Update on Cerebral Hyperperfusion Syndrome Yen-Heng Lin ,1 Hon-Man Liu2,3
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J NeuroIntervent Surg: first published as 10.1136/neurintsurg-2019-015621 on 15 May 2020. Downloaded from Hemorrhagic stroke REVIEW Update on cerebral hyperperfusion syndrome Yen- Heng Lin ,1 Hon- Man Liu2,3 ► Additional material is ABSTRACT of CHS in patients undergoing CAS, INCS, and published online only. To view Cerebral hyperperfusion syndrome (CHS) is a clinical EVT. please visit the journal online (http:// dx. doi. org/ 10. 1136/ syndrome following a revascularization procedure. In the neurintsurg- 2019- 015621). past decade, neurointerventional surgery has become SEARCH stratEGY AND SELECTION CRITERIA a standard procedure to treat stenotic or occluded CHS studies for this review were searched using 1 Medical Imaging, National cerebral vessels in both acute and chronic settings, as PubMed. The search term 'cerebral hyperperfusion' Taiwan University Hospital, well as endovascular thrombectomy in acute ischemic Taipei, Taiwan was used as the keyword, and the search was limited 2Radiology, National Taiwan stroke. This review aims to summarize relevant recent to clinical reports, clinical studies, clinical trials, and University, Taipei, Taiwan studies regarding the epidemiology, diagnosis, and reviews. The search was also limited to studies with 3 Medical Imaging, Fu Jen management of CHS as well as to highlight areas of abstracts available. The search was performed up to Catholic University Hospital, Fu uncertainty. Extracranial and intracranial cerebrovascular 30 August 2019. A total of 1490 items were iden- Jen Catholic University, New Taipei City 24352, Taiwan diseases in acute and chronic conditions are considered. tified. Using the PRISMA flowchart for guidance The definition and diagnostic criteria of CHS are diverse. (online supplementary material), titles and abstracts Correspondence to Although impaired cerebrovascular autoregulation were reviewed by the authors before requesting the Professor Hon-Man Liu, Medical plays a major role in the pathophysiology of CHS, the full text. Duplicates, reports of moyamoya disease Imaging, National Taiwan underlying mechanism is still not fully understood. Its or bypass surgery, in vitro studies, and non- English University Hospital, Taipei clinical characteristics vary in different patients. The studies were excluded. Following careful review of 10016, Taiwan; hmliu@ ntu. edu. tw current findings on clinical and radiological presentation, 135 full text articles, 56 studies focusing on updated pathophysiology, incidence, and risk factors are based information were included after careful discussion Received 12 November 2019 predominantly on carotid angioplasty and stenting by the authors. Revised 3 April 2020 studies. Hemodynamic assessment using imaging Accepted 4 April 2020 modalities is the main form of diagnosis although OVERVIEW OF CEREBRAL HYPERPERFUSION the criteria are distinct, but it is helpful for patient SYNDROME selection before an elective revascularization procedure Clinical presentation and radiological findings is conducted. After endovascular thrombectomy, a Most patients with CHS have mild symptoms and diagnosis of CHS is even more complex, and physicians signs, while some may progress to severe and life- should consider concomitant reperfusion injury. threatening symptoms. The most common clinical Management and preventative measures, including presentations include severe headache (ipsilateral to intensive blood pressure control before, during, and after the lesion side or diffuse), and eye and facial pain. revascularization procedures and staged angioplasty, are Less common and more severe symptoms include discussed in detail. focal neurological deficits, seizures, and loss of http://jnis.bmj.com/ consciousness. CHS occurred conspicuously earlier after CAS than after CEA, but the cause is unknown. The incidence of CHS peaks at 12 hours after CAS INTRODUCTION and at 6 days after CEA. Hemorrhage after CAS Cerebral hyperperfusion syndrome (CHS) is a rare was also diagnosed significantly earlier following but severe complication, and was first described as a CAS (1.7±2.1 days) than after CEA (10.7±9.9 on September 24, 2021 by guest. Protected copyright. clinical syndrome following carotid endarterectomy days) (p=0.0098).1 Despite the earlier presentation (CEA). In neurointerventional surgery, CHS may of CHS after CAS, it can delay its occurrence by up complicate extracranial carotid angioplasty and to 1 month after the procedure. stenting (CAS), and is characterized by headaches, On radiological studies, patchy or diffuse white neurological deficits, and seizures not caused by matter edema, predominantly involving the poste- cerebral ischemia. It is commonly associated with rior parieto- occipital lobe, focal infarction, and an increase in blood pressure. petechial hemorrhage (figures 1 and 2) were poten- The incidence and risk factors of CHS have tial findings, for which MRI was more sensitive. © Author(s) (or their recently been reported in several large cohorts of However, negative radiological finding cannot employer(s)) 2020. Re- use patients undergoing CAS, intracranial angioplasty exclude CHS. permitted under CC BY- NC. No and stenting (INCS), and endovascular throm- Imaging modalities also play a key role in the commercial re- use. See rights and permissions. Published bectomy (EVT). Greater familiarity with recent objective assessment and diagnosis of cerebral by BMJ. reports of the clinical symptoms, imaging features, hemodynamics in CHS. Among them, transcra- and management strategies for CHS may improve nial color duplex (TCD) is the most widely avail- To cite: Lin Y- H, Liu H- M. the vigilance necessary for effective diagnosis and able modality in practice. It measures cerebral J NeuroIntervent Surg Epub ahead of print: [please prevention. blood velocity in the middle cerebral artery, which include Day Month Year]. This review focuses on recent important studies correlates adequately with cerebral blood flow doi:10.1136/ on the presentation, diagnosis, pathophysiology, (CBF). However, TCD is operator dependent and neurintsurg-2019-015621 incidence, risk factors, prevention, and management optimal image acquisition is not always feasible. Lin Y- H, Liu H- M. J NeuroIntervent Surg 2020;0:1–7. doi:10.1136/neurintsurg-2019-015621 1 J NeuroIntervent Surg: first published as 10.1136/neurintsurg-2019-015621 on 15 May 2020. Downloaded from Hemorrhagic stroke Figure 1 (A–E) Cerebral hyperperfusion syndrome after carotid stenting. (A) CT shows regional swelling as sulcal effacement on the left temporo- parieto- occipital lobe. (B) CT angiography reveals hyperemic change on the same territory. (C) MR examination (T2 fluid attenuation inversion recovery, FLAIR) shows regional swelling without evidence of ischemic stroke (not shown). (D) Arterial spin labeling revealed relative hyperperfusion in the same region. Under strict blood pressure control, the patient improved a few days later. (E) Follow-up T2 FLAIR image 6 months later shows remission of the regional swelling. Cerebral perfusion imaging, including single photon emission Regarding CT perfusion, many criteria have been proposed, such computed tomography (SPECT), CT perfusion, and perfusion as elevated postoperative cerebral blood volume,6 mean transit weighted imaging, enables direct estimation of CBF and related time threshold <2 s or >4 s,7 increased regional cerebral blood perfusion parameters based on radioisotope or bolus injection flow and regional cerebral blood volume, and decreased mean of radioisotope or contrast agents. Among them, CT perfusion transit time along with decreased time to peak in the clinically is recommended because of good availability, relatively short related artery territory.8 The definition of CHS is highly variable acquisition time, and feasibility in critical patients. The compar- and dependent on diagnostic tools. Consensus on the definition ison of perfusion parameter to the contralateral hemisphere can and diagnostic criteria for CHS using different hemodynamic be performed by commercial workstations. (figure 3). Also, these assessment tools is warranted. new MRI techniques, such as arterial spin labeling (ASL) and quantitative MRI, can estimate CBF without the use of a contrast agent. Periprocedural imaging evaluation and prediction of CHS Pathophysiology was studied using color coded DSA, quantitative digital subtrac- Many pathophysiological mechanisms contributing to the tion tomography, and c arm derived cerebral blood volume.2–4 development of CHS have been proposed. The most accepted Using quantitative methods such as SPECT, xenon enhanced mechanism is impairment of cerebral autoregulation. Normal CT, cerebral hyperperfusion is usually considered when the cerebral autoregulation constricts the brain vessels in response revascularized territory increases CBF by 100% or more from to a sudden increase in blood flow, to maintain normal cerebral baseline values after CEA or CAS.1 This operational defini- perfusion within an acceptable range (60–160 mm Hg). Auto- tion is impractical because of the lack of pretreatment CBF regulation includes both a myogenic and a neurogenic compo- measurements. By comparing with the contralateral hemisphere, nent. The myogenic component is usually the first reaction to http://jnis.bmj.com/ an increase in CBF is generally used in defining CHS, but this a change in blood flow. If that fails, the remaining autoregula- cannot be applied to patients with contralateral stenotic disease. tion depends on the innervation of the sympathetic