Hyperacute Arterial Stroke: CT Head

History

Acute change in neurologic status; rule out stroke.

Exam

Non-Contrast Screening Head CT

Purpose:

1. Identify all areas of chronic post ischemic (or post traumatic/postoperative) damage, including encephalomalacia, subcortical leukomalacia, ischemic demyelination, shrunken gyri/ulegyria, since they will exhibit reduced blood flow on the CTA & CT perfusion;

2. Exclude abnormalities that would preclude IV or IA therapy;

3. Include evidence of hyperacute stroke findings in one or more recognizable arterial zones; include evidence of hyperdense proximal arterial segments in the high cervical, the extradural/intracranial, or intradural arterial segments. Be especially careful to analyze those proximal arteries that are accessible for embolectomy.

4. Consider venous based stroke if cytogenic edema does not conform to an arterial zone & could be a recognizable venous territory, plus, search for aggressive sinusitis/otomastoiditis/parapharyngeal infection as a cause;

5. Is the parenchymal CT density sufficiently obvious that the stroke, although present, is outside the treatment window.

Findings

Exclusionary Observations

There is evidence of recent intracranial (subarachnoid/cisternal/intraventricular) hemorrhage. [Yes/No]

There is evidence of recent intracranial parenchymal (intra axial) hemorrhage. [Yes/No]

There is evidence of recent intracranial hemorrhagic stroke conversion. [Yes/No]

There is evidence of “isodense focal mass” effect centered in the stroke-zone, which could be related to very recent hemorrhagic conversion or sequestered infarction. [Yes/No]

There may be extravasation of contrast from recent earlier CTA. [Yes/No]

There is a background CT density asymmetry between the cerebrum vs cerebellum (only evident when using narrow/high contrast window widths), which if present, is consistent with global hypoxic-ischemic (HIE) event where the cerebrum is uniformly hypodense and the cerebellum is actually normal or near normal. [Yes/No]

Generalized loss of sulci with compression of cisterns, & ventricles (not in a recognizable arterial zone) is indicative of other processes that causing asymmetric, nonfocal, brain swelling, as pseudotumor cerebri, drowning, respiratory arrest, etc. [Yes/No]

There is evidence of dural sinus thrombosis. [Yes/No]

There is evidence of major cortical or deep central vein thrombosis (these produce focal edema with a venous rather than an arterial distribution). [Yes/No]

There is evidence of aggressive otomastoid or paranasal sinus infectious disease, which could lead to cortical vein phlebothrombosis or dural sinus thrombosis. [Yes/No]

Inclusionary Observations

There is proximal arterial hyperdensity indicating acute thrombus, especially treatable stem arteries (proximal ICA, M1, intradural vertebrals, and basilar arteries), Hyperdensity could also be present in the high cervical carotid or vertebral artery thrombosis. Intrauminal hypodensity is also abnormal from subacute thrombus or dissection. [Yes/No]

There is focal effacement of GW junction from early cytogenic edema. [Yes/No]

There is evidence that the stroke-zone occupies more than 1/3 of the proximal stem artery’s expected perfusion zone. [Yes/No]

There is hyperdense CT changes in brain parenchyma, likely representing a region of dense ischemic core. [Yes/No]

There is well delineated CT hypodense change within a recognizable arterial territory indicating the stroke evolution time from ictus to imaging is at least 8 hours. [Yes/No]

There is focal effacement of sulci confirming the presence of either cytogenic edema or expanded venocapillary bed from physiologic hyperemia in the collateral zone surrounding the stroke-zone. [Yes/No]

There is focal effacement of parts of the ventricles confirming presence of local post ischemic cytogenic edema. [Yes/No]

There is protein leak into sulci (effacing the margins of the sulci) consistent with increasing blood brain barrier leak. [Yes/No]