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Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
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Bilateral Cerebral Hyperperfusion Syndrome Following Carotid Artery Stenting in Stroke - A Case Report
Nandakumar Nagaraja1, Manuel Viamonte2, Jun Yu1
1Department of Neurology, University of Florida College of Medicine, Gainesville, FL, USA.
Background:
Revascularization of the symptomatic carotid artery is performed with endarterectomy or stenting. Rarely, patients may develop cerebral hyperperfusion syndrome (CHS) following revascularization. This usually occurs in the cerebral hemisphere ipsilateral to revascularized carotid stenosis. CHS rarely involves the contralateral hemisphere.
Objective:
To present a case of CHS involving bilateral cerebral hemispheres following carotid artery stenting in acute ischemic stroke.
Case Description:
A 66-year-old woman presented with right side weakness and aphasia. National Institutes of Health stroke scale score was 27. CT angiogram/perfusion showed high grade left internal carotid artery (ICA) stenosis, left middle cerebral artery (MCA) occlusion, and increased time to peak in left MCA territory. She underwent mechanical thrombectomy with complete reperfusion. Left carotid artery stenting was performed for 85% cervical ICA stenosis with thrombus. She neurologically deteriorated and required intubation after the procedure. Follow-up CT perfusion at 18 hours after thrombectomy showed increased cerebral blood flow and early time to peak in bilateral MCA territories. CT head showed parenchymal hematoma in the left subcortical area with extension to the ventricle. Fluid-attenuated inversion recovery MRI on day 4 showed diffuse white matter hyperintensities in the entire right hemisphere, and left temporal and frontal lobes suggestive of vasogenic edema.
Conclusion:
This case highlights bilateral cerebral hyperperfusion syndrome characterized by neurological worsening, imaging findings of parenchymal hemorrhage, vasogenic edema and increased cerebral blood flow without any new ischemic lesions. The involvement of bilateral hemispheres in the absence of significant contralateral carotid stenosis is unique in this case.
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