Recurrent Hyperperfusion Syndrome and Intracerebral Hemorrhage after Recanalization of the Extracranial Carotid Artery

Thirteen months later, in November 2002, she was referred for treatment of a carotid restenosis. The patient had been asymptomatic since the first procedure. When assessed at our institution, the patient showed a residual mild, right hemiparesis. Doppl er ultrasound revealed 80% stenosis of the left ICA and common carotid artery (CCA). There was also a high-grade left external carotid artery stenosis. The vessels of the posterior circulation appeared normal. Transcranial Doppler (TCD) studies revealed reduced left middle cerebral artery (MCA) flow velocities (VL; left MCA: VL systolic 0.8 m/s, VL diastolic 0.35 m/s; right MCA: VL systolic 1.2 m/s, VL diastolic 0.4 m/s). There was no evidence of any extraintracranial collateral vascularization or cross-flow to the left ICA territory via the circle of Willis. Brain CT revealed a parenchymal defect after ICH in the left frontoparietal region. 99 Tc HMPAO-SPECT showed reduced radionuclide tracer uptake in the left ICA territory, which further decreased after acetazolamide challenge. Selective intra-arterial angiography revealed 1 80% left CCA stenosis and 1 50% left ICA stenosis according to NASCET ( fig. 1 ). The intracerebral angiogram was normal. Uneventful carotid artery stenting (CAS) was performed. On the first day after CAS, color Doppler ultrasound revealed normal VL in the region of the The term cerebral hyperperfusion syndrome (HS) was coined by Sundt et al. [1] in 1981 to describe a rare complication of carotid endarterectomy (CEA) which may appear with severe unilateral headaches, seizures and focal symptoms related to cerebral edema or intracerebral hemorrhage (ICH) and is considered to result from a major increase in ipsilateral cerebral blood flow above the metabolic demands of the brain. Obvious risk factors include long-standing hypertension, high-grade stenosis, poor collateral blood flow and contralateral carotid occlusion [2–4] . Several mechanisms such as a paralysis of cerebral autoregulatory mechanisms, a break-down of the baroreceptor-reflex and an axon-like trigeminovascular reflex have been implicated in the pathophysiology of hyperperfusion and in the evolution of the cerebral HS [2] . Once it is associated with ICH, the prognosis tends to be poor [2, 4] . We here illustrate the obvious role of endothelial damage in the development of intracerebral bleeding with the imaging findings in a rare case of a recurrent cerebral HS.