemorrhagic stroke within 6-hour

window

○ IA mechanical clot removal with retriever device

Imaging Recommendations

• Best imaging tool

○ MR + DWI, T2* GRE

• Protocol advice

○ NECT as initial study to exclude hemorrhage/mass

– CT perfusion and CTA if available

○ MR with DWI, FLAIR, GRE , MRA, PWI

○ DSA with thrombolysis in selected patients

DIFFERENTIAL DIAGNOSIS

Hyperdense Vessel Mimics

• High hematocrit (polycythemia)

• Microcalcification in vessel wall

• Diffuse cerebral edema makes vessels appear relatively hyperdense

• Normal circulating blood always slightly hyperdense to normal brain

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

• 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

– Target of thrombolysis, neuroprotective agents

• 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

CLINICAL ISSUES

Presentation

• Most common signs/symptoms

○ Focal acute neurologic deficit

○ Paresis, aphasia, decreased mental status

Demographics

• Age

○ Usually older adults

○ Consider underlying disease (sickle cell, moyamoya, NF1,

cardiac, drugs) in children, young adults

• Epidemiology

○ 2nd most common cause of death worldwide

○ #1 cause of morbidity in USA

Natural History & Prognosis

• Clinical diagnosis inaccurate in 15-20% of strokes

• Malignant MCA infarct (coma, death)

○ Up to 10% of all stroke patients

○ Fatal brain swelling with increased ICP

Treatment

• "Time is brain": IV rTPA window < 3 hours

○ IA window < 6 hours

• Patient selection most important factor in outcome

○ Symptom onset < 6 hours

○ No parenchymal hematoma on CT

○ < 1/3 MCA territory hypodensity

DIAGNOSTIC CHECKLIST

Consider

• DWI positive for acute stroke only if ADC correlates

• Rarely, ischemia or seizure may mimic tumor or encephalitis

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

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

MCA

Coronal MIP view of the CTA in the same patient shows a proximal left MCA occlusion . Minimal filling of the distal MCA branches is occurring via collaterals from the ACA and PCA.

Axial CT perfusion shows decreased cerebral blood flow in the left MCA distribution .

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

Sagittal reformatted NECT scan 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.