Evolution of a malignant right internal carotid artery infarct

Case contributed by Yaïr Glick
Diagnosis certain

Presentation

Left hemiparesis.

Patient Data

Age: 60 years
Gender: Male

CT head, day 0, several hours after symptom onset

Bilateral lacunar infarcts in the basal ganglia and external capsules. Small hypodense subcortical areas scattered in the right hemisphere, probably representing ischemic microvascular disease.
Small ovoid hypodensity centered on the genu of the right internal capsule - fresh lacunar infarct?

Post-cataract removal in both eyes. The globes are flattened, suggesting myopia.

CTA head-neck 2.5 hours later, post-thrombolysis therapy

The right internal carotid artery (RICA) is occluded immediately distal to its origin for its entire length, apparently an acute occlusion, probably due to a fresh thrombus or perhaps dissection.
The arteries of the right cerebral hemisphere are filled via the circle of Willis, albeit substantially less than the left arteries.
The rest of the neck arteries (not shown in their entirety on the axial view) are patent, with moderate atherosclerotic changes.
The right vertebral artery shows several stenoses - atherosclerotic in nature? spasm?

CT head, day 1

Acute right MCA-ACA territory infarct involving, inter alia, the head, genu and anterior body of the corpus callosum, right basal ganglia and cerebral peduncle, and causing a minimal frontal subfalcine herniation.

CT head, day 2

Right hemispheric edema more pronounced, subfalcine hernia more apparent.

CT head, day 3

Widespread right fronto-parieto-temporal edema, partially effacing the right and third ventricles. More prominent subfalcine herniation.

CT head, day 6

Ventilation tube via the mouth, nasogastric tube via the left nostril.
Yet further aggravation of the right-sided cerebral edema, with the following features:

  • widespread sulcal effacement in both cerebral hemispheres and in the cerebellum
  • severe subfalcine herniation (up to 16 mm), with effacement of the right and third ventricles
  • dilated left ventricle (hydrocephalus), with surrounding edema, most prominent around its occipital horn
  • right inferior transalar herniation
  • right descending transtentorial herniation with Kernohan phenomenon
  • severe (10 mm) cerebellar tonsillar herniation
  • both transtentorial and tonsillar herniation cause effacement of the fourth ventricle
  • falx cerebri and tentorium cerebelli appear hyperdense (as do blood vessels in the right hemisphere), probably artifactually due to cerebral edema; however, parafalcine and tentorial subdural hematoma cannot be confidently ruled out

Case Discussion

This case shows the evolution of a malignant ICA (i.e. MCA-ACA) infarction to the point where cerebral edema is so great that there are at least four types of herniation involved:

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