10254nam 2200505 450 991061928170332120230305193657.03-031-08068-8(MiAaPQ)EBC7119903(Au-PeEL)EBL7119903(CKB)25179636800041(OCoLC)1348490266(PPN)265861500(EXLCZ)992517963680004120230305d2022 uy 0engurcnu||||||||txtrdacontentcrdamediacrrdacarrierCortical spreading depression of leao from mitochondrial function to brain metabolic score (BMS) /Avraham Mayevsky and Judith SonnCham, Switzerland :Springer,[2022]©20221 online resource (429 pages)Print version: Mayevsky, Avraham Cortical Spreading Depression of Leao Cham : Springer International Publishing AG,c2022 9783031080678 Includes bibliographical references (pages 411-417) and index.Intro -- Preface 1 -- Preface 2 -- Aim of the Book -- Acknowledgments -- I -- II -- Contents -- Chapter 1: Introduction and Historical Background -- 1.1 Leão' Cortical Spreading Depression (CSD) -- 1.1.1 Aristides Leão: Life History -- 1.1.2 The Discovery of the "Spreading Depression" -- 1.1.3 Back to Brazil -- 1.1.4 Conclusion -- 1.1.5 Aristides Leão: The Four Seminal Publications (1944-1947) -- 1.2 Oxygen Homeostasis in the Brain -- 1.2.1 The Discovery of Oxygen -- 1.2.2 The Discovery of the Mitochondrial Function -- 1.3 Monitoring of Brain Mitochondrial Function in Vivo -- 1.4 Brain Energy Metabolism and Mitochondrial Function During CSD -- References -- Chapter 2: Basic Principles and Technology of NADH and Multiparametric Monitoring Used in Studying Cortical Spreading Depression (CSD) -- 2.1 Introduction -- 2.2 From NADH Monitoring to Multiparametric Monitoring Systems -- 2.2.1 Fiber-Optic-Based Fluorometer/Reflectometer -- 2.2.2 Simultaneous Monitoring of NADH by DC Fluorometer Reflectometer Together with Monitoring of Systemic Blood Pressure and Electrocortical Activity (ECoG) -- 2.2.3 Simultaneous Monitoring of NADH Together with Extracellular K+, DC Steady Potential, and ECoG -- 2.2.4 Monitoring of Brain NADH Together with Tissue pO2 and ECoG -- 2.2.5 Multiparametric Assembly for Recording of NADH, Extracellular K+, H+, DC Steady Potential, and ECoG -- 2.2.5.1 Electrode Assembly -- 2.2.5.2 Correction for Local DC Biopotential -- 2.2.5.3 NADH Fluorescence Measurement -- 2.2.6 Monitoring of NADH, pO2, Extracellular K+, DC, and ECoG, Outside and Inside Hyperbaric Chamber -- 2.2.7 Simultaneous Real-Time Monitoring of Brain NADH, HbO2, ECoG, DC Potential, and Extracellular K+ and Ca2+ -- 2.2.8 Simultaneous Real-Time Monitoring of Brain NADH, CBF, ECoG, DC Potential, and Extracellular K+ and Ca2+.2.2.9 Simultaneous Monitoring of Brain NADH, CBF, ECoG, DC Potential, and Extracellular K+, Ca+2, H+ -- 2.2.10 Multiparametric Monitoring of Neurosurgical Patients -- 2.2.11 Monitoring of the Mechanism of CSD Propagation -- 2.2.12 Multisite Monitoring of NADH and DC Potential in Rats Under Various Conditions -- 2.2.13 Multisite Multiparametric Monitoring of NADH, CBF, and DC Potential in Rats Under Experimental Conditions -- References -- Chapter 3: Single Point and Multisite Monitoring of Brain NADH Fluorescence Under CSD -- 3.1 Introduction -- 3.2 Single Point Monitoring of NADH -- 3.3 Two Points Monitoring of NADH -- 3.4 Four Points Monitoring of NADH -- References -- Chapter 4: Sequence of Physiological Responses Recorded During Induced CSD Event -- 4.1 Introduction -- 4.2 Effects of CSD on Cerebral Blood Flow and Brain Oxygen Consumption -- 4.2.1 Introduction -- 4.2.2 Methods -- 4.2.3 Results -- 4.2.4 Discussion -- 4.3 Sequence of Events Recorded During the CSD Cycle -- 4.3.1 The Use of the MPA System -- 4.3.2 CSD Initiation and Contralateral Responses -- 4.3.3 Discussion -- References -- Chapter 5: Spontaneous Development of CSD Related to Brain Pathophysiological Conditions -- 5.1 Introduction -- 5.2 During Anoxia, Hypoxia, and Ischemia -- 5.3 During Exposure to Hyperbaric Hyperoxia (HBO) -- 5.3.1 First Study-HBO Effects on Mitochondrial Function -- 5.3.1.1 Introduction -- 5.3.1.2 Methodology -- 5.3.1.3 Results -- 5.3.1.4 Discussion -- 5.3.2 Second Study-Protection Against Oxygen Toxicity by Trimethadione -- 5.3.3 Third Study-Effects of CO2 Under HBO -- 5.3.4 More Factors Affecting HBO Toxicity -- 5.3.5 Fifth Study-Multiparametric Monitoring of CSD Under HBO -- 5.3.5.1 Introduction -- 5.3.5.2 Methods -- 5.3.5.3 Results -- 5.3.5.4 Discussion -- 5.4 During Drug-Induced Seizure Activity -- 5.5 Development of CSD During and After Head Injury.5.5.1 First Study-Development of the TBI Model -- 5.5.1.1 Introduction -- 5.5.1.2 Technological Aspects -- 5.5.1.3 Results -- 5.5.1.4 Discussion -- 5.5.2 Second Study-Level of ICP and CSD After TBI -- 5.5.2.1 Introduction -- 5.5.2.2 Methods -- 5.5.2.3 Results -- 5.5.2.4 Discussion -- References -- Untitled -- Chapter 6: The Effects of Brain Metabolic and Other Perturbations on the Responses to Induced CSD -- 6.1 Effects of Oxygen Availability -- 6.1.1 Introduction -- 6.1.2 Effects of Hypoxia and Hyperoxia on the Responses to CSD -- 6.1.3 Responses to CSD Under Ischemia -- 6.1.4 Responses to CSD Under Partial Ischemia-Statistical Analysis -- 6.2 Effect of Anesthesia on the Responses to CSD -- 6.3 Effects of Hypothermia on the Responses to CSD -- 6.3.1 Introduction -- 6.3.2 Our Studies -- 6.4 Responses to CSD in the Aging Rat -- References -- Chapter 7: Effects of Pharmacological Agents on CSD -- 7.1 Effects of Carbon Monoxide -- 7.1.1 First Study -- 7.1.1.1 Introduction -- 7.1.1.2 Methods -- 7.1.1.3 Results and Discussion -- 7.1.2 Second Study -- 7.1.2.1 Introduction -- 7.1.2.2 Methods -- 7.1.2.2.1 Data Collection and Analysis -- 7.1.2.3 Results -- 7.1.2.4 Discussion -- 7.1.3 Third Study -- 7.1.3.1 Introduction -- 7.1.3.2 Methods -- 7.1.3.3 Results -- 7.1.3.4 Discussion -- 7.1.4 Fourth Study -- 7.1.4.1 Introduction -- 7.1.4.2 Methods -- 7.1.4.3 Results -- 7.1.4.4 Discussion -- 7.2 Nitric Oxide -- 7.2.1 First Study -- 7.2.1.1 Introduction -- 7.2.1.2 Methods -- 7.2.1.3 Results -- 7.2.1.4 Discussion -- 7.2.2 Second Study: The Effect of CSD Under Nitric Oxide (NO) Synthase Inhibition -- 7.2.2.1 Introduction -- 7.2.2.2 Methods -- 7.2.2.3 Results -- 7.2.2.3.1 The Variation of the Measured Parameters in the Control Study -- 7.2.2.3.2 Results: The Effect of L-NAME Injection on the Measured Parameters.7.2.2.3.3 Results: The Effect of CSD Waves on the Measured Parameters -- 7.2.2.3.4 Results: CSD Amplitudes -- 7.2.2.3.5 Results: CSD Wave Duration -- 7.2.2.3.6 Results: Recovery from CSD Wave -- 7.2.2.4 Summary -- 7.3 Alcohol Effects -- 7.3.1 First Study -- 7.3.2 Second Study: The Effects of Ethanol on the Responses to CSD -- 7.3.2.1 Introduction -- 7.3.2.2 Methods -- 7.3.2.3 Results -- 7.3.2.3.1 Amplitude Values -- 7.3.2.3.2 Wave Frequency (FRQ) -- 7.3.2.3.3 Propagation Rate: VTP (Mm/Min) -- 7.3.2.4 Discussion -- 7.3.2.4.1 Reflectance -- 7.3.2.4.2 NADH Redox State -- 7.3.2.4.3 DC Potential -- 7.3.2.4.4 CSD Wave Frequency and Propagation Rate -- References -- Chapter 8: Clinical Monitoring of Cortical Spreading Depression (CSD) in the Human Brain -- 8.1 Introduction -- 8.2 Monitoring of NADH and Other Parameters in Patients -- 8.3 The Discovery of CSD in the Human Cerebral Cortex -- 8.3.1 Introduction -- 8.3.2 Methods -- 8.3.2.1 The Development of the Monitoring System -- 8.3.2.2 Construction of the Multiprobe Assembly (MPA) -- 8.3.2.3 Patient Preparation -- 8.3.3 Results -- 8.3.4 Discussion -- References -- Chapter 9: CSD and the LifenLight Score (LLS) -- 9.1 Introduction -- 9.1.1 The Developed Concept -- 9.1.2 Brain LifenLight Score (LLS) -- 9.2 Methodology Used -- 9.2.1 The Multiparametric Monitoring System -- 9.2.2 Time Sharing Fluorometer Reflectometer (TSFR) -- 9.2.3 Mitochondrial NADH Redox State (NADH) -- 9.2.4 Microcirculatory Blood Oxygenation -- 9.2.5 Microcirculatory Blood Flow -- 9.2.6 Animal Preparation -- 9.2.7 Real-Time Data Acquisition -- 9.2.8 LifenLight Score (LLS) -- 9.3 Results -- 9.4 Discussion -- References -- Chapter 10: Discussion and Conclusions -- 10.1 Introduction -- 10.2 The Discovery of CSD in the Human Cerebral Cortex -- 10.3 NADH Responses to CSD In Vivo vs. Isolated Mitochondria In Vitro.10.4 Cortical Spreading Depression (CSD) under Pathophysiological Conditions -- 10.5 Modeling Brain Energy Metabolism and Function -- 10.5.1 Introduction -- 10.5.2 The Mathematical Model -- 10.5.3 Results -- 10.5.4 Model Discussion -- 10.6 Future Perspectives -- References -- Appendix -- Introduction -- Chapter 1: Electrical Properties of Spreading Depression -- Spontaneous Electroencephalographic Activity -- Evoked Potentials -- Slow Potentials -- Unit Activity -- Membrane Potentials -- Impedance Changes -- Chapter 5: Chemical Aspects of Spreading Depression -- Ion and Water Transport and Distribution During Spreading Depression -- Spreading Cortical Depression and Labile Chemical Compounds in the Brain -- Amino Acids and Spreading Depression -- Biochemical Correlates of the Functional Changes Accompanying Spreading Depression -- Protein Metabolism in the Course of Spreading Depression -- Chapter 7: Mechanism of Spreading Depression -- Vascular Mechanisms -- Electric Fields -- Humoral Transmission -- Potassium Hypothesis -- Glutamic Acid Hypothesis -- Concomitant Phenomena -- References -- Index.Mitochondrial pathologyBrainMetabolismDisordersMitochondrial pathology.BrainMetabolismDisorders.616.07Mayevsky Avraham1064292Sonn JudithMiAaPQMiAaPQMiAaPQBOOK9910619281703321Cortical Spreading Depression of Leao2954967UNINA