Книги по МРТ КТ на английском языке / PLUM AND POSNER S DIAGNOSIS OF STUPOR AND COM-1

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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 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

This chapter describes the biochemical and physiologic mechanisms (where known) by which multifocal and diffuse disorders interfere with the metabolism of the brain to produce delirium,

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

Behc¸et’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

stupor, or coma. It also describes the signs and symptoms that characterize these disorders and differentiate them from localized intracranial mass lesions and unifocal destructive lesions.

Not all of the myriad disorders that cause delirium or coma can be included. Among the criteria for selection are (1) presentation to an emergency department with the acute or subacute onset of delirium or coma without a prior history that immediately explains the cause, (2) a condition that may be reversible if treated promptly but is potentially lethal otherwise, (3) an illness with characteristic clinical or laboratory findings that strongly suggest the diagnosis, or (4) a rare and unusual disorder that may be overlooked by physicians who are rushing to establish a diagnosis and start treatment.

A physician confronted by a stuporous or comatose patient must address the question, which of the major etiologic categories of dysfunction (i.e., supratentorial, subtentorial, metabolic, or psychologic) caused the coma? Chapters 3 and 4 discuss the signs that indicate whether a patient is suffering from a structural cause (supratentorial or subtentorial) of coma. This chapter describes some of the causes of diffuse and metabolic brain dysfunction. The next chapter describes psychologic dysfunction.

The initial section of this chapter describes the clinical signs of diffuse, multifocal, or metabolic disease of the brain. Once the physician has determined that the patient’s signs and symptoms indicate such an illness, he or she must determine which of the large number of specific illnesses is responsible for this particular patient’s stupor or coma. This question often requires a rapid answer because many metabolic disorders that cause coma are fully reversible if treated early and appropriately, but lethal if treatment is delayed or is inappropriate.

Table 5–1 lists some of the diffuse, multifocal, and metabolic causes of stupor and coma. It attempts to classify these causes in such a way that the table can be used as a checklist of the major causes to be considered when the physician is presented with an unconscious patient suspected of suffering from an illness in this category. Heading A concerns itself with deprivation of oxygen, substrates, or metabolic cofactors. Headings B through E are concerned with systemic diseases that cause abnormalities of cerebral metabolism (metabolic encephalopathy). Headings F and G are concerned with primary disorders of nervous system function, which, because of their diffuse involvement of brain, resemble the metabolic encephalopathies more than they do focal structural disease.

Heading H lists a variety of miscellaneous disorders whose cause is unknown. Although they represent a heterogeneous group of disorders, the diseases listed in Table 5–1, when they cause stupor and coma, can usually be distinguished by clinical signs alone from supratentorial and infratentorial focal lesions and from psychologic disorders.

One caveat: neither the neurologic examination nor the examiner is infallible, and some patients have more than one cause for coma. Hence, even when the diagnosis of metabolic disease is absolutely unequivocal, unless the response to treatment is rapid and equally robust, imaging is an essential part of a careful workup.

CLINICAL SIGNS OF METABOLIC ENCEPHALOPATHY

Each patient with metabolic coma has a distinctive clinical picture, depending on the particular causative illness, the depth of coma, and the complications provided by comorbid illnesses or their treatment. Despite these individualities, however, specific illnesses often produce certain clinical patterns that recur again and again, and once recognized, they betray the diagnosis. A careful evaluation of consciousness, respiration, pupillary reactions, ocular movements, motor function, and the electroencephalogram (EEG) may differentiate metabolic encephalopathy from psychiatric dysfunction (Chapter 6) on the one hand, and from supratentorial or infratentorial structural disease on the other (see Chapters 3 and 4). Because these general characteristics of metabolic coma are so important, they are discussed before the specific disease entities.

CONSCIOUSNESS: CLINICAL ASPECTS

In patients with metabolic encephalopathy, stupor or coma is usually preceded by delirium. Delirium is characterized by alterations of arousal (either increased or decreased),1 disorientation, decreased short-term memory, reduced ability to maintain and shift attention, disorganized thinking, perceptual disturbances, delusions and/or hallucinations, and disorders of sleep-wake cycle.2 Some workers believe that

impairment of attention is the underlying abnormality in all acute confusional states; others emphasize clouding of consciousness as the core symptom.3 The importance of these early behavioral warnings is so great that we will review briefly some of the mental symptoms that often precede metabolic coma and, by their presence, suggest the diagnosis. The mental changes are best looked for in terms of arousal, attention, alertness, orientation and grasp, cognition, memory, affect, and perception.

Tests of Mental Status

Assessing cognitive function in patients with impairment of attention and alertness is often difficult. However, careful quantitative assessment of these functions is exceedingly important, because changes in cognition often indicate whether the physician’s therapeutic efforts are improving or worsening the patient’s condition. Several validated bedside tests that can be given in a few minutes, even to confused patients, have been developed. These tests allow one to score cognitive functions and to follow

the patient’s course in quantitative fashion.4–6 One test is specifically designed for patients in intensive care units, even those on respirators.7 Table 5–2 illustrates one such scale.

Arousal can be defined as the degree of sensory stimulation required to keep the patient attending to the examiner’s question. Patients with metabolic encephalopathy always have abnormalities of arousal. Some patients are hypervigilant, whereas in others arousal is decreased. In many delirious patients arousal alternates between hyperand hypovigilance.1 Hyperaroused patients are so distractible that they cannot maintain focus on relevant stimuli, whereas hypoaroused patients need constant sensory stimulation. In addition, most delirious patients have an altered sleep-wake cycle, often sleeping during the day but becoming more confused and hyperactive at night (‘‘sundowning’’). Abnormalities of arousal can also be reflected in motor activity, with hyperaroused patients demonstrating increased but purposeless motor activity and hypoaroused patients being relatively immobile. Although certain clinical states (i.e., drug withdrawal and fever) are more likely to produce a hyperaroused state than are other

metabolic disorders such as drug intoxication and hypoxia/ischemia, in a given patient the state of arousal is not a reliable guide in diagnosis. In general, about one-quarter of patients with delirium are hyperaroused, one-quarter are hypo-

aroused, and one-half fluctuate between the two states. Although hyperaroused patients are often diagnosed earlier because of their florid behavior, their outcome appears no different from those patients who are hypoactive.8,9

ATTENTION AND ALERTNESS

Attention is a process whereby one focuses on relevant stimuli from the environment and is able to shift focus to other stimuli as they become relevant. Most observers believe that the core of delirium as an altered state of consciousness is failure of attention. Attention is assessed by the examiner during the course of the clinical examination by determining whether a patient continues to respond in an appropriate fashion to the questions posed by the examiner. Attention is tested formally by having a patient perform a repetitive task that requires multiple iterations, such as naming the days of the week or months of the year, or a random list of numbers or serial subtractions, backwards. Failure to complete the task and even inability to name what the task was indicate inattention.

Three different disorders of attention can be identified in delirious patients. The first disorder that usually occurs in patients who are hyperaroused is distractibility. Patients shift attention from the examiner to noises in the hallway or other extraneous stimuli. A second abnormality of attention is perseveration. Patients answer a new question or respond to a new stimulus with the same response they gave to the previous stimulus, failing to redirect behavior toward the new stimulus. The third abnormality is failure to focus on an ongoing stimulus. After being distracted by another stimulus, the patient will forget to return to the activity in which he or she was engaged before distraction.

Alterations of alertness preceding other changes are more characteristic of acute or subacutely developing metabolic encephalopathy than of more slowly developing dementia; demented patients tend to lose orientation and cognition before displaying an alteration in alertness. Severe metabolic encephalopathy eventually leads to stupor and finally coma, and of course, when this point is reached, mental testing no longer helps to distinguish metabolic from other causes of brain dysfunction.

unequivocal symptoms of brain dysfunction. When examining patients suspected of metabolic or cerebral disorders, one must ask specifically the date, the time, the place, and how long it takes or the route one would take to reach home or some other well-defined place. Even uneducated patients or those with limited intellect should know the month and year, and most should know the day and date, particularly if there has been a recent holiday. Patients with early metabolic encephalopathy lose orientation for time and miss the year as frequently as the month or the day. Orientation for distance is usually impaired next, and finally, the identification of persons and places becomes confused. Disorientation for person and place but not time is unusual in structural disease but sometimes is a psychologic symptom. Disorientation for self is almost always a manifestation of psychologically induced amnesia.

COGNITION

The content and progression of thought are always disturbed in delirium and dementia, sometimes as the incipient symptoms. To detect these changes requires asking specific questions employing abstract definitions and problems. As attention and concentration are nearly always impaired, patients with metabolic brain disease usually make errors in serial subtractions, and rarely can they repeat more than three or four numbers in reverse. Thus, difficulty with mental arithmetic is not a sign necessarily of impaired calculation ability; writing the problem down, which eliminates the attentional component of the task, allows assessment of the underlying cognitive function. It is important to inventory language skills (including reading and writing), arithmetic skills, and visuospatial skills (including drawing), as well as to judge whether the patient is able to cooperate and to distinguish focal cognitive impairments (suggesting a focal lesion) from more global derangement that is seen in metabolic encephalopathy.

Although attention and arousal are the first faculties to be impaired by metabolic encephalopathies, they are difficult to quantify. As a result, defects in orientation and immediate grasp of test situations often become the earliest

Loss of recent memory for recent events and inability to retain new memories for more than a few minutes is a hallmark of dementia and a frequent accompaniment of delirium. Most patients with metabolic brain disease have a