Plum and Posner's Diagnosis of Stupor and Coma 4th Edition






Fred Plum came to the University of Washington in 1952 to head up the Division of Neurology (in the Department of Medicine) that consisted of one person, Fred. The University had no hospital but instead used the county hospital (King County Hospital), now called Harborview. The only emergency room in the entire county was at that hospital, and thus it received all of the comatose patients in the area. The only noninvasive imaging available was primitive ultrasound that could identify, sometimes, whether the pineal gland was in the midline. Thus, Fred and his residents (August Swanson, Jerome Posner, and Donald McNealy, in that order) searched for clinical ways to differentiate those lesions that required neurosurgical intervention from those that required medical treatment. The result was the first edition of The Diagnosis of Stupor and Coma. Times have changed. Computed tomography (CT) and magnetic resonance imaging (MRI) have revolutionized the approach to the patient with an altered level of consciousness. The physician confronted with such a patient usually first images the brain and then if the image does not show a mass or destructive lesion, pursues a careful metabolic workup. Even the laboratory evaluation has changed. In the 1950s the only pH meter in the hospital was in our experimental laboratory and many of the metabolic tests that we now consider routine were time consuming and not available in a timely fashion. Yet the clinical approach taught in The Diagnosis of Stupor and Coma remains the cornerstone of medical care for comatose patients in virtually every hospital, and the need for a modern updating of the text has been clear for some time. 

The appearance of a fourth edition now called Plum and Posner’s Diagnosis of Stupor and Coma more than 25 years after the third edition is deserving of comment. There were several reasons for this delay. First, the introduction and rapid development of MRI scanning almost immediately after the publication of the last edition both stimulated the authors to prepare a new edition and also delayed the efforts, as new information using the new MRI methods accumulated at a rapid pace and dramatically changed the field over the next decade. At the same time, there was substantial progress in theory on the neural basis of consciousness, and the senior author wanted to incorporate as much of that new material as possible into the new edition. A second obstacle to the early completion of a fourth edition was the retirement of the senior author, who also developed some difficulty with expressive language. It became apparent that the senior author was not going to be able to complete the new edition with the eloquence for which he had been known. Ultimately, the two original authors asked two of their proteges, CBS and NDS, to help with the preparation of the new edition. Fred participated in the initial drafts of this edition, but not fully in the final product. Most important, although the technologic evaluation of patients in coma has changed in ways that were unimaginable at the time of publication of the earlier editions, the underlying principles of evaluation and management have not. The examination of the comatose patient remains the cornerstone to clinical judgment. It is much faster and more accurate than any imaging study, and accurate clinical assessment is necessary to determine what steps are required for further evaluation, to determine the tempo of the workup, and most important, to identify those patients in critical condition who need emergency intervention. Coma remains a classic problem in neurology, in which intervention within minutes can often make the difference between life and death for the patient. In this sense, the fourth edition of Plum and Posner’s Diagnosis of Stupor and Coma does not differ from its predecessors in offering a straightforward approach to diagnosis and management of these critically ill patients.


Contents
1. PATHOPHYSIOLOGY OF SIGNS AND SYMPTOMS OF COMA
ALTERED STATES OF CONSCIOUSNESS
DEFINITIONS
  • Consciousness
  • Acutely Altered States of Consciousness
  • Subacute or Chronic Alterations of Consciousness
APPROACH TO THE DIAGNOSIS OF THE COMATOSE PATIENT
PHYSIOLOGY & PATHOPHYSIOLOGY OF CONSCIOUSNESS AND COMA
  • The Ascending Arousal System
  • Behavioral State Switching
  • Relationship of Coma to Sleep
  • The Cerebral Hemispheres and Conscious Behavior
  • Structural Lesions That Cause Altered Consciousness in Humans 

2. EXAMINATION OF THE COMATOSE PATIENT
OVERVIEW
HISTORY
GENERAL PHYSICAL EXAMINATION
LEVEL OF CONSCIOUSNESS
ABC: AIRWAY, BREATHING, CIRCULATION
  • Circulation Respiration
PUPILLARY RESPONSES
  • Examine the Pupils and Their Responses
  • Pathophysiology of Pupillary Responses: Peripheral Anatomy of the Pupillomotor System
  • Pharmacology of the Peripheral Pupillomotor System
  • Localizing Value of Abnormal Pupillary Responses in Patients in Coma
  • Metabolic and Pharmacologic Causes of Abnormal Pupillary Response
OCULOMOTOR RESPONSES
  • Functional Anatomy of the Peripheral Oculomotor System
  • Functional Anatomy of the Central Oculomotor System
  • The Ocular Motor Examination
  • Interpretation of Abnormal Ocular Movements
MOTOR RESPONSES
  • Motor Tone
  • Motor Reflexes
  • Motor Responses
FALSE LOCALIZING SIGNS IN PATIENTS WITH METABOLIC COMA
  • Respiratory Responses
  • Pupillary Responses
  • Ocular Motor Responses
  • Motor
  • Responses
MAJOR LABORATORY DIAGNOSTIC AIDS
  • Blood and Urine Testing
  • Computed Tomography Imaging and Angiography
  • Magnetic Resonance Imaging and Angiography
  • Magnetic Resonance Spectroscopy
  • Neurosonography
  • Lumbar Puncture
  • Electroencephalography and Evoked Potentials 

3. STRUCTURAL CAUSES OF STUPOR AND COMA
COMPRESSIVE LESIONS AS A CAUSE OF COMA
COMPRESSIVE LESIONS MAY DIRECTLY DISTORT THE AROUSAL SYSTEM
  • Compression at Different Levels of the Central Nervous System Presents in Distinct Ways
  • The Role of Increased Intracranial Pressure in Coma
  • The Role of Vascular Factors and Cerebral Edema in Mass Lesions
HERNIATION SYNDROMES: INTRACRANIAL SHIFTS IN THE PATHOGENESIS OF COMA
  • Anatomy of the Intracranial Compartments
  • Patterns of Brain Shifts That Contribute to Coma
  • Clinical Findings in Uncal Herniation Syndrome
  • Clinical Findings in Central Herniation Syndrome
  • Clinical Findings in Dorsal Midbrain Syndrome
  • Safety of Lumbar Puncture in Comatose Patients
  • False Localizing Signs in the Diagnosis of Structural Coma
DESTRUCTIVE LESIONS AS A CAUSE OF COMA
DIFFUSE, BILATERAL CORTICAL DESTRUCTION
DESTRUCTIVE DISEASE OF THE DIENCEPHALON
DESTRUCTIVE LESIONS OF THE BRAINSTEM 

4. SPECIFIC CAUSES OF STRUCTURAL COMA
INTRODUCTION
SUPRATENTORIAL COMPRESSIVE LESIONS
EPIDURAL, DURAL, AND SUBDURAL MASSES
  • Epidural Hematoma
  • Subdural Hematoma
  • Epidural Abscess/Empyema
  • Dural and Subdural Tumors
SUBARACHNOID LESIONS
  • Subarachnoid Hemorrhage
  • Subarachnoid Tumors
  • Subarachnoid Infection
INTRACEREBRAL MASSES
  • Intracerebral Hemorrhage
  • Intracerebral Tumors
  • Brain Abscess and Granuloma
INFRATENTORIAL COMPRESSIVE LESIONS
EPIDURAL AND DURAL MASSES
  • Epidural Hematoma
  • Epidural Abscess
  • Dural and Epidural Tumors
SUBDURAL POSTERIOR FOSSA COMPRESSIVE LESIONS
  • Subdural Empyema
  • Subdural Tumors
SUBARACHNOID POSTERIOR FOSSA LESIONS
INTRAPARENCHYMAL POSTERIOR FOSSA MASS LESIONS
  • Cerebellar Hemorrhage
  • Cerebellar Infarction
  • Cerebellar Abscess
  • Cerebellar Tumor
  • Pontine Hemorrhage
SUPRATENTORIAL DESTRUCTIVE LESIONS CAUSING COMA
VASCULAR CAUSES OF SUPRATENTORIAL DESTRUCTIVE LESIONS
  • Carotid Ischemic Lesions
  • Distal Basilar Occlusion
  • Venous Sinus Thrombosis
  • Vasculitis
INFECTIONS AND INFLAMMATORY CAUSES OF SUPRATENTORIAL DESTRUCTIVE LESIONS
  • Viral Encephalitis
  • Acute Disseminated Encephalomyelitis
CONCUSSION AND OTHER TRAUMATIC BRAIN INJURIES
  • Mechanism of Brain Injury During Closed Head Trauma
  • Mechanism of Loss of Consciousness in Concussion
  • Delayed Encephalopathy After Head Injury
INFRATENTORIAL DESTRUCTIVE LESIONS
BRAINSTEM VASCULAR DESTRUCTIVE DISORDERS
  • Brainstem Hemorrhage
  • Basilar Migraine
  • Posterior Reversible Leukoencephalopathy Syndrome
INFRATENTORIAL INFLAMMATORY DISORDERS
INFRATENTORIAL TUMORS
CENTRAL PONTINE MYELINOLYSIS 

5. MULTIFOCAL, DIFFUSE, AND METABOLIC BRAIN DISEASES CAUSING DELIRIUM, STUPOR, OR COMA
CLINICAL SIGNS OF METABOLIC ENCEPHALOPATHY
CONSCIOUSNESS: CLINICAL ASPECTS
  • Tests of Mental Status
  • Pathogenesis of the Mental Changes
RESPIRATION
  • Neurologic Respiratory Changes Accompanying Metabolic Encephalopathy
  • Acid-Base Changes Accompanying Hyperventilation During Metabolic Encephalopathy
  • Acid-Base Changes Accompanying Hypoventilation During Metabolic Encephalopathy
PUPILS
OCULAR MOTILITY
MOTOR ACTIVITY
  • ‘‘Nonspecific’’ Motor Abnormalities
  • Motor Abnormalities Characteristic of Metabolic Coma
DIFFERENTIAL DIAGNOSIS
  • Distinction Between Metabolic and Psychogenic Unresponsiveness
  • Distinction Between Coma of Metabolic and Structural Origin
ASPECTS OF CEREBRAL METABOLISM PERTINENT TO COMA
CEREBRAL BLOOD FLOW
GLUCOSE METABOLISM
  • Hyperglycemia
  • Hypoglycemia
ANESTHESIA
MECHANISMS OF IRREVERSIBLE ANOXIC-ISCHEMIC BRAIN DAMAGE
  • Global Ischemia
  • Focal Ischemia
  • Hypoxia
EVALUATION OF NEUROTRANSMITTER CHANGES IN METABOLIC COMA
  • Acetylcholine
  • Dopamine
  • Gamma-Aminobutyric Acid
  • Serotonin
  • Histamine
  • Glutamate
  • Norepinephrine
SPECIFIC CAUSES OF METABOLIC COMA
ISCHEMIA AND HYPOXIA
  • Acute, Diffuse (or Global) Hypoxia or Ischemia
  • Intermittent or Sustained Hypoxia
  • Sequelae of Hypoxia
DISORDERS OF GLUCOSE OR COFACTOR AVAILABILITY
  • Hypoglycemia
  • Hyperglycemia
  • Cofactor Deficiency
DISEASES OF ORGAN SYSTEMS OTHER THAN BRAIN
  • Liver Disease
  • Renal Disease
  • Pulmonary Disease
  • Pancreatic
  • Encephalopathy
  • Diabetes Mellitus
  • Adrenal Disorders
  • Thyroid
  • Disorders
  • Pituitary Disorders
  • Cancer
EXOGENOUS INTOXICATIONS
  • Sedative and Psychotropic Drugs
  • Intoxication With Other Common Medications
  • Ethanol Intoxication
  • Intoxication With Drugs of Abuse
  • Intoxication With Drugs Causing Metabolic Acidosis
ABNORMALITIES OF IONIC OR ACID-BASE ENVIRONMENT OF THE CENTRAL NERVOUS SYSTEM
  • Hypo-osmolar States
  • Hyperosmolar States
  • Calcium
  • Other Electrolytes
  • Disorders of Systemic Acid-Base Balance
DISORDERS OF THERMOREGULATION
  • Hypothermia
  • Hyperthermia
INFECTIOUS DISORDERS OF THE CENTRAL NERVOUS SYSTEM: BACTERIAL
  • Acute Bacterial Leptomeningitis
  • Chronic Bacterial Meningitis
INFECTIOUS DISORDERS OF THE CENTRAL NERVOUS SYSTEM: VIRAL
  • Overview of Viral Encephalitis
  • Acute Viral Encephalitis
  • Acute Toxic Encephalopathy During Viral Encephalitis
  • Parainfectious Encephalitis (Acute Disseminated Encephalomyelitis)
  • Cerebral Biopsy for Diagnosis of Encephalitis
CEREBRAL VASCULITIS AND OTHER VASCULOPATHIES
  • Granulomatous Central Nervous System Angiitis
  • Systemic Lupus Erythematosus
  • Subacute Diencephalic Angioencephalopathy
  • Varicella-Zoster Vasculitis
  • Behcet’s Syndrome
  • Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy
MISCELLANEOUS NEURONAL AND GLIAL DISORDERS
  • Prion Diseases
  • Adrenoleukodystrophy (Schilder’s Disease)
  • Marchiafava-Bignami Disease
  • Gliomatosis Cerebri
  • Progressive Multifocal Leukoencephalopathy
  • Epilepsy Mixed Metabolic Encephalopathy
ACUTE DELIRIOUS STATES
  • Drug Withdrawal Delirium (Delirium Tremens)
  • Postoperative Delirium Intensive Care Unit Delirium
  • Drug-Induced Delirium

6. PSYCHOGENIC UNRESPONSIVENESS
CONVERSION REACTIONS
CATATONIA
PSYCHOGENIC SEIZURES
CEREBELLAR COGNITIVE AFFECTIVE SYNDROME
‘‘AMYTAL INTERVIEW’’

7. APPROACH TO MANAGEMENT OF THE UNCONSCIOUS PATIENT
A CLINICAL REGIMEN FOR DIAGNOSIS AND MANAGEMENT PRINCIPLES OF EMERGENCY MANAGEMENT
  • Ensure Oxygenation, Airway, and Ventilation
  • Maintain the Circulation
  • Measure the Glucose
  • Lower the Intracranial Pressure
  • Stop Seizures
  • Treat Infection
  • Restore Acid-Base Balance
  • Adjust Body Temperature
  • Administer Specific Antidotes
  • Control Agitation
  • Protect the Eyes
EXAMINATION OF THE PATIENT
  • Verbal Responses
  • Respiratory Pattern
  • Eye Opening
  • Pupillary Reactions
  • Spontaneous Eye Movement
  • Oculocephalic Responses
  • Caloric Vestibulo-Ocular Responses
  • Corneal Responses
  • Motor Responses
  • Tendon Reflexes
  • Skeletal Muscle Tone
GUIDES TO SPECIFIC MANAGEMENT
  • Supratentorial Mass Lesions
  • Infratentorial Mass Lesions
  • Metabolic Encephalopathy
  • Psychogenic Unresponsiveness
A FINAL WORD

8. BRAIN DEATH
DETERMINATION OF BRAIN DEATH
CLINICAL SIGNS OF BRAIN DEATH
  • Brainstem Function
  • Confirmatory Laboratory Tests and Diagnosis
  • Diagnosis of Brain Death in Profound Anesthesia or Coma of Undetermined Etiology
  • Pitfalls in the Diagnosis of Brain Death

9. PROGNOSIS IN COMA AND RELATED DISORDERS OF CONSCIOUSNESS, MECHANISMS UNDERLYING OUTCOMES, AND ETHICAL CONSIDERATIONS
INTRODUCTION
PROGNOSIS IN COMA
PROGNOSIS BY DISEASE STATE
  • Traumatic Brain Injury
  • Nontraumatic Coma
  • Vascular Disease
  • Central Nervous System Infection
  • Acute Disseminated Encephalomyelitis
  • Hepatic Coma
  • Depressant Drug Poisoning
VEGETATIVE STATE
  • Clinical, Imaging, and Electrodiagnostic Correlates of Prognosis in the Vegetative State
MINIMALLY CONSCIOUS STATE
  • Late Recoveries From the Minimally Conscious State
LOCKED-IN STATE
MECHANISMS UNDERLYING OUTCOMES OF SEVERE BRAIN INJURY: NEUROIMAGING STUDIES AND CONCEPTUAL FRAMEWORKS
FUNCTIONAL IMAGING OF VEGETATIVE STATE AND MINIMALLY CONSCIOUS STATE
  • Atypical Behavioral Features in the Persistent Vegetative State
  • Neuroimaging of Isolated Cortical Responses in Persistent Vegetative State Patients
POTENTIAL MECHANISMS UNDERLYING RESIDUAL FUNCTIONAL CAPACITY IN SEVERELY DISABLED PATIENTS
  • Variations of Structural Substrates Underlying Severe Disability
  • The Potential Role of the Metabolic ‘‘Baseline’’ in Recovery of Cognitive Function
  • The Potential Role of Regionally Selective Injuries Producing Widespread Effects on Brain Function
ETHICS OF CLINICAL DECISION MAKING AND COMMUNICATION WITH SURROGATES
  • Surrogate Decision Making, Perceptions, and Needs
  • Professional Obligations and Diagnostic Discernment
  • Time-Delimited Prognostication and Evolving Brain States: Framing the Conversation
  • Family Dynamics and Philosophic Considerations
Index 


Book Details 
 
  • Hardcover: 400 pages
  • Publisher: Oxford University Press, USA; 4 edition (June 11, 2007)
  • Language: English
  • ISBN-10: 0195321316
  • ISBN-13: 978-0195321319
  • Product Dimensions: 10.3 x 7.2 x 1 inches
List Price: $84.95 
 
 

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