Wk 1, Case 5 - Review

Patient History

A 65-year-old woman with a history of atrial flutter, hypertension, coronary artery disease, and hyperlipidemia presents with acute-onset left-sided weakness, facial droop, slurred speech, and aphasia.

CT Head:

The ventricles and sulci are prominent but normal in size and configuration for age.

There are moderate chronic microvascular ischemic changes within the white matter of both hemispheres.

There are chronic lacunar infarcts in the left striatocapsular region, left corona radiata, and right thalamus. A small dystrophic calcification is present in the left frontal lobe.

There are vascular calcifications within the cavernous carotid and vertebral arteries bilaterally.

Hyperdensities in the right P1 segment and left sylvian fissure likely represent atherosclerosis or possibly calcified intraluminal thrombus.

The patient is status post bilateral cataract surgery.

CT Perfusion:

Study shows delayed Tmax volume of 61 cc. It is centered in the right posterior cerebral artery territory affecting the right occipital lobe. The CBF less than 30% volume is 0 cc.

CTA Head and Neck:

Angiographic images demonstrate atherosclerotic change at the aorta and origins of the innominate artery and left common carotid artery. The left common carotid artery is unremarkable. At the carotid bifurcation, there is both hard and soft plaque but no evidence of high-grade stenosis.

The right common carotid artery is also unremarkable. There is calcified plaque at the carotid bifurcation without high-grade stenosis.

The upper cervical portions of the internal carotid arteries are unremarkable. The petrous internal carotid artery shows normal appearance. There is mild atherosclerotic change in the cavernous carotid arteries bilaterally.

The right proximal V1 segment of the vertebral artery is identified. There is nonopacification of the V2 segment from approximately C3 to C6. There is distal reconstitution of the V3 and V4 segments.

The left vertebral artery shows no evidence of stenosis at its origin and it is affected by degenerative change in the cervical spine only. The left vertebral artery is seen in its entirety through its V2, V3, and V4 segments. The basilar artery is small in caliber.

There is a 3 mm filling defect in the proximal P1 segment of the right posterior cerebral artery with additional areas of non-opacification and stenosis involving the P2 segment. There also appears to be a branch of the left middle cerebral artery that does not opacify in the sylvian proximal segment.

Head and neck imaging demonstrates posterior pleural thickening and an infiltrate in the right upper lobe. There are mediastinal lymph nodes bilaterally. Lower neck supraclavicular lymphadenopathy is also present.

There is degenerative change with facet and uncovertebral joint degenerative changes most notably at the C3-4 level bilaterally, the right C2-4-5 level, bilateral C5-6 level, and bilateral C6-7 levels. These impinge on the foramen transversarium of the vertebrae.

Conclusion

1. Filling defect in the P1 segment of the right posterior cerebral artery measuring 3 mm with stenosis and areas of occlusion distally. Associated Tmax perfusion deficit in the right occipital lobe. Recommend clinical correlation for left homonymous hemianopia.

2. Probable clot in the left M2 branch of the middle cerebral artery without associated perfusion deficit.

3. Moderate parenchymal volume loss and moderate chronic small vessel ischemic changes. Small old lacunar infarcts. No hemorrhage, mass lesion, or acute infarction.