Wk 1, Case 3 - Review

Patient History
Cluster headache, not intractable, unspecified chronicity pattern.
Findings
Non-contrast CT head:

These images show abnormal hypoattenuation involving the right anterior insula, right lentiform nucleus and head of the right caudate nucleus, as well as the right frontal operculum with cortical involvement and loss of gray-white distinction with sulcal effacement involving the right frontoparietal brain as well as the right inferior frontal gyrus. Smaller focus of involvement of the posterior insula is contiguous with hypoattenuation in the right frontoparietal operculum. Subcortical focus of encephalomalacia is seen involving the postcentral gyrus.There is mild extrinsic impression upon the right frontal horn. Otherwise no shift of midline structures is noted. No evidence of hemorrhagic transformation is seen. No evidence of acute intracranial hemorrhage or extra-axial fluid collection present.

There is slightly increased density of the right middle cerebral artery, with punctate hyperdensity involving a branch vessel of the posterior portion of the sylvian fissure. Basal cisterns are patent. No focal abnormality seen in the posterior fossa. Atherosclerotic calcifications are present within the vertebral arteries as well as the right greater than left cavernous carotids.

Impressions
1. These images demonstrate multiple areas of hypoattenuation and loss of gray-white distinction involving the right frontal lobe and the right-sided basal ganglia as well as the right insula, consistent with acute infarctions involving the right MCA distribution.

2. Mildly hyperdense appearance of the right middle cerebral artery as well as a posterior branch compatible with clots.

3. Focus of encephalomalacia seen in the right postcentral gyrus that may represent a focus of chronic ischemia.

Findings
CTA Head and Neck:

The origin of the right common carotid artery is normal in appearance. There is minimal atherosclerotic change in the right common carotid artery anterior wall. At the carotid bifurcation there is high-grade stenosis where the luminal diameter of the proximal right internal carotid artery narrows to 0.1 mm. Its more distal luminal diameter measures 3.5 mm compatible with greater than 70% stenosis. There is also atherosclerotic calcification associated with the carotid bifurcation and the soft plaque associated with it.

The caliber of the distal right internal carotid artery in the neck and in the petrous portion and cavernous portion is diminished. There appears to be clot in the cavernous carotid artery on the right side. Supraclinoid right internal carotid artery is narrowed in caliber. There is clot in the M1 and M2 segment of the middle cerebral arteries on the right side. The anterior cerebral artery has a more normal caliber. Distal right middle cerebral artery branches appear to be partially supplied by posterior cerebral artery collaterals.

The origins of the vertebral arteries are normal in appearance. Their course through the neck is remarkable for narrowing of the right cervical vertebral artery at the neural foramen of the C3-4 level from uncovertebral joint degenerative changes. The remainder of the evaluation of the vertebral artery shows minimal V4 calcification on the left side intracranial portion after the posterior inferior cerebellar artery has taken off. The basilar artery is normal in appearance.

The left common carotid artery shows minimal atherosclerotic change in its cervical portion. At the carotid bifurcation there is calcified plaque with narrowing of the lumen of the proximal left internal carotid artery to a width of 1.5 mm. The distal internal carotid artery luminal width is 5 mm, calculated as borderline 70% stenosis. The petrous and cavernous left internal carotid artery show minimal atherosclerotic change.

The aerodigestive system is unremarkable. The cervical spine shows degenerative changes most notably at the C3-4, C5-6, and C6-7 levels in the cervical spine. Foraminal narrowing is present at C4-5, left greater than right, bilaterally at C5-6, and bilaterally at C6-7. Moderate to severe posterior osteophyte and uncovertebral joint degenerative changes are present at C3-4. This is the level where the vertebral artery is slightly narrowed from degenerative spurring.

Impressions
Clot in the cavernous, supraclinoid portions of the right internal carotid artery as well as the right M1 and M2 middle cerebral artery as expected from the hyperdense right middle cerebral artery sign. Right middle cerebral artery distribution stroke persists.

Severe atherosclerotic narrowing of the proximal right internal carotid artery just above the bifurcation measuring 80-90%.

Narrowing of the right cervical vertebral artery at the C3-4 level from degenerative uncovertebral joint spurring.

Approximately 70% stenosis of the left internal carotid artery at the bifurcation.

Findings
MRI brain:

Corresponding roughly in volume with the regions of hypodensity demonstrated on the CT scan performed last evening just before 7:30 there are regions of predominantly cortical and to a lesser extent subcortical T2-weighted/FLAIR signal hyperintensity as well as swelling. These involve not only the right ventral lateral frontal cortical convexity but also the striatocapsular structures on the right, the insular cortex, the right postcentral gyrus, the right inferior and the right superior parietal lobules. There is no gross hemorrhagic conversion. There is mild mass effect, as evidenced by indentation on the lateral aspect of the rostral body and the frontal horn of the right lateral ventricle, but these findings were also demonstrated on the CT from last evening.

Within the regions of presumably infarcted territory, there are scattered foci of post gadolinium T1-weighted signal hyperintensity, likely representing slow flow within vessels. There are also scattered foci of post gadolinium T1-weighted signal hyperintensity within the brain parenchyma, most prominently within the white matter immediately deep to the posterior aspect of the right superior frontal sulcus. These probably represent changes related to infarction.

Susceptibility weighted images demonstrate markedly reduced signal along the expected course of the M1 segment of the right middle cerebral artery, extending slightly into what is likely the trunk of the inferior division of the right middle cerebral artery, although this vessel appears to exhibit at least some flow void on T2-weighted images.

Cerebral blood flow is reduced throughout the region of infarction, and also within the small gaps in the diffusion weighted signal abnormality involving the ventral lateral most aspect of the right precentral gyrus. There is also slight reduction in cerebral blood flow or posterior within the right inferior parietal lobule within the posterior most extent of the reduced diffusivity, and similarly anteriorly within the right ventral lateral frontal lobe anterior to the anterior most extent of the reduced diffusivity, but these reductions in cerebral blood flow are slight. There is also slightly increased cerebral blood volume in these anterior and posterior regions that exhibited slightly reduced cerebral blood flow, compatible with an element of compensatory hyperemia. However, in the central core of the infarcted region there is both reduction in cerebral blood flow and and several blood volume.

The T2-weighted images demonstrate loss of flow void within the petrous segment of the right internal carotid artery, as well as narrowing and reduction in flow void within the cavernous and juxta clinoid segments of this vessel, compatible with slow flow. Otherwise, the flow voids appear normal.

The orbital contents appear normal.There is patchy mucosal thickening throughout the paranasal sinuses but there are no fluid levels.The mastoid air cells and the labyrinthine structures appear normal.

Impressions
Extensive right cerebral hemispheric infarction in territories supplied by both the superior and inferior division of the right middle cerebral artery as well as lenticulostriate vessels. Mild mass effect. No hemorrhagic conversion.