Manual of neurologic therapeutics - part 1 pot

Author(s): Martin A Samuels MD, FACP, FAAN Edition: Seventh ISBN: 0-7817-4646-9 Pub Date: March 2004 Pages: 592 By quack008 Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition Edited by Martin A. Samuels M.D., M.A.C.P., F.A.A.N. Neurologist-in-Chief and Chairman Department of Neurology, Brigham and Women ’ s Hospital, Professor of Neurology, Harvard Medical School, Boston, Massachusetts Secondary Editors James D. Ryan Acquisitions Editor Grace R. Caputo Developmental Editor Frank Aversa Production Editor Colin J. Warnock Manufacturing Manager Patricia Gast Cover Designer Compositor: Techbooks R. R. Donnelley – Crawfordsville Printer CONTRIBUTING AUTHORS Anthony A. Amato M.D. Associate Professor of Neurology Harvard Medical School; Chief, Neuromuscular Division, Vice-Chairman, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Robert W. Baloh M.D. Professor of Neurology University of California Medical School; Director, Neurootology Laboratory, University of California Medical Center, Los Angeles, California Donald C. Bienfang M.D. Assistant Professor of Ophthalmology Harvard Medical School; Chief, Division of Neuroophthalmology, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Edward B. Bromfield M.D. Assistant Professor of Neurology Harvard Medical School; Chief, Division of Epilepsy and Electroencephalography, Brigham and Women ’ s Hospital, Boston, Massachusetts Kirk R. Daffner M.D. Associate Professor of Neurology Harvard Medical School; Chief, Division of Cognitive and Behavioral Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts David M. Dawson M.D. Professor of Neurology Harvard Medical School; Senior Neurologist, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Steven K. Feske M.D. Assistant Professor of Neurology Harvard Medical School; Director, Stroke Division, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Robert B. Fogel M.D. Instructor in Medicine Harvard Medical School; Physician, Division of Sleep Medicine, Brigham and Women ’ s Hospital, Boston, Massachusetts Robert D. Helme F.R.A.C.P., Ph.D. Professor of Neurology University of Melbourne, Carlton, Victoria; Neurologist, Barbara Walker Centre for Pain Management, St. Vincent ’ s Hospital, Fitzroy, Victoria, Australia Galen V. Henderson M.D. Instructor in Neurology Harvard Medical School; Director, Critical Care and Emergency Neurology, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Santosh Kesari M.D., Ph.D. Instructor in Neurology Harvard Medical School; Associate Neurologist, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Ian Yi-Onn Leong M.B.B.S., M.R.C.P. Clinical Tutor Department of Medicine, National University of Singapore, Singapore; Associate Consultant, Department of Geriatric Medicine, Tan Tock Seng Hospital, Singapore Christina M. Marra M.D. Professor Department of Neurology and Medicine — Infectious Diseases, University of Washington School of Medicine, Seattle, Washington Michael Ronthal M.B.B.Ch., F.R.C.P., F.R.C.P.E. Associate Professor of Neurology Harvard Medical School; Senior Neurologist, Department of Neurology, Beth Israel — Deaconess Medical Center, Boston, Massachusetts Martin A. Samuels M.D., M.A.C.P., F.A.A.N. Professor of Neurology Harvard Medical School; Neurologist-in-Chief and Chairman, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Egilius L.H. Spierings M.D., Ph.D. Associate Clinical Professor of Neurology Harvard Medical School; Consultant, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Lewis R. Sudarsky M.D. Associate Professor of Neurology Harvard Medical School; Director, Movement Disorders Division, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts Patrick Y. Wen M.D. Associate Professor of Neurology Harvard Medical School; Director, Division of Neurooncology, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts David A. Wolk M.D. Instructor in Neurology Harvard Medical School; Associate Neurologist, Department of Neurology, Brigham and Women ’ s Hospital, Boston, Massachusetts John W. Winkelman M.D., Ph.D. Assistant Professor of Psychiatry Harvard Medical School; Medical Director, Sleep Health Center, Newton, Massachusetts; Physician, Division of Sleep Medicine, Department of Medicine, Brigham and Women ’ s Hospital, Boston, Massachusetts Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition DEDICATION This book is dedicated to the original contributors to the Manual of Neurologic Therapeutics. They were all members of a single group of residents in the neurology training program at the Massachusetts General Hospital when the idea was hatched almost 30 years ago. They have all gone on to distinguished careers in neurology. Telmo M. Aquino Raymond J. Fernandez Robert D. Helme Daniel B. Hier Richard C. Hinton Stephen M. Sagar Thomas M. Walshe Howard D. Weiss Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition FOREWORD It is to the classic monographs of Erb, Hughings Jackson, Gowers, K. Wilson, and their contemporaries that all scholars of neurology turn for knowledge of many of the common diseases of the human nervous system. These writings summarize the personal observations—clinical and pathological—of the author himself, expressed in the lucid and elegant language of the era. The author’s reputation attested to the verity of the observations. But perusal of these landmark documents reveals little in the nature and future prospects of therapy or means of prevention. As a consequence, neurology became known as a large branch of medicine with a multitude of diagnosable diseases bereft of therapy. All this has changed. Because of prodigious advances in biochemistry, neuropathology, and genetics, new methods of therapy have been devised, or at least conceptualized, for many of the previously recognized diseases as well as new disorders disclosed by the application of these methods. In fact, such an aggregation of new information about therapies of neurologic diseases has emerged that several neurologists have judged that a monograph devoted to the subject was warranted. This was surely the reasoning of Professor Martin A. Samuels, who undertook this task many years ago. The success of his venture is reflected in the continued demand for the Manual of Neurologic Therapeutics, now in its 7th edition. Professor Samuels, like many others who had received their specialty education in our residency program at the Massachusetts General Hospital, brings to his subject a keen knowledge of neurology and a high motivation to advance the understanding of established methods of therapy in neurology. As a member of the staff of the neurology service of the Massachusetts General Hospital, I have enjoyed and benefited from my association with Professor Samuels both during the period when he was a graduate student and later, as an esteemed faculty colleague. I applaud his latest medical literary contribution. Raymond D. Adams M.D. Boston, Massachusetts Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition PREFACE TO THE FIRST EDITION Until very recently the neurologist’s primary task was to categorize and organize the structure and pathologic alterations of the nervous system. In fact, neurology has long been known as a discipline with elegantly precise and specific diagnostic capabilities but little or no therapeutic potentiality. Further, many surgeons, pediatricians, and internists have traditionally thought of the neurologist as an impractical intellectual who spends countless hours painstakingly localizing lesions while ignoring pragmatic considerations of treatment. Perhaps this conception is largely attributable to the peculiar complexity of the nervous system and the consequent relative naivete of physicians in their understanding of its functions. Many of the classic descriptions of disease states in other medical disciplines were completed in the last century; in neurology, these have only been described in the past generation, and only in the last ten years has neurology begun to be characterized by subcellular mechanistic concepts of disease. This maturity has meant that the neurologist is now as much involved in the therapeutic aspects of his specialty of medicine as any of his colleagues. Certain neurologic diseases, such as epilepsy, have been treatable for relatively long periods of time, but understanding of the subcellular mechanisms of other diseases has led to newer, more effective forms of therapy. An example of this is the enlarged understanding we now have of the biochemical alterations in Parkinson disease, and the resultant therapeutic implications. Now, much as the endocrinologist treats diabetes with insulin and the cardiologist treats congestive heart failure with digitalis, the neurologist treats Parkinson disease with l-dopa. In all these situations, the underlying condition is not cured; rather, an attempt is made to alter the pathophysiologic processes by utilizing a scientific understanding of the function of the diseased system. This manual embodies a practical, logical approach to the treatment of neurologic problems, based on accurate diagnosis, that should prove useful to both clinician and student. No attempt is made to reiterate the details of the neurologic examination; it is assumed that the reader is competent to examine the patient — although particularly important or difficult differential diagnostic points are mentioned when appropriate. In this regard, it should be emphasized that this manual is only a guide to diagnosis and therapy, and each patient must be treated individually. The manual is organized to best meet the needs of the clinician facing therapeutic problems. Thus, the first seven chapters are concerned with symptoms, such as dizziness and headache, while the last ten consider common diseases, such as stroke and neoplasms. I thank the many colleagues and friends whose criticism and comments were useful in the preparation of this book, in particular Drs. G. Robert DeLong, C. Miller Fisher, George Kleinman, James B. Lehrich, Steven W. Parker, Henry C. Powell, E. P. Richardson, Jr., Maria Salam, Bagwan T. Shahani, Peter Weller, James G. Wepsic, and Robert R. Young. In addition I am indebted to Sara Nugent and Helen Hyland for their assistance in the preparation of the many manuscripts, and to Diana Odell Potter, formerly of Little, Brown and Company, for her editorial skills. Jane Sandiford, formerly of Little, Brown, and Kathleen O ’ Brien and Carmen Thomas of Little, Brown provided invaluable assistance in the final preparation of this material. Deep appreciation goes to Lin Richter, Editor-in-Chief of the Medical Division, Little, Brown and Company, for her support throughout this effort. I further thank Jon Paul Davidson, also fo rmerly of Little, Brown, for his valuable encouragement and help early in the course of this project. Much support and encouragement was derived from my new colleagues in the Peter Bent Brigham Hospital Neurology Section, The Longwood Avenue Neurology Program, and the West Roxbury Veterans Administration Hospital. A great deal of inspiration came from the birth of my daughter Marilyn, and my deepest thanks go to my wife, Linda, who provided constant encouragement, editorial skill, and infinite patience. Martin A. Samuels Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition PREFACE Once the last bastion of therapeutic nihilism, neurology has now clearly entered the era of intense therapy for virtually every class of disease that affects the nervous system. Consequently, the modern neurology department is now subdivided into a dozen clinical subspecialties, each with its own group of experts, often with their own postresidency specialized fellowship training programs. General neurology still exists but it is usually practiced in a consultative mode in either the hospital or the ambulatory setting. Now, the movement disorder specialist is as different from the epileptologist as the hematologist is from the endocrinologist. Basic research in the neurosciences is routinely translated into new drugs, devices, and procedures aimed at ameliorating disorders in almost all the major categories of disease. Even neurodegeneration, traditionally the most therapeutically resistant class of disease, is beginning to crack under the influence of molecular genetics and its translation into drugs that may slow or prevent cell death. In this context, the original contributors to the Manual of Neurologic Therapeutics all agreed that the 7 th edition would require a major reorganization and that the sections needed to be written by experts who had dedicated their careers to each of the various areas of concentration. Furthermore, to be optimally accessible in both office and bedside venue, the Manual needed to be presented in a format conducive to electronic presentation as well as print reproduction. Thus, the information contained here is presented in a more consistent format than previously, with better use of headings and less reliance on a traditional outline. The 7 th edition contains an entire chapter on neurologic intensive care, now a well-defined subspecialty. Epilepsy management currently involves not only an array of new drugs but also innovative strategies such as vagal nerve stimulation and a greater emphasis on earlier surgical treatment. Neurootology encompasses the common complaint of dizziness, emphasizing both pharmacologic and physical therapy approaches to treatment. Back and neck pain, still among the most common complaints in all of medicine, are now evaluated with much improved diagnostic tests, which lead to more precise treatment. An entire chapter is dedicated to sleep disorders, an enormous area of disability in which major new advances in therapy have occurred. Cancer neurology now involves a complex array of chemotherapy, radiation therapy, and new cutting edge treatments using monoclonal antibodies. No area has changed more substantively than multiple sclerosis, in which fresh magnetic resonance imaging-influenced diagnostic criteria and several immunomodulatory drugs have substantively altered the clinical course of the disease. The area of neuromuscular diseases has been influenced enormously by the use of potent treatment for immune-mediated diseases and better diagnostic precision using molecular techniques applied to blood and muscle biopsy specimens. Pain management has become an art and science of its own, deserving of its own chapter in this edition. The triptan drugs, currently numbering seven, have changed the approach to migraine, and many other headache syndromes are now more clearly classified and specifically treated. The management of acute stroke has dramatically changed even in the four years since the 6 th edition, with widespread use of not only intravenous thrombolytic drugs but also sophisticated interventional techniques aimed at extracting cerebral emboli and opening narrowed vessels with angioplasty and stenting. The advances in Parkinson disease and other movement disorders reflect the widespread availability of new dopamine receptor agonists and the use of deep brain stimulation in advanced and drug-resistant disease. Even Alzheimer disease is now treated with some success using a class of anticholinesterase drugs, and other dementias are more clearly classified and managed. Neuroophthalmology has become a major segment of neurologic practice, a fact that is reflected in an entire chapter now dedicated to that group of disorders. The most prevalent of the toxic and metabolic disorders have undergone an alteration in approach based on a better understanding of the nervous system ’ s reaction to perturbations in its milieu. Moreover, the array of infectious agents affecting the nervous system continues to change as new diseases emerge and the approach with antibiotics undergoes reassessment. The 17 chapters of the 7 th edition of the Manual of Neurologic Therapeutics are all brand new; all written by noted experts in the particular area. Emphasis has been placed on practical management, with consideration of the essentials of diagnosis and pathophysiology. The impressive progress in neurologic therapeutics is seen in the increased bulk of the book, now twice its original size. To complete the quarter century cycle since the book was first published, the foreword to the 7 th edition is written by Dr. Raymond D. Adams, to whom the 1 st edition was dedicated. Martin A. Samuels Boston, Massachusetts 1 Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition Coma, Head Trauma, and Spinal Cord Injury Galen V. Henderson z COMA z HEAD INJURY z ACUTE SPINAL CORD INJURY z BRAIN DEATH 6 — — Obeys 5 — Oriented Localizes to pain 4 Spontaneous Confused Withdraws to pain 3 To speech Inappropriate Flexion (decorticate) 2 To pain Unintelligible Extensor (decerebrate) 1 None None None a. This scale attempts to quantitate the severity of trauma on the basis of patient's best response in three areas: eye opening, motor activity, and language. b. The GCS scores range from 3 to 15. When the total score is 8 or less, the patient is considered to be in coma. Components of the Examination 1. Level of consciousness should be described according to a. Unresponsive. b. Unresponsive to pain. c. Responsive to voice. d. Lethargic but spontaneously responsive classifications are best supplemented by a description of the stimuli used and the nature of the responses. 2. Examination of the eyes a. Ocular motility 1. Pupil size and reactivity. 2. Pupils are the most reliable means of distinguishing metabolic from structural disease. 3. Preserved pupillary reflexes with absent eye movements to vestibular stimulation or even respiratory depression implicate metabolic coma. 4. Absent pupillary light reflexes indicate structural brainstem damage with important qualifications. 5. Symmetric or asymmetric impairment of the pupil's reaction to light usually indicates structural brainstem disease. Pontine infarction or hemorrhages sometimes cause small, “ pinpoint ” pupils, but they can be seen to react to light under magnification. 6. Drugs affecting pupillary function a. Anticholinergic atropine-like drugs, profound anoxia, hypothermia, or severe barbiturate intoxication can paralyze pupillary reactions. b. Atropine-like drugs, tricyclic antidepressants, and lithium toxicity cause large poorly reactive pupils. Such pharmacologic mydriasis can be confirmed by failure of the pupils to constrict to 1% pilocarpine eye drops. c. Narcotic intoxication also causes very small pupils. Naloxone administration may be used to reverse this intoxication. d. Hallucinogens such as lysergic acid diethylamide (LSD) can dilate the pupils by their sympathomimetic effect. b. Optic fundi: If the pupils are small, dilation to view the fundi should be deferred until stability of the patient's condition is assured and a probable cause of unresponsiveness is determined. I do not encourage the dilation of pupils with eye drops, but if it is performed, all caregivers should be notified, a notation made on the chart, and a banner placed on the wall at the head of the bed. P.3 1. Papilledema indicates raised intracranial pressure (ICP), but is often absent in the elderly patient and more sensitive in pediatric patients with high cerebrospinal fluid (CSF) pressure. 2. Retinal hemorrhages and optic disc edema may signify hypertensive encephalopathy. 3. Massive trauma may cause cumulus cloud infiltrates from fat embolism. 4. Subhyaloid blood or a black view indicates retinal bleeding into the vitreous (Terson syndrome) after massive abrupt subarachnoid hemorrhage. 5. Retinal infarcts (cotton-wool spots) indicate vasculitis, intravenous (IV) drug use, or septic emboli. c. Eyelids and corneal reflexes 1. The eyes are closed in coma, as in sleep, by tonic contraction of the orbicularis oculi and by inhibition of the levator palpebrae. 2. Absence of orbicularis tonus or failure of lid closure indicates seventh nerve involvement, either central or peripheral. Conversely, the presence of good lid closure and tone indicates that the caudal pons is spared. 3. Reflex spasm of the lids, blepharospasm, occurs with metabolic encephalopathy or posterior fossa lesions. 4. Spontaneous blinking implies sparing of the pontine reticular formation. Occasionally in cases of postictal coma, blinking continues while the lids are closed. 5. Blinking in response to a bright light, even through closed lids, does not indicate sparing of the visual cortex since this reflex may be mediated at a brainstem level. 6. Blinking in response to a loud sound indicates integrity of the lower pons. 7. Absence of blinking to sound, threat, or light indicates severe metabolic compromise or structural damage of the pontine tegmentum. 8. Bilateral lid closure and upward deviation of the eyes in response to strong corneal stimulation assures function from the rostral midbrain right down to the medulla oblongata. 9. A combination of failure of lid closure with spared eye deviation on corneal stimulation signifies destruction of the facial nerve or nucleus. 10. Loss of both lid closure and eye deviation on corneal (pain) stimulation is of little diagnostic help other than indicating that brainstem depression is severe. 3. Skeletal motor and reflex signs a. Patients who have hemispheric lesions typically lie in comfortable-appearing, relatively normal postures. b. Patients who have brainstem lesions often display abnormal postures. The symmetry of spontaneous movement may give a clue about the side of a focal lesion. Postures with some localizing significance are usually fragmentary and may be elicited by noxious stimuli. c. The terms decorticate and decerebrate rigidity refer to experimental studies of animals and do not accurately reflect the clinicopathologic correlations that they imply. 1. Decorticate posturing: lower extremity extensions and internal rotation with flexion of both upper extremities 2. Decerebrate posturing: lower and upper extremity extensions d. Upper extremity flexion reflects more superficial, less severe, and more chronic lesions at the level of the diencephalon or above. Upper and lower extremity extension will often accompany brainstem lesions; however, as mentioned, the upper extremity extension depends on the degree and acuteness of the lesion and being reflexively driven, on the stimulus applied at the time of the examination. The responsible lesions may also be reversible, as in severe toxic and metabolic encephalopathies. e. Deep tendon reflexes and plantar responses may also suggest a lateralized lesion, but they, too, are often misleading signs. Careful observation for subtle movements suggesting nonconvulsive seizures should be sought in all cases of coma. P.4 4. Responses respiratory pattern a. Hyperventilation is common and has poor localizing value. Differential diagnosis includes 1. Fever 2. Sepsis 3. Metabolic acidosis 4. Drug toxicity 5. Cardiopulmonary disease b. Cheyne – Stokes respirations refer to a periodic breathing pattern of alternating hyperpnea and apnea. c. Apneustic. 1. Characterized by a prolonged pause at the end of inspiration and is also called “ inspiratory cramp. ” 2. It does localize to a lesion in the mid to caudal pons. d. Biot breathing 1. Characterized by chaotic or ataxic breathing pattern with loss of regularity of alternating pace and depth of inspirations and expirations that may occur when the neurons in the respiratory center are damaged. 2. Such patients are prone to apnea. 3. A variety of lesions may cause this pattern. Level of Consciousness 1. Structural coma can result from primary cerebral hemispheric or primary brainstem involvement. [...]... role of decompressive craniotomy in the treatment, or avoidance, of intracranial hypertension? 2 In 19 95, the Brain Trauma Foundation, the American Association of Neurological Surgeons (AANS), and the Joint Section on Neurotrauma and Critical Care of the AANS and Congress of Neurological Surgeons first published an evidence-based tome to improve nonpenetrating TBI care Table 1- 4 is a brief outline of. .. a fixed posture, often with abduction of the shoulders and partial flexion of the elbows; usual duration 10 to 20 seconds, but often cluster; EEG pattern of rapid, diffuse polyspikes, often following a slow wave f Tonic–clonic (grand mal, convulsion): Stereotyped sequence of bilateral stiffening followed by clonic contractions; usual duration, 50 to 12 0 seconds; EEG pattern of low-amplitude polyspikes... be identified in an individual patient 4 Several of the epilepsy syndromes listed in Table 2 -1 , in a modified version of the 19 89 ILAE classification, are discussed at greater length at the end of this chapter TABLE 2 -1 MODIFIED INTERNATIONAL LEAGUE AGAINST EPILEPSY CLASSIFICATION OF EPILEPSY SYNDROMES Localization related (partial, focal) epilepsies 1 Idiopathic: Benign childhood epilepsy with centrotemporal... Compared with typical absence, often less complete but longer and more gradual behavioral arrest and recovery; EEG pattern of slow (1. 5–2.5 Hz) spike–wave complexes c Myoclonic: Brief, shock-like jerking of muscles on both sides of body; duration, less than 1 second; EEG pattern of generalized polyspike–wave complex d Clonic: Series of myoclonic jerks; duration variable; EEG pattern of repeated myoclonic jerks... disorders that threaten life and independent functions (Tables 1- 2 and 1- 3 ) TABLE 1- 2 APPROACH TO THE ASSESSMENT AND MANAGEMENT OF ACUTE COMA Stabilization • Airway control • Oxygenation and ventilation • Adequate circulation (includes avoidance of hypotention in strokes) • Cervical stabilization Immediate therapies given to all patients • Thiamine 10 0 mg IV • Dextrose 50% 50 mL IV (may be held if immediate... TOMOGRAPHY SCANS AND LEVEL OF CONSCIOUSNESS True Dimensions from Midline (mm) Level of Consciousness Pineal Septum Pellucidum Awake 0–3 2–7 Drowsy 3–6 2 10 Stupor 6–9 7 14 Coma 9 15 12 18 From Ropper AH Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass N Engl J Med 19 86; 314 :953–958, with permission c When these mechanisms become exhausted, intracranial... level of consciousness, in whom early signs of neurologic deterioration cannot be appreciated 3 The goal of ICP monitoring is to detect abnormal physiologic events before the loss of the neurologic function, therefore allowing clinicians to intervene and avoid additional brain injury TREATMENT Physiologic Principles 1 Intracranial anatomy a The components of volume within the nondistensible cranium of. .. instead Concussion 1 Patients may or may not have loss of consciousness 2 Patients should have “normal” CT scan findings P .11 3 Patients commonly complain of headache, dizziness, irritability, short-term memory loss, and/or short attention span These “minor” head injuries may have sequelae that may be devastating to activities of daily living Contusion 1 A contusion is bruising of brain tissue 2 Contusions... volume lead to dramatic elevations of ICP (Fig 1- 1 ) FIG 1- 1 Intracranial compliance curve d Intracranial compliance can be described as change in volume divided by the change in pressure 3 Cerebral perfusion and autoregulation a Brain tissue requires constant perfusion to ensure adequate delivery of substrate, principally oxygen and glucose b The hemodynamic response of the brain has the capacity to... range of systemic blood pressures c CPP, defined as the mean systemic arterial pressure (MAP) minus the ICP, provides the driving force for circulation across the capillary beds of the brain d Autoregulation refers to the physiologic response whereby CBF remains relatively constant over a wide range of blood pressures as a consequence of alterations of cerebrovascular resistance (Fig 1- 2 ) FIG 1- 2 Cerebral . Martin A. Manual of Neurologic Therapeutics, 7th Edition DEDICATION This book is dedicated to the original contributors to the Manual of Neurologic Therapeutics. They were all members of a single. Edition: Seventh ISBN: 0-7 81 7-4 64 6-9 Pub Date: March 2004 Pages: 592 By quack008 Copyright ©2004 Lippincott Williams & Wilkins Samuels, Martin A. Manual of Neurologic Therapeutics, 7th Edition. antibiotics undergoes reassessment. The 17 chapters of the 7 th edition of the Manual of Neurologic Therapeutics are all brand new; all written by noted experts in the particular area. Emphasis has been