Wk 2, Case 1 - Review

Patient History

A 90-year-old female presents to the emergency department after a ground level fall with altered mental status.

Findings

CT Head:

Within the left subinsular region, there is a hyperdense region (Hounsfield unit 40), suggestive of blood products. There is surrounding hypodensity extending superiorly within the periventricular white matter to the centrum semiovale.

Additional scattered periventricular and subcortical hypodensities are nonspecific, but likely related to chronic microvascular ischemic change.

There is age-related cortical volume loss with ventricular and sulci prominence.

The gray-white differentiation is otherwise preserved. Ventricles are otherwise unremarkable and basal cisterns are patent.

There is trace mucosal thickening within a few ethmoid air cells and the maxillary sinuses. The paranasal sinuses are otherwise clear. The mastoid air cells are clear. Opacities within the external ear canals likely represent impacted cerumen. There is a partially empty sella turcica.

There is right temporoparietal scalp and periorbital soft tissue swelling. Scalp and calvarium are otherwise unremarkable. Hyperostosis frontalis interna is present.

Patient is status post bilateral cataract lens replacements. There is an ovoid hypoattenuating soft tissue mass in the right fossa for lacrimal gland. There is asymmetric enlargement of the right superior ophthalmic vein relative to the left side.

CTA Head and Neck:

Four-vessel branching aortic arch present with left vertebral artery arising directly from the aortic arch. There are atherosclerotic calcifications of the aortic arch, descending thoracic aorta, ascending aorta, and branches of ascending aorta.

The common and external carotid arteries are patent without evidence of aneurysm, high-grade stenosis, or dissection. Retropharyngeal course of the common carotid arteries present.

There are minimal atherosclerotic calcifications of the proximal aspect of the cervical segment of the right internal carotid artery, with less than 25% narrowing by NASCET criteria. In contrast, there is approximately 50% stenosis of the proximal aspect of the cervical segment of the left internal carotid artery secondary to atherosclerotic calcified and noncalcified plaque.

The cervical segments of the internal carotid arteries are otherwise unremarkable.

There is severe narrowing of the V1 segment of the left vertebral artery, which may be exacerbated by tortuosity of the vessel. The V1, V2, and V3 segments of the left vertebral artery are otherwise unremarkable. The V1, V2, and V3 segments of the right vertebral artery are unremarkable. The right vertebral artery is dominant.

There is asymmetric fusiform dilation of the supraclinoid segment of the left internal carotid artery relative to the right side, (5 mm on the left versus 3 mm in the right). There are atherosclerotic calcifications of the cavernous, clinoid, and supraclinoid segments of the internal carotid arteries with associated moderate narrowing.

The anterior cerebral arteries are patent, with asymmetric hypoplastic right A1 segment relative to the left side. The anterior communicating artery is unremarkable.

There is abrupt cut off of the M1 segment of the left middle cerebral artery just beyond its origin. Notably, there is evidence of collateral flow within the left cerebral hemisphere, with some opacification of the M3 and M4 segments of the left MCA.

Right dominant vertebrobasilar system with patent V4 segments of the vertebral arteries and patent basilar artery.

The posterior inferior cerebellar arteries are patent. The anterior inferior cerebellar arteries are not visualized and likely diminutive in caliber. The superior cerebellar arteries are patent.

There is severe narrowing of the P2 segment of the right posterior cerebral artery. The posterior cerebral arteries are otherwise patent. The posterior communicating arteries are not visualized, likely congenitally hypoplastic or absent.

CTP Head and Neck:

In the left MCA territory, there is elevated Tmax and mean time to transit with decreased cerebral blood flow and normal cerebral blood volume. Findings are compatible with large area of ischemic penumbra without core infarct by strict criteria.

RAPID analysis: Mismatch volume = 101 cc; CBF <30% = 0 cc; Tmax >6s = 101 cc

MRI Brain:

There are multifocal areas of elevated DWI signal with decreased ADC values primarily involving the left MCA territory as well as a portion of the left ACA territory.

The most notable infarcts involve the left lentiform nucleus and extend to the corona radiata and the lateral ventricular margin. Infarcts also demonstrate foci of susceptibility artifact and isointense T1 signal, compatible with microhemorrhage within the acute infarct as seen on prior CT.

There is an additional cortical infarct along the medial left frontoparietal cortex in the paracentral lobule.

Associated T2 FLAIR hyperintense signal is compatible with cytotoxic edema. There is no extra-axial fluid collection.

No acute infarct within the right cerebral hemisphere, brainstem, or cerebellum.

ASL perfusion imaging demonstrates multifocal areas of decreased cerebral blood flow within the left MCA territory relative to the right side. Overall there is limited evaluation on the ASL perfusion with signal changes related to susceptibility.

Additional periventricular and subcortical T2 FLAIR hyperintensities are nonspecific but likely related to chronic microvascular ischemic disease. The gray-white matter differentiation is otherwise preserved.

There is age-related global parenchymal volume loss with ventricular and sulcal prominence.

The ventricular system is otherwise unremarkable. The major intracranial flow voids are intact. There is a partially empty sella turcica.

The visualized paranasal sinuses are clear. A small left mastoid effusion is present. The right mastoid air cells are clear.

Partially visualized cervical spine appears unremarkable. There is susceptibility artifact from dental hardware.

Conclusion

1. Abrupt cut off of the M1 segment of the left MCA, compatible with thrombus. Associated large ischemic penumbra within the left MCA territory. RAPID quantitative analysis as detailed above.

2. Multifocal acute to subacute infarcts within the left MCA territory with evidence of internal microhemorrhage. This is predominantly in the perforator distribution involving the lentiform nucleus and corona radiata.

3. Additional acute infarct within the left ACA territory (left paracentral lobule).