Научно-практический журнал
«Клиническая физиология кровообращения»

Главный редактор

Лео Антонович Бокерия, доктор медицинских наук, профессор, академик РАН и РАМН, директор ФГБУ «НМИЦССХ им. А.Н. Бакулева» МЗ РФ

Церебральный гиперперфузионный синдром: проблема разграничения близких синдромов, вероятные механизмы развития, клинические проявления и факторы риска

Авторы: Емец Е.В., Шумилина М.В.

Организация:
1 Институт подготовки кадров высшей квалификации и профессионального образования ФГБУ «Национальный медицинский исследовательский центр сердечно-сосудистой хирургии им. А.Н. Бакулева» (президент – академик РАН и РАМН Л.А. Бокерия) Минздрава России, Рублевское ш., 135, Москва, 121552, Российская Федерация
2 БУЗ Воронежской области «Воронежская областная клиническая больница № 1, Московский пр-т, 151, Воронеж, 394066, Российская Федерация

Для корреспонденции: Сведения доступны для зарегистрированных пользователей.

Раздел: Обзоры

DOI: https://doi.org/10.24022/1814-6910-2021-18-2-118-127

УДК: 616.831-005

Библиографическая ссылка: Клиническая физиология кровообращения. 2021; 2 (18): 118-127

Цитировать как: Емец Е.В., Шумилина М.В. . Церебральный гиперперфузионный синдром: проблема разграничения близких синдромов, вероятные механизмы развития, клинические проявления и факторы риска. Клиническая физиология кровообращения. 2021; 2 (18): 118-127. DOI: 10.24022/1814-6910-2021-18-2-118-127

Ключевые слова: церебральный гиперперфузионный синдром, нарушения венозного оттока, артериовенозный баланс

Поступила / Принята к печати:  26.02.2021 / 01.03.2021

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Аннотация

Обзор посвящен обобщению современных данных о церебральном гиперперфузионном синдроме (ЦГС). ЦГС сходен с синдромом избыточной перфузии, гипертонической энцефалопатией, синдромом задней обратимой энцефалопатии и cиндромом обратимой церебральной вазоконстрикции. Рассматривается проблема разграничения ЦГС и близких синдромов. Обсуждаются вероятные механизмы развития ЦГС после операций реваскуляризации каротидных и других артерий: 1) повышенный церебральный кровоток; 2) нарушение церебральной авторегуляции; 3) повреждение церебральных сосудов свободными радикалами; 4) разрушение рефлекторного механизма барорецептора; 5) связь ЦГС с тригеминоваскулярным рефлексом; 6) связь ЦГС с церебральным артериовенозным дисбалансом. Подчеркивается важность изучения артериовенозного дисбаланса как механизма развития ЦГС. Рассматриваются факторы риска развития ЦГС после каротидной эндартерэктомии и стентирования каротидных артерий.

Литература

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****
  1. Radak D.M., Ševković M., Babić S. How to identify risk for cerebral hyperperfusion syndrome after carotid revascularization procedures? Vojnosanit. Pregl. 2019; 76 (8): 834–8. DOI: 10.2298/VSP170910154R
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  3. Abou-Chebl A., Yadav J.S., Reginelli J.P., Bajzer C., Bhatt D., Krieger D.W. Intracranial haemorrhage and hyperperfusion syndrome following carotid artery stenting. J. Am. Coll. Cardiol. 2004; 43 (9): 1596–601. DOI: 10.1016/j.jacc.2003.12.039
  4. Ogasawara K., Sakai N., Kuroiwa T., Hosoda K., Iihara K., Toyoda K. et al. Japanese Society for Treatment at Neck in Cerebrovascular Disease Study Group. Intracranial hemorrhage associated with cerebral hyperperfusion syndrome following carotid endarterectomy and carotid artery stenting: retrospective review of 4494 patients. J. Neurosurg. 2007; 107 (6): 1130–6. DOI: 10.3171/JNS-07/12/1130
  5. Hobson R.W. 2nd, Mackey W.C., Ascher E., Murad M.H., Calligaro K.D., Comerota A.J. et al. Society for Vascular Surgery. Management of atherosclerotic carotid artery disease: clinical practice guidelines of the Society for Vascular Surgery. J. Vasc. Surg. 2008; 48 (2): 480–6. DOI: 10.1016/j.jvs.2008.05.036
  6. Sundt T.M., Sandok B.A., Whisnant J.P. Carotid endarterectomy. Complications and preoperative assessment of risk. Mayo Clin. Proc. 1975; 50 (1): 301–6.
  7. Lin Y.-H., Liu H.-M. Update on cerebral hyperperfusion syndrome. J. Neurointervent. Surg. 2020; 12: 788–93. DOI: 10.1136/neurintsurg-2019-015621
  8. Delgado M.G., Bogousslavsky J. Cerebral hyperperfusion syndrome and related conditions. Eur. Neurol. 2020; 83: 453–7. DOI: 10.1159/000511307
  9. Lassen N.A. The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet. 1966; 2 (7473): 1113–5. DOI: 10.1016/s0140-6736(66)92199-4
  10. Cho A.H., Cho Y.P., Lee D.H., Kwon T.W., Kwon S.U., Suh D.C. et al. Reperfusion injury on magnetic resonance imaging after carotid revascularization. Stroke. 2014; 45 (2): 602–4. DOI: 10.1161/STROKEAHA. 113.003792
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  12. Bernstein M., Fleming J.F., Deck J.H. Cerebral hyperperfusion after carotid endarterectomy: a cause of cerebral hemorrhage. Neurosurgery. 1984; 15 (1): 50–6. DOI: 10.1227/00006123-198407000-00010
  13. Moulakakis K.G., Mylonas S.N., Sfyroeras G.S., Andrikopoulos V. Hyperperfusion syndrome after carotid revascularization. J. Vasc. Surg. 2009; 49 (4): 1060–68. DOI: 10.1016/j.jvs.2008.11.026
  14. Spetzler R.F., Wilson C.B., Weinstein P., Mehdorn M., Townsend J., Telles D. Normal perfusion pressure breakthrough theory. Clin. Neurosurg. 1978; 25: 651–72. DOI: 10.1093/neurosurgery/25.cn_suppl_1.651
  15. Naylor A.R., Evans J., Thompson M.M., London N.J., Abbott R.J., Cherryman G. et al. Seizures after carotid endarterectomy: hyperperfusion, dysautoregulation or hypertensive encephalopathy? Eur. J. Vasc. Endovasc. Surg. 2003; 26 (1): 39–44. DOI: 10.1053/ejvs.2002.1925
  16. Hinchey J., Chaves C., Appignani B., Breen J., Pao L., Wang A. et al. A reversible posterior leukoencephalopathy syndrome. N. Engl. J. Med. 1996; 334 (8): 494–500. DOI: 10.1056/NEJM199602223340803
  17. Ay H., Buonanno F.S., Schaefer P.W., Le D.A., Wang B., Gonzalez R.G. et al. Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI. Neurology. 1998; 51 (5): 1369–76. DOI: 10.1212/wnl.51.5.1369
  18. Bartynski W.S. Posterior reversible encephalopathy syndrome. Part 2: controversies surrounding pathophysiology of vasogenic edema. Am. J. Neurorad. 2008; 29: 1043–9. DOI: 10.3174/ajnr.A0929
  19. Fugate J.E., Rabinstein A.A. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol. 2015; 14 (9): 914–25. DOI: 10.1007/s12028-012-9733-x
  20. Levitt A., Zampolin R., Burns J., Bello J.A., Slasky S.E. Posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome. Distinct clinical entities with overlapping pathophysiology. Radiol. Clin. North Am. 2019; 57 (6): 1133–46. DOI: 10.1016/j.rcl.2019.07.001
  21. Calabrese L.H., Dodick D.W., Schwedt T.J., Singhal A.B. Narrative review: reversible cerebral vasoconstriction syndromes. Ann. Intern. Med. 2007; 146 (1): 34–44. DOI: 10.7326/0003-4819-146-1-200701020-00007
  22. Ducros A. Reversible cerebral vasoconstriction syndrome. Lancet Neurol. 2012; 11 (10): 906–17. DOI: 10.1016/S1474-4422(12)70135-7
  23. Ducros A., Bousser M.G. Reversible cerebral vasoconstriction syndrome. Pract. Neurol. 2009; 9 (5): 256–67. DOI: 10.1136/jnnp.2009.187856
  24. Ogasawara K., Inoue T., Kobayashi M., Endo H., Yoshida K., Fukuda T. et al. Cerebral hyperperfusion following carotid endarterectomy: diagnostic utility of intraoperative transcranial Doppler ultrasonography compared with single-photon emission computed tomography study. Am. J. Neuroradiol. 2005; 26 (2): 252–7.
  25. Mitrasinović A., Kolar J., Radak S., Nenezić D., Kupresanin I., Aleksić N. Ultrasonografic monitoring of hemodynamic parameters in symptomatic and asymptomatic patients with high-grade carotid stenosis prior and following carotid endarterectomy. Vojnosanit. Pregl. 2012; 69 (5): 399–404 (Serbian). DOI: 10.2298/VSP1205399M
  26. Henderson R.D., Phan T.G., Piepgras D.G., Wijdicks E.F. Mechanisms of intracerebral hemorrhage after carotid endarterectomy. J. Neurosurg. 2001; 95 (6): 964–9. DOI: 10.3171/jns.2001.95.6.0964
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Об авторах

  • Емец Екатерина Викторовна, врач функциональной диагностики; ORCID
  • Шумилина Маргарита Владимировна, доктор мед. наук, профессор кафедры кардиологии и функциональной диагностики, заведующая группой ультразвуковых исследований сердечно-сосудистой и органной патологии; ORCID

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