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Record Nr. |
UNINA9910483040803321 |
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Titolo |
Moyamoya disease : current knowledge and future perspectives / / Satoshi Kuroda, editor |
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Pubbl/distr/stampa |
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Singapore : , : Springer, , [2021] |
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©2021 |
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ISBN |
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Descrizione fisica |
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1 online resource (xv, 341 pages) : illustrations |
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Disciplina |
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Soggetti |
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Nervous system - Surgery |
Malalties cerebrovasculars |
Neurocirurgia |
Llibres electrònics |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Nota di contenuto |
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Intro -- Foreword -- Preface -- Contents -- Part I: Concept of Moyamoya Disease -- 1: History of Disease Entity and Diagnosis Criteria -- 1.1 Introduction -- 1.2 History of Moyamoya Disease -- 1.3 Diagnosis Criteria of Moyamoya Disease -- References -- 2: Moyamoya Syndrome -- 2.1 Terminology -- 2.2 Epidemiology -- 2.2.1 Japan -- 2.2.2 Taiwan -- 2.2.3 China -- 2.2.4 Korea -- 2.2.5 United States of America -- 2.2.6 Germany -- 2.3 Associated Conditions -- 2.3.1 Neurofibromatosis Type 1 (von Recklinghausen's Disease) -- 2.3.2 Down Syndrome (Trisomy 21) -- 2.3.3 Thyroid Disease -- 2.3.4 Sickle Cell Disease -- 2.3.5 Others -- 2.3.6 Acquired Conditions -- 2.4 Surgical Revascularization and Outcome -- 2.5 Future Perspectives in Diagnosis and Patient Care -- References -- 3: Unilateral Moyamoya Disease: A Distinct Entity? -- 3.1 Introduction -- 3.2 Definition of Unilateral Moyamoya Disease -- 3.3 Clinical and Radiological Features -- 3.4 Biomarkers -- 3.5 Differentiation of Moyamoya Disease from Non-moyamoya Arteriopathy, Including FCA -- 3.6 Contralateral Progression -- 3.7 PCA Involvement -- 3.8 Perspectives -- References -- Part II: Genetic Aspect of Moyamoya Disease -- 4: RNF213 as a Susceptibility Gene for Moyamoya Disease |
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has Multifunctional Roles in Biological Processes -- 4.1 Introduction: RNF213 and Moyamoya Disease -- 4.2 Functional Properties of RNF213 and its Variants -- 4.2.1 Upregulation of RNF213 by Inflammatory Substances -- 4.2.2 Inhibitory Effects of RNF213 Variants on EC Functions and Cell Division -- 4.2.2.1 EC Dysfunction -- 4.2.2.2 Abnormal Mitosis -- 4.2.3 Stabilizing Effect of RNF213 on Cytoplasmic Lipid Droplets -- 4.2.4 NFκB Activation and Apoptosis by RNF213 Variants -- 4.2.5 Roles Played by RNF213 Domains and Variants -- 4.3 Susceptibilities Related to RNF213. |
4.3.1 Hypoxia and Hypoperfusion -- 4.3.2 Endoplasmic Reticulum Stress in Diabetes -- 4.3.3 Lipotoxicity -- 4.4 Relationship with Infection and Immune Function in MMD -- 4.5 Conclusions and Perspectives -- References -- 5: RNF213 and Clinical Feature -- 5.1 Introduction -- 5.2 RNF213 p.R4810K Genotype-Phenotype Correlation in Moyamoya Disease in East Asia -- 5.2.1 Japan and Korea -- 5.2.2 China -- 5.3 The Other Rare Variants of RNF213 -- 5.4 RNF213 Variant in Caucasian -- 5.5 RNF213 and Diseases Other than Moyamoya Disease -- 5.6 Conclusion -- References -- 6: RNF213 Variant as a Biomarker of Cerebrovascular Disease -- 6.1 Ring Finger Protein 213 (RNF213) -- 6.2 RNF213 and Intracranial Artery Stenosis -- 6.3 Variants of RNF213 Other than p.Arg4810Lys Associated with ICAS -- 6.4 Features of ICAS with the RNF213 p.Arg4810Lys Variant -- 6.5 Associations of General Ischemic Stroke and the RNF213 p.Arg4810Lys Variant -- 6.6 Associations of Systemic Vascular Diseases with the RNF213 p.Arg4810Lys Variant -- 6.7 Functional Analysis of the RNF213 Gene -- 6.8 Future Perspectives and Issues -- References -- Part III: Pathophysiology of Moyamoya Disease -- 7: TIA and Headache in Pediatric Moyamoya Disease -- 7.1 Introduction -- 7.2 Transient Ischemic Attack -- 7.2.1 Clinical Features and Mechanism -- 7.2.2 Natural Course of TIA -- 7.3 Headache Attack -- References -- 8: Ischemic Stroke -- 8.1 Introduction -- 8.2 Symptomatology -- 8.3 Radiological Features: Locations and Collateral Flows -- 8.4 Cerebral Hemodynamic Compromise -- 8.4.1 Compensatory Mechanisms against Cerebral Perfusion Pressure Decrease -- 8.4.2 Evaluation of Cerebral Perfusion Pressure Decrease -- 8.5 Ivy Sign -- 8.6 Surgical Indications -- 8.7 Antiplatelet Therapy for Ischemic MMD -- References -- 9: Hemorrhagic Stroke and the Japan Adult Moyamoya Trial. |
9.1 Introduction -- 9.2 The JAM Trial -- 9.3 Primary Results of the JAM Trial -- 9.4 Prespecified Subgroup Analysis of the JAM Trial -- 9.5 Mechanism of Bleeding in Moyamoya Disease: Periventricular Anastomosis -- 9.6 Why Does the Posterior Hemorrhage Group Have a Poor Natural Prognosis? -- 9.7 The Mechanism of Bypass Surgery in Preventing Hemorrhage -- 9.8 Additional Sub-analyses of the JAM Trial -- 9.9 Summary -- References -- 10: Cognitive Function in Pediatric Moyamoya Disease -- 10.1 Introduction -- 10.2 Clinical Features -- 10.3 Effects of Surgical Revascularization on Intellectual Outcome -- 10.4 Pathophysiology -- 10.5 Conclusion -- References -- 11: Cognitive Dysfunction in Adults -- References -- 12: Asymptomatic Moyamoya Disease -- 12.1 Introduction -- 12.2 Definition and Epidemiology -- 12.3 Radiological Findings -- 12.4 Natural Course -- 12.5 Asymptomatic Moyamoya Registry (AMORE) Study -- 12.6 Conclusion -- References -- Part IV: Update on Neuroradiology in Moyamoya Disease -- 13: Periventricular Anastomosis -- 13.1 Anatomy -- 13.2 Relationship between Periventricular Anastomosis and Bleeding -- 13.3 Radiological Findings -- 13.3.1 Lenticulostriate Anastomosis -- 13.3.2 Thalamic Anastomosis -- 13.3.3 Choroidal Anastomosis -- References -- 14: |
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Arterial Shrinkage -- 14.1 Introduction -- 14.2 Arterial Shrinkage in Carotid Fork -- 14.3 Arterial Shrinkage in Posterior Cerebral Artery -- 14.4 Arterial Shrinkage in Moyamoya Syndrome -- 14.5 Clinical Significance of Arterial Shrinkage in Moyamoya Disease -- 14.5.1 Endovascular Treatment -- 14.5.2 Differential Diagnosis of Moyamoya Disease -- References -- 15: Disease Progression -- 15.1 Introduction -- 15.2 Suzuki's Angiographic Staging as an Intrinsic Temporal Nature of Physiological Compensatory Reorganization in MMD -- 15.3 Disease Progression in Adult MMD. |
15.4 Significance of Progressive Stenosis in Posterior Cerebral Artery (PCA) -- References -- 16: Postoperative Hyperperfusion -- 16.1 Introduction -- 16.2 Incidence of HP -- 16.3 Clinical Features -- 16.4 Diagnosis -- 16.5 Intraoperative Evaluations -- 16.5.1 Indocyanine Green Videoangiography -- 16.5.2 Flow Meters -- 16.5.3 Caliber Mismatch of Donor and Recipient Arteries -- 16.5.4 Hemodynamic Sources of Recipient Arteries -- 16.6 Postoperative Imaging -- 16.6.1 SPECT/PET -- 16.6.2 MRI -- 16.7 3 MRA -- 16.8 Pathogenesis -- 16.9 Perioperative Management of HP -- References -- 17: Postoperative FLAIR Imaging Changes -- 17.1 Introduction -- 17.2 Radiological Features of the Hyperintense Signal -- 17.3 The Role of Cerebral Hemodynamics -- 17.3.1 Preoperative Cerebral Hemodynamics -- 17.3.2 Postoperative Hyperperfusion -- 17.4 Future Perspective -- References -- Part V: Real World of Surgical Revascularization for Moyamoya Disease -- 18: Overview of Surgical Revascularization and Long-Term Outcome in Japan -- 18.1 Introduction -- 18.2 Surgical Procedures -- 18.2.1 Indirect Bypass Surgery -- 18.2.2 Direct Bypass Surgery -- 18.2.3 Combined Bypass Surgery -- 18.3 Long-Term Outcome in Japan -- References -- 19: Perioperative Complications -- 19.1 Background -- 19.2 Frequency and Pathophysiology of Perioperative Complications -- 19.2.1 Classification -- 19.3 Perioperative Stroke -- 19.3.1 Ischemic Complications -- 19.4 Hemorrhagic Complications -- 19.4.1 Postoperative Hyperperfusion -- 19.5 Procedure-Related Complications -- 19.6 Perioperative Management to Prevent Complications -- 19.7 Discussion -- References -- 20: Long-Term Outcome in Europe -- 20.1 Moyamoya Disease in Europe: Overview -- 20.2 Surgical Treatment of Moyamoya Patients in our Institute -- 20.3 Long-Term Outcome of Moyamoya Patients in Europe. |
20.4 Conclusion -- References -- 21: Long-Term Outcomes in the USA -- 21.1 Introduction -- 21.2 Epidemiology of Moyamoya Disease in the USA -- 21.3 Presentation -- 21.4 Natural History in the USA -- 21.5 Treatment Trends -- 21.6 Outcomes -- 21.7 Conclusions -- References -- 22: Long-Term Outcome in China -- 22.1 Introduction -- 22.2 Epidemiology -- 22.2.1 General Epidemiology -- 22.2.2 Genetic Epidemiology -- 22.3 Treating Modality -- 22.3.1 Revascularization -- 22.3.2 Varied Kinds of Revascularization -- 22.3.3 Modified Revascularization -- 22.4 Ischemic Moyamoya Disease in China and Its Long-Term Outcomes -- 22.4.1 Cognitive Status of MMD in China -- 22.4.2 Long-Term Outcomes of Ischemic MMD in China -- 22.4.2.1 Overall Outcomes -- 22.4.2.2 Neurocognitive and Neuroimaging Outcomes -- 22.5 Long-Term Outcomes in Hemorrhagic MMD -- 22.5.1 Natural History of Hemorrhagic MMD in China -- 22.5.2 Long-Term Outcome of Surgically Treated Hemorrhagic MMD in China -- 22.5.2.1 Direct Revascularization -- 22.5.2.2 Indirect Revascularization -- 22.5.2.3 Combined Revascularization -- 22.6 Long-Term Outcomes in Pediatric MMD -- 22.6.1 Treatments -- 22.6.2 Long-Term Clinical Outcome -- 22.7 Conclusion -- References -- 23: Long-Term Outcome |
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of Revascularization Surgery for Moyamoya Disease in Korea -- 23.1 Introduction -- 23.2 Procedure of RVS -- 23.3 Indication of RVS -- 23.4 Selection of the RVS Procedure -- 23.5 Long-term Outcome of RVS for Patients with MMD in Korea (Table 23.1) -- 23.6 Conclusion -- References -- 24: Indirect Bypass Surgery for Moyamoya Disease -- 24.1 Introduction -- 24.2 History and Mechanism of Indirect Bypass Surgery -- 24.3 The Hemodynamic Characteristics of Moyamoya Disease -- 24.4 Pre-Operative Neuroimaging for Precise Application of Indirect-Bypass Surgery. |
24.5 Surgical Procedure of Indirect Bypass Surgery. |
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