EEG and Evoked Potentials in Psychiatry and Behavioral Neurology

John R. Hughes, William P. Wilson

• Publisher: Butterworth-Heinemann
• Year: 2013
• Print ISBN: 9780409950625
• eBook ISBN: 9781483164502
• Topic: Medicine
• Subtopic: Diseases & Allergies

EEG and Evoked Potentials in Psychiatry and Behavioral Neurology discusses the two techniques of examining brain function: electroencephalography (EEG) and evoked potentials. The book also addresses conditions that fall under the umbrella term ""behavioral sciences"" and are associated with psychiatry and neurology. The book begins by discussing current definitions of organic brain syndrome in order to delineate more clearly the processes whose EEG correlates are to be described. It then outlines the various EEG correlates of impaired central nervous system (CNS) dysfunction for a variety of specific organic etiologies. Separate chapters cover EEG studies of schizophrenia, affective disorders, alcoholism, mental retardation, childhood psychiatric disorders, and changes in CNS function caused by psychtropic drugs. The various aspects of EEG pertinent to electroconvulsive therapy are also discussed, including the role of a baseline EEG, beneficial and adverse changes, neurophysiologic mechanisms, and the nature of the seizures themselves. This book is intended for the neurologist dealing actively with psychiatric or mental disorders; the electroencephalographer who is generally concerned with behavioral neurology or especially interested in various controversial EEG patterns; and the psychiatrist interested in organicity in general or EEG in particular.

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EEG IN ORGANIC BRAIN SYNDROME

Richard D. Weiner

Publisher Summary

This chapter focuses on the use of electroencephalogram (EEG) in organic brain syndrome. EEG has always been utilized in the evaluation of patients with possible organic dysfunction of the central nervous system. The third edition of the Diagnostic and Statistical Manual (DSM-III) divides organic brain syndromes into three categories: (1) delirium, (2) dementia, and (3) specific organic syndromes. In each case, the diagnosis is ascertained by means of the clinical presentation rather than with respect to the underlying organic etiology. Delirium represents an acute or subacute state of diffuse cellular metabolic dysfunction. Its hallmark is clouding of consciousness, often present to a fluctuating degree. Dementia is an insidious neuropathologic process that disrupts higher cortical functions rather than the level of consciousness. DSM-III allows for the presence of a variety of organic brain syndromes that do not include either clouding of consciousness or loss of major intellectual abilities. These disorders include the amnestic syndrome, delusional syndrome, organic hallucinosis, organic affective syndrome, and organic personality syndrome.

The electroencephalogram (EEG) has always been utilized in the evaluation of patients with possible organic dysfunction of the central nervous system (CNS), and there still remains a good rationale for its continued use, particularly in helping to differentiate between psychiatric and neurologic disorders. This brief review outlines the various EEG correlates of impaired CNS dysfunction for a variety of specific organic etiologies. Because organic brain disease is typically prevalent in the elderly, some attention is also given to a description of EEG changes associated with the normal aging process. Before any of this can be accomplished, however, it is necessary to discuss the current definitions of organic brain syndrome so as to delineate more clearly the processes whose EEG correlates are to be described.

A DEFINITION OF ORGANIC BRAIN SYNDROME

Current psychiatric nomenclature, as typified by the third edition of the Diagnostic and Statistical Manual, or DSM-III, (APA, 1980) divides organic brain syndromes into three categories: delirium, dementia, and specific organic syndromes. In each case, the diagnosis is ascertained by means of the clinical presentation, rather than with respect to the underlying organic etiology. This was done in order to simplify diagnosis and represents a clear departure from previous diagnostic systems.

Delirium

Delirium represents an acute or subacute state of diffuse cellular metabolic dysfunction. Its hallmark is clouding of consciousness, often present to a fluctuating degree. If testable, evidence of both disorientation and memory impairment is also present. In addition, at least two of the following symptoms must occur: perceptual disturbance, incoherent speech, disturbance of the sleep-wake cycle, or altered psychomotor activity. Finally, there must be evidence from the medical history or from the physical or laboratory examination of a specific etiologic factor.

Delirium appears to be both a relatively common and an underreported clinical entity. Lipowski (1980) reported its occurrence in 5 to 10% of hospitalized medical/surgical patients, and Robinson (1956) has suggested that for hospitalized geriatric patients its prevalence may be as high as 40%. As we shall see, the use of the EEG is particularly indicated in the evaluation of delirium, where it is nearly always abnormal and where its level of abnormality is often well correlated with the level of clinical impairment.

Dementia

Unlike delirium, dementia is an insidious neuropathologic process, which disrupts higher cortical functions rather than the level of consciousness (Wells, 1977, 1978; McEvoy, 1981). This impairment in higher cortical function may take the form of any or all of the following: diminished capacity for abstraction, poor judgment, aphasia, apraxia, agnosia, and personality change. As with delirium, memory dysfunction must also be present. Although the presence of an objectively defined organic etiology is helpful, it is not required for the diagnosis of dementia (APA, 1980).

Dementia is a very common disorder among the elderly. It has been estimated, for example, that 1,000,000 Americans over the age of 65 years are so afflicted (McEvoy, 1981). Over 50% of cases of dementia are secondary to senile or presenile pathologic changes of the Alzheimer type, with the second most prevalent etiology being that of a vascular nature (multi-infarct dementia). Although in the past some have attempted to discriminate delirium and dementia on the basis of the reversibility of the underlying disease process, it is now clear that such is not the case. Although delirium is more likely to be associated with a reversible etiology, Wells (1978) has pointed out that 15% of dementias are also potentially reversible and that a further 20 to 25% of cases, for example, in which the dementia is secondary to hypertension, thromboembolic disease, drug abuse, infections, brain tumors, and normal pressure hydrocephalus (NPH), can be medically palliated. Finally it should be pointed out that delirium and dementia often coexist and that the occurrence of one does not therefore preclude the presence of the other.

Specific Organic Syndromes

DSM-III (APA, 1980) allows for the presence of a variety of organic brain syndromes that do not include either clouding of consciousness or loss of major intellectual abilities. In each case, however, objective evidence for the presence of a specific organic etiologic factor must be present. These disorders include the following: amnestic syndrome (Benson, 1978), delusional syndrome, organic hallucinosis, organic affective syndrome, and organic personality syndrome. In each case the nomenclature makes clear the descriptive nature of the clinical presentation. The specific organic syndromes are less common than either delirium or dementia and are less likely to be associated with EEG changes.

THE GENERAL ROLE OF EEG IN EVALUATION OF ORGANIC BRAIN SYNDROMES

EEG changes associated with organic brain syndromes are typically nonspecific, the most common effects being generalized regular and irregular slowing. Exceptions to the nonspecificity rule include Jakob-Creutzfeldt disease, herpes encephalitis, hepatic encephalopathy, and some types of drug intoxication, all of which will be discussed later. Although EEG changes frequently occur in organic brain syndromes, such changes, particularly in the early stage of the disease, may not reflect a clearly discernible shift to an abnormal morphology (Pro and Wells, 1977). For this reason the use of serial EEGs in the evaluation of such disorders is highly indicated.

It is not surprising that delirium, which represents an acute and diffuse cerebral metabolic impairment sufficient to disrupt consciousness to some degree, also disrupts the scalp-recorded manifestations of cerebral neurophysiologic functioning. Romano and Engel (1944) were among the first to show not only that the presence and degree of EEG slowing were correlated with clinical impairment in delirious patients, but also that decreases in the level of slowing correlated well with improvement in behavioral function. Since then, these findings have in general been corroborated (e.g., Engel and Romano, 1959; Lipowsky, 1967). With dementia, such a correlation between severity of clinical impairment and degree of EEG changes is less impressive. Kiloh et al (1981) have attempted to explain this on the basis of the acuteness of the underlying disease process, claiming that the extent of EEG abnormality appears to be related more to the rate of progress of the dementia than to the degree. Harner (1975), on the other hand, has suggested that the presence of EEG abnormality may be a measure of the potential reversibility of the condition. Still, it is probably unwise to generalize such claims to individual cases at the present time, given the relative absence of definitive research data.

Markand (1979) has provided a rough gradation of EEG changes with respect to behavioral level of CNS dysfunction. With only mild behavioral impairment, the initial EEG changes consist of slowing of the posterior alpha rhythm, followed by generalization of theta slowing, decrease in the level of EEG reactivity, and, finally, loss of fast (alpha and beta) activity along with a buildup in diffuse very slow (delta) activity. A moderate level of behavioral impairment, according to such a schema, is heralded by fluctuating amounts of frontal intermittent rhythmic delta activity (FIRDA) superimposed upon a slow background, whereas with severe impairment, such as that seen in comatose states, low-voltage irregular delta activity is typically seen, along with suppression-burst activity as the disease continues to progress.

Markand points out that such findings may prove helpful in a variety of etiologic discriminations, e.g., generalized versus focal disease and epileptic versus nonepileptic states. Such use is often extremely valuable; still, one must keep in mind the occurrence of exceptions. The presence of focal EEG findings does not necessarily rule out the presence of a primary generalized disturbance such as delirium or dementia, as a diffuse cerebral metabolic impairment, for example, can easily bring subliminal focal alterations to the fore. Similarly, focal disease, such as an acute hemispheric infarct, may initially present with diffuse EEG findings. Furthermore, the presence of epileptiform activity, even focal in distribution, may occur with certain types of nonepileptic disorders, whether metabolic or structural. Finally, postictal states in epileptics, and occasionally even the ictal episodes themselves, may be marked by EEG slowing rather than by distinct sharp-contoured epileptiform EEG transients.

A correlation between the nature of EEG changes and the distribution of neuropathologic alterations has been postulated for degenerative encephalopathies by Gloor et al (1968). According to this hypothesis, diseases involving only the cortical gray matter, like Alzheimer and Pick disease, present primarily with low-voltage irregular slowing, ...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• PREFACE
• CONTRIBUTING AUTHORS
• Chapter 1: EEG IN ORGANIC BRAIN SYNDROME
• Chapter 2: EEG IN SCHIZOPHRENIA
• Chapter 3: EEG IN AFFECTIVE DISORDERS
• Chapter 4: EEG, ALCOHOL, AND ALCOHOLISM
• Chapter 5: EEG AND PSYCHOTROPIC DRUGS
• Chapter 6: EEG RELATED TO ELECTROCONVULSIVE THERAPY
• Chapter 7: ELECTROENCEPHALOGRAPHIC SLEEP CHANGES IN PSYCHIATRIC PATIENTS
• Chapter 8: CONTINGENT NEGATIVE VARIATION AND OTHER SLOW POTENTIALS IN ADULT PSYCHIATRY
• Chapter 9: EVOKED POTENTIALS IN ADULT PSYCHIATRY
• Chapter 10: EEG AND EVOKED POTENTIALS IN LEARNING DISABILITIES
• Chapter 11: EEG IN MENTAL RETARDATION
• Chapter 12: EEG IN CHILDHOOD PSYCHIATRIC DISORDERS
• Chapter 13: A REVIEW OF THE POSITIVE SPIKE PHENOMENON: RECENT STUDIES
• Chapter 14: A REVIEW OF THE 6/SEC SPIKE AND WAVE COMPLEX
• Chapter 15: A REVIEW OF SMALL SHARP SPIKES
• Chapter 16: THE MEDICOLEGAL EEG
• INDEX