Revascularization of Concurrent Renal and Cerebral Artery Stenosis in a 14-Year-Old Girl with Takayasu Arteritis and Moyamoya Syndrome

Concurrent involvement of bilateral renal and cerebral arteries, usually incurred as stenosis, is rare in childhood-onset Takayasu arteritis (c-TA). We report the case of a 14-year-old girl, with c-TA, presenting with transient ischemic attack after endovascular revascularization for renal artery stenosis and cerebrovascular stroke after surgical revascularization for cerebral artery stenosis associated with childhood-onset moyamoya syndrome. We deem that decrease of blood pressure by endovascular revascularization and improvement of cerebral perfusion by surgical revascularization may have jeopardized the cerebral deep watershed zone to cerebral ischemia followed by cerebral hyperperfusion syndrome and caused transient ischemic attack and cerebrovascular stroke in our patient. Revascularization could be a double-edge sword for c-TA patients presenting with concomitant renal artery stenosis and cerebral artery stenosis, and should be performed with caution. Quantitative analysis of cerebral blood flow by brain magnetic resonance imaging and angiography should be performed within 48 hours after surgical revascularization in c-TA.

Delayed Cerebral Hyperperfusion Syndrome after Carotid Artery Stenting: the Finding of Multimodal MRI

A 78-year-old right handed man with hypertension presented with sudden onset dysarthria and right hemiparesis. Magnetic resonance angiography revealed near-occlusion of left proximal internal carotid artery. Emergent carotid stenting was performed. On the 17th day after carotid stenting, he showed decreased consciousness. Magnetic resonance imaging (MRI) showed edematous change with high signal and increased perfusion in the left hemisphere. Our case shows that delayed cerebral hyperperfusion syndrome can occur even 2 weeks after carotid artery stenting and multimodal MRI can help accurate diagnosis.

Acute Subdural Hematoma after Carotid Artery Stenting

Cerebral hyperperfusion syndrome is a major cause of morbidity and mortality following carotid artery stenting (CAS). We present a case of acute subdural hematoma (SDH) 2 hours after CAS. In this case, arterial origin of bleeding was verified during operation. To our knowledge, there is no prior case report of SDH without intraparenchymal nor subarachnoid hemorrhage subsequent to CAS. We postulate that SDH was caused by sudden rise in intracranial pressure due to the hyperperfusion which disrupted a corticodural bridging artery.

Fatal Propofol Infusion Syndrome Associated with Refractory Partial Status Epilepticus in a Patient with Cerebral Hyperperfusion Syndrome

Status epilepticus is rare complication of cerebral hyperperfusion syndrome and is a critical medical emergency that requires potent anesthetics. Propofol has the advantages of being rapid-acting and possessing a weaker cardiopulmonary suppression profile, but its use is associated with serious propofol infusion syndrome. We report herein a case of cerebral hyperperfusion syndrome after carotid endarterectomy presenting with refractory partial status epilepticus and fatal outcome associated with propofol infusion syndrome.

Delayed Cerebral Hyperperfusion Syndrome Three Weeks after Carotid Artery Stenting Presenting as Status Epilepticus

Cerebral hyperperfusion syndrome (CHS) is increasingly recognized as an uncommon, but serious, complication subsequent to carotid artery stenting (CAS) and carotid endarterectomy (CEA). The onset of CHS generally occurs within two weeks of CEA and CAS, and a delay in the onset of CHS of over one week after CAS is quite rare. We describe a patient who developed CHS three weeks after CAS with status epilepticus.

Post-Carotid Endarterectomy Cerebral Hyperperfusion Syndrome : Is It Preventable by Strict Blood Pressure Control?

OBJECTIVE: Cerebral hyperperfusion syndrome (CHS) is a serious complication after carotid endarterectomy (CEA). However, the prevalence of CHS has decreased as techniques have improved. This study evaluates the role of strict blood pressure (BP) control for the prevention of CHS. METHODS: All 18 patients who received CEA from February 2009 through November 2012 were retrospectively reviewed. All patients were routinely managed in an intensive care unit by a same protocol. The cerebral perfusion state was evaluated on the basis of the regional cerebral blood flow (rCBF) study by perfusion computed tomography (pCT) and mean velocity by transcranial doppler (TCD). BP was strictly controlled (100% increase in the rCBF by pCT or in the mean velocity by TCD compared with preoperative values) or CHS was detected, BP was maintained below 120/80 mm Hg. RESULTS: TCD and pCT data on the patients were analyzed. Ipsilateral rCBF was significantly increased after CEA in the pCT (p=0.049). Post-CEA hyperperfusion was observed in 3 patients (18.7%) in the pCT and 2 patients (12.5%) in the TCD study. No patients developed clinical CHS for one month after CEA. Furthermore, no patients developed additional neurological deficits related to postoperative cerebrovascular complications. CONCLUSION: Intensive care with strict BP control (<140/90 mm Hg) achieved a low prevalence of post-CEA hyperperfusion and prevented CHS. This study suggests that intensive care with strict BP control can prevent the prevalence of post-CEA CHS.

Hyperperfusion Syndrome after Carotid Stent-Supported Angioplasty in Patients with Autonomic Dysfunction

Cerebral hyperperfusion syndrome (CHS) is a rare, serious complication of carotid revascularization either after carotid endarterectomy or carotid stent placement. Although extensive effort has been devoted to reducing the incidence of CHS, little is known about the prevention. Postprocedural hypertension is very rare due to autoregulation of carotid baroreceptors but may occur if presented with autonomic dysfunction. We present two cases of CHS after cerebral revascularization that presented autonomic dysfunction.

Hyperacute hyperperfusion intracerebral hemorrhage complicating carotid endarterectomy: A case report

Most complications of carotid endarterectomy originate from either thrombotic or embolic ischemia. Although the incidence of hemorrhagic hyperperfusion syndrome after carotid endarterectomy is extremely rare, it can cause significant morbidity and mortality. Several mechanisms are involved in the pathophysiology of cerebral hyperperfusion syndrome including impaired cerebral autoregulation and normal pressure breakthrough. Presently, a different mechanism is suggested. Unfortunately, suggestions for prevention are limited to strict perioperative control of hypertension in patients with critical stenosis and chronic cerebral hypoperfusion. We report hypertensive-like ipsilateral basal ganglia hemorrhage after carotid endarterectomy.