Specific Imaging Findings

Chronic infarcts are areas of variable size, shape, and location, usually with cortical and subcortical involvement, characterized by CSF-like density on CT and signal intensity on MRI. There is shrinking and/or amputation of the cerebral parenchyma, with passive (ex vacuo) dilation of adjacent CSF-containing spaces (such as ventricles and cortical sulci). Along the edges of the CSF-like area of encephalomalacia, there is an ill-defined rim of relatively higher CT attenuation, representing gliosis. FLAIR images show to better advantage the gliotic margins, which are bright between the CSF-like encephalomalacia and isointense normal white matter. Chronic infarct is also bright on ADC maps. CT and T2*WI may show chronic microhemorrhages and rarely distrophic calcifications, as bright and dark areas, respectively. There is no contrast enhancement and vascular paucity is usually present in the affected area. Curvilinear hyperintensity of the cerebral cortex corresponding to laminar necrosis may be seen on T1-weighted and FLAIR images, especially if the underlying white matter was not infarcted. Infarcts affecting large white matter tracts also show atrophy along the entire tract, remote from the primary injury (Wallerian degeneration). Atypical location and distribution of encephalomalacia and gliosis should raise possibility of a different etiology, such as prior traumatic contusion, surgery, venous infarct, vasculitis or metabolic disorders.

Pertinent Clinical Information

History of stroke with chronic stable neurological deficit is the most commonly encountered clinical scenario, but incidental finding of chronic infarcts also occurs in patients with minimal or absent symptoms and signs. This is explained by compensation (especially for in-utero or early postnatal lesions), and/or involvement of non-eloquent areas. Cardio-cerebro-vascular risk factors should be investigated in patients with cerebral infarcts, in order to reduce risk of new injuries or progressive deterioration. Location and shape of the lesion can suggest the causative mechanism: thromboembolic events of major arteries distal to the circle of Willis show a wedge or rectangular shape, within the corresponding vascular distribution; occlusions of perforating arteries cause subcortical (lacunar) infarcts, confined to the deep gray matter and/or white matter; embolic and hemodynamic infarcts, caused by occlusion of arteries proximal to the circle of Willis or emboli from these vessels or the heart, tend to involve the border zones between adjacent vascular territories (“watershed” areas).