Imaging description

Internal carotid artery (ICA) dissection may be clinically unsuspected as a cause of subacute ischemic stroke, but there are imaging manifestations that suggest this diagnosis. A watershed distribution of hypodensity (Figure 8.1A) in a patient presenting with acute neurologic deficit is highly suspicious for ischemic infarct from an ipsilateral ICA dissection. MRI typically demonstrates restriction (bright signal) on diffusion-weighted images and decreased signal on the apparent diffusion coefficient (ADC) map which corresponds to acute cytotoxic edema in the areas of hypodensity (Figure 8.1B). Additionally, finding intrinsic high T1 and FLAIR signal outlining the affected cortex (Figure 8.1C and 8.1D) is consistent with laminar necrosis, as these signal abnormalities take 10–14 days to appear after the ischemic event. This indicates subacute ischemia. Corresponding gyriform or superficial enhancement in the affected cortex and subcortical white matter (Figure 8.1E and 8.1F) can help differentiate the process from other diseases. Gyriform enhancement is usually caused by vascular or inflammatory processes and is rarely neoplastic.

Finding bright signal within the ipsilateral carotid artery on T1-weighted images, corresponding to loss of the normally visualized signal void, suggests slow flow or thrombus as the etiology for the acute ischemic event (Figure 8.1G). If the vascular flow voids are normal on the brain MR study, MR angiography (MRA) of the neck vasculature will often reveal the source of the ischemic event.

In the majority of cases, carotid artery dissection involves the extracranial ICA, sparing the bifurcation. Time-of-flight MRA will show signal loss in the ipsilateral ICA (Figure 8.1H), consistent with a flow-related abnormality secondary to dissection and possible thrombosis. Three-dimensional maximum intensity projection images will usually demonstrate flow-related signal loss or smooth tapering of the ICA lumen distal to the bifurcation. On CTA, ICA dissection is characterized by eccentric luminal narrowing with an increase in the external diameter of the artery from mural thrombus, producing a target appearance [1].