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(BQ) Part 1 book “Neurosurgery rounds - Questions and answers” has contents: Basic neurosciences, neuroanatomy, neurophysiology, spine and peripheral nerve, anesthetics, analgesics, and antiinflammatories, intensive care - vasogenic and hematologic,… and other contents.
Neurosurgery Rounds Questions and Answers Neurosurgery Rounds Questions and Answers Mark R Shaya, MD, FACS Chief Executive Officer Neurosurgical Institute of Florida University of Miami Hospital Miami, Florida Remi Nader, MD, CM, FRCSC, FACS, FAANS Chief, Neurosurgery Section Director, Neuroscience Clinical Effectiveness Program Memorial Hospital at Gulfport Affiliate Assistant Professor of Neurosurgery University of Mississippi Medical Center Attending Neurosurgeon Gulf Coast Brain and Spine Institute Gulfport, Mississippi Jonathan S Citow, MD Lake County Neurosurgery Chief of Neurosurgery, Condell Medical Center Libertyville, Illinois Associate Clinical Professor Rosalind Franklin University North Chicago, Illinois Hamad I Farhat, MD Section Head Neurovascular and Neuroendovascular Surgery NorthShore Medical Group, Neurosurgery Evanston Hospital Evanston, Illinois Assistant Clinical Professor University of Chicago Chicago, Illinois Abdulrahman J Sabbagh, MD, FRCSC Deputy Chairman, Department of Neurosurgery Director, Neurosurgery Residency Program Neurosciences Center King Fahd Medical City—Ministry of Health Riyadh, Saudi Arabia Thieme New York • Stuttgart Thieme Medical Publishers, Inc 333 Seventh Ave New York, NY 10001 Executive Editor: Kay D Conerly Managing Editor: Lauren Henry Editorial Director: Michael Wachinger Production Editor: Marcy Ross International Production Director: Andreas Schabert Vice President, International Marketing and Sales: Cornelia Schulze Chief Financial Officer: James W Mitos President: Brian D Scanlan Compositor: MPS Limited, a Macmillan Company Printer: Sheridan Press Library of Congress Cataloging-in-Publication Data: Available from the publisher upon request Copyright © 2011 by Thieme Medical Publishers, Inc This book, including all parts thereof, is legally protected by copyright Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation without the publisher’s consent is illegal and liable to prosecution This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage Important note: Medical knowledge is ever-changing As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may be required The authors and editors of the material herein have consulted sources believed to be reliable in their efforts to provide information that is complete and in accord with the standards accepted at the time of publication However, in view of the possibility of human error by the authors, editors, or publisher of the work herein or changes in medical knowledge, neither the authors, editors, nor publisher, nor any other party who has been involved in the preparation of this work, warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or for the results obtained from use of such information Readers are encouraged to confirm the information contained herein with other sources For example, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this publication is accurate and that changes have not been made in the recommended dose or in the contraindications for administration This recommendation is of particular importance in connection with new or infrequently used drugs Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain Printed in the United States of America 54321 ISBN 978-1-58890-499-7 Contents nc e sci r Neu o asic I B e s Preface vii Contributors ix Neuroanatomy Cranial Spine and Peripheral Nerve Cases Neurophysiology 63 General 64 Cases 90 Neuropathology Congenital Trauma Epilepsy Neoplastic Degenerative Neuropharmacology Neurotransmitters Epilepsy Anesthetics, Analgesics, and Antiinflammatories Antimicrobials Intensive Care: Vasogenic and Hematologic Toxicology e 42 55 97 98 102 104 110 123 127 128 133 135 142 145 149 s e nc sci Neu o r linical C II Cranial Neurosurgery 153 General 154 Trauma and Emergencies 175 Neoplasms 187 Endocrine 207 Radiation Therapy 213 Infections 215 Vascular 218 Congenital and Pediatric 240 Pain and Functional 252 Cases 255 vi Contents Spine 281 Spinal Anatomy and Surgical Technique 282 Trauma 305 Degenerative 324 Neoplastic, Infectious, Vascular 332 Congenital and Pediatric 342 Cases 346 Peripheral Nerves 357 General 358 Upper Extremity 370 Lower Extremity 379 Cases 385 Neurology General Emergencies and Epilepsy Infectious and Inflammatory Congenital and Pediatric Functional and Pain Cases Neuroradiology 423 Cranial 424 Spinal 433 391 392 394 397 404 411 413 Index 443 Preface v The front cover of this text shows neurosurgical pioneer Dr Harvey Cushing on rounds almost a century ago with residents, students, and nurses examining a patient after a craniotomy It is truly extraordinary to see this patient without all the bedside machines, monitors, and tubes we are used to seeing today Although the science and technologic armamentarium have progressed over the years, the true didactics of neurosurgery remain essentially as they were at the time this picture was taken The amount of information required to complete neurosurgery residency training can be very intimidating and broad The diagnosis and management of neurosurgical diseases is an ever-advancing field that remains challenging for both the trainees and mentors The purpose of this book is to provide diversified coverage of the multiple disciplines that are involved and intertwined in the understanding, care, and treatment of neurosurgical patients Although its primary use will be for review purposes by the trainee, resident, or medical student prior to being “pimped” by their mentor about topics in neurosurgery, the book also provides a handy reference guide that the reader can fall back upon in reviewing specific topics as they relate to simple and complex neurosurgery and neuroscience issues The book is divided into two sections including basic and clinical neurosciences The sections are further composed of four to five subsections including neuroanatomy, neurophysiology, neuropathology, neuropharmacology, cranial neurosurgery, spine, peripheral nerves, neurology, and neuroradiology By providing this organization we have attempted to cover all categories involved in the practice and understanding of neurosurgical diseases, both from a basic science and clinical standpoint With 23 authors, contributors, and collaborators from four countries, including not only neurosurgeons but also specialists in neuropathology, neuroradiology, orthopedic surgery, anesthesiology, and neurology, we have attempted to cover as broadly as possible—yet in a concise manner—specific topics that will come up in the day-to-day evaluation and treatment of neurosurgical patients This book was edited as a combined effort from the experts in the now new field of neurosurgical review to bring to the reader the optimal didactic experience We ii viii Preface have attempted to present material in a way to best facilitate the retention and understanding of complex concepts and rare diseases by breaking them down to their bare essentials We hope that you enjoy reading this book as much as we did putting it together Mark Shaya, MD Remi Nader, MD Contributors Nazek Ahmad, MD (Cranial Neurosurgery–Pediatric) Neurosurgery Resident Department of Neurosurgery Neurosciences Center King Fahd Medical City Riyadh, Saudi Arabia Mohammd Alfawareh, MD (Spine) Subspecialty Consultant Spine Surgeon, Pediatric Spine Surgeon, Musculoskeletal Oncology Surgeon Spine Surgery Department Neurosciences Center Part-time Orthopedic Surgery Section, Department of Surgery King Fahd Medical City Riyadh, Saudi Arabia - Aisha Nassr Al-Hajjaj, MD (Neuroradiology) Subspecialty Consultant Neurosurgeon, Neuro endovascular Interventionist Department of Neurosurgery Neurosciences Center King Fahd Medical City Riyadh, Saudi Arabia Tamer Altay, MD (Neuroradiology) Assistant Professor Department of Neurosurgery University of Arkansas for Medical Sciences Little Rock, Arkansas Gmaan Alzahrani, MD (Cranial Neurosurgery–Pediatric) Neurosurgery Resident Department of Neurosurgery Neurosciences Center King Fahd Medical City Riyadh, Saudi Arabia Walid I Attia, MD, MSc, PhD (Spine) Subspecialty Consultant Neurosurgery Department, Spine Surgery Department Director, Spine Fellowship Program Neurosciences Center King Fahd Medical City Riyadh, Saudi Arabia ix 138 I Basic Neurosciences 47 What are the neurologic side effects of steroids? Mental agitation, “steroid psychosis,” spinal epidural lipomatosis, multifocal leukoencephalopathy, and pseudotumor cerebri2,3 48 What is the mechanism of action of opioid analgesics? Opioid receptors are of multiple subtypes, all G-protein linked Activation of presynaptic opioid receptors causes inhibition of Ca2+ influx through voltage-regulated ion channels, decreasing neurotransmitter release Activation of postsynaptic opioid receptors results in increased Kefflux causing inhibition.1,2 49 Mention important characteristics of opioid analgesics Overdose is possible with potential seizure and respira tory depression Physical and psychological tolerances may develop They have no ceiling effects.2,3 50 List examples of weak opioids, their dosage, and delivery times Codeine 30 to 60 mg IM/PO every hours as needed (PRN) Propoxyphene to tablets PO every to hours PRN Tramadol 50 to 100 mg PO every to hours PRN This opioid binds to μ-opioid receptors inhibiting the reuptake of serotonin and norepinephrine.2,3 51 Discuss dosages, onset, and duration of the most common opioids used in neurosurgery and spine surgery See Table 4.3 for details.2,3 Dose and Route Duration Comments Abbreviations: APAP, acetaminophen; CNS, central nervous system; IM, intramuscularly; IV, intravenously; MAOI, monamine oxidase inhibitor; PO, orally, Hydrocodone 10 mg + 325 mg APAP 1–2 tab every 4–6 h Do not exceed 4000 mg of APAP in 24 h 4–6 h mg + 500 g APAP 1–2 tab every 4–6 h Codeine 130 mg IM, 200 mg PO 3.5 h Morphine 20–60 mg PO or 10 mg IM or 2–3 mg IV 4–7 h Respiratory depression Morphine oral is a long-acting PO form Hydromorphone 7.5 mg PO; 1.5 mg IM 3h Meperidine 75 mg IM, 300–400 mg PO 4–6 h Long-term or high doses not recommended because its metabolites can cause agitation and CNS hyperactivity (delirium and seizures); severe encephalopathy if given with MAOIs Oxycodone 15 mg IM; 30 mg PO 2–3 h for acetaminophen and 12 h for oxycodone Fentanyl Patch patch 72 h Not for postop analgesic due to risk of respiratory depression Drug Name Table 4.3 Most Common Opioids Used in Neurosurgery (the Doses Are Equianalgesic for Severe Pain)2,3 140 I Basic Neurosciences 52 What is the antidote for morphine? Naloxone2 53 What is the primary indication for dexmedetomidine (Precedex; Hospira, Inc., Lake Forest IL), its mechanism of action, and most common side effect? Dexmedetomidine (Precedex) is indicated to treat anxiety; it provides opioid sparing analgesia and sedation without respiratory depression It is approved for use in intubated and nonintubated patients It is a highly selective α-2 agonist with a common side effect of bradycardia.9,10 54 Why is dexmedetomidine useful in functional neurosurgery? It provides successful sedation without interfering with electrophysiologic monitoring, thus allowing brain mapping during awake craniotomy and microelectrode recording during implantation of deep-brain stimulators.9,10 55 What are the effects of dexmedetomidine in traumatic spinal cord injury? It decreases inflammation Serum levels of TNF-α and IL-6 were significantly reduced in Wistar Rats postspinal cord injury after treatment with dexmedetomidine.9,10 56 Is the innate immune response potentiated by dexmedetomidine? Yes, in the presence of inflammation, a sedative such as dexmedetomidine may act in an anti- rather than proinflammatory manner.9 57 What are the two types of antiemetics and their characteristics? Phenothiazine and nonphenothiazine Phenothiazine antiemetics, promethazine and prochlorperazine, lower the threshold for seizures and should be used with caution following craniotomy and head injury Other alternatives are trimethobenzamide, which is very effective for nausea related to posterior fossa surgery, dimenhydrinate, and diphenhydramine Metoclopramide may cause extrapyramidal symptoms that respond to diphenhydramine Ondansetron is the most common drug used to treat nausea and vomiting related to chemotherapy and surgery.2,3 4 Neuropharmacology: Anesthetics 141 58 Why is the use of acid inhibitors in neurosurgery patients important? The risk of stress ulcers is high in patients with CNS pathology These pathologies include brain and spinal cord injury, brain tumors, intracerebral hemorrhage, syndrome of inappropriate antidiuretic hormone secretion (SIADH), CNS infection, and ischemic stroke Other nonneurologic factors that contribute are the use of steroids, burns, hypotension, respiratory failure, coagulopathies, renal/hepatic failure, and sepsis Diencephalon and brainstem pathologies may reduce the vagal output that leads to hypersecretion of gastric acid and pepsin.3,8 59 What are the acid inhibitors commonly used in neurosurgery patients? Ranitidine 150 mg PO twice daily or 50 mg IV every hours Famotidine 40 mg PO daily—this drug may cause thrombocytopenia Omeprazole inhibits the final step in acid secretion by gastric parietal cells It should not be used long term as the trophic effects may lead to gastric carcinoid tumors; it decreases the effectiveness of prednisone and the clearance of warfarin and phenytoin Doses are 20 to 40 mg twice daily Sucralfate appears to be superior to H2 antagonists with a lower incidence of pneumonia; doses are g PO four times daily on an empty stomach Cimetidine is not recommended because of its interactions with multiple other medications.3,8 60 What is the mechanism of action of ondansetron? It inhibits 5HT3 receptors found in the area postrema and the peripheral sensory and enteric nerves Its activation opens ion channels It decreases emesis in chemotherapy and postoperatively.2,3 142 I Basic Neurosciences Antimicrobials 61 What are the main physiochemical properties influencing antimicrobial penetration into the CNS? Ionization: Ionized (polar) compounds are less likely to cross the BBB Lipophilicity: High lipophilic drugs penetrate the CNS more (unequal distribution, high lipophilic drugs will accumulate in lipid-rich brain structures and minimally in cerebrospinal fluid [CSF] and extracellular spaces) Molecular weight: Substance > 500 to 800 Daltons penetrate with difficulty the BBB (e.g., vancomycin or amphotericin B), especially an intact barrier Protein binding: Highly protein-bound drugs have reduced CNS penetration Active transport: Active transport cells in the choroid plexus may excrete drugs.11 62 What are the factors to be considered when starting empiric antimicrobial therapy? The most likely infectious agent, which in turn depends on patient age, immune status, and setting (community or nosocomial).11 63 Is antibiotic prophylaxis for ventilated patients necessary to prevent pneumonia? Studies have demonstrated the use of cefuroxime 1500 mg for doses or ampicillin-sulbactam g for days after intubation reduces the incidence of subsequent pneumonia.11 64 What is the pharmacologic approach in the case of suspected ventriculitis/meningitis associated with a neurosurgical procedure including an external ventricular drain (EVD), head trauma, or shunt infection? EVD and/or shunt infections frequently involve grampositive organisms (S epidermidis and S aureus, including methicillin-resistant S aureus) Around 25% of these infections are secondary to gram-negative organisms, such as E coli, Klebsiella, Acinetobacter, and Pseudomonas species Vancomycin plus cefepime or meropenem is 4 Neuropharmacology: Antimicrobials 143 recommended Any infected hardware should be replaced, removed, or externalized Intraventricular and intrathecal administration of antibiotics may be necessary.11 65 What is important to remember when treating a brain abscess? Always obtain a specimen The type of pathogen depends on patient-specific risk factors A brain abscess is often polymicrobial (around 60%), with anaerobic bacteria in up to 49% of cases Organisms frequently isolated are Streptococcus milleri, Bacteroides species, Enterobacteriaceae, and S aureus Initial coverage for immunocompetent patients is vancomycin, ceftriaxone or cefotaxime, and metronidazole Keep metronidazole even if an anaerobic source is not identified on culture Patients who had recent neurosurgery or head injury with a possible nosocomial source should be treated with a third- or fourth-generation cephalosporin with antipseudomonal activity (ceftazidime or cefepime) along with vancomycin and metronidazole Treatment should continue for to weeks.11 66 What is the rationale for the use of steroids in bacterial meningitis? Experimental data have shown that an inflammatory response in the subarachnoid space contributes significantly to morbidity and mortality Dexamethasone given before or with the first dose of antibiotics and then every hours for days improves outcome There are no data to support steroids in patients who have meningitis related to CSF shunts and postneurosurgical procedures.11 67 Name some of the antibiotics for intrathecal and intraventricular use They include vancomycin with doses of 10 to 20 mg/day for a few days until the cultures become negative, gentamicin and tobramycin with doses of to 10 mg/day, and amikacin 10 to 20 mg/day Preservative-free formulations should be used for intraventricular administration No antimicrobial agent has been approved by the Food and Drug Administration for intraventricular use.11 68 What are the side effects of intraventricular vancomycin? Ototoxicity, CSF eosinophilia, seizures, altered mental status, and local tissue irritation11 144 I Basic Neurosciences 69 What are the alternatives in the case of multidrugresistant Acinetobacter and Pseudomonas ventriculitis? Polymyxin B and colistimethate with doses of to 20 mg/ day—the optimal duration is unknown11 70 Which vitamin should be coadministered with isoniazid for tuberculosis treatment? Pyridoxine, vitamin B6, should be administered to prevent peripheral neuropathy.11 71 What is the main side effect of ethambutol? Optic neuritis that can lead to blindness11 4 Neuropharmacology: Intensive Care 145 Intensive Care: Vasogenic and Hematologic 72 What are the best options to treat hypertension when high intracranial pressure is present (e.g., traumatic brain injury [TBI])? Sympathomimetic-blocking agents drugs such as β-blocking drugs (propranolol, esmolol, labetalol) or centrally acting α receptor agonists (clonidine or α-methyldopa)12 73 Why is nicardipine a good alternative to manage hypertension in neurovascular pathologies (e.g., TBI, subarachnoid hemorrhage, intraparenchymal hemorrhages)? It is a short-acting continuous-infusion agent with a reliable dose–response relationship and favorable safety profile It has been shown to reverse vasospasm.12 74 Which of the following vasodilating antihypertensive agents cross the BBB: nitroprusside, calcium channel blockers, hydralazine, adenosine, nitroglycerin? They all As vasodilating antihypertensive agents these drugs have the potential to increase cerebral blood flow, impair autoregulation, and increase intracranial pressure.12,13 75 Besides nimodipine, what are other effective options for vasospasm prophylaxis? In addition to the standard course for vasospasm prophylaxis, that is, nimodipine 60 mg every hours or 30 mg every hours, the following can also be used: HMG Co A (3-hydroxy-3-methyl-glutaryl-CoA) reductase inhibitors (statins) have been shown to reduce inflammation, increase production of nitric oxide through upregulation of nitric oxide synthase and prevent thrombogenesis Animal as well as human research studies have reported decreased vasospasm-related ischemic deficits after subjects received statins either before or after subarachnoid hemorrhage Pravastatin or simvastatin in 40 mg or 80 mg daily doses respectively are commonly used Continuous infusions of magnesium have been effective in reducing cerebral vasospasm—specific doses and serum target levels are still under investigation.12,14 146 I Basic Neurosciences 76 What is the specific mechanism of nimodipine? Nimodipine blocks L-type calcium channels The L-type channel is the major influx route for calcium ions in smooth muscle 77 In addition to nimodipine and the Triple-H therapy, are there any more options to treat vasospasm? Intraventricular nicardipine, intraarterial milrinone, nitric oxide, and clazosentan are new alternatives for the treatment of refractory vasospasm 78 How is intraventricular nicardipine used in the treatment of vasospasm? Intraventricular nicardipine can be used to treat severe vasospasm in doses of mg every 12 hours for to 17 days.15 79 What is the clinical use of milrinone? Intraarterial followed by systemic milrinone for 14 days demonstrated a significant enlargement in diameter of vasospastic intracranial arteries The systemic dose started at 50 μg/kg/min and was titrated to 1.5 μg/kg/min.16 80 What is the mechanism of action of clazosentan? Clazosentan, an endothelin receptor antagonist, has been shown to decrease moderate and severe vasospasm and is currently being evaluated in phase III trials.17 81 What is the treatment for SIADH? Fluid restriction (800–1000 mL/day) An alternative is demeclocycline, which is an antibiotic that inhibits ADH’s action on the collecting duct of the kidney, producing water diuresis.12 82 What is the treatment for cerebral salt wasting (CSW)? Replacement of intravascular volume with normal saline12 83 What is the treatment for diabetes insipidus (DI)? Most of the time, DI is transient and does not require management other than to monitor inputs and outputs If necessary, desmopressin at 2–4 μg every to 12 hours IM or IV can be given 4 Neuropharmacology: Intensive Care 147 84 What is another clinical use of desmopressin? Desmopressin (0.3 μg/kg) can be used in thrombocytopenia or platelet dysfunction including platelet dysfunction related to acetylsalicylic acid (aspirin) or clopidogrel Desmopressin releases von Willebrand factor from the endothelium.12 85 What is the mechanism of action of warfarin? It inhibits the hepatic synthesis of vitamin K-dependent clotting factors: I, VII, IX, and X It has no effect on factors already synthesized.18 86 What are the options to reverse the effects of warfarin? Vitamin K (10 mg IV or IM for a few days), factor VII, and protein C activation peptide (PCP; factor IX).18 87 For emergent reversal of anticoagulation in war farin-consuming patients, will factor VIIa correct the international normalized ratio (INR) and the underlying coagulopathy? No, factor VIIa will reverse the INR, but will not replace the vitamin K-dependent factors (II, VII, IX, X) Factor VIIa is thought to act by binding to the surface of activated platelets, forming a stable clot The optimal dose for the reversal of warfarin is not known and ranges from 10 to 20 μg/kg Vitamin K and fresh frozen plasma are required to replace inactivated factors.18 88 Which medications and foods can increase the levels of warfarin? Cimetidine, metronidazole, trimethoprim-sulfamethoxazole, fluconazole, amiodarone, and grapefruit—they share in common the liver enzyme CYP3A418 89 What is the mechanism of action of heparin? It inhibits the activity of several clotting factors (IIa, IXa, Xa, Xia, XIIa) via activation of antithrombin III.3 90 What are the side effects of heparin? Bleeding, osteoporosis, heparin-induced thrombocytopenia, and hypersensitivity Low-molecular-weight heparins 148 I Basic Neurosciences can be used in case of hypersensitivity, but the risk of thrombocytopenia is still present 91 What is the mechanism of action of acetylsalicylic acid (aspirin) and for how long will the effects last? Acetylsalicylic acid (aspirin) blocks irreversibly the enzymatic conversion (by inhibiting cyclooxygenase [COX-1]) of arachidonic acid to prostaglandins and thromboxanes, lasting to 10 days, the lifespan of platelets 92 What is the mechanism of action of clopidogrel (Plavix)? It blocks ADP receptors on platelets decreasing its activation Its effects can be reversed by the administration of platelets and desmopressin (DDAVP).3 93 What are the treatment options for von Willebrand disease? Cryoprecipitate—which is rich in factors VII, XIII, fibrinogen, and VW factor, and desmopressin (DDAVP)—facilitates the release of von Willebrand factor from epithelial cells 4 Neuropharmacology: Toxicology 149 Toxicology 94 Name the antidote for organophosphates, lead, iron, and arsenic Atropine/pralidoxime, ethylenediaminetetraacetic acid (EDTA), deferoxamine, and dimercaprol, respectively2,3 95 What is the antidote for copper, iron, lead, and mercury intoxication? Penicillamine2,3 96 What is the antidote for carbon monoxide intoxication? Oxygen 97 What are the mechanisms of action of cocaine? It blocks dopamine, norepinephrine, and serotonin reuptake in the CNS causing tachycardia, hypertension, mydriasis, hyperactivity, psychotic episodes, hallucinations, dyskinesias, and decreased appetite Complications resulting from toxicity are arrhythmias, myocardial infarction, stroke, subarachnoid hemorrhage, convulsions, which can lead to death.19 98 What is the common presentation and time course of stroke associated with cocaine? Seventy percent of strokes postintranasal and post-IV cocaine use are hemorrhagic Most strokes tend to occur within an hour of use, especially for “crack” (freebase form, smokable) and IV injection Others occur within hours Infarction of the brain, spinal cord (usually anterior spinal artery), or retinal artery occur less frequently than hemorrhage, but are more common with smoking “crack” cocaine Patients tend to develop their infarct within a few hours of use or wake up with a deficit the morning after.19 99 What are the mechanisms of action of amphetamines? They block the reuptake of norepinephrine and dopamine, and release amines into the circulation Amphetamines have similar effects and toxicity as cocaine.19 150 I Basic Neurosciences ■ References Kandel E, Schwartz J, Jessell T Principles of Neural Science New York, NY: McGraw-Hill Medical; 2000 Katzung BG Basic & Clinical Pharmacology Stamford, CT: Appleton & Lange; 2000 Brunton L, Blumenthal D, Buxton I Goodman and Gilman’s Manual of Pharmacology and Therapeutics New York, NY: McGraw-Hill Professional; 2007 Abou Khaled KJ, Hirsch LJ Updates in the management of seizures and status epilepticus in critically ill patients Neurol Clin 2008;26(2):385–408, viii Vasile B, Rasulo F, Candiani A, Latronico N The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome Intensive Care Med 2003;29(9): 1417–1425 Coffey RJ, Edgar TS, Francisco GE, et al Abrupt withdrawal from intrathecal baclofen: recognition and management of a potentially life-threatening syndrome Arch Phys Med Rehabil 2002;83(6):735–741 Deer TR, Raso LJ, Coffey RJ, Allen JW Intrathecal baclofen and catheter tip inflammatory mass lesions (granulomas): a reevaluation of case reports and imaging findings in light of experimental, clinicopathological, and radiological evidence Pain Med 2008;9(4):391–395 Greenberg MS Handbook of Neurosurgery 6th ed New York, NY: Thieme Medical Publishers; 2006 Gertler R, Brown HC, Mitchell DH, Silvius EN Dexmedetomidine: a novel sedative-analgesic agent Proc (Bayl Univ Med Cent) 2001;14(1):13–21 10 Rozet I Anesthesia for functional neurosurgery: the role of dexmedetomidine Curr Opin Anaesthesiol 2008; 21(5): 537–543 11 Ziai WC, Lewin JJ III Update in the diagnosis and management of central nervous system infections Neurol Clin 2008;26(2):427–468, viii 12 Rangel-Castilla L, Gopinath S, Robertson CS Management of intracranial hypertension Neurol Clin 2008; 26(2): 521–541, x 13 Urrutia VC, Wityk RJ Blood pressure management in acute stroke Neurol Clin 2008;26(2):565–583, x–xi 14 Sillberg VA, Wells GA, Perry JJ Do statins improve outcomes and reduce the incidence of vasospasm after aneurysmal subarachnoid hemorrhage: a meta-analysis Stroke 2008;39(9): 2622–2626 15 Goodson K, Lapointe M, Monroe T, Chalela JA Intraventricular nicardipine for refractory cerebral vasospasm after subarachnoid hemorrhage Neurocrit Care 2008;8(2): 247–252 16 Fraticelli AT, Cholley BP, Losser MR, Saint Maurice JP, Payen D Milrinone for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage Stroke 2008;39(3):893–898 4 Neuropharmacology: References 151 17 Macdonald RL, Kassell NF, Mayer S, et al; CONSCIOUS-1 Investigators Clazosentan to overcome neurological ische mia and infarction occurring after subarachnoid hemor rhage (CONSCIOUS-1): randomized, double-blind, placebo- controlled phase dose-finding trial Stroke 2008;39(11): 3015–3021 18 Aiyagari V, Testai FD Correction of coagulopathy in warfarin associated cerebral hemorrhage Curr Opin Crit Care 2009;15(2):87–92 19 Enevoldson TP Recreational drugs and their neurological consequences J Neurol Neurosurg Psychiatry 2004;75 (Suppl 3):iii9–iii15 ... 55 97 98 10 2 10 4 11 0 12 3 12 7 12 8 13 3 13 5 14 2 14 5 14 9 s e nc sci Neu o r linical C II Cranial Neurosurgery. .. labyrinthine artery (Fig 1. 13 )19 39 What are the major parts of the temporal bone? Squamous and petrous parts1 40 The cribriform plate is part of what bone? The ethmoid bone1 1 Neuroanatomy: Cranial ... cranial fossas (Fig 1. 11) Foramen ovale Foramen spinosum 1 Neuroanatomy: Cranial Internal acoustic meatus Foramen lacerum Jugular foramen Hypoglossal canal Posterior fossa Fig 1. 11 Interior view