Acute Cerebral Infarction: CT Imaging, Diagnosis, and Evolution

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 Acute Cerebral Infarction: CT Imaging, Diagnosis, and Evolution

Expert Radiologic Review with Case Discussion

Acute cerebral infarction (ACI), more commonly known as an ischemic stroke, remains a leading cause of death and long-term disability globally. Early diagnosis through neuroimaging—especially CT—plays a vital role in patient prognosis and management. In this post, we explore the imaging characteristics, differential diagnosis, and evolution of cerebral infarction based on a clinical CT case of right hemispheric infarction, accompanied by comparative normal anatomy.

What Causes Acute Cerebral Infarction?

Etiology and Pathophysiology

Acute cerebral infarction results from the sudden interruption of cerebral blood flow, leading to irreversible ischemia and infarction. The most common causes include:

  • Large vessel atherosclerosis
  • Cardioembolism (e.g., atrial fibrillation)
  • Small vessel disease (lacunar infarcts)

The cascade begins with cellular energy failure due to oxygen and glucose deprivation, followed by cytotoxic edema, ion pump failure, and excitotoxicity. Ultimately, neuronal death ensues, with imaging changes becoming evident over time.

Epidemiology

  • Globally, stroke is the second leading cause of death, with ischemic strokes accounting for ~87% of all cases.
  • Incidence increases with age and comorbidities such as hypertension, diabetes, and hyperlipidemia.
  • In Korea, the prevalence of cerebral infarction is estimated at 3.5 per 1,000 population, with a rising trend due to aging demographics.

Clinical Presentation

Typical symptoms of ACI include:

  • Sudden unilateral weakness or numbness
  • Aphasia or dysarthria
  • Vision disturbances
  • Loss of coordination or balance
  • Altered mental status

The case highlighted involves left facial weakness due to right hemispheric infarction, confirming contralateral symptom expression.

Imaging Features on CT

Early CT Findings:

  • Loss of gray-white differentiation
  • Hypodensity (Low-Density Area; LDA) in cortical or subcortical regions
  • Obscuration of the lentiform nucleus
  • Effacement of sulci and Sylvian fissure

Evolution Over Time:

  • Day 0-3: Cytotoxic edema causes clear low attenuation in cortex and subcortex.
  • Day 5: Well-demarcated infarct zone, maximal edema.
  • Day 11: "Fogging phenomenon" may obscure lesions—appears transiently isodense.

These changes are visible in the serial CTs included in the case. Notably, the right frontal lobe triangular hypodensity signals early infarction.

Differential Diagnosis

Distinguishing ACI from:

  • Multiple Sclerosis (MS): Presents with multifocal demyelinating lesions on MRI, often periventricular.
  • Metastatic Brain Tumor: Ring-enhancing lesions with surrounding vasogenic edema.
  • Seizure or migraine aura: May mimic stroke symptoms but have transient or migratory imaging findings.

Treatment and Prognosis

Acute Management:

  • IV tPA (alteplase) within 4.5 hours of symptom onset
  • Endovascular thrombectomy for large vessel occlusions up to 24 hours
  • Blood pressure control, antiplatelet therapy (aspirin), and anticoagulation (if cardioembolic)

Long-term:

  • Physical rehabilitation
  • Risk factor control (HTN, DM, dyslipidemia)
  • Antithrombotic secondary prevention

Prognosis depends on infarct size, location, and promptness of reperfusion. Without early intervention, irreversible damage and permanent neurological deficits can result.

Figures & CT Comparison


  • Normal axial CT anatomy through the body of the lateral ventricles.
  • A triangular hypodense area in the right frontal lobe suggests acute infarction.
  • Serial CT showing progression and fogging phenomenon.

Quiz

1. What does the “fogging phenomenon” refer to in CT imaging of cerebral infarction?

A. Contrast enhancement of necrotic tissue
B. Reversal of ischemia due to treatment
C. Temporary normalization of infarcted tissue density
D. Hemorrhagic transformation of infarct

Answer: C
Explanation: Fogging refers to the infarct becoming isodense with normal brain parenchyma around 1–3 weeks post-infarction, leading to false-negative CT.

2. Which of the following is the most likely cause of sudden left facial weakness in a right-handed patient?

A. Left pontine hemorrhage
B. Right hemispheric cerebral infarction
C. Migraine with aura
D. Bell’s palsy

Answer: B
Explanation: A right hemispheric infarct causes contralateral (left) facial weakness, especially if cortical motor fibers are involved.

3. Which imaging feature helps distinguish multiple sclerosis from acute infarction?

A. Diffuse low attenuation on CT
B. Well-demarcated enhancing lesion
C. Periventricular T2-hyperintense lesions on MRI
D. Hypodensity in basal ganglia

Answer: C
Explanation: MS is best visualized on MRI as multiple periventricular plaques with T2 Hyperintensity, often in different stages of evolution.

References

  1. Wardlaw, J. M., et al. "Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration." Lancet Neurology 2013;12(8):822–838.
  2. Lansberg, M. G., et al. "Time to treatment with endovascular thrombectomy and outcomes from ischemic stroke: a meta-analysis." JAMA 2016;316(12):1279–1288.
  3. Powers, W. J., et al. "Guidelines for the early management of patients with acute ischemic stroke." Stroke 2018;49(3):e46–e110.
  4. Bivard, A., et al. "Evolution of brain infarction after stroke and reperfusion." Stroke 2014;45(3):993–999.
  5. Bang, O. Y., et al. "Pathophysiology of ischemic stroke and neurovascular unit." Journal of Stroke 2016;18(3):231–239.
  6. Donnan, G. A., et al. "Stroke." Lancet 2008;371(9624):1612–1623.
  7. Hacke, W., et al. "Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke." New England Journal of Medicine 2008;359(13):1317–1329.

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