Wk 5, Case 3 - Review

Patient History

Episode of decreased responsiveness.

Findings

CT Head:

Brain Parenchyma: Minimal patchy white matter hypoattenuation with preserved gray-white distinction. No hemorrhage, cerebral edema, acute cortical infarction, mass, mass effect, or midline shift.

Ventricles and Sulci: Diffusely prominent. Normal for age.

Extra-Axial Spaces: No extra-axial fluid collection or hematoma.

CT Perfusion Head:

No asymmetries in the mean transit times, cerebral blood flow, or cerebral blood volume to suggest an autoregulatory compromise.

Slightly increased Tmax in the right PCA territory, likely insignificant and likely related to the anatomical variations of the intracranial circulation where the left PCA receives its flow predominantly from the anterior circulation. The right PCA and branches appear patent.

AIF/VOF Placement: Technically Adequate

Stroke Location: Not present.

CBF<30% volume (mL): 0

Tmax>6.0s volume (mL): 0

Mismatch volume (mL): 0

Mismatch ratio: None

CTA Head and Neck:

Extracranial

Great Vessels: Patent.

Common carotid arteries: Patent. Atherosclerotic calcification of carotid bulbs without hemodynamically significant stenosis.

Right ICA: No flow limiting stenosis. No dissection.

Left ICA: No flow limiting stenosis. No dissection.

Vertebral Arteries: Normal bilaterally. Dominant left vertebral artery. No dissection.

Bilateral osteophytes at C5-C6 with indentation upon the vertebral arteries.

Left vertebral artery at the C3-C4 level demonstrates a loop with a medial course extending through a narrowed left neural foramen (hypertrophic facet arthropathy) with a short segment extradural intraspinal course. No significant narrowing although this segment of the vessel. Mild tortuosity of the smaller right vertebral artery.

Intracranial

Intracranial ICAs: Patent bilaterally from the skull base to the carotid terminus. Left internal carotid artery is larger than the right. Atherosclerotic calcifications of cavernous and paraclinoid ICAs with no more than a mild narrowing. No evidence of a hemodynamically significant stenosis.

MCAs: Patent bilaterally.

ACAs: Severely hypoplastic or absent right A1 segment. Patent dominant left A1 segment with bilateral A2 segments of the anterior cerebral artery receiving blood from the left.

ACom: Present

P-Comms: Prominent left posterior communicating artery with no visualized right-sided vessel. Fetal origin of the left PCA

PCAs: Hypoplastic, small P1 segment on the left with the distal P2 and P3 segments of the left posterior cerebral artery receiving blood predominantly from the left posterior communicating artery. Patent right posterior cerebral artery throughout its P1, P2 and P3 segments with no significant stenosis.

Basilar artery: Patent.

Vertebral arteries: Scattered atherosclerotic calcification of V4 segments without hemodynamically significant stenosis. Left dominant vertebral artery.

Conclusion

1. No acute infarct. No acute intracranial hemorrhage.

2. Intracranial and extracranial carotid and vertebral arterial vasculature is patent without stenosis, dissection, or aneurysm. Atherosclerotic changes at the carotid bifurcations and involving the cavernous and clinoid segments of the internal carotid arteries with no more than mild narrowing.

3. Anatomical variation of the circle of Willis with the left posterior cerebral artery and bilateral anterior cerebral artery distribution supplied predominantly from the left internal carotid artery. Hypoplastic or absent right A1 segment, and a very small/hypoplastic left P1 segment.

4. No significant abnormality seen on the CT perfusion imaging. Subjective/slight prolongation of Tmax in the right posterior cerebral artery distribution that likely represents the difference between the transit time on the posterior circulation vessel as compared to the anterior circulation flow through the left PCA, given the anatomical variation of the circle of Willis described in #3 above.