Presentation
Patient with a prior history of infarction of left frontal lobe and a known obstruction of internal carotid artery on both sides with an intact circle of Willis. Now the patient presents with semi-acute swallowing disorder and hoarseness.
Patient Data
Axial slice shows a large tissue defect left frontal, due to an infarction. Retrospectively there is subtle swelling of the right occipital lobe with diminished grey-white matter differentiation.
A large defect of left frontal lobe and some small defects in the cerebellum are preexistent.
In the right occipital lobe a new abnormality is present:
enlarged arachnoidal spaces indicating tissue loss
cortical thinning an loss of subcortical white matter
gyral T1 hyperintensity of the cortex and subcortical T2 and FLAIR hyperintensity
facilitated diffusion restriction
Case Discussion
Cortical mineralization on CT and/or T1 signal hyperintensity is fairly common following stroke and should not be mistaken for true pure cortical laminar necrosis which refers to damage limited to specific layers of the cortex. It should be noted, however, that area of cortical laminar necrosis may exist adjacent to large territorial infarcts.
In the literature there is some debate about the pathophysiology leading to the signal changes; some authors suggest the T1-shortening might be due to hemorrhagic components or calcifications. Other case series, however, report no signs of hemorrhage or calcifications on imaging. Some case series include autopsy and in these, no signs of hemorrhage were found as well. Based on in vivo and postmortem evaluation the T1 and FLAIR hyperintensity is thought to result from the deposition of lipid-laden macrophages in the area of subcortical necrosis. Signal changes occur in the cortical and subcortical area because the grey matter is most vulnerable to ischemia and hypoperfusion. Why these tissue changes occur and why in some but not all patients remains to be resolved.
Unable to process the form. Check for errors and try again.