Fact-sheet: Infarction of brain


Updated on 04/07/2026 at 8:44 AM

Note : 9.5/10 ( 2 notes )
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Definition

Perfusion disturbance leading to cerebral ischemia, most often of atheromatous origin (carotid or vertebral artery stenosis), more rarely secondary to a cardioembolic cause, intracranial atherosclerosis, arterial dissection, or vasculitis

Clinical features

Focal neurological deficit corresponding to the ischemic territory.

5-10% seizure incidence within the first 24 hours.

Former definition of TIA = if symptoms resolve within 24 hours, this is a Transient Ischemic Attack (TIA).

New definition of TIA = short-lived deficit of presumed ischemic origin, with symptoms typically lasting less than 1 hour and no MRI evidence of recent infarction.
If the deficit persists or diffusion MRI is positive, this is termed a completed stroke or infarction.

Radiography

Chest X-ray: look for aspiration pneumonia in case of fever

Ultrasound

Duplex ultrasound of the neck vessels: search for carotid or vertebral artery stenosis

Transcranial Doppler: search for intracranial stenosis or arterial vasospasm

Echocardiography if cardiac arrhythmia: search for an atrial mural thrombus

CT

Non-contrast brain CT: - May be normal in the first hours - Early signs of cerebral ischemia: effacement of cortical sulci, spontaneous hyperdensity of a cerebral artery, effacement of the lentiform nucleus, loss of gray-white matter differentiation and effacement of the insular ribbon, mass effect - Look for mass effect - Describe the extent of the ischemic lesions and the territory involved - Search for hemorrhagic transformation, spontaneously hyperdense Fogging phenomenon: 2nd or 3rd week post ischemic stroke. - Return of the ischemic lesions to a density similar to that of normal brain parenchyma due to replacement of cellular edema by lipids and macrophages, capillary proliferation. --> temporary "disappearance" of the ischemic lesions on non-contrast CT. --> Formation of an encephalomalacic cavity thereafter with reappearance of hypodensity. If in doubt: brain MRI or contrast-enhanced CT: blood-brain barrier breakdown.

MRI

Diffusion: diffusion hyperintensity and decreased ADC, visible as early as the first hour.

Perfusion: useful early, prior to thrombolysis, to estimate the hypoperfused but non-infarcted territory and the size of the ischemic penumbra (diffusion-perfusion mismatch)

FLAIR-T2: more sensitive than T2 for supratentorial ischemic lesions, seen as T2-FLAIR hyperintensity

T2: remains superior to FLAIR for infratentorial lesions

T2* gradient echo: search for a hemorrhagic component in hyposignal

MRA of the supra-aortic trunks: search for and evaluation of stenosis of the cerebral vasculature

Special case: Percheron artery occlusion.

  • This is a variant of thalamo-mesencephalic vascularization, corresponding to a single trunk supplying the bilateral paramedian thalamic territory and sometimes the thalamo-mesencephalic territory.
  • Clinical presentation: polymorphic. The most frequently encountered signs are impaired consciousness (coma 47%, hypersomnia 29%), cognitive disturbances (memory impairment 63%, confusion 55%, and behavioral disturbances 29%), and oculomotor disturbances (vertical gaze palsy and Parinaud syndrome 61%). Motor deficits (13%) and dysarthria (29%) are less common.
  • Severe impairment of consciousness usually resolves rapidly within hours to days.
  • CT: Same as infarction, with hypodensities of the paramedian thalamic nuclei +/- the cerebral peduncles.
  • MRI: Diffusion hyperintensity of the thalami, decreased ADC in acute lesions, T2 FLAIR hyperintensity in established lesions. No hemorrhagic changes on T2 GE. Normal circle of Willis.

Differential diagnosis

Differential diagnoses of Percheron artery occlusion

- In cases of bilateral involvement, always consider dural sinus thrombosis in the territory of the internal cerebral veins. In this case, the edema will be vasogenic (normal or increased ADC) and more extensive, involving the thalami and other basal ganglia. Venous MRA will establish the diagnosis.

- Metabolic causes: Wernicke encephalopathy, central and extrapontine myelinolysis.

- Creutzfeldt-Jakob disease, bithalamic gliomas.