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EEG and Evoked Potentials in Psychiatry and Behavioral Neurology

EEG and Evoked Potentials in Psychiatry and Behavioral Neurology

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EEG and Evoked Potentials in Psychiatry and Behavioral Neurology

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750 pages
Oct 22, 2013


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.
Oct 22, 2013

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EEG and Evoked Potentials in Psychiatry and Behavioral Neurology - Elsevier Science




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.


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 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.


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.


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, while cerebral white matter diseases, like multifocal leukoencephalopathy, present with high-voltage polymorphic delta activity. Conditions such as Jakob-Creutzfeldt disease, which affect both cortical and subcortical gray matter, on the other hand, present with either FIRDA or bilaterally synchronous epileptiform complexes. Although such pathophysiologic correlates are conceptually appealing, their general utility in the practice of clinical EEG remains rather limited.


The EEG is often very useful in discriminating between a functional and an organic etiology for mental status changes, particularly when supplemented by a good clinical history. A common case is that of depressive pseudodementia, where an apparent dense organic brain syndrome may instead represent an atypical manifestation of affective disorder. Patients with conversion disorders may not only mimic cases of focal neurologic disease, for example with symptoms of hemiplegia or visual disturbances, but can also present with confusion, disorientation, memory disturbances, and diminished cognitive performance. This is even more likely to be the case with functional dissociative reactions, where such symptomatology may occur in conjunction with hysterical seizures, pseudocoma, or fugue states. It must also be remembered, as mentioned earlier, that psychotic, affective, and characterologic impairment may reflect an organic etiology in addition to the usual functional correlates.

In most such cases, at least with a history of acute onset, a normal EEG is consistent with a functional cause, whereas an abnormal EEG indicates the presence of organicity. Although the discriminative capacity of the EEG is generally high in these circumstances, a couple of exceptions should be noted. The first is the possibility that an organic brain syndrome and functional disorder coexist, as in a mildly demented patient with a major depressive episode. Second, some types of delirium (e.g., alcohol withdrawal) and dementia (e.g., senility) may not be associated with distinct EEG abnormalities. Keeping these caveats in mind will greatly increase the usefulness of the EEG in this regard. It is true that the majority of psychiatric patients do not require an EEG, but the use of this noninvasive and relatively inexpensive evaluative tool is certainly indicated when the possibility of organic brain dysfunction is being considered.


Since most common types of organic brain disease occur more often in the elderly, it is important to consider first what types of EEG changes are associated with the normal aging process; otherwise discriminating between normal and abnormal EEG patterns may prove difficult. In the 1950s and 1960s, Busse, Obrist, and coworkers carried out careful longitudinal studies (reviewed by Obrist and Busse, 1965, and Obrist, 1976) which served to dispel the prevalent myth, based upon studies involving an ill elderly population, that abnormal EEGs were consistent with normal aging. They found instead that diffuse slowing was not seen in elderly persons with normal cognitive functioning and that, although the predominant posterior alpha frequency does in fact decrease with age, particularly over the ninth decade, it generally remains 8 Hz. More recently Hubbard et al (1976) reported similar findings for a cohort of centenarians.

A specific age-dependent EEG finding of these investigators, however, is the presence of brief runs of irregular focal anterior temporal slowing in the theta and delta range, particularly on the left, occasionally mixed with some sharp components (Busse and Obrist, 1963). This focal slowing was seen in 30 to 40% of normal volunteers aged over 60 years but did not appear to increase in incidence with further aging. It was also found to be maximal during drowsiness and to disappear during sleep. As no correlation between focal slowing and intellectual or cognitive functioning could be demonstrated, it was concluded that such changes, when present to a mild degree, should not be considered pathologic in this population. Continuous levels of anterior temporal slowing, or focal slowing with alternative topographic distributions do appear to be associated with focal CNS disease, however.

A further characteristic of the normal elderly EEG is the relative integrity of anterior irregular beta activity in the frequency band of 18 to 30 Hz. The occurrence of this activity increases during early adulthood to plateau during middle age. Mundy-Castle et al (1954), among others, specifically point this out as a means of discrimination between normal and senile elderly, particularly as prominent slowing is not always a feature of the latter.

Finally it has been reported that the EEG in normal elderly persons shows a decreased reactivity to sensory stimulation, particularly with respect to the posterior alpha rhythm (Obrist and Busse, 1965). Consistent with this is the finding that photic recruiting responses appear to diminish with age, as does the EEG response to hyperventilation.


Senile and Presenile Dementia of the Alzheimer Type

Senile dementia represents the most common type of organic brain syndrome encountered in clinical practice. It is now generally recognized that the only clinical differences between senile and presenile dementia of the Alzheimer type relate to age of onset and rapidity of course, the presenile variety showing a more fulminant progression. This is indeed true for EEG changes as well, with virtually all patients with presenile dementia demonstrating pathologic EEG activity on the initial recording (Letemendia and Pampiglione, 1958; Gordon and Sim, 1967). With early, and occasionally even late, senile dementia, EEG changes, though often present, may not yet be in the pathologic range.

The earliest EEG alterations with senile or presenile dementia are a decrease in the frequency of the posterior rhythm along with diminution of the amplitude of all background activity (Harner, 1975). Later, a buildup of generalized irregular slowing and disappearance of fast activity can be seen (Weiner and Schuster, 1956), though it should be noted that the appearance of such changes often lags behind deterioration in the clinical presentation. In severely demented patients, paroxysmal or even triphasic patterns may occasionally be seen. Focal slowing is uncommon, being present in only 10% of the cases.

The presence and extent of generalized slowing and also the disappearance of fast activity both appear to be correlated with the degree of cognitive deterioration. In addition, there is some evidence that they may also serve as prognostic measures, particularly with respect to life expectancy (Obrist and Henry, 1958). The degree of slowing, however, also appears to be related to the speed at which the dementia is progressing, with very insidious cases tending to show the least such changes. The occurrence of positive findings on neurologic examination also appears to be associated with greater amounts of EEG slowing.

Although it is easy to discriminate normal and demented elderly on the basis of such EEG changes on a group basis (Soininen et al, 1982), such a determination may prove difficult in individual cases. Harner (1975) has suggested instead that the utility of the EEG in senile demented patients is to alert the clinician to the presence of an underlying toxic or metabolic disorder in cases where marked EEG changes are present early in the course, or to discriminate between organic and functional etiologies when a normal EEG is recorded alongside of fulminant cognitive alterations.

Both senile and presenile Alzheimer disease also affect the sleep EEG to some degree. At some point during its progression, again particularly with presenile dementia, sleep spindles, K-complexes, and even the sleep stage itself often becomes disrupted. In addition, the slowing seen during the waking state is accentuated by drowsiness, as was described earlier for age-related slowing.

The degree of EEG slowing in demented patients is well correlated with objective measures of cognitive deterioration (Obrist and Busse, 1965). A similar correlation with respect to pathologic changes, specifically regarding ventricular enlargement, however, has not yet been demonstrated, although this may relate to the fact that only advanced cases were considered in the study which undertook such a comparison (Stefoski et al, 1976). The use of hyperbaric oxygenation appears to affect neither the cognitive changes nor the EEG abnormalities associated with Alzheimer disease. Finally, it should be noted that although patients with Alzheimer disease usually present with coarse diffuse dementive symptomatology, the disorder may occasionally be at least initially manifested by an organic delusional or personality syndrome.

Other Degenerative Disorders

Pick disease, which selectively affects frontal regions rather than the more diffuse pattern of Alzheimer disease, is much less likely to be associated with EEG pathology. Gordon and Sim (1967) found, for example, that only one-third of Pick patients had abnormal EEGs as opposed to all those with presenile Alzheimer disease.

The EEG hallmark of Huntington disease is a gradual flattening of the EEG to the point where only very low voltage irregular theta and delta activity is present (Shista et al, 1974), although this is not invariably the case. The degree to which this phenomenon occurs appears to correlate well with the extent of cortical atrophy (Scott et al, 1972). The disruption of sleep spindles and K-complexes with Huntington disease is even greater than that seen in Alzheimer patients. A relatively frequent occurrence in Huntington cases is for the disorder to present initially as an organic personality syndrome.

Approximately half of the patients with Wilson disease have abnormal EEGs (Westmoreland et al, 1974). This is manifested by both generalized irregular and paroxysmal slowing except when significant hepatic dysfunction is present, in which case triphasic EEG complexes may be seen. There does not appear to be a good correlation between EEG changes and degree of clinical symptomatology. EEG findings with cerebellar degeneration consist of the same nonspecific pattern of generalized EEG slowing, but again, these are not seen consistently.

Patients with certain forms of progressive myoclonus epilepsy typically develop seizures during adolescence followed by an evolving dementive picture over the next 2 to 10 years. Along with nonspecific regular and irregular slowing, the EEG in such cases often also displays bilaterally synchronous epileptiform activity of various morphologies (Janeway et al, 1967). In addition, markedly elevated somatosensory evoked potentials may be seen (Halliday, 1967).

Many patients with Parkinson disease also present with dementia. In addition, Hirano et al (1961) have reported a specific Parkinson/dementia syndrome prevalent on the island of Guam. The EEG is reported to be abnormal in 36% of those with Parkinson disease (Yeager et al, 1966). Again, the most typical finding is generalized slowing, although occasional focal frontotemporal slowing may also occur. Patients who have had stereotactic surgery for treatment of this disorder are more likely to demonstrate EEG changes. A decreased amount of slow-wave sleep is also often seen with Parkinson disease. When recording the EEG in patients with this condition, one should be careful to keep in mind the 4- to 5-Hz tremor artifact which is frequently present.

Multiple sclerosis (MS), particularly late in the disease, often presents with dementia or one of the specific organic brain syndromes. The EEG is abnormal in 50% of MS patients, revealing either focal or generalized slowing but is never found to be abnormal in the absence of CNS symptomatology (Hoefer and Guttman, 1944). The recent utilization of sensory evoked potentials has demonstrated a far greater applicability for these techniques in the evaluation of MS patients than does the standard EEG.


The discrimination between senile or presenile Alzheimer disease and multi-infarct dementia is generally made on the basis of clinical course and objective evidence of underlying cerebrovascular disease. The multiple small infarcts associated with the typical stairstep deterioration reported with multi-infarct dementia may be manifested in the EEG by either focal or generalized slowing or by both. The presence of focal EEG findings in a demented patient therefore strongly indicates the presence of a multi-infarct dementia rather than Alzheimer disease (Soininen et al, 1982). The degree to which EEG abnormalities are seen depends upon the amount of cortex involved, the extent to which the region is adjacent to scalp electrodes, and the potency of collateral circulation (Wilson et al, 1977). Occasionally a delirious state may occur, and in such cases frontal intermittent rhythmic delta activity (FIRDA) may be seen to coexist with generalized slowing. Van der Drift (1972) has speculated that this may reflect anterior diencephalic ischemia.

Cerebral infarctions may present with either dementia or delirium. In clearly demarcated focal lesions, slowing of relatively high amplitude can be seen initially, gradually diminishing in amplitude and anatomic extent over time. With a more massive hemispheric infarct (carotid/middle cerebral artery circulation), generalized slowing is initially present, with focal or hemispheric findings often not observed until later in the course. Occasionally, however, the only EEG changes to occur may consist of low-voltage slowing and/or suppression of fast activity. Particularly if infarcts have occurred previously, accurate localization or even lateralization on the basis of the EEG may be difficult (Birchfield et al, 1959). Still, lateralization can be made in approximately 80% of cases. An additional EEG finding seen with acute severe hemispheric infarcts is periodic lateralized epileptiform discharges (PLEDs), which are a transient phenomenon consisting of regularly occurring complexes with a hemispheric predominance (Chatrian et al, 1964). Vertebral or basilar artery infarcts are much less likely to be associated with EEG abnormalities (Phillips, 1964). When EEG changes are seen, they usually consist of either bilateral posterior theta activity (Birchfield et al, 1959) or asymmetrical attenuation of background activity.

Acute subdural hematomas, particularly if large, may be accompanied by a delirious state, whereas late in the course a dementive syndrome may be seen. Because an electrically inactive mass lies between the scalp electrodes and the cerebral cortex in cases of subdural hematoma, EEG evaluation is fraught with difficulty (Harner, 1975). Although ipsilateral or generalized EEG slowing often occurs, ipsilateral attenuation of EEG activity (particularly of faster rhythms), no abnormality, or even contralateral findings may also be observable. Because of this, the echoencephalogram or, more recently, the computerized tomographic (CT) scan are more viable diagnostic tools.

In patients with Sturge-Weber disease, a prominent unilateral attenuation of background EEG activity over the involved hemisphere is often seen, frequently accompanied by epileptiform activity (Brenner and Sharbrough, 1976).


Metabolic disorders are a common cause of delirium, dementia, and specific organic brain syndromes. EEG evaluation in such cases is strongly indicated. As opposed to the case of senile dementia, for example, prominent EEG changes are generally recognizable very early in the clinical course. This is particularly important since a great many of these disorders are potentially reversible. Except as will be noted below, the predominant EEG changes found with metabolic disorders consist of generalized regular or irregular slowing, although in cases of preexisting CNS disease, focal findings may occur.

Electrolyte, pH, and Temperature Disturbances

Except for calcium imbalance, electrolyte disturbances have little effect upon the EEG. Hypocalcemia is associated with irregular and paroxysmal slowing, along with epileptiform activity and seizures (Markand, 1979), while hypercalcemia is known to produce generalized slowing and, occasionally, FIRDA and triphasic activity. Although acidosis is not associated with distinct EEG changes, marked slowing and FIRDA may be seen in cases of alkalosis (Kiloh et al, 1981). Similarly, although dehydration does not affect the EEG, water intoxication may lead to major pathophysiologic changes, predominantly consisting of generalized slowing and FIRDA. Possibly related to electrolyte and/or fluid and acid/base alterations, postcardiotomy delirium is associated with EEG slowing which precedes the development of the behavioral signs and continues past apparent return to baseline (Sachdev et al, 1967). The EEG effects of hyperthermia have not been adequately separated from those due to the underlying etiology. Hypothermia, on the other hand, produces slowing and attenuation of background activity beginning at 25°C, reaching an isoelectric baseline between 10° and 20°.

Disorders of Glucose Metabolism

Hypoglycemia is well known for its EEG correlates, yet it should be pointed out that these do not generally occur until the blood glucose falls to between 40 and 60 mg/dl. The initial EEG signs of hypoglycemia are reduction of posterior alpha frequency and increased sensitivity to hyperventilation (Markand, 1979). With further decrease in blood glucose levels, generalized theta and delta slowing occur, and even some degree of focal slowing may also be present, particularly with underlying cerebrovascular disease. When the hypoglycemic insult is severe and/or prolonged, permanent EEG changes, including generalized slowing and both focal and generalized epileptiform activity, may be observed.

Fewer EEG changes are generally found with hyperglycemia, except that some degree of generalized slowing can occur with increasing obtundation of the mental status. Well-compensated diabetics tend to have normal EEGs. In nonketotic hyperglycemic hyperosmolar coma, however, where metabolic derangement in addition to hyperglycemia is present, the EEG is usually quite abnormal (Maccario et al, 1965). Along with generalized slowing, focal slowing and even epileptiform activity may be seen in such cases.

Endocrine Disturbances

Thyroid dysfunction has been the most carefully studied endocrine disturbance with respect to the EEG (Wilson, 1965). Hypothyroidism is associated most prominently with slowing of the posterior alpha frequency and attenuation of the amplitude of the background activity, although some degree of generalized irregular slowing is often present, particularly in severe cases (Browning et al, 1954). Lesser amounts of EEG abnormality are seen with thyrotoxicosis, where, again, the most prominent effect is generally on the alpha rhythm, which increases in frequency. An increased amount of beta activity and occasional scattered irregular theta activity may also be seen.

In mild cases of hypoparathyroidism, only some degree of diminution of alpha activity and low-amplitude irregular slowing occurs (Clark et al, 1962). In more severe cases, greater amounts of generalized slowing, along with paroxysmal slowing or sharp activity, may be produced. Similar EEG findings have been reported with pseudohypoparathyroidism, although the occurrence of epileptiform activity in this variant appears to be more likely (Dickson et al, 1960). Hyperparathyroidism has not been as well investigated as the deficiency disorder, but EEG changes appear to be those described as pertaining to hypercalcemia (Wilson, 1965).

In cases of Addison disease, the EEG is typically normal or shows mild generalized slowing (Nishitani, 1962). The changes with Cushing disease are even less striking, with only minimal slowing or an elevation in fast activity being noted (Glaser, 1976). Hypopituitarism produces EEG changes similar to those seen with Addison disease except when mental obtundation is present, in which case more prominent generalized slowing occurs. In these and, for that matter, most types of metabolic encephalopathies, EEG changes generally show a rapid return to baseline upon adequate therapeutic correction of the specific imbalance. When mental impairment is present, the EEG in acute porphyria also shows some degree of generalized slowing. Occasionally some lateralization or even epileptiform activity may also occur.

Vitamin Deficiencies

Vitamin deficiencies of the B group may be associated with some degree of generalized EEG slowing (Kiloh et al, 1981). Serial EEG follow-up in cases of pernicious anemia has been used to provide a good objective measure of recovery following vitamin B12 replacement therapy (Walton et al, 1954). Chronic ethanol abuse, discussed elsewhere in this volume (Chapter 4), which leads to a thiamine deficiency state, is frequently not associated with EEG abnormalities other than an excess of beta activity (Coger et al, 1978). When Wernicke’s encephalopathy is present, however, some degree of generalized slowing is common; Victor et al (1972) reported an incidence of 50%.


EEG grading of anoxic brain injury has shown a good correlation with clinical prognosis (Prior, 1973). With a mild insult, only a minimal amount of scattered irregular theta activity is present, while more severe episodes are associated with larger amounts of generalized slowing along with disappearance of fast activity. Very severe injuries may produce a persistent vegetative state and more striking EEG findings, such as suppression-burst activity. Chronic respiratory insufficiency may lead to some degree of generalized slowing, less commonly accompanied by FIRDA and triphasic waves (Glaser, 1976). These findings are also seen in patients with pickwickian syndrome, many of whom also present with sleep apnea.


Patients with hepatic disease demonstrate a variety of EEG findings which correlate quite well with clinical status (Parson-Smith et al, 1957). With mild dysfunction, disorganization of background activity followed by a decrease in the amplitude and frequency of the alpha rhythm and buildup of generalized irregular theta activity can be seen. More severe impairment, at which point the patient is generally rather obtunded, is associated with delta slowing and the presence of triphasic waves. These complexes are high-amplitude broad transients that occur bilaterally, synchronously, and symmetrically in runs lasting up to tens of seconds or more (Bickford and Butt, 1955). A characteristic anterior-to-posterior phase lag is typically present. Although long considered an EEG hallmark of hepatic encephalopathy, triphasic waves may, as alluded to earlier, also occur in certain other conditions, where they often have atypical morphologic or distributional properties. Simsarian and Harner (1972) pointed out that triphasic waves are seen in only 20% of cases of hepatic encephalopathy and that they represent a poor prognosis. The EEG has been highly utilized as an objective measure of encephalopathic impairment in cases of Reye syndrome (Aoki and Lombroso, 1973).


The use of the EEG has proved more fruitful in cases of renal disease than in any other form of metabolic disorder. Hughes (1980) reported 36% of records to be abnormal, generally manifesting slowing of both background activity and the posterior rhythm. A good correlation between the level of EEG slowing and both blood urea nitrogen and levels of consciousness and cognitive impairment has been found. Triphasic activity is seen in 22% of the cases (Simsarian and Harner, 1972), mainly with moderately severe impairment. Bourne et al (1975) made use of serial computerized spectral analysis to follow the course of uremic patients through remissions and exacerbations of their disease.

During dialysis, with its rapid interchange of metabolic products, a dialysis disequilibrium syndrome has been reported (Kennedy et al, 1963). This is associated with high-amplitude rhythmic delta activity but has become relatively uncommon since certain refinements in dialysis technique became prevalent. An insidiously developing subacute progressive dialysis encephalopathy, otherwise described as dialysis dementia, occasionally occurs among those receiving chronic dialysis (Chokroverty et al, 1976). In such cases quite prominent EEG slowing, along with FIRDA and occasionally frontocentral spike and wave activity, may be seen.


The EEG following carbon monoxide poisoning of sufficient severity to cause behavioral CNS sequelae often shows some degree of generalized slowing (Lennox and Petersen, 1958). Diffuse or focal epileptiform activity may occasionally also occur, particularly in patients with seizures. Similar findings have been reported in cases of heavy metal, organic solvent, organophosphorus, and bromide intoxication (Freund and Niedermeyer, 1982).

Most forms of drug-induced encephalopathies show a good correlation between level of EEG impairment and level of mental status alteration (Kurtz, 1976). In general, diffuse slowing and prominent beta activity are the usual early features, with intermittent rhythmic bursts of delta activity seen as the patient becomes increasingly obtunded. In comatose states, diffuse delta, suppression-burst activity, or even an isoelectric record can be found. Such effects occur with sedative/hypnotic agents, neuroleptics, antidepressants, lithium, anxiolytics, CNS stimulants, anticonvulsants, narcotics, anticholinergic agents, steroids, and some antibiotics, along with a host of other compounds (Bauer, 1982; Itil, 1982; see also Chapter 5 on psychotropic drugs). With many of these drugs, severe intoxication may also be accompanied by epileptiform activity. It should be noted that sedative hypnotic and anxiolytic agents produce rhythmic beta activity, particularly in the frontocentral areas. Withdrawal from these drugs leads to slowing and paroxysmal activity except in the case of ethanol, where low-voltage fast activity is usually the prominent finding (Wikler et al, 1956). Many toxic drug effects on the EEG often persist past apparent return to clinical baseline.

CNS stimulants and hallucinogenic agents, especially in low to moderate doses, have the interesting property of increasing the amount of fast activity while having the opposite effect upon any level of ongoing background slowing. This presumably has some relationship to the observed behavioral changes (Toman and Davis, 1949). Marijuana has no effect upon the EEG (Rodin et al, 1970).


Cerebral infections manifest themselves, if acute, with delirium and, if chronic or if residua are present, with dementia or a specific organic brain syndrome. Herpes encephalitis, which specifically affects temporal lobe structures, is of particular interest, as patients who recover from this fulminant disease may show signs of an amnestic

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