Neuroanesthesia and Neurocritical Care Textbook PDF

Textbook of Neuroanesthesia and Neurocritical Care Volume I - Neuroanesthesia Hemanshu Prabhakar Zulfiqar Ali Editors https://t.me/Anesthesia_Books 123 Textbook of Neuroanesthesia and Neurocritical Care Hemanshu Prabhakar Zulfiqar Ali Editors Text...

Textbook of Neuroanesthesia and Neurocritical Care Volume I - Neuroanesthesia Hemanshu Prabhakar Zulfiqar Ali Editors https://t.me/Anesthesia_Books 123 Textbook of Neuroanesthesia and Neurocritical Care Hemanshu Prabhakar Zulfiqar Ali Editors Textbook of Neuroanesthesia and Neurocritical Care Volume I - Neuroanesthesia Editors Hemanshu Prabhakar Zulfiqar Ali Department of Neuroanaesthesiology Division of Neuroanesthesiology and Critical Care Department of Anesthesiology All India Institute of Medical Sciences Sher-i-Kashmir Institute of Medical New Delhi Sciences India Soura, Srinagar Jammu and Kashmir India ISBN 978-981-13-3386-6    ISBN 978-981-13-3387-3 (eBook) https://doi.org/10.1007/978-981-13-3387-3 Library of Congress Control Number: 2019934709 © Springer Nature Singapore Pte Ltd. 2019 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Singapore Pte Ltd. The registered company address is: 152 Beach Road, #21-01/04 Gateway East, Singapore 189721, Singapore Foreword Neuroanaesthesia and neurocritical care continue to evolve and develop as specialities, presenting those of us responsible for patient care with ever more challenges. Within the operating theatre, technological advances in surgical techniques and imaging have necessitated changes both in the way we work and also where we work. Advances in interventional neuroradiology have led to a greater demand for anaesthetic and critical care input outside of the oper- ating theatre, often in remote sites, with all the associated challenges. An ever-increasing number of surgical procedures of greater complexity along- side an aging population have led to increased demands on the neurocritical care unit. Fortunately, advances in neuroanaesthesia, neurocritical care and neuromonitoring have recognised and facilitated these changes. It has often been said that neuroanaesthesia is a speciality where the knowl- edge and skill of the anaesthetist directly influences patient outcome. This remains true today. To this end, the Textbook of Neuroanaesthesia and Neurocritical Care edited by Hemanshu Prabhakar covers all aspects of patient care. Volume I rightly begins with the fundamentals of neuroanaesthesia including anatomy, physiology and pharmacology, an understanding of which is essential to underpin good care. There is detailed guidance on the process of anaesthesia for neurosurgery includ- ing coexisting problems, special considerations, pain management and near misses. A special topics section includes recent innovations such as robotic sur- gery, gene delivery and expression, intra-arterial drug delivery and simulation in neuroanaesthesia. In volume II, the complexities of critical care are thoroughly addressed, starting with the fundamentals of neurocritical care through to the intensive care management of specific conditions, neuromonitoring, pain man- agement, ethical considerations and near misses. Again, there is a special topics section on recent advances including research and evidence-based practice. This comprehensive textbook is an authoritative and practical clinical text. It covers the breadth and depth of the complex specialities of neuroanaesthe- sia and critical care and includes chapters by many leading names in neuro- anaesthesia who have lent their expertise to this work. It will be essential reading for trainees, clinicians and researchers involved in neurosciences. Despite the ever-increasing challenges facing us, this book should provide the reader with the necessary knowledge to enhance their practice and provide optimal neuroanaesthesia and neurocritical care. Consultant Neuroanaesthetist, Judith Dinsmore Department of Anaesthesia St George’s University Hospitals NHS Foundation Trust, London, UK v Preface The editors feel pleased to present the first edition of Textbook of Neuroanesthesia and Neurocritical Care. This book has tried to cover the basic concepts of neuroanaesthesia and neurocritical care along with the major changes that have evolved in the field of neurosciences in the last decade. An attempt has been made by the authors to present an updated pre- sentation of the subject. The book is available in two volumes: volume I focuses on the foundation of neuroanaesthesiology, and volume II focuses on the understanding of the neurocritical care. We hope that this book will be of immense use for readers, who are more focused on gaining an advanced understanding in the field of neurosciences. We thank the authors for doing an outstanding job of producing authorita- tive chapters. We feel privileged to have compiled this first edition and are enthusiastic about everything it offers to our readers. We learned much in the process of editing this textbook and hope that you will find this textbook a valuable source of educational resource in the field of neurosciences. New Delhi, India Hemanshu Prabhakar Srinagar, India  Zulfiqar Ali vii Contents Part I Fundamentals of Neuroanesthesia 1 Neuroanatomy   3 Ravi K. Grandhi and Alaa Abd-Elsayed 2 Physiology for Neuroanesthesia 17 Thomas M. Price, Catriona J. Kelly, and Katie E. S. Megaw 3 Pharmacological Considerations in Neuroanesthesia 33 Sabine Kreilinger and Eljim P. Tesoro Part II Neuromonitoring 4 Intraoperative Monitoring of the Brain 43 Hironobu Hayashi and Masahiko Kawaguchi 5 Intraoperative Neuromonitoring for the Spine  63 Dhritiman Chakrabarti and Deepti Srinivas Part III Anesthesia for Neurosurgery 6 Anesthesia for Supratentorial Brain Tumor (SBT) 77 Fenghua Li and Reza Gorji 7 Anesthesia for Infratentorial Lesions 95 Barkha Bindu and Charu Mahajan 8 Anesthesia for Aneurysmal Subarachnoid Hemorrhage 115 Nicolas Bruder, Salah Boussen, and Lionel Velly 9 Anesthesia for Cerebrovascular Lesions 131 Shiwani Jain and Manish Kumar Marda 10 Anesthesia for Pituitary Lesions 145 Tullio Cafiero 11 Anesthesia for Epilepsy Surgery 159 Sujoy Banik and Lashmi Venkatraghavan 12 Anesthesia for Functional Neurosurgery  171 Zulfiqar Ali and Hemanshu Prabhakar ix x Contents 13 Anesthesia for Endoscopic Third Ventriculostomy 177 Abdelazeem Ali El-Dawlatly 14 Anesthesia for Spine Surgery 189 Andres Zorrilla-Vaca, Michael C. Grant, and Marek A. Mirski 15 Anesthesia for Traumatic Brain Injury  201 Rachel Kutteruf 16 Anesthesia for Traumatic Spine Injury 225 Onat Akyol, Cesar Reis, Haley Reis, John Zhang, Shen Cheng, and Richard L. Applegate II Part IV Co-existing Problems 17 Co-Existing Hypertension in Neurosurgery 235 Ramamani Mariappan and Rajasekar Arumugam 18 Co-existing Diabetes Mellitus in Neurosurgical Patients  253 Manikandan Sethuraman Part V Special Considerations 19 Pregnancy and Neuroanesthesia 265 Monica S. Tandon and Aastha Dhingra 20 Pediatric Neuroanesthesia 291 Jue T. Wang and Craig McClain 21 Geriatric Neuroanesthesia 311 Kiran Jangra and Shiv Lal Soni Part VI Allied Considerations 22 Interventional Neuroradiology  327 Ravi Bhoja, Meghan Michael, Jia W. Romito, and David L. McDonagh 23 Anesthesia for Gamma Knife Surgery  341 Summit Dev Bloria, Ketan K. Kataria, and Ankur Luthra 24 Infection Control in Operating Rooms: Sterilization and Disinfection Practices 351 Purva Mathur 25 Intravenous Thrombolysis 359 Vasudha Singhal and Jaya Wanchoo Contents xi Part VII Transfusion Practice 26 Fluid Management in Neurosurgical Patients 373 Wojciech Dabrowski, Robert Wise, and Manu L. N. G. Malbrain 27 Blood Transfusion in Neurosurgery  383 Kavitha Jayaram and Shibani Padhy Part VIII Near Misses 28 Near Misses in Neuroanesthesia  403 Zakir Hajat and Zoe Unger 29 Near Misses in the Intraoperative Brain Suite 413 Cory Roeth, Nicoleta Stoicea, and Sergio D. Bergese 30 Complications of Neuroanesthesia  419 Emily Farrin, Brett J. Wakefield, and Ashish K. Khanna Part IX Pain Management 31 Pain Management Following Craniotomy  437 Chia Winchester and Alexander Papangelou 32 Post-operative Pain Management in Spine Surgery  447 Ravi K. Grandhi and Alaa Abd-Elsayed 33 Trigeminal Neuralgia 457 Nidhi Gupta Part X Special Topics 34 Postoperative Cognitive Dysfunction  483 Suparna Bharadwaj and Sriganesh Kamath 35 Enhanced Recovery After Neurosurgical Procedures (Craniotomies and Spine Surgery)  493 Juan P. Cata, Katherine Hagan, and Mauro Bravo 36 Robot-Assisted Neurosurgery  503 Indu Kapoor, Charu Mahajan, and Hemanshu Prabhakar 37 Gene Therapy for Neuroanesthesia 511 Ellen S. Hauck and James G. Hecker 38 Intra-arterial Drug Delivery for Brain Diseases  523 Jason A. Ellis and Shailendra Joshi Contributors Alaa Abd-Elsayed Department of Anesthesiology, UW Health Pain Services, University of Wisconsin-Madison, Madison, WI, USA Shiwani Agarwal Department of Neuroanaesthesia and Critical Care, Max Super Specialty Hospital Vaishali, Ghaziabad, India Onat Akyol Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA Department of Anesthesiology, Bağcılar Training and Research Hospital, İstanbul, Turkey Zulfiqar Ali Division of Neuroanesthesiology, Department of Anesthesiology, Sher-i-Kashmir Institute of Medical Sciences Soura, Srinagar, Jammu and Kashmir, India Richard L. Applegate II Anesthesiology and Pain Medicine, University of California Davis Health, Sacramento, CA, USA Rajasekar Arumugam Surgical Intensive Care Unit, Christian Medical College Vellore, Vellore, India Sujoy Banik Department of Anesthesia and Pain Medicine, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada Sergio D. Bergese Department of Anesthesiology, The Ohio State University Wexner Medical Center, Columbus, OH, USA Department of Neurological Surgery, The Ohio State University Wexner Medical Center, Columbus, OH, USA Suparna Bharadwaj Department of Neuroanaesthesia and Neurocritical Care, National Institute of Mental Health and Neurosciences, Bengaluru, India Ravi Bhoja Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas, TX, USA Barkha Bindu Department of Neuroanaesthesiology and Neuro-Critical Care, All India Institute of Medical Sciences, New Delhi, India Summit Dev Bloria Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India xiii xiv Contributors Salah Boussen Department of Anesthesiology and Intensive Care, CHU Timone, AP-HM, Aix-Marseille University, Marseille, France Mauro Bravo Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Anesthesiology and Surgical Oncology Research Group, Houston, TX, USA Nicolas Bruder Department of Anesthesiology and Intensive Care, CHU Timone, AP-HM, Aix-Marseille University, Marseille, France Tullio Cafiero Department of Anesthesia and Postoperative Intensive Care, Antonio Cardarelli Hospital, Napoli, Italy Juan P. Cata Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Anesthesiology and Surgical Oncology Research Group, Houston, TX, USA Dhritiman Chakrabarti Department of Neuroanaesthesiology and Neurocritical Care, National Institute of Mental Health and Neuro Sciences, Bangalore, India Shen Cheng Department of Neurosurgery, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Wojciech Dabrowski Department of Anaesthesiology and Intensive Therapy, Medical University of Lublin, Lublin, Poland Aastha Dhingra Department of Anaesthesia, Max Super-specialty Hospital, Ghaziabad, India Abdelazeem Ali El-Dawlatly College of Medicine, King Saud University, Riyadh, Saudi Arabia Jason A. Ellis Department of Neurosurgery, Hofstra Northwell School of Medicine, Lenox Hill Hospital, New York, NY, USA Emily Farrin Anesthesiology Institute, Cleveland Clinic, Cleveland, OH, USA Reza Gorji Department of Anesthesiology, SUNY Upstate Medical University, Syracuse, NY, USA Ravi K. Grandhi Department of Anesthesiology, Maimonides Medical Center, Brooklyn, NY, USA Michael C. Grant Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Hospital, Baltimore, MD, USA Nidhi Gupta Department of Neuroanaesthesia, Indraprastha Apollo Hospitals, New Delhi, India Katherine Hagan Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA Anesthesiology and Surgical Oncology Research Group, Houston, TX, USA Contributors xv Zakir Hajat Department of Anesthesia, University Health Network, Toronto Western Hospital, Toronto, ON, Canada Ellen S. Hauck Department of Anesthesiology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA Hironobu Hayashi Department of Anesthesiology, Nara Medical University Hospital, Kashihara, Japan James G. Hecker Department of Anesthesiology and Pain Medicine, Harborview Medical Center, Seattle, WA, USA Kiran Jangra Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India Kavitha Jayaram Department of Anesthesiology and Critical Care, Nizams Institute of Medical Sciences, Hyderabad, India Shailendra Joshi Department of Anesthesia, Columbia University Medical Center, New York, NY, USA Sriganesh Kamath Department of Neuroanaesthesia and Neurocritical Care, National Institute of Mental Health and Neurosciences, Bengaluru, India Indu Kapoor Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi, India Ketan K. Kataria Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India Masahiko Kawaguchi Department of Anesthesiology, Nara Medical University Hospital, Kashihara, Japan Catriona J. Kelly Department of Neuroanaesthesia, Royal Victoria Hospital, Belfast, Belfast, UK Ashish K. Khanna Anesthesiology Institute, Cleveland Clinic, Cleveland, OH, USA Wake Forest University School of Medicine, Winston-Salem, NC, USA Sabine Kreilinger Department of Anesthesiology, University of Illinois at Chicago, Chicago, IL, USA Rachel Kutteruf Department of Anesthesiology, U.S. Anesthesia Partners— Washington, Seattle, WA, USA Fenghua Li Department of Anesthesiology, SUNY Upstate Medical University, Syracuse, NY, USA Ankur Luthra Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India Charu Mahajan Department of Neuroanaesthesiology and Neuro-Critical Care, All India Institute of Medical Sciences, New Delhi, India xvi Contributors Manu L. N. G. Malbrain Intensive Care Unit, University Hospital Brussels (UZB), Jette, Belgium Faculty of Medicine and Pharmacy, Vrije Unoversiteit Brussel (VUB), Brussels, Belgium Manish Kumar Marda Department of Neuroanaesthesia and Critical Care, Max Super Specialty Hospital Vaishali, Ghaziabad, India Ramamani Mariappan Department of Anaesthesia, Christian Medical College Vellore, Vellore, India Purva Mathur JPNA Trauma Center, All India Institute of Medical Sciences, New Delhi, India Craig McClain Department of Anesthesiology, Critical Care and Pain Medicine, Harvard Medical School, Boston Children’s Hospital, Boston, MA, USA David L. McDonagh Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas, TX, USA Katie E. S. Megaw Department of Neuroanaesthesia, Royal Victoria Hospital, Belfast, Belfast, UK Meghan Michael Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas, TX, USA Marek A. Mirski Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Hospital, Baltimore, MD, USA Shibani Padhy Department of Anesthesiology and Critical Care, Nizams Institute of Medical Sciences, Hyderabad, India Alexander Papangelou Department of Anesthesiology, Emory University Hospital, Atlanta, GA, USA Hemanshu Prabhakar Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences, New Delhi, India Thomas M. Price Department of Neuroanaesthesia, Royal Victoria Hospital, Belfast, Belfast, UK Cesar Reis Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA Department of Preventive Medicine, Loma Linda University Medical Center, Loma Linda, CA, USA Haley Reis Loma Linda School of Medicine, Loma Linda, CA, USA Cory Roeth Boonshoft School of Medicine, Dayton, OH, USA Department of Anesthesiology, The Ohio State University Wexner Medical Center, Columbus, OH, USA Jia W. Romito Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas, TX, USA Contributors xvii Manikandan Sethuraman Division of Neuroanesthesia, Department of Anesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India Vasudha Singhal Department of Neuroanesthesiology and Critical Care, Medanta, The Medicity, Gurgaon, India Shiv Lal Soni Department of Anaesthesia and Intensive Care, Postgraduate Institute of Medical Education and Research, Chandigarh, India Deepti Srinivas Department of Neuroanaesthesiology and Neurocritical Care, National Institute of Mental Health and Neuro Sciences, Bangalore, India Nicoleta Stoicea Department of Anesthesiology, The Ohio State University Wexner Medical Center, Columbus, OH, USA Monica S. Tandon Department of Anesthesiology and Intensive Care, G. B. Pant Institute of Postgraduate Medical Education and Research, New Delhi, India Eljim P. Tesoro Department of Pharmacy Practice, University of Illinois at Chicago, Chicago, IL, USA Zoe Unger Department of Anesthesia, University Health Network, Toronto Western Hospital, Toronto, ON, Canada Lionel Velly Department of Anesthesiology and Intensive Care, CHU Timone, AP-HM, Aix-Marseille University, Marseille, France Lashmi Venkatraghavan Department of Anesthesia and Pain Medicine, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada Brett J. Wakefield Anesthesiology Institute, Cleveland Clinic, Cleveland, OH, USA Jaya Wanchoo Department of Neuroanesthesiology and Critical Care, Medanta, The Medicity, Gurgaon, India Jue T. Wang Department of Anesthesiology, Critical Care and Pain Medicine, Boston Children’s Hospital, Boston, MA, USA Chia Winchester Department of Anesthesiology, Emory University Hospital, Atlanta, GA, USA Robert Wise Department of Anaesthetics, Critical Care and Pain Management, Pietermaritzburg Metropolitan, Pietermaritzburg, South Africa Discipline of Anaesthesiology and Critical Care, Clinical School of Medicine, University of KwaZulu-Natal, Durban, South Africa John Zhang Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA Andres Zorrilla-Vaca Department of Anesthesiology, Universidad del Valle, School of Medicine, Cali, Colombia About the Editors Hemanshu Prabhakar is a professor in the Department of Neuroanaesthesiology and Critical Care at All India Institute of Medical Sciences (AIIMS), New Delhi, India. He received his training in neuroanes- thesia and completed his PhD at the same institute. He is a recipient of the AIIMS Excellence award for notable contributions in academics and has more than 200 publications in peer-reviewed national and international jour- nals to his credit. Dr. Prabhakar serves as a reviewer for various national and international journals. He is also a review author for the Cochrane Collaboration and has a special interest in evidence-based practice in neuroanesthesia. Dr. Prabhakar is a member of several national and international neuroanesthesia societies and is past secretary of the Indian Society of Neuroanesthesia and Critical Care. He serves on the editorial board of the Indian Journal of Palliative Care and is the executive editor of the Journal of Neuroanaesthesiology and Critical Care. Zulfiqar Ali is an associate professor in the Division of Neuroanesthesiology and Neurocritical Care at Sher-i-Kashmir Institute of Medical Sciences, Srinagar, India. He received his training in neuroanesthesia from All India Institute of Medical Sciences, New Delhi, and the National Institute of Mental Health and Neurosciences, Bengaluru. His areas of interest include neuro- critical care and chronic pain management. He has many publications in peer- reviewed national and international journals to his credit. Dr. Ali is a member of various national and international neuroanesthesia societies and is a past executive committee member of the Indian Society of Neuroanesthesia and Critical Care. He serves as an associate editor of the Indian Journal of Anesthesia and co-editor of Northern Journal of ISA. In addition, he is a reviewer for several national and international journals. xix  Part I Fundamentals of Neuroanesthesia  Neuroanatomy 1 Ravi K. Grandhi and Alaa Abd-Elsayed 1.1 Overview 1.2 Central Nervous System The nervous system is made up of two parts: the 1.2.1 Brain central nervous system (CNS) and the peripheral nervous system (PNS). The brain and spinal cord The brain can be divided into the supratentorial form the majority of the CNS. The CNS inte- and the infratentorial compartments. The supra- grates, processes, and coordinates incoming sen- tentorial compartment contains the cerebral sory data and outgoing motor functions that alter hemispheres and the diencephalon (thalamus and the activities of the end organs or muscles. The hypothalamus). The infratentorial compartment brain is also the part of the body where higher is made up of the brain stem and the cerebellum. cognitive activities occur, while the cranial and spinal nerves form the majority of the PNS. The 1.2.1.1 Supratentorial Compartment PNS delivers sensory information to the CNS and carries motor commands from the CNS to the Cerebrum peripheral tissues and systems. The two systems The cerebrum makes up the largest part of the are in close communication with each other. And brain. It is made up of a right and left hemisphere. when one of the two systems is altered in any The hemispheres are made up of numerous sulci fashion, the other one may be affected. This or fissures and gyri or folds. The two sides of the chapter will review the significant anatomical brain are connected via the corpus callosum, considerations in each of the two systems which is a collection of white matter fibers. Based (Fig. 1.1). on functional differences, the cerebrum is divided into four lobes: frontal, parietal, temporal, and occipital lobes. The frontal lobe is separated from the parietal lobe via the central sulcus (Rolandic fissure). The frontal lobe is separated from the temporal lobe via the lateral sulcus (Sylvian fis- R. K. Grandhi (*) sure). The frontal and parietal lobes are separated Department of Anesthesiology, Maimonides Medical from the temporal lobe via the lateral sulcus. And Center, Brooklyn, NY, USA finally, the parieto-occipital sulcus divides the A. Abd-Elsayed parietal lobe from the occipital lobe. Department of Anesthesiology, UW Health Pain The cerebrum is made up of numerous func- Services, University of Wisconsin-Madison, tional areas that each provide a particular activity Madison, WI, USA © Springer Nature Singapore Pte Ltd. 2019 3 H. Prabhakar, Z. Ali (eds.), Textbook of Neuroanesthesia and Neurocritical Care, https://doi.org/10.1007/978-981-13-3387-3_1 4 R. K. Grandhi and A. Abd-Elsayed Nervous System Central Nervous Peripheral System Nervous System Somatic Nervous Autonomic Brain Spinal Cord System Nervous System Sympathetic Supratentorial Infratentorial Nervous System Cerebral Parasympathetic Diencephalon Brainstem Cerebellum Hemispheres Nervous system Thalamus Pons Hypothalamus Medulla Midbrain Fig. 1.1 Overall anatomical organization of the nervous system essential to survival. The frontal lobe, which is other areas. Also, within the cerebrum are Broca’s made up of primary motor cortex, executes and Wernicke’s areas, which are responsible for actions. Adjacent to this cortex is also the premo- speech and comprehension. Broca’s area is tor cortex and other supplementary motor areas, located in the frontal lobe, while Wernicke’s is which are involved in selecting voluntary move- located at the temporoparietal junction. These ments. There are also sensory areas within the two areas are closely linked by arcuate fibers. cortex, which help integrate the different stimuli Damage to any one of these parts can cause prob- from the senses. These areas work closely with lems either with speech or comprehension. The the thalamus. Each of the hemispheres receives cerebrum also works closely with the hippocam- information about the contralateral side of the pus to form memories. Neurodegenerative dis- body. The primary somatosensory cortex located eases such as Alzheimer’s affect the cerebrum. in the lateral parietal lobe, which integrates the touch signal, is often illustrated as a homunculus. Cortex The homunculus is a deformed human, where The outermost surface of the cerebrum is the cor- there are different sized body parts reflecting the tex that has a grayer appearance and, as a result, relative density of their innervation. Areas with is called gray matter. The cortex is a folded struc- lots of innervation such as the fingertips and lips ture, and each one of these folds is referred to as require more cortical processing compared to a gyrus. Each one of the grooves is called a 1 Neuroanatomy 5 s­ ulcus. These folds allow the brain to occupy a Diencephalon smaller cranial volume and store increased func- The diencephalon is made up of the thalamus, tional areas. Below the cortex are myelinated epithalamus, subthalamus, and hypothalamus. axons, which give the characteristic appearance and often referred to as white matter. Thalamus The thalamus integrates sensory and motor Limbic System inputs and transmits the information to the ipsi- The limbic system is the medial portion of the lateral cerebral cortex. There is reciprocal feed- temporal lobe. It is vital in forming memories, back that projects to the thalamic subnuclei. It emotions, and behaviors. The limbic system receives significant inputs from all the senses coordinates actions between different parts of the except for smell. The thalamus may also serve brain including the cortex, brain stem, thalamus, as a filter, trying to simplify the information and hypothalamus. The limbic system is made up received and process it to convey the best over- of the amygdala, hippocampus, fornix, mammil- all impression. There are a number of nuclei in lary bodies, cingulate gyrus, and parahippocam- the thalamus that play key roles in the function- pal gyrus. These structures communicate with ing of the body. The anterior thalamic nuclei each other via the Papez circuit. The amygdala is work closely with the limbic system, which is a collection of the nuclei that receives multiple also connected with the cingulate gyrus and sensory nerve signals. The amygdala integrates mammillary bodies. Medial nuclei are associ- this information, ignores some stimuli, and cre- ated with the frontal association cortex and pre- ates outputs via the hypothalamus, thalamus, hip- motor cortex. Ventral anterior and lateral nuclei pocampus, brain stem, and cortex. The amygdala have inputs from the globus pallidus and project also plays a role in mediating emotional responses to the motor cortex. Ventral posteromedial and associated with memories particularly the fear ventral posterolateral nuclei function as sensory response. The hippocampus is most important transmitters associated with the face and body, to memory formation, particularly declarative respectively. Another part of the thalamus is the memory. Declarative memory is the ability to medial and lateral geniculate bodies, which pro- recall previous life events. Overtime, certain cess auditory and visual information. Finally, declarative memories can be independently the thalamus is also the primary entrance recalled without the hippocampus. The hip- through which additional information from the pocampus is also important in learning. reticular formation reaches the cerebral cortex. Animals with a damaged thalamus often suffer Basal Ganglia in a permanent coma. The basal ganglia (or basal nuclei) are made up of the caudate nucleus, putamen, globus pallidus, Epithalamus nucleus accumbens, olfactory tubercle, ventral The epithalamus connects the limbic system to pallidum, subthalamic nucleus, and substantia the rest of the brain. The pineal gland is a part of nigra. The basal ganglia work with the motor the epithalamus. The pineal gland secretes mela- cortex, premotor cortex, and motor nuclei of the tonin, which is involved in the regulation of the thalamus. It modulates voluntary movements, circadian rhythm. procedural learning, and routine behaviors or habits. The substantia nigra forms the dopa- Subthalamus mine necessary for basal ganglia function. The The subthalamus has efferent connections to the subthalamic nucleus is the only part of the basal striatum (caudate nucleus and putamen), dorsal ganglia to produce the excitatory neurotransmit- thalamus, substantia nigra, and red nucleus. It ter glutamate. A number of motor-related dis- also has afferent connections from the substantia eases have pathology in the basal ganglia, nigra and striatum. It is often involved in move- including Parkinson’s and Huntington’s disease. ment control. 6 R. K. Grandhi and A. Abd-Elsayed Hypothalamus rior pituitary does not synthesize but secretes The hypothalamus mediates the endocrine, antidiuretic hormone and oxytocin. autonomic, visceral, and homeostatic functions. It is the highest center for regulation of visceral 1.2.1.2 Infratentorial Compartment functions. The hypothalamus connects the ner- The infratentorial compartment is the area under vous system to the endocrine system via the the tentorium cerebelli. The primary component pituitary gland. The hypothalamus is made up of is the cerebellum. Nerves C1–C3 innervate this a number of nuclei, each of with particular area. nuclei that function to regulate the body. Anterior nuclei include preoptic, supraoptic, Cerebellum and paraventricular. Anterior nuclei function in The cerebellum is made up of tightly folded layer thermoregulation via sweating or panting, vaso- of the cortex, with several deep nuclei embedded pressin release, oxytocin release, thyroid-releas- in the white matter underneath and a fluid-filled ing hormone release, and corticotropin-releasing ventricle in the middle. Signals in the cerebellum hormone release. Middle nuclei include infun- flow in a unidirectional fashion. The cerebellum dibular, tuberal, dorsomedial, ventromedial, and plays a major role in motor functions, in particu- lateral. They function in the regulation of blood lar coordination, posture, and balance. pressure, heart rate, gastrointestinal stimulation, Damage to the cerebellum leads to motor distur- satiety, growth hormone-releasing hormone bances. There is decreased muscle tone ipsilat- release, and feeding. Posterior nuclei include eral to the lesion site. The cerebellum is an supramammillary, mammillary, intercalate, and anatomically distinct portion from the cerebrum. posterior. They function in arousal, learning, It is made up of fine grooves, with several differ- memory, energy balance, and sleep. Lateral ent types of neurons in a very regular distribu- nuclei are the location where hypocretin is tion. The most important types of cells in the released, which functions in arousal, tempera- cerebellum are the Purkinje and granule cells. All ture regulation, blood pressure, hunger, and of the output from the cerebellum passes through wakefulness. Anterior and medial nuclear a couple of small deep nuclei lying within the groups provide parasympathetic control, white matter. whereas sympathetic control is performed by The three lobes of the cerebellum are flocculo- the posterior and lateral nuclei. The hypothala- nodular lobe, anterior lobe, and posterior lobe. mus is also connected with other areas in the The latter two lobes are also split into the midline brain to help coordinate different functions. cerebellar vermis and lateral cerebral hemi- spheres. The flocculonodular lobe regulates bal- Pituitary ance and eye movements. It receives vestibular Pituitary gland is located below the hypothalamus input from both the semicircular canals and the at the base of the brain. The hypothalamus works vestibular nuclei and sends fibers back to the closely with the pituitary to initiate endocrine medial and lateral vestibular nuclei. It also responses. The pituitary regulates the majority of receives visual input from the superior colliculi body functions, including blood pressure, water and from the visual cortex. balance, thyroid levels, breast milk production, The cerebellar vermis and paravermis regulate sexual organ function, and growth. The pituitary body and limb movements. It receives proprio- has three parts: anterior, intermediate, and poste- ception input from the dorsal columns of the spi- rior. The anterior pituitary synthesizes and secretes nal cord and trigeminal nerve, as well as visual prolactin, growth hormone, adrenocorticotropic and auditory systems. It also sends fibers to the hormone, thyroid-­stimulating hormone, luteiniz- deep cerebellar nuclei which in turn project to ing hormone, and follicle-stimulating hormone. both the cerebral cortex and brain stem, thus pro- The anterior and intermediate pituitary together viding modulation of the descending motor sys- release melanocyte-­releasing hormone. The poste- tems. This area also has sensory maps because it 1 Neuroanatomy 7 receives data on the position of various body vertebral arteries are formed from the subclavian parts in space. This information is also used to artery. The posterior communicating arteries anticipate the future position of the body (also (PCOM) connect the PCAs and also connect to known as “feed forward”). the anterior circulation. The PCA supplies most The lateral hemispheres are involved in the of the blood to the occipital lobe and inferior por- planning movement and evaluating sensory infor- tion of the temporal lobe. mation for action. It receives input from the cere- Three arteries perfuse the cerebellum: supe- bral cortex particularly the parietal lobe via the rior cerebellar arteries (SCA), anterior inferior pontine nuclei and dentate nucleus and sends cerebellar artery (AICA), and posterior inferior fibers to the ventrolateral thalamus and red cerebellar artery (PICA). The SCA branches off nucleus. This area is also involved in planning the the lateral portion of the basilar artery, just infe- movement that is about to occur. rior to its bifurcation into the posterior cerebral artery. It also supplies blood to the pons before Blood Supply reaching the cerebellum. The SCA supplies blood Cerebral blood flow to the brain makes up about to most of the cerebellar cortex, the cerebellar 15% of cardiac output. The brain is vulnerable to nuclei, and the superior cerebellar peduncles. factors that acutely decrease perfusion; as a result The AICA branches off the lateral portion of the the brain has many safeguards including auto- basilar artery, just superior to the junction of the regulation and redundancy within the blood sup- vertebral arteries. ply. Autoregulation is the phenomenon of Symptoms associated with infarctions vary maintaining a constant blood flow despite a based on the artery infarcted in the brain and the change in perfusion pressure. The consequence area of the brain supplied by that particular artery. of a compromise in blood flow, which is known MCA infarctions or strokes are the most com- as a stroke, can be devastating. The arterial mon. MCA infarctions present with sensory and blood supply is divided into anterior and poste- motor disturbances of the contralateral face, arm, rior portions. The anterior part is via the left and and leg. They can also present with aphasias if right internal carotid arteries, while the posterior the dominant hemisphere is affected. If the ACA portion is the vertebrobasilar artery. The anasto- is infarcted, it can present with leg weakness mosis of these systems forms the circle of Willis more than arm weakness. If the PCA is infarcted, and helps to create a redundant system of blood then it presents with visual field abnormalities. supply to help protect against ischemia. However, Lacunar strokes present with pure sensory or it is important to note that the system doesn’t pure motor abnormalities. Vertebrobasilar infarc- always protect against ischemia and is not com- tions present with brain stem dysfunction, which pletely redundant. Once the internal carotid arter- can include vertigo, ataxia, and dysphagia. ies enter the cranial vault, they branch into the The venous drainage system helps remove the anterior cerebral artery (ACA) and eventually blood from the brain. It is made up of two parts: form the middle cerebral artery (MCA). The the superficial and deep sinuses. The superficial anterior cerebral arteries are connected via the system is composed of the sagittal sinuses and anterior communicating artery (ACOM). The cortical veins that are located on the surface of ACA supplies the majority of the midline por- the cerebrum. The most prominent of these tions of the frontal and superior medial parietal sinuses is the superior sagittal sinus, which is lobes. The MCA supplies most of the lateral por- located midline along the fal x cerebri. The deep tions of the hemispheres. The ACA, MCA, and venous drainage system is composed of the lat- ACOM form the anterior circulation of the circle eral sinuses, sigmoid sinuses, straight sinus, and of wills. The posterior circulation begins when draining deep cerebral veins. All the veins in the the basilar artery, which is formed from the right deep venous drainage system combine to form and left vertebral arteries, branches into the left the vein of Galen. Both of these ­systems combine and right posterior cerebral artery (PCA). The to drain into the internal jugular veins. 8 R. K. Grandhi and A. Abd-Elsayed Brain Stem a baroreceptor. And finally, the medulla is impor- The brain stem is considered the most ancient tant in managing the reflex centers of vomiting, part of the brain. It is made up of three parts: the coughing, sneezing, and swallowing. medulla oblongata, pons, and midbrain. The brain stem primarily provides motor and sensory Pons innervation to the face and neck via the cranial The pons is located between the medulla and nerves. It also plays a key role in connecting the midbrain. The pons contains the tracts that carry motor and sensory systems of the brain, which signals that travel from the cerebrum to the includes the corticospinal tract, posterior medulla and on to the cerebellum. It also contains column-­medial lemniscus pathway, and the spi- the tracts that carry important sensory signals up nothalamic tract. Finally, the brain stem plays a to the thalamus. Posteriorly, there are cerebellar key role in the regulation of cardiac and respira- peduncles that connect the pons to the cerebel- tory function. It also regulates the CNS helping lum and midbrain. The pons also has the respira- to maintain consciousness and regulating the tory pneumotaxic center and apneustic centers, sleep cycle. which are vital in maintaining respiration and transitioning from inspiration to expiration. The Medulla Oblongata pons also has the nuclei that coordinate with The medulla oblongata is a structure that is sleep, swallowing, respiration, and bladder con- located superior to the cervical spinal cord. On trol. The pons also coordinates the activities of the external surface, the prominent structure is the cerebral hemispheres. It also plays an impor- the anterior median fissure. On either side of this tant role in control of cranial nerves of 5–8, which are the medullary pyramids. The pyramids are includes hearing, equilibrium, taste, and facial made up of the corticospinal and corticobulbar sensations. tracts originating from the spinal cord. At the caudal part of the medulla, these tracts cross over Midbrain to form the decussation of the pyramids. The The midbrain is made up of four parts: tectum, anterior external arcuate fibers lie on top of this. cerebral peduncles, tegmentum, and cerebral The area between the anterolateral and postero- aqueduct. The tectum forms the upper border of lateral sulcus is the olivary bodies. These bodies the midbrain. It is comprised of the superior and are formed by the inferior olivary nuclei. The inferior colliculi. The inferior colliculi are the posterior medulla contains the gracile fasciculus principal midbrain nuclei of the auditory path- and the cuneate fasciculus. Together, they make way. Above the inferior colliculi are the super up the posterior funiculi. Just above these tuber- colliculi, which are involved in vision, in particu- cles is the triangular fossa, which forms the lower lar the vestibulo-ocular reflex. Together they floor of the fourth ventricle. The fossa is bound form the corpora quadrigemina. These structures by the inferior cerebral peduncle, which connects help to decussate the fibers of the optic nerve. Of the medulla to the cerebellum. note, the trochlear nerve comes out of the poste- The medulla plays an important role in con- rior midbrain below the inferior colliculi. The trolling the autonomous nervous system. The dorsal covering of the cerebral aqueduct is also medulla regulates respiration via interaction with part of the midbrain. the carotid and aortic bodies. These receptors The tegmentum, which forms the floor of the detect changes in pH; thus, if the blood is acidic, midbrain, is made up of several nuclei, substantia the medulla sends signals to the respiratory mus- nigra, and reticular formation. The ventral teg- culature to increase the respiratory rate to reoxy- mentum is composed of cerebral peduncles, genate blood. The medulla also plays an important which serve as the transmission axons of the role in regulating the parasympathetic and sym- upper motor neurons. The reticular formation is a pathetic nervous systems, which play a key role large area of the midbrain that has multiple regu- in the cardiovascular system. It also plays as latory functions. It plays a key role in arousal, 1 Neuroanatomy 9 sleep-wake cycling, and maintaining conscious- which becomes the forebrain. The forebrain ness [13, 14]. It also contains the locus coeruleus, divides into two parts: the telencephalon and which is involved in alertness modulation and diencephalon. The telencephalon goes on to form autonomic reflexes. Serotonin is also made in the the cerebral cortex, basal ganglia, and other reticular formation, which is a key regulator of structures. The diencephalon forms the thalamus mood. The reticular formation also plays a key and hypothalamus. The hindbrain goes on to role in regulation of the cardiovascular system, develop into the metencephalon and myelen- along with the medulla. Finally, the reticular for- cephalon. The metencephalon forms the cerebel- mation is important in habituation, which is the lum and pons. The myelencephalon forms the process by which the brain begins to ignore medulla oblongata. The developing brain is repetitive meaningless stimuli, but remains vigi- more vulnerable to injury in comparison to the lant to new sounds. The red nucleus is closely developed or adult brain. When the development involved in motor coordination. Another impor- of the brain is delayed by an external influence or tant part of the tegmentum is the substantia nigra, toxin, there is virtually no regeneration or repair. which is closely associated with the basal gan- This can lead to lifelong disability. As a result, glia. Dopamine produced in the substantia nigra minimizing exposures to a developing brain is and ventral tegmental area plays a role in excita- vital. tion, motivation, and habituation. Dysfunction is One of the most defining features of the brain associated with Parkinson’s disease. is the gyri that define the outer surface. In womb, The cerebral aqueduct is involved with the the brain starts off smooth, but with time the fis- movement of CSF. It is surrounded by gray mat- sures start to form. The fissures form because of ter, which is known as the periductal gray. In this the rapidly growing hemispheres, which rapidly area, there are neurons involved in the pain increase in size due to the expansion of the gray desensitization pathway that interact with the matter. The underlying white matter does not reticular activating system. When the neurons grow at the same rate as the hemispheres. here are stimulated, they cause activation of the nucleus raphe magnus. The neurons project into 1.2.1.3 Spinal Cord the posterior gray column of the spinal cord and The spinal cord is a bundle of nervous tissue that prevent pain sensitization transmission. extends from the medulla oblongata in the brain stem to the lumbar region of the vertebral col- Development umn. The spinal cord connects the brain to the In utero, the brain starts to develop at the begin- peripheral nervous system. The spinal cord is ning of the third week as the ectoderm forms the encased in a bony shell made up of the cervical neural plate. By the fourth week, the neural plate vertebrae. The spinal cord transmits nerve signals has widened to give a broad cephalic end and a from the motor cortex to the musculature and narrower caudal end. The swellings represent the from the afferent fibers of the sensory neurons to beginning of the forebrain, midbrain, and hind- the sensory cortex. The spinal cord also plays a brain. Neural crest cells make up the lateral edge key role in coordinating reflexes and contains of the plate at the neural folds. By the end of the numerous reflex arcs (ankle jerk, knee jerk, fourth week, the neural plate folds and closes to biceps jerk, forearm jerk, triceps jerk). The spinal form the neural tube, which brings together the cord is made up of 31 segments; at each level neural crest cells. Cells at the cephalic end give there are 1 pair of sensory nerve roots and 1 pair rise to the brain, while cells at the caudal end give of motor nerve roots. rise to the spinal cord. With time the tube flexes The spinal cord and brain are covered by three giving rise to the crescent-shaped cerebral hemi- protective layers of the meninges. The dura mater spheres. These cerebral hemispheres first appear is the outermost layer and forms a tough protec- on day 32. During this fourth week, the cephalic tive coating. Between the vertebrae and dura part bends forward forming the cephalic flexure, mater is the epidural space. The epidural space is 10 R. K. Grandhi and A. Abd-Elsayed made up of adipose tissue and has numerous and sensory axons. The columns of white matter blood vessels. The arachnoid mater is the middle carry information up or down the spinal cord layer that is located underneath the dura mater.. The white matter is made up of the dorsal The arachnoid mater is named for its open, spid- white matter, ventral white matter, and lateral erlike appearance. The space between the arach- white matter. The dorsal white matter has the noid mater and pia mater is the subarachnoid ascending tracts, while the ventral white matter space. The subarachnoid space has cerebrospinal has the descending tracts. The dorsal column fluid (CSF), which is accessed in neuraxial anes- below T6 has the gracile fasciculus, which has thesia. The CSF is made in the brain’s lateral ven- input from the lower body. And above T6, there tricles and flows through the foramen of Monro is both input from the lower body and upper into the third ventricle and through the cerebral body, which is also known as the cuneate fasci- aqueduct to the fourth ventricle. It passes into the cle. The lateral white matter has both and is subarachnoid space through three openings in the mainly involved with pain and movement. The roof of the fourth ventricle. The two lateral open- absolute amount of white matter decreases as ings are the foramen of Luschka and a median you progress caudally through the spinal cord. opening called the foramen of Magendie. The Lesions at the dorsal and ventral roots present as CSF then flows through the subarachnoid space strictly sensory or motor deficits; while lesions around the brain and drains into the superior sag- at the peripheral nerves more often present with ittal sinus through the arachnoid granulations. deficits in both the sensory and motor The pia mater is tightly adhered to the spinal pathways. cord. The cord is stabilized within the dura mater The spinal cord terminates at the conus by connecting denticulate ligaments, which medullaris, while the pia mater continues via extend from the enveloping pia mater laterally the filum terminale, which anchors the spinal between dorsal and ventral roots. The dural sac cord to the coccyx. The cauda equina is a collec- ends at the level of the second sacral vertebrae. tion of nerves below the conus medullaris that travel in the vertebral column to the coccyx. The Spinal Cord Segments cauda equina forms because the spinal cord The gray column (matter) at the center of the spi- stops elongating at about age 4, even though the nal column is shaped like a butterfly and consists vertebral column continues to lengthen until of cell, bodies of interneurons, motor neurons, adulthood. neuroglia cells, and unmyelinated axons. The There are 31 spinal cord segments in the spi- gray matter consists of longitudinal columns of nal cord – 8 cervical segments, 12 thoracic seg- cells, with a segmental relationship to the spinal ments, 5 lumbar segments, 5 sacral segments, nerve fibers. These columns are grouped into the and 1 coccygeal segment. In the fetus, vertebral dorsal (posterior) horn, ventral (anterior) horn, segments correspond with spinal cord segments. and intermediate gray. The dorsal roots are affer- In adults, the spinal cord ends around the L1/L2 ent fascicles, receiving sensory information. The vertebral level, which corresponds to the conus roots terminate in dorsal root ganglia, which are medullaris. As a result, the spinal cord segments made up of the respective cell bodies. The ventral do not correspond with the vertebral segments nerve roots are made up of efferent fascicles that especially in the lower spinal cord. The cervical arise from motor neurons whose cell bodies are enlargement, stretching from the C5 to T1 verte- found in the ventral horns of the spinal cord. brae, is the location for the sensory and motor The ventral horn also includes interneurons, output associated with the arms and trunk. This which are involved in the processing of motor enlargement corresponds with the brachial information. The intermediate gray contains the plexus. The lumbar enlargement, located between interneurons for primitive connections. L1 and S3, handles sensory input coming from The white matter is located adjacent to the and going to the legs. This corresponds with the gray matter and is made up of myelinated motor lumbosacral enlargement. 1 Neuroanatomy 11 Development Over the course of the cell division process, There are four stages of spinal cord develop- groups of cells break off from the neural plate and ment: neural plate, neural fold, neural tube, and become a part of the mesoderm. Slowly, these neu- spinal cord. At the end of the third week, the ral crest cells migrate away from the neural tube ectoderm located at the midline of thickens to and form a number of different tissues including form the neural plate. Slowly, the lateral edges of the neurons of the dorsal root ganglion and post- the neural plate began to move dorsally and synaptic cells of the sympathetic and parasympa- medially. When the edges meet, they form the thetic nervous systems. When these cells fail to neural tube. As the neural tube begins to develop, appropriately migrate, it forms diseases such as the notochord begins to secrete sonic hedgehog Hirschsprung’s disease. Hirschsprung’s occurs (SHH). This helps to establish the ventral when there is a portion of the digestive system that pole in the developing fetus. As a result, the can’t perform peristalsis. floor plate also begins to secrete SHH, which induces the basal plate to develop motor neu- Blood Supply rons. During the maturation of the neural tube, The blood supply of the spinal cord is made of lateral walls thicken and form the longitudinal three longitudinal arteries, which are the anterior groove of the sulcus limitans. This extends the spinal artery, right posterior spinal artery, and left length of the spinal cord into dorsal and ventral posterior spinal artery. The anterior spinal artery portions. At the same time, the ectoderm secretes provides blood flow to the anterior 2/3 of the spi- bone morphogenetic protein (BMP). These two nal cord. These arteries travel in the subarach- opposing gradients help the cells divide along noid space and send branches into the spinal the dorsal ventral axis. This release of the cord. They form connections via the anterior and BMP also induces the roof plate to secrete BMP, posterior segmental medullary arteries, which which leads to the formation of the sensory neu- enter the spinal cord at various points. The blood rons. Simultaneously, the lumen of the neural flow through these arteries provides sufficient tube begins to narrow to help form the central blood supply primarily to the cervical spinal canal of the spinal cord. Further, the floor plate cord. Beyond that region, the spinal cord derives secretes netrins. The netrins act as chemoattrac- much of its blood supply from the anterior and tants, which lead to the decussation of pain and posterior radicular arteries, which run into the temperature sensory neurons in the alar plate spinal cord alongside the dorsal and ventral nerve across the anterior white commissure. These roots. The largest of the anterior radicular arteries fibers ascend toward the thalamus. Once the cau- is the artery of Adamkiewicz, which usually dal neuropore and formation of the brain’s ven- arises between L1 and L2. Impaired blood flow to tricles with the choroid plexus is completed, the these radicular arteries can result in spinal cord central canal of the caudal spinal cord is filled infarction and paraplegia. with CSF. Closure of the neural tube progresses both cranially and caudally. Malformations of Somatosensory Organization the neural tube closure can lead to abnormal The somatosensory system is primarily con- development of the central nervous system. cerned with transmitting the sensory information Failure of the cranial tube to close completely at from the integumentary and musculoskeletal sys- the cranial end may manifest as exencephaly, tems of the body. This system can be divided into anencephaly, or cranioschisis. The complete clo- the dorsal column-medial lemniscus (DCML) sure of the lumbar region of the neural tube may and the anterolateral system (ALS). The DCML lead to rachischisis or myeloschisis, which is plays the main role in the touch, proprioception, where the spinal cord is exposed to the outside. and vibration, while the ALS plays the key role in More mild defects may present as spina bifida, pain and temperature. Both sensory pathways use which is the result of an incomplete vertebral three different nerves to transmit the information arch. from the sensory receptors in the periphery to the 12 R. K. Grandhi and A. Abd-Elsayed cerebral cortex. In both pathways, the primary to the reticular formation in the midbrain. The sensory neuron cell bodies are found in the dorsal reticular formation is connected with the hippo- root ganglion and their central neurons project campus to create memories and centromedian into the spinal cord. nucleus to create diffuse non-specific pain sensa- In the DCML, a primary neuron’s axon enters tion. Further, the ALS axons help inhibit the ini- the dorsal column of the spinal cord. If the pri- tial pain signal via projections to the mary axon enters below level T6, the axon travels periaqueductal gray in the pons and nucleus in the fasciculus gracilis, which is the medial part raphe magnus. of the cord. If the primary axon enters above level T6, it travels in the fasciculus cuneatus, which is located more lateral. Through both these path- Motor Component ways, the primary axon ascends to the caudal The corticospinal tract is the motor pathway for medulla, where it leaves the fasciculi and syn- the upper motor neurons (UMN) coming from apses with a secondary neuron in one of the dor- the cerebral cortex and from the primitive brain sal column nuclei, either the nucleus gracilis or stem motor nuclei. The cortical upper motor neu- nucleus cuneatus, respectively. The first process- rons originate from Brodmann areas 1, 2, 3, 4, ing of discriminative touch information occurs in and 6. Majority originate from Brodmann area 4, the caudal medulla. The secondary axons syn- which is premotor frontal area. They descend apse with these nuclei. These secondary axons down the posterior limb of the internal capsule, are known as the internal arcuate fibers. The into the cerebral peduncles, and then into the internal arcuate fibers decussate and ascend as medullary pyramids, where about 90% of axons the contralateral medial lemniscus. Axons from cross to the contralateral side at the decussation the medial lemniscus terminate in the ventral of the pyramids. Then the neurons descend as the posterolateral nucleus of the thalamus. In the lateral corticospinal tract. The axons synapse thalamus, neurons synapse with tertiary neurons, with lower motor neurons (LMN) in the ventral which eventually ascend in the posterior limb of horns. Most of the axons will cross to the contra- the internal capsule to the primary sensory cor- lateral side of the cord before they synapse. The tex. Further, the axons that enter the dorsal col- midbrain nuclei include four motor tracts that umns also give rise to collaterals that terminate in send UMN axons down the spinal cord to the spinal cord. These collaterals play an impor- LMN. These four tracts are the rubrospinal tract, tant role in modulating simple motor behaviors. vestibulospinal tract, tectospinal tract, and reticu- The ALS has a different anatomical pathway lospinal tract. Damage to the UMN of the corti- compared to the DCML. The primary axons of cospinal tract can lead to paralysis, paresis, the ALS enter the spinal cord and ascend 1–2 lev- hypertonia, hyperreflexia, or spasticity. els ipsilaterally before synapsing with the sub- The LMN have two divisions: the lateral corti- stantia gelatinosa. Once synapsing, the secondary cospinal tract and the anterior corticospinal tract. axons decussate in the ventral white commissure The lateral tract contains fibers that are involved and ascend as a part of the anterolateral spinotha- with distal limb control. Thus, these neurons are lamic tract. This tract travels through the medulla only found at the cervical and lumbosacral and eventually synapses in the thalamus and fur- enlargements. There is no decussation of the lat- ther similar to the DCML. In syringomyelia with eral corticospinal tract after decussation at the pathologic cavitation, there is often bilateral loss medullary pyramids. The lateral corticospinal of pain and temperature sensations in the derma- tract forms the majority of connections in the cor- tomes at the level of the lesion because of the ticospinal tract. The anterior corticospinal tract proximity of the ventral white commissure to the descends ipsilaterally in the anterior column and central canal of the spinal cord. synapses ipsilaterally in the ventromedial It is important to note that some of the pain nucleus. These nerves control the large postural fibers in the ALS deviate away from this pathway muscles of the trunk and axial skeleton. 1 Neuroanatomy 13 Spinocerebellar Tract except for the optic nerve. The optic nerve is con- Proprioceptive information, which are the stimuli sidered a tract of the diencephalon. However, that affect muscle joints or other deep tissues, the remaining ten cranial nerves extend outside travel in the spinal cord via three tracts based on of the brain and are considered a part of the the spinal cord level. These receptors are respon- PNS. The autonomic nervous system is involved sible for the perception of motion and position of in involuntary self-regulation via the sympathetic the body. They carry unconscious proprioceptive and parasympathetic nervous systems. The sym- information about the body position from the pathetic and parasympathetic systems are periphery to the cerebellum. Above T1, proprio- antagonists. ceptive primary axons enter the spinal cord and ascend ipsilaterally until synapsing in the acces- 1.2.1.5 Somatic Nervous System sory cuneate nucleus. The secondary axons pass The somatic nervous system (SoNS) is made up into the cerebellum via the inferior cerebellar of the sensory and somatosensory nervous sys- peduncle, where they synapse with the cerebellar tem. The SoNS is made up of afferent neurons deep nuclei. This is part of the cuneocerebellar (sensory) and efferent nerves (motor). The affer- tract. From the levels of T1–L2, propriocep- ent nerves relay information from the body to the tive information enters the spinal cord and CNS, while the efferent nerves are responsible ascends ipsilaterally until synapsing with for stimulating muscle contraction. The efferent Clarke’s nucleus (nucleus dorsalis). Below the nerves include all the non-sensory neurons con- level of L2, proprioceptive information travels nected with the skeletal muscles and skin. The via the fasciculus gracilis and DCML, until efferent SoNS involves an initial signal that reaching Clarke’s nucleus. Neurons within begins in the upper cell bodies of motor neurons Clarke’s nucleus give rise to second-order sen- within the precentral gyrus. Stimuli from the pre- sory fibers that ascended the ipsilateral dorsal central gyrus are transmitted down the cortico- part of the lateral funiculus of the spinal cord. At spinal tract to control the skeletal muscles. These the medulla, these fibers enter the cerebellum via stimuli are conveyed from the upper motor neu- the inferior peduncle. Lesions or deficits to the rons (UMN) through the ventral horn of the spi- cerebellum manifest with ataxia of the extremi- nal cord and across synapses to be received by ties on the same side of the lesion. It is often hard the sensory receptors of alpha motor neuron, to damage just the spinocerebellar tracts. which are large lower motor neurons, of the brain stem and spinal cord. UMN release acetylcholine 1.2.1.4 Peripheral Nervous System from their axonal terminal knobs, which are The peripheral nervous system (PNS) is made up received by the nicotinic receptors of the lower of the nerves and ganglia that are located outside motor neurons. These signals are further relayed of the brain and spinal cord. The primary func- to the end organ. In contrast to this pathway, the tion of the peripheral nervous system is to con- SoNS is also made up of reflex arcs. The reflex nect the CNS to the limb and organs. However, arc is a shorter neuronal circuit creating direct unlike the CNS, the PNS is not protected by the connections between the sensory input and a spe- vertebral column and skull or by the blood-brain cific motor output. Reflex arcs have various lev- barrier. Thus, the nerves are more exposed to tox- els of complexity; some involve just two nerves, ins, mechanical injuries, and other pathological while others have three nerves, with the addition processes. The peripheral nervous system is of an interneuron. Some of the reflexes are pro- divided into the somatic nervous system and tective, while others contribute to regular behav- autonomic nervous system. The somatic nervous ior. This leads to a shorter response time. system is involved with voluntary control of the In the head and neck, 12 cranial nerves carry muscles. Of note, the sensory nervous system is somatosensory data. Ten of the cranial nerves origi- part of the somatic nervous system. In the somatic nate from the brain stem and also control the ana- system, the cranial nerves are part of the PNS tomic functions in the head. The nuclei of the 14 R. K. Grandhi and A. Abd-Elsayed Table 1.1 Cranial nerves Cranial nerve Location of exit Structures supplied I: Olfactory nerve Cribriform plate Olfactory mucosa II: Optic Optic foramen Rods and cones of the retina III: Oculomotor Superior orbital fissure Superior rectus, medial rectus, inferior rectus, inferior oblique, and sphincter oblique IV: Trochlear Superior orbital fissure Superior oblique V: Trigeminal Superior orbital fissure, Muscles of mastication, tensor tympani, tensor palati foramen rotundum, foramen ovale VI: Abducens Superior orbital fissure Lateral rectus VII: Facial Internal auditory canal Posterior external ear canal, anterior 2/3 of the tongue, facial muscles, salivary glands, lacrimal glands VIII: Vestibulocochlear Internal auditory canal Cochlea and vestibule of the inner ear IX: Glossopharyngeal Jugular foramen Posterior 1/3 of the tongue (sensory and taste), middle ear, carotid body/sinus, stylopharyngeus, parotid gland X: Vagus Jugular foramen External ear, aortic arch/body, epiglottis, soft palate, pharynx, larynx, lungs XI: Accessory Jugular foramen Trapezius, sternocleidomastoid XII: Hypoglossal Hypoglossal canal Muscles of the tongue olfactory and optic nerves lie in the forebrain and superior trunk and innervates the rhomboid mus- thalamus. The vagus nerve receives sensory infor- cles which retract the scapula. The subclavian mation from the organs in the thorax and abdomen. nerve, which branches from C5 and C6, innervates The cranial nerves are summarized in Table 1.1. the subclavius muscle that lifts the ribs during res- piration. The long thoracic nerve, which originates 1.2.1.6 Cervical Spinal Nerves (C1–C4) from the C5, C6, and C7, innervates the serratus Spinal nerve C1 (suboccipital nerve) provides and is vital in lifting up the scapula. innervation to the nerves at the base of the skull. The trunks split into divisions and then form C2 and C3 form many nerves in the neck, provid- cords, which are named in relation to their positon ing both motor and sensory controls. These with the axillary artery. The three cords are the nerves include greater occipital nerve, lesser posterior, lateral, and medial cords. The cords occipital nerve, greater auricular nerve, and lesser lead to the formation of the terminal branches. auricular nerve. The phrenic nerve is a nerve, The terminal branches are musculocutaneous which arises from C3, C4, and C5, that is vital to nerve, axillary nerve, radial nerve, median nerve, survival by supplying the thoracic diaphragm and ulnar nerve. Because both the musculocuta- enabling breathing. It is important to note that if neous and median nerve originate from the lateral the cervical spine is transected above C3, then the cord, they are well connected. The musculocuta- patient will not be able to spontaneously breathe. neous nerve innervates the skin of the anterolat- eral forearm along with the brachialis, biceps 1.2.1.7 Brachial Plexus (C5–T1) brachii, and coracobrachialis. The median The brachial plexus, which is made up of the last nerve innervates the skin of the lateral 2/3 of the four cervical nerves (C5–C8 and T1), innervates hand and the tips of digits 1–3. It also innervates the upper limb and upper back. It is made up of the forearm flexors, thenar eminence, and lumbri- five roots, three trunks, six divisions (three anterior cals of the hand 1–2. The axillary nerve and three posterior), three cords, and five branches innervates the sensory portion of the lateral shoul-. The five roots come together to form five der and upper arm and also plays a role innervat- trunks (superior trunk, middle trunk, and inferior ing the deltoid and teres minor muscles. The trunk). The dorsal scapular nerve comes from the radial nerve innervates the sensory portion of the 1 Neuroanatomy 15 posterior lateral forearm and wrist. It also inner- result of the parasympathetic system, there is vates the triceps brachii, brachioradialis, anco- decreased heart rate and other sympathetic neus, and extensor muscles of the posterior arm response, while there is increased digestion, uri- and forearm. The ulnar nerve innervates the nation, and defecation. Humans have some con- skin of the palm and medial side of the hand and trol over the parasympathetic system. digits 3–4. It also innervates the hypothenar emi- nence, some forearm flexors, the thumb adductor, lumbricals 3–4, and the interosseous muscles 1.3 Conclusion. Brachial plexus injuries affect the cutaneous sensation and the muscular motions depending on The nervous system is made up of two key parts: the nerve that has been affected. CNS and PNS. The relationship and interaction between the two are as important as each indi- 1.2.1.8 Lumbosacral Plexus vidual part. Damage to one area can be minor or (L1-Coccygeal Nerve) devastating for the welfare of the individual. The lumbosacral plexus is made up of three key Disturbances during development in utero can be parts: lumbar plexus, sacral plexus, and pudendal particularly profound affecting a number of dif- plexus. Often times bone injuries in the pelvic ferent areas of the nervous system. Anatomy region can affect these nerves. plays a key role in determining function and pathology. Clearly identifying the different struc- 1.2.1.9 Autonomic Nervous System (ANS) tures and function can help predict the deficiency The ANS controls involuntary responses to regu- found upon damage. late physiologic functions, in particular those that have smooth muscle. This includes the heart, bladder, and other exocrine or endocrine organs Key Points via ganglionic neurons. The ANS is always The nervous system is made up of two active. Depending on the situation, either the parts: the central nervous system and sympathetic or parasympathetic system domi- peripheral nervous system. The two sys- nates. This leads to the release of neurotransmit- tems work closely together to coordi- ters, which affect the organs in different ways. nate function. The other division of the ANS is the enteric ner- Pathology in one portion can lead to vous system. The enteric nervous system dysfunction in the end organs. Stresses surrounds the digestive tract and, as a result, or dysfunction during development can allows for local control of the gastrointestinal lead to diffuse debility. system. However, the sympathetic and para- Some of the pathological changes are sympathetic provide input. amenable to correction, while others are The sympathetic system is involved in “flight not. or fight,” which is a stress response mediated by norepinephrine and epinephrine. This often occurs when the body feels that it is under great stress. The norepinephrine and epinephrine References increase the heart rate and blood flow to certain 1. Rakic P. Evolution of the neocortex: a perspective areas such as the muscles while also decreasing from developmental biology. Nat Rev Neurosci. the activities of noncritical functions such as 2009;10(10):724–35. digestion. 2. Pessoa L. Emotion and cognition and the amyg- The parasympathetic system is in many ways dala: from “what is it?” to “what’s to be done?”. Neuropsychologia. 2010;48(12):3416–29. the opposite of the sympathetic system. The pri- 3. Spreng RN, Mar RA. I remember you: a role for mem- mary neurotransmitter involved is acetylcholine, ory in social cognition and the functional neuroanat- which allows the body to “rest and digest.” As a omy of their interaction. Brain Res. 2012;1428:43–50. 16 R. K. Grandhi and A. Abd-Elsayed 4. Curlik DM 2nd, Shors TJ. Training your brain: do 13. Steriade M. Arousal--revisiting the reticular activat- mental and physical (MAP) training enhance cogni- ing system. Science. 1996;272(5259):225–0. tion through the process of neurogenesis in the hip- 14. Evans BM. Sleep, consciousness and the spontaneous pocampus? Neuropharmacology. 2013;64:506–14. and evoked electrical activity of the brain. Is there a 5. Fix J. Board review series: neuroanatomy. 4th ed. cortical integrating mechanism? Neurophysiol Clin. Baltimore: Lippincott Williams & Wilkins; 2007. 2003;33(1):1–10. 6. Stocco A, Lebiere C, Anderson JR. Conditional rout- 15. Guo X, Tang XC. Roles of periaqueductal gray and ing of information to the cortex: a model of the basal nucleus raphe magnus on analgesia induced by lap- ganglia's role in cognitive coordination. Psychol Rev. paconitine, N-deacetyllappaconitine and morphine. 2010;117(2):541–74. Zhongguo Yao Li Xue Bao. 1990;11(2):107–12. 7. Fix J. High-yield neuroanatomy. 4th ed. Baltimore: 16. Echelard Y, Epstein DJ, St-Jacques B, Shen L, Mohler Lippincott Williams & Wilkins; 2008. J, McMahon JA, et al. Sonic hedgehog, a mem- 8. Fine EJ, Ionita CC, Lohr L. The history of the devel- ber of a family of putative signaling molecules, is opment of the cerebellar examination. Semin Neurol. implicated in the regulation of CNS polarity. Cell. 2002;22(4):375–84. 1993;75(7):1417–30. 9. Budohoski KP, Czosnyka M, Kirkpatrick PJ, 17. Than-Trong E, Bally-Cuif L. Radial glia and neural Smielewski P, Steiner LA, Pickard JD. Clinical rel- progenitors in the adult zebrafish central nervous sys- evance of cerebral autoregulation following sub- tem. Glia. 2015;63(8):1406–28. arachnoid haemorrhage. Nat Rev Neurol. 2013; 18. Melissano G, Bertoglio L, Rinaldi E, Leopardi M, 9(3):152–63. Chiesa R. An anatomical review of spinal cord blood 10. Bahr M, Frotscher M. Duus’ topical diagnosis in neu- supply. J Cardiovasc Surg. 2015;56(5):699–706. rology: anatomy - physiology - signs - symptoms. 5th 19. Mai J, Paxinos G. The human nervous system. 3rd ed. ed. New York: Teachers, Parents, Students; 2012. Waltham: Academic; 2011. 11. Guyenet PG, Koshiya N, Huangfu D, Baraban SC, 20. Anatomy SK. Physiology: the unity of form and func- Stornetta RL, Li Y-W. Role of medulla oblongata in tion. New York: McGraw Hill; 2007. generation of sympathetic and vagal outflows. Prog 21. Laight D. Overview of peripheral nervous system Brain Res. 1996;107:127–44. pharmacology. Nurse Prescr. 2013;11(9):448–54. 12. Hughes T. Neurology of swallowing and oral feed- 22. Matic A. Introduction to the nervous system - part 2: ing disorders: assessment and management. J Neurol autonomic nervous system and central nervous sys- Neurosurg Psychiatry. 2003;74(90003):48iii–52. tem. AMWA J. 2014;29(2):51–5.  Physiology for Neuroanesthesia 2 Thomas M. Price, Catriona J. Kelly, and Katie E. S. Megaw 2.1 Cerebral Metabolism 2.1.2  erobic and Anaerobic A Metabolism 2.1.1 Introduction The main energy substrate of the brain is glucose, The primary function of the brain is to develop accounting for 25% of the total glucose con- action potentials in response to stimulation to sumption within the body (30 mg/100 g/min). allow the propagation of neuronal transmission In addition to acting as an energy substrate, glu-. In order to maintain this function, the brain cose is a precursor for the neurotransmitters requires considerable energy supply, together γ-aminobutyric acid (GABA), acetylcholine, and with the effective removal of waste products. glutamate. Glucose initially crosses the blood-­ Energy is primarily used for the maintenance of brain barrier by facilitated diffusion using functioning ion channels, such as the Na+/K+ GLUT1 glucose transporter system before uptake ATPase ion pump, to maintain the resting mem- into cells occurs via GLUT1 into astrocytes, brane potential and therefore neuronal function. GLUT3 into neurons, and GLUT5 into microg- In addition, energy is required for the mainte- lial cells. nance of cellular structure and integrity and for Around 70% of glucose entering the cells the production of neurotransmitters. Under nor- undergoes oxidation using the glycolytic and citric mal conditions supply of energy substrate acid cycle, with the remaining 30% being con- exceeds demand, but under certain conditions verted to amino acids, proteins, and lipids. The supply fails to meet demand, and neuronal dam- glycolytic pathway converts glucose to pyruvic age can occur. This section will look at cerebral acid, a process that generates two molecules of metabolism under aerobic and anaerobic condi- adenosine triphosphate (ATP). In the presence of tions and adaptations during periods of stress and oxygen, pyruvic acid enters the mitochondria and ischemia. is oxidized within the citric acid cycle to carbon dioxide and water, a process that generates the coenzymes reduced nicotine adenine dinucleotide (NADH), flavin adenosine dinucleotide, and gua- nosine triphosphate (GTP). These coenzymes then T. M. Price (*) · C. J. Kelly · K. E. S. Megaw undergo oxidative phosphorylation within the Department of Neuroanaesthesia, Royal Victoria electron transport chain, allowing the generation of Hospital, Belfast, Belfast, UK a maximum of 38 molecules of ATP for each mol- e-mail: [email protected]; ecule of glucose metabolized. [email protected] © Springer Nature Singapore Pte Ltd. 2019 17 H. Prabhakar, Z. Ali (eds.), Textbook of Neuroanesthesia and Neurocritical Care, https://doi.org/10.1007/978-981-13-3387-3_2 18 T. M. Price et al. In the absence of adequate oxygen supply, 95%. This results in ion channel disruption anaerobic glycolysis occurs with the conversion of and altered ionic homeostasis and leads to neuro- pyruvic acid to lactic acid, yielding two molecules nal depolarization and the release of intracellular of ATP. Although less energy efficient than aerobic calcium and excitatory neurotransmitters such as metabolism, the lactic acid generated acts as a key glutamate. During these periods, lactate utiliza- energy substrate during periods of high metabolic tion from anaerobic metabolism acts as an alter- activity and stress. It is hypothesized that within native energy source to ensure ATP production astrocytes, lactate produced by glycolysis is continues. exported via the monocarboxylate transport pro- tein and taken up by adjacent neurons for oxida- tion and further energy production, a process 2.1.4  erebral Metabolic Rate C termed astrocyte-neuron lactate shuttle [3, 4]. and Flow-Metabolism Coupling Cerebral metabolic rate (CMR) is the rate at 2.1.3  erebral Metabolic Changes C which the brain utilizes metabolic substrates During Periods of Stress (oxygen (CMRO2), glucose (CMRglu)) or gener- ates by-products (CMRlact). Oxygen con- While the brain has considerable energy expendi- sumption of the brain is considerable, accounting ture, the metabolic reserves are very limited, and for 20% of basal oxygen consumption (50 mL/ periods of dysglycemia are tolerated poorly, in min) at rest: particular, hypoglycemia. Glycogen stores within the brain are exhausted after 2–3 min. Blood CMRO 2 = sugar levels P1 (shown in red) Normal Compliance Reduced Compliance P1>P2 P2>P1 Time in ICP, such as in traumatic brain injury. Compensatory mechanisms occur through increased cerebral venous outflow, decreased cerebral blood flow (CBF), and compression of intracranial venous sinuses. CSF volume buffer- Intracranial Pressure se ing occurs through “spatial compensation,” Pha whereby intracranial CSF is displaced into the tion spinal canal. This occurs more slowly and is sig- ensa nificant in slow increases in ICP such as intra- cranial tumor growth. omp Once these compensatory mechanisms are Compensation Phase Dec exhausted, ICP increases rapidly. This decom- pensation phase leads to a reduction in CPP and focal brain compression. This can lead to cere- bral ischemia, foramen magnum herniation, and brain stem death (Fig. 2.5). Intracranial Volume Historically CSF and cerebral blood volume compensation have been given equal weighting Fig. 2.5 Intracranial pressure-volume curve. Initial com- pensatory mechanisms ensure intracranial compliance within the Monro-Kellie doctrine, but this may (ΔV/ΔP) remains high. Once these compensatory mecha- be misleading to the dynamic reality, due to the nisms are exhausted, decompensation occurs as compli- disproportionately large cerebral blood flow ance reduces and intracranial pressure rapidly increases (700 mL/min, 14% of cardiac output) in com- parison to CSF production (0.35–0.40 mL/min) pathic intracranial hypertension) and extracra-. Afferent cerebral arterial inflow has tradi- nial causes (cervical and thoracoabdominal tionally been the focus of ICP management, venous obstruction). Extracranial causes through CPP manipulation. However, the con- are of particular relevance to the neuroanesthe- tribution of the cerebral venous efferent drain- tist. Cervical spine flexion and rotation cause a age is significant and undervalued. Failure of significant increase in ICP , and raised adequate venous drainage to match afferent intrathoracic (e.g. positive pressure ventilation) arterial inflow can lead to large increases in and intra-abdominal pressure (e.g., prone posi- ICP. Causes of venous obstruction can be classi- tioning, abdominal compartment syndrome) fied into focal intracranial causes (skull fracture, will also increase cerebral venous pressure, venous sinus thrombosis, cerebral edema, idio- thereby increasing ICP. 2 Physiology for Neuroanesthesia 25 Table 2.2 Causes of raised intracranial pressure descends across the temporal incisura, causing A. Increase in brain stem and posterior cerebral artery compression. brain B. Increase in The oculomotor nerve and corticospinal tracts are parenchyma cerebral blood C. Increase in volume volume CSF volume compressed, manifesting as unilateral papillary Cerebral edema Increased cerebral Reduced CSF dilatation and contralateral