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 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral hyperperfusion syndrome after carotid endarterectomy is an uncommon but distressing complication. Findings in nearly all these patients include the presence of ipsilateral high-grade carotid artery stenosis, postoperative ipsilateral headache followed by seizures, and transient neurologic deficits. It appears to be caused by the loss of autoregulation within the brain, usually occurring between 5 and 7 days postoperatively.
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PMID:Cerebral hyperperfusion syndrome: an etiology of seizures following carotid endarterectomy. 825 34

Cerebral hyperperfusion syndrome after carotid endarterectomy (CEA) is a rare but well-known phenomenon. Percutaneous transluminal angioplasty (PTA) is being widely evaluated for treatment of selected stenoses of the extracranial arteries. Its benefits and risks still need to be established. Hyperperfusion injury (HI) after PTA of cerebral arteries has not been reported. We describe two patients with severe HI, one with a small putaminal haemorrhage and the other with diffuse basal subarachnoid haemorrhage. In both cases, a typical clinical hyperperfusion syndrome with headache, confusion, vomiting and seizures occurred. Patient 1 underwent PTA of the left carotid artery, both subclavian arteries and proximal vertebral arteries, patient 2 had carotid angioplasty only. Transcranial Doppler ultrasound displayed markedly elevated blood-flow velocities. HI may occur after PTA of extracranial arteries. The pathogenesis might be similar to reperfusion injury after CEA. Our findings suggest that: (1) HI may occur after PTA; (2) patients should be monitored after PTA for HI; (3) further risk factors for HI need to be identified.
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PMID:Cerebral hyperperfusion injury after percutaneous transluminal angioplasty of extracranial arteries. 912 Apr 91

Cerebral hyperperfusion syndrome as a complication of carotid endarterectomy (CEA) has been widely reported in the surgical literature. It may occur within hours to 3 weeks after CEA and is characterized by symptoms ranging from headaches, fits, confusion, focal neurological signs to intracerebral hemorrhage. Although percutaneous transluminal angioplasty (PTA) and stenting are increasingly performed as an alternative to CEA in the treatment of carotid artery stenosis, few cases of cerebral hyperperfusion injury following carotid stenting have been reported. We describe 2 cases of cerebral hyperperfusion syndrome following PTA and stenting for high-grade internal carotid artery (ICA) stenosis. Both cases involved a lesion of 95% in severity. The first case was a 73-year-old man who developed generalized convulsion 7 h following stenting to the left ICA. The second case was an 80-year-old woman who developed recurrent right periorbital headache and confusion 16 h after stenting to the right ICA, followed by left upper limb seizure 14 days later. Both patients fully recovered without any intracerebral hemorrhage or infarction. To our knowledge, this is the first report of cerebral hyperperfusion injury after carotid stenting without associated intracranial hemorrhage and with full recovery. In the patient with neurological symptoms following carotid stenting, it is important to consider cerebral hyperperfusion syndrome as a differential diagnosis to embolic or hemorrhagic stroke since early recognition and meticulous control of blood pressure may prevent progression to cerebral hemorrhage and death.
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PMID:Epileptic seizures attributed to cerebral hyperperfusion after percutaneous transluminal angioplasty and stenting of the internal carotid artery. 1097 Oct 23

Cerebral hyperperfusion syndrome (CHS) after carotid endarterectomy is characterised by ipsilateral headache, hypertension, seizures, and focal neurological deficits. If not treated properly it can result in severe brain oedema, intracerebral or subarachnoid haemorrhage, and death. Knowledge of CHS among physicians is limited. Most studies report incidences of CHS of 0-3% after carotid endarterectomy. CHS is most common in patients with increases of more than 100% in perfusion compared with baseline after carotid endarterectomy and is rare in patients with increases in perfusion less than 100% compared with baseline. The most important risk factors in CHS are diminished cerebrovascular reserve, postoperative hypertension, and hyperperfusion lasting more than several hours after carotid endarterectomy. Impaired autoregulation as a result of endothelial dysfunction mediated by generation of free oxygen radicals is implicated in the pathogenesis of CHS. Treatment strategies are directed towards regulation of blood pressure and limitation of rises in cerebral perfusion. Complete recovery happens in mild cases, but disability and death can occur in more severe cases. More information about CHS and early institution of adequate treatment are of paramount importance in order to prevent these potentially severe complications.
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PMID:Cerebral hyperperfusion syndrome. 1629 45

Cerebral hyperperfusion syndrome is a rare but well-described complication following carotid endarterectomy or stenting. Clinical signs are ipsilateral, throbbing, unilateral headache with nausea or vomiting, seizures, and neurological deficits, with or without intracerebral abnormalities on CT scan, such as brain edema or intracerebral hemorrhage. Subarachnoidal hemorrhage is rarely described especially if it occurs isolated. We describe a 74-year-old man with a history of high blood pressure, hypercholesterolemia, atrioventricular block with pacemaker, and ischemic cardiopathy with coronary bypass. He underwent right carotid endarterectomy for a 90% NASCET asymptomatic stenosis. Four days after surgery, he complained of unusual headaches with right, throbbing hemicrania. Nine days after surgery, he presented with left hemiplegia and a partial motor seizure. He had fluctuant altered consciousness, left hemiplegia, and left visual and sensory neglect. Brain CT showed right frontal subarachnoidal hemorrhage without parenchymal bleeding. Cerebral angiography found no cerebral aneurysm, no vascular malformation, but a vasospasm of the left middle cerebral artery. Transcranial Doppler confirmed this vasospasm. Evolution was favorable with no recurrence of seizures but with an improvement of the neurological deficits and vasospasm. Physicians should bear in mind this very rare complication of endarterectomy and immediately perform neuroimaging in case of unusual headache following endarterectomy or angioplasty.
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PMID:Isolated Subarachnoidal Hemorrhage following Carotid Endarterectomy. 2067 62

Cerebral hyperperfusion syndrome (CHS) after carotid surgery, although rare, is a well-described phenomenon. Although originally described after carotid endarterectomy, it has now also been described after carotid artery stenting. It is classically described as an acute neurologic deficit occurring several days after a carotid procedure, associated with severe hypertension and preceded by a severe headache. CHS represents a spectrum of clinical symptoms ranging from severe unilateral headache, to seizures and focal neurologic defects, to intracerebral hemorrhage in its most severe form. The exact mechanism leading to CHS is unknown; however, it seems to be related to increased regional cerebral blood flow secondary to loss of cerebrovascular autoregulation. Given the significant morbidity associated with CHS, researchers have been trying to identify which patients are most at risk. This is a difficult task given the rarity of the disease and the multiple confounding factors in the patient population who undergo carotid intervention. The goal was to determine those patients most at risk preoperatively, so that they may be more closely monitored postoperatively to prevent the development of CHS and its associated morbidity. The purpose of this review was to summarize the data currently available in the literature on CHS, with emphasis on pathophysiology, risk factor assessment, diagnostic modalities, and disease management, to provide insight for future research to better elucidate how to reduce the morbidity and mortality caused by CHS.
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PMID:Cerebral hyperperfusion syndrome after carotid intervention: a review. 2218 61

Moyamoya disease (MMD) is a progressive occlusive disease of the distal internal carotid artery that is primarily treated by superficial temporal artery-middle cerebral artery (STA-MCA) bypass. Despite its effectiveness, several postoperative complications have been reported with STA-MCA bypass. Cerebral hyperperfusion syndrome (CHS) after STA-MCA has attracted considerable attention as a hemodynamics-related complication because more cases of CHS after STA-MCA bypass are reported in MMD than in non-MMD patients. The mechanisms underlying CHS after revascularization in MMD patients are poorly understood. This report presents a comprehensive review of the literature on CHS after revascularization in MMD patients, focusing on the pathogenesis, clinical features, imaging techniques, treatment, and prognosis of CHS. Impaired cerebrovascular autoregulation has been implicated in the pathogenesis of CHS, which is characterized by unilateral headache, face and eye pain, seizures, and focal neurological deficits secondary to cerebral edema, and intracranial hemorrhage. Imaging techniques, such as single photon emission computed tomography (SPECT), 3-T magnetic resonance imaging/angiography, and selective arterial spin-labeling magnetic resonance imaging, are valuable for identifying patients at risk for CHS. Treatment strategies include strict blood pressure control, intracranial hemorrhage prevention, and free oxygen radical scavenger administration. Most patients can achieve a satisfying prognosis after effective treatment.
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PMID:Cerebral hyperperfusion syndrome after revascularization surgery in patients with moyamoya disease. 2346 48

Cervical artery dissection (CeAD) occurs preferentially in the middle-aged, and its annual incidence rate is 2.6 to 3.0 per 100,000.(1) Manifestations of internal carotid artery dissection (ICAD) include ischemic stroke and TIA (>70% of patients), headache, neck pain, Horner syndrome, cranial nerve palsy, pulsatile tinnitus, and, rarely, subarachnoid hemorrhage.(2) Cerebral hyperperfusion syndrome is known to occur after carotid artery revascularization procedures and it is thought to result from the combination of several factors that impair cerebral vascular autoregulatory mechanisms.(3.)
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PMID:Cerebral hyperperfusion syndrome: a novel presentation of internal carotid artery dissection. 2382 78

Cerebral hyperperfusion syndrome is a well-recognized and potentially fatal complication of carotid revascularization. However, the occurrence of non-aneurysmal subarachnoid hemorrhage as a manifestation of cerebral hyperperfusion syndrome post-carotid endarterectomy is uncommon. We report a case of a patient who presented with headache following carotid endarterectomy for a critically occluded common carotid artery. This progressed to deteriorating consciousness and seizures. Investigations revealed a left cortical non-aneurysmal subarachnoid hemorrhage. Non-aneurysmal subarachnoid hemorrhage is a rare post-operative complication of carotid endarterectomy. Immediate management with aggressive blood pressure control is key to prevent permanent neurological deficits. Cerebral hyperperfusion syndrome (CHS) after carotid revascularization procedures is an uncommon and potentially fatal complication. Pathophysiologically it is attributed to impaired autoregulatory mechanisms and results in disruption of cerebral hemodynamics with increased regional cerebral blood flow (Cardiol Rev 20:84-89, 2012; J Vasc Surg 49:1060-1068, 2009). The condition is characterized by throbbing ipsilateral frontotemporal or periorbital headache. Other symptoms include vomiting, confusion, macular edema, focal motor seizures with frequent secondary generalization, focal neurological deficits, and intraparenchymal or subarachnoid hemorrhage (SAH) (Lancet Neurol 4:877-888, 2005). The incidence of CHS varies from 0.2% to 18.9% after carotid endarterectomy (CEA), with a typical reported incidence of less than 3% in larger studies (Cardiol Rev 20:84-89, 2012; Neurosurg 107:1130-1136, 2007). Uncontrolled hypertension, an arterially isolated cerebral hemisphere, and contralateral carotid occlusion are the main risk factors (Lancet Neurol 4:877-888, 2005; J Neurol Neurosurg Psychiatry 83:543-550, 2012). We present a case of non-aneurysmal SAH after CEA, with focus on its presentation, risk factors, and management.
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PMID:Cortical non-aneurysmal subarachnoid hemorrhage post-carotid endarterectomy: a case report and literature review. 2425 64

Cerebral hyperperfusion syndrome (CHS) describes a syndrome of sudden onset focal neurological features, unilateral headache, and systemic hypertension. Recurrent CHS in the same patient has not been described to date. We describe a 55-year-old woman who first developed CHS post intracranial stenting with sudden-onset right focal seizures and associated acute focal edema on imaging. After one and half years, the patient developed symptomatic in-stent restenosis and underwent repeat angioplasty with stenting. Postprocedure, the patient had another episode of CHS in the form of acute bleed in the basal ganglia and died. A review of literature of patients for CHS postintracranial angioplasty and stenting also was performed. The present case describes a rare clinical scenario where the patient had recurrent CHS with different clinical and imaging features.
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PMID:Recurrent cerebral hyperperfusion syndrome after intracranial angioplasty and stenting: case report with review of literature. 2430 88


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