Hyperacute Arterial Stroke X - Clinical Case Summary
Hyperacute Arterial Stroke X - Clinical Case Summary
Hyperacute Arterial Stroke X - Clinical Case Summary
SummaryHistory
Exams performed
Prior available imaging reports
Initial Non-Contrast Head CT
1. Acute thrombus in the high cervical and vertical intrapetrous segments of the left cervical ICA without evidence of acute cerebral stroke. The history of acute upper neck pain makes dissection a likely possibility. Head was negative for hyperacute stroke changes
Initial MRA of the Neck
1. Acute dissection of the high cervical ICA on the left with high-grade luminal stenosis. There is limited persistent antegrade blood flow and evidence of EC-IC collateral.
Initial MRA of the Head
1. There is evidence of an acute, high cervical, ICA dissection on the left; there is collateralization related to minimal antegrade blood, & patent EC-IC connections. There is an incomplete circle of Willis limiting retrograde perfusion from the PCA to the left carotid circulation.
Initial Head MR
1. The diffusion was MR diffusion positive for evidence of a recent seizure event within the left hippocampus. It was negative for stroke.
9 Days Later Limited MR (only diffusion sequences) obtained after new symptoms
1. The initial prior MR diffusion at presentation was normal for stroke but positive for seizure (presented in Case 9A). The 9 day follow up MR diffusion (presented here in Case 9B) demonstrates multiple focal areas of acute ischemic changes (secondary embolic shower) in the left splenium and body of the corpus callosum (distal ACA-pericallosal perfusion zone), in one mesial and one lateral lenticulostriate perforator, and in several distal Lt. anterior insular M3 branches. These thromboembolic ischemic sites are all positive on both the DWI & ADC maps confirming their hyperacute timeframe.
10 Day Follow up CTA
1. The 10 day followup CTA demonstrated substantial recanalization of the thrombi in the right A1/2 clot, and the left M1/2 clot leaving only minimal to moderate residual luminal narrowing in the proximal inferior division MCA. The P1 was developmentally hypoplastic (fetal variant) and not thrombosed.
Overall impression
2. The follow-up CTA (obtained 11 days after initial CTA) demonstrates recanalization of the prior sites of intraluminal thrombus. There is minimal residual clot along the wall of in the left MCA producing only minimal stenosis. The sites of positive MR diffusion appear as completed infarctions on the CTA.
3. The left hippocampal, post seizure, edema has largely cleared leaving only minimal residual changes.
Lessons to be learned
2. This case illustrates how fluid the clinical situation is in stroke cases. Within 9 days after the initial presentation, new symptoms developed, which were the result of intercurrent acute post embolic strokes. Thus, the initial MR diffusion was negative for stroke and positive for seizure, while the followup MR diffusion has become positive. This exam reveals multiple new secondary thromboemboli causing strokes in the left insula, the left lateral basal ganglia, the left mesial basal ganglia, and the left corpus callosum. The new strokes were obviously the result of interval proximal clot lysis and secondary downstream embolization.
3. The CTA obtained at 10 days after presentation and one day after the followup MR diffusion, illustrates the effectiveness of the delayed CTA in detecting sites of completed infarction based on persistently very low CT density within the venocapillary pool in these areas clearly matches the concurrent MR diffusion. The 3 month follow up FLAIR demonstrates how both of the the entire left centrum semiovale stroke proceeded to liquefactive necrosis, where as only a very small part of the left spenium stroke proceeded to liquefactive necrosis. Most of the corpus callosum stroke remained solid and demonstrated parenchymal hemosiderin within the stroke-zone. Thus, the outcome for both is completed stroke but the outcome is liquefactive necrosis for the centrum semiovale stroke (ultimately had reflow) and chronic sequestered infarction for the corpus callosum stroke (ultimately never developed reflow necessary to remove the infarcted tissue-hence the name).