42 year old male with right sided numbness and neck pain; history of seizures and hypertension.
 

Noncontrast CT head; MRA of the neck; MRA of the head; MR diffusion; MR flair; MR susceptibility

CT head
1. Hyperdense left ICA is evident in its’ high cervical segment and evidence of lucency within the lumen of the adjacent high cervical ICA (likely intraluminal hyperacute thrombus). Brain CT density is NL without CT evidence of stroke.

CT perfusion was not acquired

MRA of the neck
1. Acute dissection of the high cervical and vertical intrapetrous ICA on the left with intraluminal thrombus producing high-grade luminal stenosis (or occlusion) leaving at best minimal residual antegrade blood flow. Patent EC-IC collateral likely provides most of the extradural ICA collateral flow.
2. Given a history of seizures, this spontaneous left ICA dissection may have been the result of a recent grand mal type of seizure. No underlying vasculopathy is evident.

MRA of the head
1. High cervical and intrapetrous ICA arterial dissection on the left with intraluminal thrombus evident. There is functional EC-IC collateral accounting for the abrupt transition between the thrombus and the patent ICA.
2. Multiple sites of acute thromboemboli are evident (right A1/A2 junction, left M1/2 junction, and left proximal P1 segment.

CTA venocapillary pool was not acquired

MR Diffusion
1. Abnormal diffusion is evident in the left hippocampus consistent with very recent seizure. No sites of positive diffusion are present to confirm stroke.

MR Flair
1. Abnormal FLAIR is evident in the  left hippocampus and in the columns of the fornix consistent with very recent seizure. No other sites of positive FLAIR are present to confirm stroke.
2. There is positive FLAIR signal in the wall of the high left ICA consistent with dissection. There is positive intraluminal FLAIR within the intrapetrous left ICA consistent with intraluminal thrombosis over a short segment. There is a clear delineation between this thrombus and the remaining patent ICA. The source of the patent cavernous segment is likely functional EC-IC collateral.

MR  susceptibility (SWI)
1. There is positive SWI signal in the left M1/M2 segments of the MCA and in the proximal A1/A2 segments. The left P1-PCA thrombus and the extradural ICA thrombi are obscured by bone artifact.
2. There is venous  left cerebral hyperemia, which could be a response to the proximal flow limiting ICA dissection or could be post ictal hyperemia or both. No CT perfusion is available to differentiate between these two possibilities.

1. High cervical, left, ICA dissection. It extends into the vertical segment intrapetrous ICA canal. It recanalizes in the horizontal intrapetrous, ICA canal, likely from vidian artery collaterals.

2. Acute thromboembolic stenoses with clot in the proximal segment of the right ACA. Note the right A1 segment is developmentally hypoplastic. There is a second clot is located at the left M2-MCA bifurcation of the superior and inferior divisions. There is at least minimal antegrade filling in both sites of luminal stenosis. There is also evidence of functional pial collateralization.

3. MR diffusion is negative for an acute ischemic event within the cerebrum. However, there is acute cytogenic edema limited to the left hippocampus consistent with a very recent seizure event. The hippocampal edema is unlikely to be an ischemic (i.e. anterior choroidal artery perfusion zone) hippocampal injury, because there is no concurrent ischemic injury in the adjacent parahippocampal gyrus nor in the uncus (also supplied by the anterior choroidal artery). Basis for the acute seizure is indeterminate by imaging.

1. This case illustrates how the initial symptoms in this case were most likely to be related to a seizure (acute post ictal findings were evident on the MR diffusion and FLAIR). It is also likely that the epileptic event caused the left high cervical ICA dissection (evident on the FLAIR). The dissection resulted in a short segment occluding thrombus in the intrapetrous left ICA (also visualized on FLAIR). Clot lysis likely produced the intradural left cerebral emboli.  Currently, there is no acute stroke relative to the sites of emboli. Therefore, the initial symptoms were likely post ictal. 

2. We actually had a limited outside CTA preceeding our MR and MRA by 10 hours. It demonstrated the intrapetrous dissection, but clearly demonstrated a normal appearance to the intracranial arteries. The MRA presented in this case now has evidence of thromboemboli in multiple arteries.  This case demonstrates how quickly clot lysis of the original thrombus can produce secondary emboli.

3. The SWI demonstrates venous hyperemia and evidence of recent thrombus in most of the embolic sites. The hyperemia is nonspecific and could be physiologic in response to proximal flow limitation at the dissection site, or could be related to post ictal hyperemia, or both.

4. Currently, there is no positive diffusion to confirm stroke at this time. Since DWI is very sensitive to the earliest ischemic injury and none is evident, the presenting symptoms are likely related to the seizure event.

5. Finally, always be aware that stroke symptoms are not specific and multiple other problems causing similar symptoms are possible, as in this case. However this is not the end of this case. The patient developed new symptoms a few days later and new imaging was obtained producing new imaging findings. Proceed to Case 9B, which is the same patient as in this Case 9A.

Watch the included summary video for this instructional case.