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高血圧性脳症

著者: 野川茂 東海大学医学部付属八王子病院脳神経内科

監修: 内山真一郎 国際医療福祉大学臨床医学研究センター

著者校正/監修レビュー済:2021/03/31
患者向け説明資料

概要・推奨   

【概要】
  1. 高血圧性脳症は高血圧緊急症のひとつに含まれ、本来脳血管自動調節能(cerebral autoregulation)を有する脳血管に閾値を超えた高血圧負荷がかかり、脳血管のvasospasmおよび血液脳関門(BBB)のbreak-through現象による血管原性浮腫を生じ、可逆的あるいは非可逆的な組織学的変化が起きる状態である。
  1. 従来、このような病態はCTのみでは同定しにくいこともあったが、近年、MRI、MRA、脳還流画像などにより、reversible cerebral vasoconstriction syndrome(RCVS)PRES(posterior reversible encephalopathy syndrome)といったダイナミックな病態として捉えられるようになり、正しい診断が迅速な治療に結びつくようになってきた。
  1. 高血圧性脳症は、脳、心、腎、大血管などの標的臓器に不可逆的な変化をもたらす「高血圧緊急症」のひとつとされ[1][2]、速やかに適切に治療されなければ、脳血管障害(脳梗塞、脳出血、くも膜下出血)などの後遺症を残し、死に至ることもある疾患である。
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
野川茂 : 特に申告事項無し[2021年]
監修:内山真一郎 : 特に申告事項無し[2021年]

改訂のポイント:
  1. 脳卒中治療ガイドライン2015[追補2019]、高血圧治療ガイドライン 2019に基づき改訂を行った。
 

病態・疫学・診察

疾患情報  
  1. 高血圧性脳症とは、血圧の急激な上昇に伴う神経障害で、脳血管自動調節能の逸脱による脳血管のvasospasmおよびBBBのbreak-thorough現象による血管性浮腫が原因と考えられている。
  1. 長期の高血圧患者では、220/110 mmHg以上(JNC7[3]の定義)で発症することが多いが、正常血圧者では160/100 mmHgでも発症することがある[4]
  1. 主症状は激しい頭痛、悪心・嘔吐、視力障害、痙攣、意識障害などである。
  1. 本疾患では、後方循環の白質に浮腫性病変を来すことが多く、後方可逆性白質脳症症候群(posterior reversible encephalopathy syndrome、PRES[5])、あるいは可逆性後白質脳症症候群(reversible posterior leukoencephalopathy syndrome、RPLS[6])とも呼ばれる。これらは同義であるため、併記されることもある(RPLS/PRES)。
  1. 高血圧により二次的に可逆性脳血管攣縮症候群(reversible cerebral vasoconstriction syndrome、RCVS[7])を呈することがあり、本疾患の類縁疾患と考えられる。
  1. 高血圧の原因は様々であり( >詳細情報 参照)、受診時には必ずしも、高血圧を呈しているとは限らない。症状の詳細な聴取、PRES、RCVSを含めたMRI所見などの解析が重要である。
  1. 脳卒中などの各種神経疾患との鑑別が重要であるため、必要であれば脳神経内科医または脳神経外科医にコンサルトする。
  1. また、子癇および子癇前症は高血圧性脳症と類似しているが、血管の蛋白透過性の亢進なども加わった病態であり、必すしも高血圧を呈さないこともある[8][9]
  1. 高血圧性脳症は、治療の遅滞が非可逆的な脳障害や、ときに致死的転帰を招く高血圧緊急症である。
  1. 治療には降圧薬の点滴静注による速やかな降圧が必要であるため、原則として集中治療室(ICU)かそれに類する環境下での治療を要する。
 
概念・病態生理  
  1. 高血圧性脳症とは、1928年にOppenheimerらが提唱した概念で、急激な血圧上昇、あるいは持続的な高度の高血圧により神経症状が引き起こされた病態である[10]。脳血管には全身血圧の変化に関わらず、脳血流を一定に保つ脳血管自動調節能autoregulationが存在することが知られている。一般には、脳血管自動調節能の働く全身平均血圧は60-150 mmHg程度とされており、その上限を超えた際に高血圧性脳症を生じるとされる[11]
  1. その機序としては、従来2種類の説が報告されている。

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文献 

著者: Aram V Chobanian, George L Bakris, Henry R Black, William C Cushman, Lee A Green, Joseph L Izzo, Daniel W Jones, Barry J Materson, Suzanne Oparil, Jackson T Wright, Edward J Roccella, Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program Coordinating Committee
雑誌名: Hypertension. 2003 Dec;42(6):1206-52. doi: 10.1161/01.HYP.0000107251.49515.c2. Epub 2003 Dec 1.
Abstract/Text The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

PMID 14656957  Hypertension. 2003 Dec;42(6):1206-52. doi: 10.1161/01.H・・・
著者: C J Vaughan, N Delanty
雑誌名: Lancet. 2000 Jul 29;356(9227):411-7. doi: 10.1016/S0140-6736(00)02539-3.
Abstract/Text A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage. Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, beta-blockers, labetelol, or calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists.

PMID 10972386  Lancet. 2000 Jul 29;356(9227):411-7. doi: 10.1016/S0140・・・
著者: W S Bartynski, J F Boardman
雑誌名: AJNR Am J Neuroradiol. 2007 Aug;28(7):1320-7. doi: 10.3174/ajnr.A0549.
Abstract/Text BACKGROUND AND PURPOSE: Although the term posterior reversible encephalopathy syndrome (PRES) was popularized because of the typical presence of vasogenic edema in the parietal and occipital lobes, other regions of the brain are also frequently affected. We evaluated lesion distribution with CT and MR in a large cohort of patients who experienced PRES to comprehensively assess the imaging patterns identified.
MATERIALS AND METHODS: The locations of the PRES lesion at toxicity were comprehensively identified and tabulated in 136 patients by CT (22 patients) and MR (114 patients) imaging including the hemispheric, basal ganglial, and infratentorial locations. Clinical associations along with presentation at toxicity including blood pressure were assessed.
RESULTS: Vasogenic edema was consistently present in the parietal or occipital regions (98%), but other locations were common including the frontal lobes (68%), inferior temporal lobes (40%), and cerebellar hemispheres (30%). Involvement of the basal ganglia (14%), brain stem (13%), and deep white matter (18%) including the splenium (10%) was not rare. Three major patterns of PRES were noted: the holohemispheric watershed (23%), superior frontal sulcal (27%), and dominant parietal-occipital (22%), with additional common partial or asymmetric expression of these primary PRES patterns (28%).
CONCLUSION: Involvement of the frontal lobe, temporal lobe, and cerebellar hemispheres is common in PRES, along with the occasional presence of lesions in the brain stem, basal ganglia, deep white matter, and splenium. Three primary PRES patterns are noted in the cerebral hemispheres, along with frequent partial or asymmetric expression of these PRES patterns. Awareness of these patterns and variations is important to recognize PRES neurotoxicity more accurately when present.

PMID 17698535  AJNR Am J Neuroradiol. 2007 Aug;28(7):1320-7. doi: 10.3・・・
著者: Anne Ducros
雑誌名: Lancet Neurol. 2012 Oct;11(10):906-17. doi: 10.1016/S1474-4422(12)70135-7.
Abstract/Text Recurrent thunderclap headaches, seizures, strokes, and non-aneurysmal subarachnoid haemorrhage can all reveal reversible cerebral vasoconstriction syndrome. This increasingly recognised syndrome is characterised by severe headaches, with or without other symptoms, and segmental constriction of cerebral arteries that resolves within 3 months. Reversible cerebral vasoconstriction syndrome is supposedly due to a transient disturbance in the control of cerebrovascular tone. More than half the cases occur post partum or after exposure to adrenergic or serotonergic drugs. Manifestations have a uniphasic course, and vary from pure cephalalgic forms to rare catastrophic forms associated with several haemorrhagic and ischaemic strokes, brain oedema, and death. Diagnosis can be hampered by the dynamic nature of clinicoradiological features. Stroke can occur a few days after initial normal imaging, and cerebral vasoconstriction is at a maximum on angiograms 2-3 weeks after clinical onset. The calcium channel blocker nimodipine seems to reduce thunderclap headaches within 48 h of administration, but has no proven effect on haemorrhagic and ischaemic complications.

Copyright © 2012 Elsevier Ltd. All rights reserved.
PMID 22995694  Lancet Neurol. 2012 Oct;11(10):906-17. doi: 10.1016/S14・・・
著者: K Yamaguchi, Y Fukuuchi, S Nogawa, T Dembo, Y Tomita, K Tanaka
雑誌名: Keio J Med. 2000 Feb;49 Suppl 1:A71-4.
Abstract/Text A 23-year-old woman presented in our hospital with toxemia, underwent cesarean section at about 36 weeks gestation, and became eclamptic in the immediate postpartum period. Following a complex partial seizure a few hours after the cesarean section, the patient experienced drowsiness, then cortical blindness. Cranial computed tomography (CT) performed at about 24 hours after the onset of the seizure showed low density areas in the bilateral occipital lobes. Intravenous magnesium sulfate was given, and the neurological symptoms disappeared within three weeks. Xenon/CT cerebral blood flow (CBF) was measured during the acute and chronic stages of the patient's eclampsia and compared with cranial magnetic resonance imaging (MRI) performed at about the same time. In the acute stage, MRI showed abnormal T2-hyperintensity signals in the head of the left caudate nucleus and in the bilateral occipital lobes, predominantly in the white matter. Xenon/CT CBF measurement showed decreased local cerebral blood flow (LCBF) in the area of the left anterior cerebral artery (ACA), the bilateral posterior cerebral arteries (PCAs), and the watershed areas of the left hemisphere. In the chronic stage, abnormal T2-hyperintensity signals remained in that part of the left occipital lobe where, in the acute stage, a marked decrease in LCBF had been detected. The main mechanism of eclampsia in this patient is thought to be a reactive vasoconstriction against hypertension rather than a vasodilatation.

PMID 10750343  Keio J Med. 2000 Feb;49 Suppl 1:A71-4.
著者: Masami Shimoda, Shinri Oda, Hideaki Shigematsu, Kaori Hoshikawa, Masaaki Imai, Fuminari Komatsu, Akihiro Hirayama, Takahiro Osada
雑誌名: Cephalalgia. 2018 Oct;38(12):1864-1875. doi: 10.1177/0333102418762471. Epub 2018 Mar 1.
Abstract/Text Introduction We previously reported centripetal propagation of vasoconstriction at the time of thunderclap headache remission in patients with reversible cerebral vasoconstriction syndrome. Here we examine the clinical significance of centripetal propagation of vasoconstriction. Methods Participants comprised 48 patients who underwent magnetic resonance angiography within 72 h of reversible cerebral vasoconstriction syndrome onset and within 48 h of thunderclap headache remission. Results In 24 of the 48 patients (50%), centripetal propagation of vasoconstriction occurred on magnetic resonance angiography at the time of thunderclap headache remission. The interval from first to last thunderclap headache in patients with centripetal propagation of vasoconstriction (14 ± 10 days) was significantly longer than that of patients without centripetal propagation of vasoconstriction (4 ± 2 days). In the patients with centripetal propagation of vasoconstriction at the time of thunderclap headache remission, the incidence of another cerebral lesion (38%, 9 of 24 cases) was significantly higher than in patients without centripetal propagation of vasoconstriction (0%). From findings of sequential magnetic resonance angiography before and after thunderclap headache remission, we observed tendencies in which centripetal propagation of vasoconstriction gradually progressed after the onset of reversible cerebral vasoconstriction syndrome and peaked at the time of thunderclap headache remission. The progress of centripetal propagation of vasoconstriction concluded with thunderclap headache remission. Conclusions Centripetal propagation of vasoconstriction has clinical significance as an indicator of the severity of reversible cerebral vasoconstriction syndrome. The presence of centripetal propagation of vasoconstriction is associated with an increased risk of brain lesions and a longer interval from first to last thunderclap headache. Moreover, repeat magnetic resonance angiography to assess centripetal propagation of vasoconstriction during the time from onset to thunderclap headache remission can help diagnose reversible cerebral vasoconstriction syndrome.

PMID 29495882  Cephalalgia. 2018 Oct;38(12):1864-1875. doi: 10.1177/03・・・
著者: P W Schaefer, F S Buonanno, R G Gonzalez, L H Schwamm
雑誌名: Stroke. 1997 May;28(5):1082-5. doi: 10.1161/01.str.28.5.1082.
Abstract/Text BACKGROUND: The pathophysiology of eclampsia remains unclear. While the majority of patients develop reversible T2 hyperintense signal abnormalities on MR scans and reversible neurological deficits, some patients do develop infarctions (permanent T2 hyperintense abnormalities) and permanent neurological impairment. Routine MRI cannot prospectively differentiate between these two patient groups. Echo-planar diffusion-weighted imaging, however, is a new technique that clearly differentiates between cytotoxic and vasogenic edema.
CASE DESCRIPTION: A 30-year-old woman developed symptoms consistent with eclampsia 24 hours after delivering premature twins. An MRI demonstrated extensive, diffuse T2 hyperintense signal abnormalities involving subcortical white matter and adjacent gray matter with a posterior predominance, consistent with either infarction or hypertensive ischemic encephalopathy. Diffusion-weighted images demonstrated increased diffusion, consistent with vasogenic edema and hypertensive ischemic encephalopathy.
CONCLUSIONS: Unlike routine MRI, diffusion-weighted imaging reliably differentiates between vasogenic edema and cytotoxic edema. Consequently, in eclamptic patients diffusion-weighted imaging can afford clear differentiation between hypertensive ischemic encephalopathy and infarction, two very different entities with very different treatment protocols. Diffusion-weighted imaging should be performed in all eclamptic patients and should greatly affect their management.

PMID 9158653  Stroke. 1997 May;28(5):1082-5. doi: 10.1161/01.str.28.5・・・
著者: K Weingarten, D Barbut, C G Filippi, C Filippi, R D Zimmerman
雑誌名: AJR Am J Roentgenol. 1994 Mar;162(3):665-70. doi: 10.2214/ajr.162.3.8109519.
Abstract/Text OBJECTIVE: The purpose of this study was to investigate the findings on spin-echo and gradient-echo MR images obtained in patients with hypertensive encephalopathy.
SUBJECTS AND METHODS: The MR images of 36 patients with clinically documented acute (< 72 hr) hypertensive encephalopathy were prospectively examined. Brain swelling on short TR images, hyperintensity on long TR images, and hypointensity on long TR and gradient-echo images were assessed.
RESULTS: The most common finding was hyperintensity in the supratentorial white matter (n = 32), representing hypertensive encephalopathy-induced reversible edema, irreversible infarction, or preexisting ischemic disease. These entities were difficult to distinguish on the basis of the initial examination. A more characteristic finding was edema (swelling on short TR images and hyperintensity on long TR images) in the basal ganglia (n = 22), brainstem (n = 15), and cerebellum (n = 11). Punctate foci of hypointensity, seen on long TR spin-echo images but optimally visualized on gradient-echo images, were the most distinguishing feature of this disorder.
CONCLUSION: MR imaging is efficacious in revealing deep ganglionic and posterior fossa edema, which is characteristic of hypertensive encephalopathy. Serial MR studies are necessary to distinguish transient edema from permanent zones of infarction. Gradient-echo MR imaging is particularly valuable in visualizing petechial hemorrhages, the presence of which distinguishes nonspecific white matter disease from an acute or prior episode of hypertensive encephalopathy and serves as a permanent marker of this disease.

PMID 8109519  AJR Am J Roentgenol. 1994 Mar;162(3):665-70. doi: 10.22・・・
著者: Bo Gao, Hui Liang, Feng-li Liu, Cui Lv
雑誌名: Clin Neuroradiol. 2012 Dec;22(4):341-4. doi: 10.1007/s00062-012-0162-1. Epub 2012 Aug 11.
Abstract/Text
PMID 22886172  Clin Neuroradiol. 2012 Dec;22(4):341-4. doi: 10.1007/s0・・・

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