Neurocritical Care for the Advanced Practice Clinician PDF

Jessica L. White Kevin N. Sheth Editors Neurocritical Care for the Advanced Practice Clinician 123 Neurocritical Care for the Advanced Practice Clinician Jessica L. White Kevin N. Sheth Editors Neurocritical Care for the Advanced Practice Clinician Editors Jessica L....

Jessica L. White Kevin N. Sheth Editors Neurocritical Care for the Advanced Practice Clinician 123 Neurocritical Care for the Advanced Practice Clinician Jessica L. White Kevin N. Sheth Editors Neurocritical Care for the Advanced Practice Clinician Editors Jessica L. White Kevin N. Sheth Neuroscience Intensive Neurosciences Intensive Care Unit Care Unit Yale New Haven Hospital Yale School of Medicine New Haven, Connecticut New Haven, Connecticut USA USA ISBN 978-3-319-48667-3  ISBN 978-3-319-48669-7 (eBook) DOI 10.1007/978-3-319-48669-7 Library of Congress Control Number: 2017946839 © Springer International Publishing AG 2017 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, repro- duction on microfilms or in any other physical way, and transmission or infor- mation 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 war- ranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neu- tral with regard to jurisdictional claims in published maps and institutional affiliations. Printed on acid-free paper This Springer imprint is published by Springer Nature The registered company is Springer International Publishing AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Dedicated to our colleagues in the Neuro ICU – the nurses, physicians, and advanced practice clinicians who commit themselves to providing compassionate care for the neurologically ill. And to our patients and their families – the practice and art of critical care neurology is our service to them. Acknowledgment This project strives to highlight the professional collaboration between advanced practice clinicians and physicians as part of a multidisciplinary team. We are grateful to our contributors for exemplifying this collaboration by generously sharing their expertise and experience in the field of neurocritical care. We would like to thank the Yale University Neurocritical Care faculty and APC staff for their encouragement and feed- back through this process. And special thanks to Guido Falcone for his editorial assistance. We are privileged to work everyday with such a phenomenal team. vii Contents 1 The Role of Advanced Practice Clinicians in the Neuroscience ICU......................... 1 Jessica L. White and Kevin N. Sheth 2 Neuroanatomy.................................. 5 Laura A. Lambiase, Elizabeth M. DiBella, and Bradford B. Thompson 3 Neuroradiology................................. 29 Susan Yeager, Mohit Datta, and Ajay Malhotra 4 Aneurysmal Subarachnoid Hemorrhage.......... 55 Jessica L. White and Charles Matouk 5 Intracerebral Hemorrhage....................... 75 Devra Stevenson and Kevin N. Sheth 6 Acute Ischemic Stroke........................... 93 Karin Nyström and Joseph Schindler 7 Mechanical Thrombectomy for Acute Ischemic Stroke................................. 117 Ketan R. Bulsara, Jennifer L. Dearborn, and Jessica L. White ix x Contents 8 Malignant Ischemic Stroke and Hemicraniectomy............................... 137 Julian Bösel 9 Cerebral Venous Thrombosis..................... 151 Gretchen Crabtree and Chad Miller 10 Traumatic Brain Injury.......................... 165 Megan T. Moyer and Monisha A. Kumar 11 Intracranial Pressure Management............... 183 Danielle Bajus and Lori Shutter 12 Seizures and Status Epilepticus................... 201 Catherine Harris and Emily Gilmore 13 Neurological Infections.......................... 223 Brian A. Pongracz, Douglas Harwood, and Barnett R. Nathan 14 Brain Tumors................................... 251 Raoul J. Aponte, Ankur R. Patel, and Toral R. Patel 15 Spinal Cord Injury.............................. 269 Jennifer Massetti and Deborah M. Stein 16 Neuromuscular Disease.......................... 289 Peter Reuter and Alejandro Rabinstein 17 Hypoxic-Ischemic Injury After Cardiac Arrest..... 307 Jodi D. Hellickson and Eelco F.M. Wijdicks 18 Brain Death and Organ Donation................ 321 Dea Mahanes and David Greer Contents xi 19 Goals of Care and Difficult Conversations......... 343 Christine Hudoba and David Y. Hwang 20 Multimodality Monitoring....................... 363 Richard Cassa and Nils Petersen 21 Airway and Ventilation Management............. 387 Matthew Band and Evie Marcolini 22 Pharmacology................................... 407 Kent A. Owusu and Leslie Hamilton 23 Common Complications in the Neuro ICU........ 439 Jennifer L. Moran and Matthew A. Koenig 24 Helpful Links and Resources..................... 467 David Tong and Jessica L. White Chapter 1 The Role of Advanced Practice Clinicians in the Neuroscience ICU Jessica L. White and Kevin N. Sheth The field of neurocritical care encompasses a broad range of neurological pathology and requires a multidisciplinary approach to provide best patient care. At institutions across the country, physicians work alongside physician assistants and nurse practitioners to care for neurologically ill patients. This collaborative relationship serves to provide an ideal comple- ment of specialized medical knowledge and experienced bed- side care. Stemming from a historical genesis in primary care practice, the fundamental education of nurse practitioners and physician assistants is general by design, including basic prin- ciples of medical science and clinical management. This educa- tional foundation offers the benefit of professional flexibility and the ability to adapt to a myriad of subspecialties; however, such adaptation requires continued focused learning when entering a subspecialty to acquire advanced understanding of patient care. Recognizing this challenge, we embarked on a J.L. White, PA-C (*) K.N. Sheth, MD Yale University, New Haven, CT, USA e-mail: [email protected]; [email protected] © Springer International Publishing AG 2017 1 J.L. White, K.N. Sheth (eds.), Neurocritical Care for the Advanced Practice Clinician, DOI 10.1007/978-3-319-48669-7_1 2 J.L. White and K.N. Sheth project to meet the knowledge needs of physician assistants and nurse practitioners that have selected neurocritical care as their field of practice. Many terms have been used to describe the collective role of physician assistants and nurse practitioners—midlevel provider, nonphysician provider, and advanced practice provider among them. For the purposes of this project, the term advanced practice clinician (APC) is used to encompass both professions. The role of APCs has evolved considerably over the past several decades. Both professions were developed in the 1960s to adjunct a short- age of primary care providers in the United States. The imple- mentation of restrictions on house staff work hours in the 1990s set the stage for the rapid expansion of the APC role into the hospital setting [1, 2]. This role of APCs working in inpatient medicine has grown substantially since that shift. In 1995 the acute care nurse practitioner certification was developed for the purpose of focusing training on caring for critically ill patients. This certification now represents the fifth most common area of practice for nurse practitioners. Similarly, a hospital medicine specialty certification is available for physician assistants and ~25% of these professionals now work in hospital settings. As the medical community is faced with continued projections of physician shortages across the board, the role of APCs in the inpatient realm is projected to increase [1, 2, 5]. The field of neurocritical care has experienced significant growth in recent years, outpacing the growth of residency and fellowship training programs. Across the country, this rapid expansion has provided a considerable opportunity for APCs to enter the field of neuro- critical care and work in a dynamically evolving area. Given this shift in scope of practice, it has been imperative to provide APCs with the training and experience necessary to provide exemplary care to the critically ill. In intensive care units across the country, it has been shown that nurse practitio- ners and physician assistants provide appropriate medical care to ICU patients, as measured in rates of morbidity and mortality [6, 7]. Beyond these measurements, there are also established 1 The Role of Advanced Practice 3 benefits of integrating APCs into intensive care units. APCs offer a unique level of experience and continuity of care that can result in improved compliance with clinical guidelines , decreased length of stay, and overall cost savings [9–11]. Intensive care units have integrated APCs in a variety of ways—some by developing units staffed by APCs alone, others by creating multidisciplinary teams of APCs and physicians. Regardless of the chosen structure, APC staffing can aid in pro- viding sustained clinical expertise to bedside care, particularly in settings where house staff work on rotating schedules. In the challenging environment of the intensive care unit, the presence of seasoned clinicians to give support to physicians-in-training provides significant benefits. Survey data from academic insti- tutions indicate that APCs are perceived as an effective comple- ment to physicians-in-training, enhancing patient care through improved communication and continuity of care. Furthermore, APCs contribute to the training of residents by reducing their workload, reducing patient-to-provider ratios, and increasing didactic educational time. The neurocritical care community has experienced this shift in staffing along with the rest of the critical care realm. In keep- ing with broader trends, APCs working in neurocritical care are seen as promoting effective communication, a team environ- ment, and, most importantly, timely identification of patients with neurological deterioration. However, this impact does not come without dedicated learning and experience. The field of neurocritical care includes a unique spectrum of neurological disease and much of the expertise required to skillfully care for neuroscience ICU patients is not addressed in the general educa- tion of the APCs. The purpose of this book is to bridge the gap between the foundational medical education of APCs and the fundamentals of the neurocritical care subspecialty. By discuss- ing common neurocritical topics as presented by a multidisci- plinary collection of leaders in the field, we hope to engage and empower the continued expansion of the role of advanced prac- tice clinicians in neurocritical care. 4 J.L. White and K.N. Sheth References 1. Gordon CRCR. Care of critically ill surgical patients using the 80-hour accreditation Council of Graduate Medical Education work-week guidelines: a survey of current strategies. Am Surg. 2006;72(6): 497–9. 2. Cooper RAR. Health care workforce for the twenty-first century: the impact of nonphysician clinicians. Annu Rev Med. 2001;52(1):51–61. 3. Kleinpell RR. American Academy of nurse practitioners National Nurse Practitioner sample survey: focus on acute care. J Am Acad Nurse Pract. 2012;24(12):690–4. 4. Assistants AAoP. 2013 AAPA annual survey report. 2013. 5. Colleges AoAM The complexities of physician supply and demand: projections through 2025. http://www.tht.org/education/resources/ AAMC.pdf. 6. Costa DKDK. Nurse practitioner/physician assistant staffing and criti- cal care mortality. Chest. 2014;146(6):1566. 7. Gershengorn HBHB. Impact of nonphysician staffing on outcomes in a medical ICU. Chest. 2011;139(6):1347. 8. Gracias VHVH. Critical care nurse practitioners improve compliance with clinical practice guidelines in "semiclosed" surgical intensive care unit. J Nurs Care Qual. 2008;23(4):338–44. 9. Russell DD. Effect of an outcomes-managed approach to care of neu- roscience patients by acute care nurse practitioners. Am J Crit Care. 2002;11(4):353–62. 10. Landsperger JS. Outcomes of nurse practitioner-delivered critical care: a prospective cohort study. Chest. 2015;149(5):1146–54. 11. Kleinpell RMRM. Nurse practitioners and physician assistants in the intensive care unit: an evidence-based review. Crit Care Med. 2008;36(10):2888–97. 12. Joffe AMAM. Utilization and impact on fellowship training of non-­ physician advanced practice providers in intensive care units of aca- demic medical centers: a survey of critical care program directors. J Crit Care. 2014;29(1):112–5. 13. Dies NN. Physician assistants reduce resident workload and improve care in an academic surgical setting. JAAPA Montvale NJ. 2016; 29(2):41–6. 14. Robinson JJ. Neurocritical care clinicians' perceptions of nurse practi- tioners and physician assistants in the intensive care unit. J Neurosci Nurs. 2014;46(2):E3–7. Chapter 2 Neuroanatomy Laura A. Lambiase, Elizabeth M. DiBella, and Bradford B. Thompson 2.1 Skull, Fossae, and Meninges The cranium is composed of multiple bones that act as a protec- tive container for the brain (Figs. 2.1 and 2.2). It is composed of the frontal bone, which articulates with the two parietal bones at the coronal suture. The parietal bones meet at the midline and are joined by the sagittal suture. The temporal bones lie inferior to the parietal bones and posterior to the greater wing of the sphenoid bone. The occipital bone meets the parietal bones at the lambdoid suture and protects the posterior surface of the brain. At the base of the occipital bone, there is a large opening, the foramen magnum, through which the spinal cord connects to the brainstem. A series of smaller bones including the zygo- matic, ethmoid, maxilla, mandible, nasal, vomer and lacrimal bones comprise the complex facial surface of the skull [6, 7]. L.A. Lambiase, PA-C E.M. DiBella, PA-C B.B. Thompson, MD (*) Brown University, Providence, RI, USA e-mail: [email protected]; [email protected]; [email protected] © Springer International Publishing AG 2017 5 J.L. White, K.N. Sheth (eds.), Neurocritical Care for the Advanced Practice Clinician, DOI 10.1007/978-3-319-48669-7_2 6 L.A. Lambiase et al. Frontal bone Sphenoid bone Parietal bone Lacrimal bone Ethmoid bone Nasal bone Temporal bone Zygomatic bone Maxillary bone Mandible Fig. 2.1 Bones of the cranium (Used with permissions from Gallici et al. ) The bones of the skull articulate to form three distinct fossae: anterior, middle, and posterior (Fig. 2.3). The anterior fossa is formed by the frontal, ethmoid, and sphenoid bones and con- tains the anterior and inferior aspects of the frontal lobes. The middle fossa is formed by the sphenoid and temporal bones and contains the temporal lobes. Additionally, the sella turcica of the sphenoid bone provides a protective seat for the pituitary gland within the hypophysial fossa. The posterior fossa is 2 Neuroanatomy 7 Frontal bone Sphenoid bone Parietal bone Lacrimal bone Ethmoid bone Occipital bone Nasal bone Temporal bone Zygomatic bone Maxillary bone Mandible Fig. 2.2 Bones of the cranium (Used with permissions from Gallici et al. ) p­redominantly formed by the occipital bone with small ­contributions from the sphenoid and temporal bones—it con- tains the brainstem and the cerebellum. The brain is covered in three layers of protective meninges, which work with the skull and cerebrospinal fluid (CSF) to blunt the effects of insults to the brain. The dura mater is the thickest fibrous external layer, which adheres to the internal surface of the cranium. The dura can be dissected into two dis- tinct layers: the periosteal layer, which connects the dura to the skull, and the meningeal layer, which lies more medially. The 8 L.A. Lambiase et al. Frontal bone Sphenoid bone Parietal bone Ethmoid bone Temporal bone Occipital bone Fig. 2.3 Cranial fossa (Used with permissions from Gallici et al. ) dura mater folds in on itself in the interhemispheric fissure to create the falx cerebri. An additional dural fold c­ reates the ten- torium cerebelli, separating the cerebral ­hemispheres from the cerebellum. While these dural folds provide structure to the brain, they constitute sites of potential herniation in the setting of space occupying lesions or ­cerebral edema. The arachnoid mater lies medial to the dura mater. The sub- arachnoid space separates the arachnoid and pia mater. Small fibrous strands called trabeculae tether the arachnoid and pia to one another. The CSF in this space serves as another protective buffer for the brain. The pia mater is the thinnest meningeal 2 Neuroanatomy 9 layer and is adherent to the brain. This layer is highly vascular and provides oxygen and nutrients to the brain [6, 7, 15]. Clinical Correlate With traumatic injury, there is potential for bleeding between the skull and dura (epidural hematoma), between the dura and arachnoid meninges (subdural hematoma), or within the subarachnoid space (subarach- noid hemorrhage). (See Chap. 10 for further clinical information). An epidural hematoma occurs most commonly when a temporal bone fracture severs the middle meningeal artery, although venous bleeding can also be a cause. A subdural hematoma is most often caused by tearing of the bridging veins in the subdural space. Subarachnoid hemorrhage can occur in a number of conditions, including rupture of a cerebral aneurysm and trauma. 2.2 Cerebrum The cerebrum constitutes the bulk of the brain and is the area responsible for intellectual thought and function. The cerebral cortex is the circumferential gray matter on the surface of the brain that covers the white matter and the deeper gray matter structures. The cortex folds to create raised gyri and sunken grooves called sulci. The cerebrum is separated into two hemispheres by the ­interhemispheric fissure and connected by a bundle of nerves called the corpus callosum. Each hemisphere contains a frontal, parietal, temporal, and occipital lobe (Fig. 2.4). The frontal lobe 10 L.A. Lambiase et al. Caudate nucleus Frontal lobe Corona radiata Body of the lateral ventricle Parietal Corpus callosum lobe Superior sagittal sinus Occipital lobe Fig. 2.4 Cerebrum (Flair sequence MRI brain) is anterior to the central sulcus that separates the frontal and parietal lobes. The frontal lobe is the site of abstract reasoning, judgment, behavior, creativity, and initiative. The parietal lobe is involved in language, maintaining attention, memory, spatial awareness, and integrating sensory information including ­tactile, visual, and auditory senses. The lateral (or Sylvian) fissure ­separates the parietal and frontal lobes from the temporal lobe. The temporal lobe processes sensory input such as language, visual input, and emotions. Tucked deep within the lateral ­fissure lays the insula, which is involved with emotion and ­consciousness. The occipital lobe is the most posterior lobe of the cerebrum and is separated from the parietal and temporal lobes by the parieto-occipital fissure. The occipital lobe con- 2 Neuroanatomy 11 tains the primary visual cortex and is involved in sight and interpretation of visual stimuli. On the medial surface of each cerebral hemisphere, the limbic cortex modulates emotion, behavior, and long-term memory. Clinical Correlate In a majority of people, the left hemisphere is domi- nant, being responsible for language production and comprehension. This is true for both right-handed (90% left dominance) and left-handed individuals (70% left dominance). In the dominant hemisphere, Broca’s area in the frontal lobe is responsible for fluent speech. Damage to this region causes expressive aphasia. Wernicke’s area, located in the temporal lobe of the dominant hemi- sphere, is responsible for comprehension. Damage to Wernicke’s area causes receptive aphasia. Damage to the nondominant hemisphere can cause uni- lateral neglect of the contralateral side and apraxia, which can impact activities of daily living and lead to spatial disorientation. 2.3 Diencephalon The diencephalon is composed of the thalamus and hypothala- mus. The thalami are bilateral relay stations for sensory informa- tion located medial to the internal capsule and lateral to the third ventricle. They initiate reflexes in response to visual and auditory stimuli. Sensory fibers ascend from the brainstem to the thalamus and then their signals are relayed to the cortex. 12 L.A. Lambiase et al. The hypothalamus is connected inferiorly to the pituitary gland; together, these structures regulate many hormonal ­activities within the body. The anterior lobe of the pituitary gland (adeno- hypophysis) secretes hormones including adrenocorticotrophic hormone, thyroid-stimulating hormone, luteinizing ­ hormone, follicle-stimulating hormone, prolactin, and melanocyte-stimulat- ing hormone in response to signals from the hypothalamus. The posterior lobe (neurohypophysis) contains axons extending from the hypothalamus that secrete oxytocin and vasopressin. Clinical Correlate After pituitary surgery, central diabetes insipidus can develop due to reduced secretion of antidiuretic hor- mone (vasopressin). Patients develop excessive urine output with resultant hypovolemia and hypernatremia. 2.4 Basal Ganglia The basal ganglia are the deep gray matter structures consisting of the caudate nucleus, globus pallidus, and putamen (Fig. 2.5). The basal ganglia relay information from the cortex and work with the cerebellum to coordinate movement. They are respon- sible for the initiation and termination of movements, preven- tion of unnecessary movement, and modulation of muscle tone. 2.5 Brainstem The brainstem consists of three components: midbrain, pons, and medulla. It contains critical structures, such as the cranial nerve nuclei, regulates several autonomic functions and basic reflexes, and determines the level of consciousness (Figs. 2.6–2.9). 2 Neuroanatomy 13 Frontal lobe Frontal horns of lateral ventricles Corpus callosum Sylvian fissure Caudate nucleus Globus pallidus Putamen Internal capsule rd 3 ventricle Temporal Thalamus lobe Posterior horns of lateral ventricles Corpus callosum Occipital lobe Fig. 2.5 Basal ganglia (Flair sequence MRI brain) The descending motor and ascending sensory pathways pass through the brainstem. The reticular activating system resides in the rostral brainstem and projects to the thalami and then the cortex to maintain wakefulness. Damage to this structure results in decreased level of arousal or coma. 2.6 Cerebellum The cerebellum is located posterior to the brainstem (Figs. 2.7, 2.8 and 2.9). The cerebellum works in tandem with the basal ganglia to provide smooth coordinated movement. Damage to the cerebellum causes limb ataxia, vertigo, and gait disturbances. 14 L.A. Lambiase et al. Frontal lobes Temporal tip of lateral ventricles Suprasellar cistern Cerebral Interpeduncular aqueduct cistern Temporal lobe Midbrain Ambient cistern Ambient cistern Quadrigeminal cistern Superior sagittal sinus Cerebellum Occipital lobes Fig. 2.6 Midbrain and cisterns (Flair sequence MRI brain) 2.7 Cerebral Vasculature The arterial supply to the brain is divided into anterior and pos- terior circulations. The anterior circulation originates from bilateral internal carotid arteries (ICA). Each ICA travels supe- riorly through the neck and enters the cranium via the carotid canal within the temporal bone. The ICA then bifurcates into the anterior cerebral artery (ACA) and the middle cerebral artery (MCA). The ACA supplies the anterior medial surface of the brain, which includes the frontal and anterior parietal lobes. The 2 Neuroanatomy 15 Temporal lobe Internal carotid arteries Basilar artery Prepontine 4th ventricle cistern Pons Cerebellum Fig. 2.7 Pons and posterior fossa (Flair sequence MRI brain) MCA supplies the bulk of the cerebral hemisphere. It typically divides into superior and inferior divisions as it passes through the lateral fissure. These divisions supply the cortex superior and inferior to the lateral fissure, respectively. Prior to this bifur- cation, several small vessels called the lenticulostriate arteries arise from the MCA. These vessels provide the blood supply for a majority of the basal ganglia and internal capsule. The posterior circulation is supplied by bilateral vertebral arteries (VA). They travel superiorly through the transverse 16 L.A. Lambiase et al. Medulla Cerebellum Fig. 2.8 Medulla and posterior fossa (Flair sequence MRI brain) processes of the cervical vertebrae and then the foramen magnum to enter the skull. The VAs then merge to form the basilar artery (BA), which in turn branches into bilateral posterior cerebral arteries (PCA). The PCAs supply the inferior and medial temporal lobes as well as the occipital lobes. There are three major paired branches which arise from the posterior ­circulation to perfuse the brainstem and cerebellum. The posterior inferior cerebellar artery (PICA) arises from the VA and supplies the lateral medulla and 2 Neuroanatomy 17 Frontal Parietal lobe lobe Limbic cortex Corpus callosum Quadrigeminal cistern Cerebellum Pituitary gland Cerebral aqueduct Midbrain 4th ventricle Prepontine cistern Pons Occipital lobe Medulla Spinal cord Fig. 2.9 Sagittal view (Flair sequence MRI brain) inferior cerebellum. The anterior inferior cerebellar artery (AICA) arises from the lower BA and supplies part of the pons, the middle cerebellar peduncle, and an anterior strip of the cerebellum. The superior cerebellar artery (SCA) arises near the top of the BA and supplies the upper pons, the superior cerebellar peduncle, and the superior half of the cerebellum. The BA also supplies the brainstem directly via small perforating arteries. The two halves of the anterior circulation are connected at the ACAs via the anterior communicating artery. The anterior and posterior circulations are connected via bilateral posterior com- municating arteries which join the ICAs and the PCAs. Together, these arteries form an anastomotic ring at the base of the brain which is referred to as the Circle of Willis. (Fig. 2.10). 18 L.A. Lambiase et al. ACOMM ACA ACA MCA MCA PCA PCA BA ICA ICA VA Fig. 2.10 Vascular anatomy (MRA) Clinical Correlate Large-vessel occlusions, due to embolism (such as from atrial fibrillation) or in situ thrombosis, lead to specific stroke syndromes. For example, a left MCA infarction results in aphasia, right hemiparesis, and left gaze preference amongst other symptoms. Chronic hypertension causes damage to the lenticulo- striate and pontine perforator arteries. This can lead to 2 Neuroanatomy 19 a lacunar infarct or vessel rupture, resulting in intrapa- renchymal hemorrhage. The branch points of the Circle of Willis are typical sites of aneurysm formation. Aneurysmal rupture leads to subarachnoid hemorrhage. Venous drainage is more variable than arterial supply. The anterior and superior cortical veins drain into the superior ­sagittal sinus (Fig. 2.6), which traverses posteriorly between the falx cerebri and the skull. At the level of the tentorium cerebelli it divides into two transverse sinuses at the confluence of sinuses (torcula). Each transverse sinus receives direct drainage from more inferior and lateral cortical veins. They then each continue inferiorly to become the sigmoid sinuses and ulti- mately the internal jugular veins. Other superficial veins drain into the cavernous sinuses along either side of the sella turcica. The cavernous sinuses drain into the superior petrosal sinus and then the transverse sinus, or into the inferior petrosal sinus and then the internal jugular vein. The deep cerebral veins drain into the internal cerebral veins, the basal veins of Rosenthal, and the great vein of Galen. The great vein of Galen then joins the inferior sagittal sinus to form the straight sinus, which joins the superior sagittal sinus at the confluence of sinuses. 2.8 Ventricles The main role of the ventricular system and the CSF within it is to cushion the brain (Figs. 2.4, 2.5 and 2.7). Within the ven- tricles, the choroid plexus produces approximately 450 mL of 20 L.A. Lambiase et al. CSF each day, which circulates through the ventricular system and subarachnoid space before being drained into the venous system, where it is reabsorbed by the arachnoid granulations. At any given time, there is approximately 150 mL of CSF within the ventricular system. The two lateral ventricles are large, C-shaped structures that lie within the cerebral hemi- spheres and connect to the third ventricle through the intraven- tricular foramina (foramina of Monro). The third ventricle lies midline within the diencephalon and projects posteroinferiorly to the cerebral aqueduct in the midbrain. The cerebral aque- duct connects to the fourth ventricle between the brainstem and the ­cerebellum. CSF then drains from the fourth ventricle into the subarachnoid space through the median aperture (foramen of Magendi) and two lateral apertures (foramina of Lushka). The subarachnoid space contains a series of cisterns including the cisterna magna, premedullary cistern, prepontine cistern, cerebellopontine cistern, suprasellar cistern and the perimesencephalic cisterns (ambient, quadrigeminal and inter- peduncular). Clinical Correlate Hydrocephalus occurs when CSF production outstrips CSF reabsorption or when CSF flow is obstructed. Hydrocephalus is categorized as communicating, when there is diffuse dysfunction of the arachnoid granula- tions; or noncommunicating, when there is an obstruc- tion to CSF flow within the ventricular system. Hydrocephalus can be treated with an extraventricular drain which provides an outlet for excess CSF. For long- term CSF diversion, a ventriculoperitoneal shunt may be placed. 2 Neuroanatomy 21 2.9 Cranial Nerves There are 12 pairs of cranial nerves (CN), which arise directly from the brain and exit the skull through foramina or fissures in the cranium. (See Table 2.1 Cranial nerves). Table 2.1 Cranial nerves Cranial Brainstem nucleus nerve Name location Main functions I Olfactory Smell II Optic Vision III Oculomotor Midbrain Eyelid retraction; eye elevation, adduction, depression, and external rotation; pupil constriction IV Trochlear Midbrain Eye depression and internal rotation V Trigeminal Pons (also Sensation of face; Midbrain mastication and Medulla) VI Abducens Pons Eye abduction VII Facial Pons Facial movement VIII Vestibulocochlear Pons Hearing; vestibular sense IX Glossopharyngeal Medulla Taste from posterior third of tongue; gag reflex X Vagus Medulla Swallowing; parasympathetic innervation of much of the body XI Accessory Medulla Shoulder shrug (trapezius muscle) and neck rotation (sternocleidomastoid muscle) XII Hypoglossal Medulla Tongue movement