Книги по МРТ КТ на английском языке / PLUM AND POSNER S DIAGNOSIS OF STUPOR AND COM-1
.pdfxContents
MAJOR LABORATORY DIAGNOSTIC AIDS 77
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 88
COMPRESSIVE LESIONS AS A CAUSE OF COMA 89
COMPRESSIVE LESIONS MAY DIRECTLY DISTORT THE AROUSAL SYSTEM 90
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 95
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 114 DIFFUSE, BILATERAL CORTICAL DESTRUCTION 114 DESTRUCTIVE DISEASE OF THE DIENCEPHALON 114 DESTRUCTIVE LESIONS OF THE BRAINSTEM 115
4.SPECIFIC CAUSES OF STRUCTURAL COMA 119
INTRODUCTION 120
SUPRATENTORIAL COMPRESSIVE LESIONS 120
EPIDURAL, DURAL, AND SUBDURAL MASSES 120
Epidural Hematoma Subdural Hematoma Epidural Abscess/Empyema Dural and Subdural Tumors
SUBARACHNOID LESIONS 129
Subarachnoid Hemorrhage Subarachnoid Tumors Subarachnoid Infection
INTRACEREBRAL MASSES 135
Intracerebral Hemorrhage Intracerebral Tumors Brain Abscess and Granuloma
INFRATENTORIAL COMPRESSIVE LESIONS 142
EPIDURAL AND DURAL MASSES 143
Epidural Hematoma Epidural Abscess Dural and Epidural Tumors
SUBDURAL POSTERIOR FOSSA COMPRESSIVE LESIONS 144
Subdural Empyema Subdural Tumors
Contents xi
SUBARACHNOID POSTERIOR FOSSA LESIONS 145
INTRAPARENCHYMAL POSTERIOR FOSSA MASS LESIONS 145
Cerebellar Hemorrhage Cerebellar Infarction Cerebellar Abscess Cerebellar Tumor Pontine Hemorrhage
SUPRATENTORIAL DESTRUCTIVE LESIONS CAUSING COMA 151
VASCULAR CAUSES OF SUPRATENTORIAL
DESTRUCTIVE LESIONS 152
Carotid Ischemic Lesions Distal Basilar Occlusion Venous Sinus
Thrombosis Vasculitis
INFECTIONS AND INFLAMMATORY CAUSES OF SUPRATENTORIAL DESTRUCTIVE LESIONS 156
Viral Encephalitis Acute Disseminated Encephalomyelitis
CONCUSSION AND OTHER TRAUMATIC BRAIN INJURIES 159
Mechanism of Brain Injury During Closed Head Trauma Mechanism of Loss of Consciousness in Concussion Delayed Encephalopathy After Head Injury
INFRATENTORIAL DESTRUCTIVE LESIONS 162
BRAINSTEM VASCULAR DESTRUCTIVE DISORDERS 163
Brainstem Hemorrhage Basilar Migraine Posterior Reversible
Leukoencephalopathy Syndrome
INFRATENTORIAL INFLAMMATORY DISORDERS 169
INFRATENTORIAL TUMORS 170
CENTRAL PONTINE MYELINOLYSIS 171
5.MULTIFOCAL, DIFFUSE, AND METABOLIC BRAIN DISEASES CAUSING DELIRIUM, STUPOR, OR COMA 179
CLINICAL SIGNS OF METABOLIC ENCEPHALOPATHY 181
CONSCIOUSNESS: CLINICAL ASPECTS 181
Tests of Mental Status Pathogenesis of the Mental Changes
RESPIRATION 187
Neurologic Respiratory Changes Accompanying Metabolic Encephalopathy Acid-Base Changes Accompanying Hyperventilation During Metabolic Encephalopathy Acid-Base Changes Accompanying Hypoventilation During Metabolic Encephalopathy
PUPILS 192
OCULAR MOTILITY 193
MOTOR ACTIVITY 194
‘‘Nonspecific’’ Motor Abnormalities Motor Abnormalities Characteristic of Metabolic Coma
DIFFERENTIAL DIAGNOSIS 197
Distinction Between Metabolic and Psychogenic Unresponsiveness Distinction Between Coma of Metabolic and Structural Origin
xii Contents
ASPECTS OF CEREBRAL METABOLISM PERTINENT
TO COMA 198
CEREBRAL BLOOD FLOW 198
GLUCOSE METABOLISM 202
Hyperglycemia Hypoglycemia
ANESTHESIA 205
MECHANISMS OF IRREVERSIBLE ANOXIC-ISCHEMIC
BRAIN DAMAGE 206
Global Ischemia Focal Ischemia Hypoxia
EVALUATION OF NEUROTRANSMITTER CHANGES IN
METABOLIC COMA 208
Acetylcholine Dopamine Gamma-Aminobutyric
Acid Serotonin Histamine Glutamate Norepinephrine
SPECIFIC CAUSES OF METABOLIC COMA 210
ISCHEMIA AND HYPOXIA 210
Acute, Diffuse (or Global) Hypoxia or Ischemia Intermittent or Sustained Hypoxia Sequelae of Hypoxia
DISORDERS OF GLUCOSE OR COFACTOR AVAILABILITY 220
Hypoglycemia Hyperglycemia Cofactor Deficiency
DISEASES OF ORGAN SYSTEMS OTHER THAN BRAIN 224
Liver Disease Renal Disease Pulmonary Disease Pancreatic Encephalopathy Diabetes Mellitus Adrenal Disorders Thyroid Disorders Pituitary Disorders Cancer
EXOGENOUS INTOXICATIONS 240
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 251
Hypo-osmolar States Hyperosmolar States Calcium Other Electrolytes Disorders of Systemic Acid-Base Balance
DISORDERS OF THERMOREGULATION 259
Hypothermia Hyperthermia
INFECTIOUS DISORDERS OF THE CENTRAL NERVOUS
SYSTEM: BACTERIAL 262
Acute Bacterial Leptomeningitis Chronic Bacterial Meningitis
INFECTIOUS DISORDERS OF THE CENTRAL NERVOUS SYSTEM: VIRAL 266
Overview of Viral Encephalitis Acute Viral Encephalitis Acute Toxic Encephalopathy During Viral Encephalitis Parainfectious Encephalitis (Acute Disseminated Encephalomyelitis) Cerebral Biopsy
for Diagnosis of Encephalitis
Contents xiii
CEREBRAL VASCULITIS AND OTHER VASCULOPATHIES 273
Granulomatous Central Nervous System Angiitis Systemic Lupus Erythematosus Subacute Diencephalic Angioencephalopathy Varicella-Zoster Vasculitis Behc¸et’s Syndrome Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy
MISCELLANEOUS NEURONAL AND GLIAL DISORDERS 276
Prion Diseases Adrenoleukodystrophy (Schilder’s Disease) Marchiafava-Bignami Disease Gliomatosis Cerebri Progressive Multifocal Leukoencephalopathy Epilepsy Mixed Metabolic Encephalopathy
ACUTE DELIRIOUS STATES 282
Drug Withdrawal Delirium (Delirium Tremens) Postoperative Delirium Intensive Care Unit Delirium Drug-Induced Delirium
6.PSYCHOGENIC UNRESPONSIVENESS 297
CONVERSION REACTIONS 299 CATATONIA 302 PSYCHOGENIC SEIZURES 304
CEREBELLAR COGNITIVE AFFECTIVE SYNDROME 306 ‘‘AMYTAL INTERVIEW’’ 307
7. APPROACH TO MANAGEMENT OF THE UNCONSCIOUS PATIENT 309
A CLINICAL REGIMEN FOR DIAGNOSIS AND MANAGEMENT 309
PRINCIPLES OF EMERGENCY MANAGEMENT 311
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 317
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 320
Supratentorial Mass Lesions Infratentorial Mass Lesions Metabolic
Encephalopathy Psychogenic Unresponsiveness
A FINAL WORD 327
8.BRAIN DEATH 331
DETERMINATION OF BRAIN DEATH 331
CLINICAL SIGNS OF BRAIN DEATH 333
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
xivContents
9.PROGNOSIS IN COMA AND RELATED DISORDERS OF CONSCIOUSNESS, MECHANISMS UNDERLYING OUTCOMES, AND ETHICAL CONSIDERATIONS 341
INTRODUCTION 342 PROGNOSIS IN COMA 343
PROGNOSIS BY DISEASE STATE 344
Traumatic Brain Injury Nontraumatic Coma Vascular Disease Central Nervous System Infection Acute Disseminated Encephalomyelitis Hepatic Coma Depressant Drug Poisoning
VEGETATIVE STATE 357
Clinical, Imaging, and Electrodiagnostic Correlates of Prognosis in the Vegetative State
MINIMALLY CONSCIOUS STATE 360
Late Recoveries From the Minimally Conscious State
LOCKED-IN STATE 363
MECHANISMS UNDERLYING OUTCOMES OF SEVERE BRAIN INJURY: NEUROIMAGING STUDIES AND CONCEPTUAL FRAMEWORKS 364
FUNCTIONAL IMAGING OF VEGETATIVE
STATE AND MINIMALLY CONSCIOUS STATE 365
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 372
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 (J.J. FINS) 376
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 387
PLUM AND POSNER’S DIAGNOSIS OF STUPOR AND COMA
Fourth Edition
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Chapter 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 AND 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
ALTERED STATES OF
CONSCIOUSNESS
And men should know that from nothing else but from the brain came joys, delights, laughter and jests, and sorrows, griefs, despondency and lamentations. And by this, in an especial manner, we acquire wisdom and knowledge, and see and hear and know what are foul, and what are fair, what sweet and what unsavory . . .
—The Hippocratic Writings
Impaired consciousness is among the most difficult and dramatic of clinical problems. The ancient Greeks knew that normal consciousness depends on an intact brain, and that impaired consciousness signifies brain failure. The brain tolerates only limited physical or metabolic injury, so that impaired consciousness is often a sign of impending irreparable damage to the brain. Stupor and coma imply advanced brain failure, just as, for example, uremia means renal failure, and the longer such brain failure lasts,
3
4Plum and Posner’s Diagnosis of Stupor and Coma
the narrower the margin between recovery and the development of permanent neurologic injury. The limited time for action and the multiplicity of potential causes of brain failure challenge the physician and frighten both the physician and the family; only the patient escapes anxiety.
Many conditions cause coma. Table 1–1 lists some of the common and often perplexing causes of unconsciousness that the physician may encounter in the emergency department of a general hospital. The purpose of this mono-
graph is to describe a systematic approach to the diagnosis of the patient with reduced consciousness, stupor, or coma based on anatomic and physiologic principles. Accordingly, this book divides the causes of unconsciousness into two major categories: structural and metabolic. Chapter 1 provides background information on the pathophysiology of impaired consciousness, as well as the signs and symptoms that accompany it. In Chapter 2 this information is used to define a brief but informative neurologic examination that is necessary to
Table 1–1 Cause of Stupor or Coma in 500 Patients Initially Diagnosed as ‘‘Coma of Unknown Etiology’’*
|
|
Subtotals |
|
|
|
Subtotals |
|
|
|
|
|
||
I. Supratentorial lesions |
101 |
|
B. Destructive or ischemic lesions |
53 |
||
A. Rhinencephalic and subcortical |
2 |
|
1. Pontine hemorrhage |
11 |
||
destructive lesions |
|
2. |
Brainstem infarct |
40 |
||
1. Thalamic infarcts |
2 |
3. |
Basilar migraine |
1 |
||
B. Supratentorial mass lesions |
99 |
4. |
Brainstem demyelination |
1 |
||
1. Hemorrhage |
76 |
III. Diffuse and/or metabolic |
326 |
|||
|
a. Intracerebral |
44 |
|
brain dysfunction |
|
|
|
(1) Hypertensive |
36 |
|
A. Diffuse intrinsic disorders of brain |
38 |
|
|
(2) Vascular anomaly |
5 |
|
1. ‘‘Encephalitis’’ or |
14 |
|
|
(3) Other |
3 |
|
|
encephalomyelitis |
|
|
b. Epidural |
4 |
2. |
Subarachnoid hemorrhage |
13 |
|
|
c. Subdural |
26 |
3. |
Concussion, nonconvulsive |
9 |
|
|
d. Pituitary apoplexy |
2 |
|
|
seizures, and postictal states |
|
2. |
Infarction |
9 |
4. |
Primary neuronal disorders |
2 |
|
|
a. Arterial occlusions |
7 |
|
B. Extrinsic and metabolic |
288 |
|
|
(1) Thrombotic |
5 |
|
disorders |
|
|
|
(2) Embolic |
2 |
|
1. Anoxia or ischemia |
10 |
|
|
b. Venous occlusions |
2 |
2. |
Hypoglycemia |
16 |
|
3. |
Tumors |
7 |
3. |
Nutritional |
1 |
|
|
a. Primary |
2 |
4. |
Hepatic encephalopathy |
17 |
|
|
b. Metastatic |
5 |
5. |
Uremia and dialysis |
8 |
|
4. |
Abscess |
6 |
6. |
Pulmonary disease |
3 |
|
|
a. Intracerebral |
5 |
7. |
Endocrine disorders |
12 |
|
|
b. Subdural |
1 |
|
|
(including diabetes) |
|
5. |
Closed head injury |
1 |
8. |
Remote effects of cancer |
0 |
|
II. Subtentorial lesions |
65 |
9. |
Drug poisons |
149 |
||
A. Compressive lesions |
12 |
10. |
Ionic and acid-base disorders |
12 |
||
1. |
Cerebellar hemorrhage |
5 |
11. |
Temperature regulation |
9 |
|
2. |
Posterior fossa subdural or |
1 |
12. |
Mixed or nonspecific |
1 |
|
|
extradural hemorrhage |
|
|
|
metabolic coma |
|
3. |
Cerebellar infarct |
2 |
|
IV. Psychiatric ‘‘coma’’ |
8 |
|
4. |
Cerebellar tumor |
3 |
|
A. Conversion reactions |
4 |
|
5. |
Cerebellar abscess |
1 |
|
B. Depression |
2 |
|
6. |
Basilar aneurysm |
0 |
|
C. Catatonic stupor |
2 |
|
*Represents only patients for whom a neurologist was consulted because the initial diagnosis was uncertain and in whom a final diagnosis was established. Thus, obvious diagnoses such as known poisonings, meningitis, and closed head injuries, and cases of mixed metabolic encephalopathies in which a specific etiologic diagnosis was never established are underrepresented.
Pathophysiology of Signs and Symptoms of Coma |
5 |
determine if the reduced consciousness has a structural cause (and therefore may require immediate imaging and perhaps surgical treatment) or a metabolic cause (in which case the diagnostic approach can be more lengthy and extensive). Chapters 3 and 4 discuss pathophysiology and specific causes of structural injury to the brain that result in defects of consciousness. Chapter 5 examines the broad range of metabolic causes of unconsciousness, and the specific treatments they require. Chapter 6 explores psychiatric causes of unresponsiveness, which must be differentiated from organic causes of stupor and coma. Chapter 7 provides a systematic discussion of the treatment of both structural and metabolic coma. Chapter 8 explores the outcomes of coma of different causes, including the prognosis for useful recovery and the states of long-term impairment of consciousness. Chapter 9 reviews some ethical problems encountered in treating unconscious individuals.
DEFINITIONS
Consciousness
Consciousness is the state of full awareness of the self and one’s relationship to the environment. Clinically, the level of consciousness of a patient is defined operationally at the bedside by the responses of the patient to the examiner. It is clear from this definition that it is possible for a patient to be conscious yet not responsive to the examiner, for example, if the patient lacks sensory inputs, is paralyzed (see lockedin syndrome, page 7), or for psychologic reasons decides not to respond. Thus, the determination of the state of consciousness can be a technically challenging exercise. In the definitions that follow, we assume that the patient is not unresponsive due to sensory or motor impairment or psychiatric disease.
Consciousness has two major components: content and arousal. The content of consciousness represents the sum of all functions mediated at a cerebral cortical level, including both cognitive and affective responses. These functions are subserved by unique networks of cortical neurons, and it is possible for a lesion that is strategically placed to disrupt one of the networks, causing a fractional loss of conscious-
ness.1 Such patients may have preserved awareness of most stimuli, but having suffered the loss of a critical population of neurons (e.g., for recognizing language symbol content, differences between colors or faces, or the presence of the left side of space), the patient literally becomes unconscious of that class of stimuli. Patients with these deficits are often characterized as ‘‘confused’’ by inexperienced examiners, because they do not respond as expected to behavioral stimuli. More experienced clinicians recognize the focal cognitive deficits and that the alteration of consciousness is confined to one class of stimuli. Occasionally, patients with right parietotemporal lesions may be sufficiently inattentive as to appear to be globally confused, but they are not sleepy and are, in fact, usually agitated.2
Thus, unless the damage to cortical networks is diffuse or very widespread, the level of consciousness is not reduced. For example, patients with advanced Alzheimer’s disease may lose memory and other cognitive functions, but remain awake and alert until the damage is so extensive and severe that response to stimuli is reduced as well (see vegetative state, page 8). Hence, a reduced level of consciousness is not due to focal impairments of cognitive function, but rather to a global reduction in the level of behavioral responsiveness. In addition to being caused by widespread cortical impairment, a reduced level of consciousness can result from injury to a specific set of brainstem and diencephalic pathways that regulate the overall level of cortical function, and hence consciousness (Figure 1–1). The normal activity of this arousal system is linked behaviorally to the appearance of wakefulness. It should be apparent that cognition is not possible without a reasonable degree of arousal.
Sleep is a recurrent, physiologic, but not pathologic, form of reduced consciousness in which the responsiveness of brain systems responsible for cognitive function is globally reduced, so that the brain does not respond readily to environmental stimuli. Pathologic alteration of the relationships between the brain systems that are responsible for wakefulness and sleep can impair consciousness. The systems subserving normal sleep and wakefulness are reviewed later in this chapter. A key difference between sleep and coma is that sleep is intrinsically reversible: sufficient stimulation will return the individual to a normal waking state. In contrast, if patients