Background: Cerebral hyperperfusion is a potential complication of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis for moyamoya disease, but the optimal postoperative management has not been determined. Aggressive blood pressure lowering is controversial because of the risk of ischemic complications. Objective: To establish the optimal postoperative management protocol to prevent symptomatic cerebral hyperperfusion in moyamoya disease. Methods: N-isopropyl-p-[123I]-iodoamphetamine single-photon emission computed tomography was performed 1 and 7 days after STA-MCA anastomosis on 152 hemispheres from 108 consecutive patients with moyamoya disease (2–69, mean 33.3 years). Between 2004 and 2007 (period 1), 65 patients were maintained under normotensive conditions after 93 operations, and only patients with cerebral hyperperfusion underwent blood pressure lowering. Between 2008 and 2010 (period 2), all 43 patients were prospectively subjected to intensive blood pressure lowering (<130 mm Hg of systolic blood pressure) immediately after 59 operations. Then the incidence of symptomatic cerebral hyperperfusion was compared between the two groups. Results: Systolic blood pressure the day after surgery was significantly lower in period 2 (mean, 120.9 mm Hg) than in period 1 (133.9 mm Hg) (p < 0.0001). Symptomatic cerebral hyperperfusion was seen in 22 patients during period 1 (23 hemispheres, 24.7%), but only in 4 patients during period 2 (6.7%, p = 0.0047). Multivariate analysis revealed that prophylactic blood pressure lowering was significantly associated with the prevention of symptomatic cerebral hyperperfusion (p = 0.015). Symptomatic cerebral hyperperfusion was relieved in all patients without developing a permanent neurological deficit due to cerebral hyperperfusion. Conclusion: Prophylactic blood pressure lowering prevents symptomatic cerebral hyperperfusion after STA-MCA anastomosis in patients with moyamoya disease. Accurate diagnosis of cerebral hyperperfusion and blood pressure lowering, and considering the severity of hemodynamic compromise in the contralateral and/or remote areas are essential for postoperative management of moyamoya disease.

1.
Suzuki J, Takaku A: Cerebrovascular ‘moyamoya’ disease. Disease showing abnormal net-like vessels in base of brain. Arch Neurol 1969;20:288–299.
2.
Fujimura M, Kaneta T, Tominaga T: Efficacy of superficial temporal artery-middle cerebral artery anastomosis with routine postoperative cerebral blood flow measurement during the acute stage in childhood moyamoya disease. Childs Nerv Syst 2008;24:827–832.
3.
Fujimura M, Mugikura S, Kaneta T, Shimizu H, Tominaga T: Incidence and risk factors for symptomatic cerebral hyperperfusion after superficial temporal artery-middle cerebral artery anastomosis in patients with moyamoya disease. Surg Neurol 2009;71:442–447.
4.
Guzman R, Lee M, Achrol A, Bell-Stephens T, Kelly M, Do HM, Marks MP, Steinberg GK: Clinical outcome after 450 revascularization procedures for moyamoya disease. J Neurosurg 2009;111:927–935.
5.
Houkin K, Ishikawa T, Yoshimoto T, Abe H: Direct and indirect revascularization for moyamoya disease: surgical techniques and peri-operative complications. Clin Neurol Neurosurg 1997;99(suppl 2):S142–S145.
6.
Okada Y, Shima T, Nishida M, Yamane K, Yamada T, Yamanaka C: Effectiveness of superficial temporal artery-middle cerebral artery anastomosis in adult moyamoya disease: cerebral hemodynamics and clinical course in ischemic and hemorrhagic varieties. Stroke 1998;29:625–630.
7.
Piepgras DG, Morgan MK, Sundt TM Jr, Yanagihara T, Mussman LM: Intracerebral hemorrhage after carotid endarterectomy. J Neurosurg 1988;68:532–536.
8.
Solomon RA, Loftus CM, Quest DO, Correll JW: Incidence and etiology of intracerebral hemorrhage following carotid endarterectomy. J Neurosurg 1986;64:29–34.
9.
Sundt TM Jr, Sharbrough FW, Piepgras DG, Kearns TP, Messick JM, O’Fallon WM: Correlation of cerebral blood flow and electroencephalographic changes during carotid endarterectomy: with results of surgery and hemodynamics of cerebral ischemia. Mayo Clin Proc 1981;56:533–543.
10.
Fujimura M, Kaneta T, Mugikura S, Shimizu H, Tominaga T: Temporary neurologic deterioration due to cerebral hyperperfusion after superficial temporal artery-middle cerebral artery anastomosis in patients with adult-onset moyamoya disease. Surg Neurol 2007;67:273–282.
11.
Furuya K, Kawahara N, Morita A, Momose T, Aoki S, Kirino T: Focal hyperperfusion after superficial temporal artery-middle cerebral artery anastomosis in a patient with moyamoya disease. Case report. J Neurosurg 2004;100:128–132.
12.
Kim JE, Oh CW, Kwon OK, Park SQ, Kim SE, Kim YK: Transient hyperperfusion after superficial temporal artery/middle cerebral artery bypass surgery as a possible cause of postoperative transient neurological deterioration. Cerebrovasc Dis 2008;25:580–586.
13.
Kohama M, Fujimura M, Mugikura S, Tominaga T: Temporal change of 3-T magnetic resonance imaging/angiography during symptomatic cerebral hyperperfusion following superficial temporal artery-middle cerebral artery anastomosis in a patient with adult-onset moyamoya disease. Neurosurg Rev 2008;31:451–455.
14.
Nakagawa A, Fujimura M, Arafune T, Sakuma I, Tominaga T: Clinical implications of intraoperative infrared brain surface monitoring during superficial temporal artery-middle cerebral artery anastomosis in patients with moyamoya disease. J Neurosurg 2009;111:1158–1164.
15.
Ogasawara K, Komoribayashi N, Kobayashi M, Fukuda T, Inoue T, Yamada K, Ogawa A: Neural damage caused by cerebral hyperperfusion after arterial bypass surgery in a patient with moyamoya disease: case report. Neurosurgery 2005;56:E1380.
16.
Ohue S, Kumon Y, Kohno K, Watanabe H, Iwata S, Ohnishi T: Postoperative temporary neurological deficits in adults with moyamoya disease. Surg Neurol 2008;69:281–286.
17.
Fujimura M, Shimizu H, Mugikura S, Tominaga T: Delayed intracerebral hemorrhage after superficial temporal artery-middle cerebral artery anastomosis in a patient with moyamoya disease: possible involvement of cerebral hyperperfusion and increased vascular permeability. Surg Neurol 2009;71:223–227.
18.
Fujimura M, Shimizu H, Inoue T, Mugikura S, Saito A, Tominaga T: Significance of focal cerebral hyperperfusion as a cause of transient neurologic deterioration after EC-IC bypass for moyamoya disease: Comparative study with non-moyamoya patients using 123I-IMP-SPECT. Neurosurgery 2011;68:957–965.
19.
Khan N, Schuknecht B, Boltshauser E, Capone A, Buck A, Imhof HG, Yonekawa Y: Moyamoya disease and moyamoya syndrome: experience in Europe: Choice of revascularisation procedures. Acta Neurochir (Wien) 2003;145:1061–1071.
20.
Tominaga T, Fujimura M: Outcome of revascularization surgery for moyamoya disease under standardized peri-operative management protocol. Annual Report by the Research Committee on Spontaneous Occlusion of the Circle of Willis (Moyamoya Disease) of Health and Labour Science Research Grants (in Japanese). Res Measures Intract Dis (Japan) 2009;30:5–6.
21.
Miyamoto S; Japan Adult Moyamoya Trial Group: study design for a prospective randomized trial of extracranial-intracranial bypass surgery for adults with moyamoya disease and hemorrhagic onset – the Japan Adult Moyamoya Trial Group. Neurol Med Chir (Tokyo) 2004;44:218–219.
22.
Kikuta K, Takagi Y, Nozaki K, Yamada K, Miyamoto S, Kataoka H, Arai T, Hashimoto N: Effects of intravenous anesthesia with propofol on regional cortical blood flow and intracranial pressure in surgery for moyamoya disease. Surg Neurol 2007;68:421–424.
23.
Fujimura M, Kaneta T, Shimizu H, Tominaga T: Cerebral ischemia owing to compression of the brain by swollen temporal muscle used for encephalo-myo-synangiosis in moyamoya disease. Neurosurg Rev 2009;32:245–249.
24.
Fukui M: Guidelines for the diagnosis and treatment of spontaneous occlusion of the circle of Willis (‘moyamoya’ disease). Research Committee on Spontaneous Occlusion of the Circle of Willis (Moyamoya Disease) of the Ministry of Health and Welfare, Japan. Clin Neurol Neurosurg 1997;99(suppl 2):S238–S240.
25.
Research on intractable disease of the Ministry of Health, Labour and Welfare, Japan. Recommendations for the Management of Moyamoya Disease. A Statement from Research Committee on Spontaneous Occlusion of the Circle of Willis (Moyamoya Disease) (in Japanese). Surg Cereb Stroke 2009;37:321–337.
26.
Ikeda E, Hosoda Y: Distribution of thrombotic lesion in the cerebral arteries in spontaneous occlusion of the circle of Willis: cerebrovascular moyamoya disease. Clin Neuropathol 1993;12:44–48.
27.
Heros RC, Scott RM, Ackerman RH, Conner ES: Temporary neurological deterioration after extracranial-intracranial bypass. Neurosurgery 1984;15:178–185.
28.
Kuroda S, Kamiyama H, Abe H, Asaoka K, Mitsumori K: Temporary neurological deterioration caused by hyperperfusion after extracranial-intracranial bypass: case report and study of cerebral hemodynamics. Neurol Med Chir (Tokyo) 1994;34:15–19.
29.
Yamaguchi K, Kawamata T, Kawashima A, Hori T, Okada Y: Incidence and predictive factors of cerebral hyperperfusion after extracranial-intracranial bypass for occlusive cerebrovascular diseases. Neurosurgery 2010;67:1548–1554.
30.
Ogasawara K, Inoue T, Kobayashi M, Endo H, Fukuda T, Ogawa A: Pretreatment with the free radical scavenger edaravone prevents cerebral hyperperfusion after carotid endarterectomy. Neurosurgery 2004;55:1060–1067.
31.
Huang AP, Liu HM, Yang CC, Tsai YH, Wang KC, Yang SH, Kuo MF, Tu YK: Clinical significance of posterior circulation changes after revascularization in patients with moyamoya disease. Cerebrovasc Dis 2009;28:247–257.
32.
Komoribayashi N, Ogasawara K, Kobayashi M, Saitoh H, Terasaki K, Inoue T, Ogawa A: Cerebral hyperperfusion after carotid endarterectomy is associated with preoperative hemodynamic impairment and intraoperative cerebral ischemia. J Cereb Blood Flow Metab 2005;26:878–884.
33.
Oka K, Yamashita M, Sadoshima S, Tanaka K: Cerebral haemorrhage in Moyamoya disease at autopsy. Virchows Arch A Pathol Anat Histol 1981;392:247–261.
34.
Takagi Y, Kikuta K, Nozaki K, Hashimoto N: Histological features of middle cerebral arteries from patients treated for Moyamoya disease. Neurol Med Chir (Tokyo) 2007;47:1–4.
35.
Chan PH: Role of oxidants in ischemic brain injury. Stroke1996;27:1124–1129.
36.
Kang HS, Kim JH, Phi JH, Kim YY, Wang KC, Cho BK, Kim SK: Plasma matrix metalloproteinases, cytokines and angiogenic factors in moyamoya disease. J Neurol Neurosurg Psychiatry 2010;81:673–678.
37.
Sakamoto S, Kiura Y, Yamasaki F, Shibukawa M, Ohba S, Shrestha P, Sugiyama K, Kurisu K: Expression of vascular endothelial growth factor in dura matter of patients with moyamoya disease. Neurosurg Rev 2008;31:77–81.
38.
Fujimura M, Watanabe M, Narisawa A, Shimizu H, Tominaga T: Increased expression of serum matrix metalloproteinase-9 in patients with moyamoya disease. Surg Neurol 2009;72:476–480.
39.
Mikami C, Suzuki M, Tsuiki K, Ogawa A: Effect of nicardipine and magnesium on cerebral infarction-brain surface perfusion technique. Cerebrovasc Dis 2001;11:44–50.
40.
Amenta F, Tomassoni D: Treatment with nicardipine protects brain in an animal model of hypertension-induced damage. Clin Exp Hypertens 2004;26:351–361.
41.
Kawamata T, Kawashima A, Yamaguchi K, Hori T, Okada Y: Usefulness of intraoperative laser Doppler flowmetry and thermography to predict a risk of postoperative hyperperfusion after STA-MCA bypass for moyamoya disease. Neurosurg Rev 2011;34:355–362.
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
You do not currently have access to this content.