-
Infarction: focal hypodense area, in cortical, subcortical,
or deep gray or white matter, following vascular territory,
or watershed distribution. Early subtle findings include
obscuration of gray/white matter contrast and effacement
of sulci, or "insular ribbon."
-
Hemorrhage: hyperdense image in white or deep gray matter,
with or without involvement of cortical surface (40 to
90 HU). Petechial refers to scattered hyperdense points,
coalescing to form irregularly hyperdense areas with hypodense
interruptions. Hematoma refers to a solid, homogeneously
hyperdense image.
-
Hyperdense image in major intracranial artery: suggestive
of vascular embolic material.
-
Calcification: hyperdense image within or attached to
vessel wall (>120 HU).
-
Incidental: silent infarct, subdural collection, tumor,
giant aneurysm, arteriovenous malformation.
-
Acute: Subtle low signal (hypointense) on T1, often difficult
to see at this stage, and high signal (hyperintense) on
spin density and/or T2-weighted and proton density-weighted
images starting 8 h after onset; should follow vascular
distribution. Mass effect maximal at 24 h, sometimes starting
2 h after onset, even in the absence of parenchymal signal
changes. No parenchymal enhancement with paramagnetic
contrast agent. Territorial intravascular paramagnetic
contrast enhancement of "slow-flow" arteries
in hyperacute infarcts; at 48 h, parenchymal and meningeal
enhancement can be expected.
-
Subacute (1 wk or older): Low signal on T1, high signal
on T2-weighted images. Follows vascular distribution.
Revascularization and blood-brain barrier breakdown may
cause parenchymal enhancement with contrast agents.
-
Old (several weeks to years): Low signal on T1, high
signal on T2. Mass effect disappears after 1 mo. Loss
of tissue with large infarcts. Parenchymal enhancement
fades after several months.
Stroke Education
