Cerebral Infarction

Pathology

- Interruption of blood flow through an intracranial

artery → oxygen deprivation → ischemic stroke →
cerebral infarction
- Most common cause of stroke is thrombotic or
embolic occlusion
- Risk factors of ischemic stroke: hypertension,
smoking, diabetes mellitus, hypercholesterolemia
 Cerebral Infarction

3 Major Types of Stroke: Cerebral Infarction:

1. Cerebral Infarction (80%) 1. Large vessel occlusion (40-50%)

2. Intra-cerebral hemorrhage 2. Small vessel (lacunar) (20%)
(15%) 3. Cardioembolic infarction (20%)
3. Subarachnoid hemorrhage (5%) 4. Blood disorders (5%)
5. Non-atheromatous occlusions (5%)
Classic Signs and Symptoms
Signs and Symptoms

● Hemisensory deficits
● Monocular or binocular visual loss
● Visual field deficits
● Diplopia
● Ataxia
● Vertigo (rarely in isolation)
● Nystagmus
● Sudden decrease in level of consciousness
Differential Diagnosis Rule In Rule Out
Brain Neoplasm Same manifestations as CT Scan, CBC, electrolytes,
infarction like weakness, metabolic panel
diplopia, ataxia
Hypoglycemia Same manifestations like Glucose and electrolyte levels
weakness, light
headedness
Hyponatremia Weakness, decreased Urine osmolality, serum osmolality,
level of consciousness urine sodium concentration
Subarachnoid Dizziness, diplopia, visuao CT Scan, Lumbar puncture
hemorrhage loss
Migraine Headache Nausea, vomiting, Ruled out clinically, diagnostic
unilateral weakness tests can be performed to rule out
diseases that may mimic migraine
 Hyperacute infarction ( less than 4-6 hours)

On CT:
● 60 % of CT scans obtained within first few hours
appear normal
● Early signs can be seen in 4-6 hours:
○ Hyperdense MCA (dense MCA sign)
○ Hyperdense basilar artery ( dense basilar artery
sign)
● INSULAR RIBBON SIGN
○ Loss of gray-white matter junction along the
lateral insula
● Loss of gray-white matter junction along the cortex
● VANISHING BASAL GANGLIA SIGN
○ Loss of density of the basal ganglia nuclei, such
as lentiform nucleus
Acute Infarction (12 hours to 5
days )
On CT:
● Hypodensity is confined within the vascular
teritory and involves the grey and white matter
● There is little or no mass effect evident during
the 1st 24 hours
● Sulcal effacement
MRI
INFARCTION ON MRI

● MRI are more sensitive than CT in identification

and localization
● On T2W1, highs signal intensity may be seen
approximately 6 hours
● FLAIR images
○ Can be seen within 3 hours
○ Demonstrate intraarterial signal that is
hyperintense or isointense to grey matter
● High signal DWI and low signal ADC - maps within
minutes
● DWI
○ considered to be the most reliable marker of
ischemic core and detect ischemia within 30
mins
○ May demonstrate high signal for several weeks,
due to T2 weighted effects apparent diffusion in
early & subacute infarction “T2 shine through”,
confirmation with ADC map is needed to
confirm abnormal DWI
ADC
● Peaks by 3 days and pseudonormalize during
subacute period between 7th and 11th day of
infarction
● More accurate assessment of infarct age
Acute Infarction (12 hours to 5
days
On MRI:)

● Vascular flow related abnormalities

● Absence of normal flow void and slow flow with
intravascular arterial enhancement
● T2WI & T2 flair- hyperintensity
● T1WI - hypointensity
● Mass effect increases
● Limited diffusion on DWI ( appears bright in DWI
and dark on ADC)
● Between 3-5 days
○ Becomes more hypodense and with sharper
margins
○ Swelling or mass effect is maximum at this
time
T1WI T2WI
T2 Flair DWI
Comparison of T2WI and DWI:

● In acute phase
○ T2W1 will be normal but in time
infarcteed area will be hyperintense
○ T2Wi reach maximum at 7-30 days
● DWI
○ Infarction appears hyperintense
during acute phase
○ Becomes bright maximum of 7 days
○ (+) 3 weeks after onset
● ADC
○ Low signal intensity with maximum at
24 hours
○ Increase signal intensity & become
bright (hyperintense in chronic stage
Subacute Infarction (6 to 17 days)
● On CT
○ Wedge-shaped hypodense lesion
○ Involves both the gray and white matter in a
vascular distribution
○ Mass effect initially increases then begins to
diminish after 7 to 10 days
○ Gyral enhancement in contrast
○ (+) signs of petechial hemorrhage
 Subacute Infarction (6 to 17 days)

Image reference: https://radiopaedia.org/cases/subacute-cerebral-infarction-1

Subacute Infarction (6 to 17 days)
● Fogging effect
○ Change from HYPODENSE to ISODENSE
○ Due to influx of lipid-laden macrophages,
decreased water content, proliferation of
capillaries, reperfusion and petechial hemorrhage
○ Usually seen 2-3 weeks post ictus and should
resolve on subsequent imaging
 Subacute Infarction (6 to 17 days)

Fogging effect

Image reference: https://radiopaedia.org/cases/subacute-cerebral-infarction-1

Subacute Infarction (6 to 17 days)
● On MRI
○ Hypointensity on T1 and hyperintensity on T2
○ DWI remains hyperintense due to T2 shine
through
○ ADC pseudonormalization occurs in the 2nd
week. It continues to appear hyperintense even
after 2 weeks
 Subacute Infarction (6 to 17 days)
● On MRI

Image reference: https://radiopaedia.org/cases/subacute-cerebral-infarction-with-mr-spectroscopy

 Subacute Infarction (6 to 17 days)
● On MRI

Image reference: https://radiopaedia.org/cases/subacute-cerebral-infarction-with-mr-spectroscopy

Chronic Infarction (months to years)
● On CT,
○ Encephalomalacic changes
○ Hypodensity becomes more homogenous
approaching the density of CSF
(encephalomalacia)
○ If the lesion is near a ventricle, dilatation of
adjacent ventricle
○ Sulcal enlargement
Chronic Infarction (months to years)
 Chronic Infarction (months to years)

Image reference: https://www.slideshare.net/thamir22/radiology-of-brain-hemorrhage-vs-infarction

Chronic Infarction (months to years)
● On MRI,
○ Encephalomalacic changes
○ ADC is high, DWI is low
○ T2 hyperintensity
 Chronic Infarction (months to years)

Image reference: https://www.slideshare.net/thamir22/radiology-of-brain-hemorrhage-vs-infarction

 Chronic Infarction (months to years)

Image reference: https://www.slideshare.net/thamir22/radiology-of-brain-hemorrhage-vs-infarction

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