Electroencephalography and Evoked Potentials

The techniques of applied electrophysiology are of practical importance in diagnosing and managing certain categories of neurological disease. Modern instrumentation permits the selective investigation of the functional aspects of the central and peripheral nervous systems. The electroencephalogram (EEG) and evoked potentials are measures of electrical activity generated by the central nervous system (CNS). Despite the introduction of positron emission tomography (PET), functional magnetic resonance imaging (fMRI), and magnetoencephalography (MEG), electroencephalography and evoked potential studies are currently the only readily available laboratory tests of brain physiology. As such, they are generally complementary to anatomical imaging techniques such as computed tomography (CT) or MRI, especially when it is desirable to document abnormalities that are not associated with detectable structural alterations in brain tissue. Furthermore, EEG provides the only continuous measure of cerebral function over time.

This chapter is not intended as a comprehensive account of all aspects of EEG and evoked potentials. Rather, the intent is to provide clinicians with an appreciation of the scope and limitations of these investigations as currently used.

Electroencephalography

Physiological Principles of Electroencephalography

The cerebral cortex generates EEG signals. Spontaneous EEG activity reflects the flow of extracellular space currents generated by the summation of excitatory and inhibitory synaptic potentials occurring on thousands or even millions of cortical neurons. Individual action potentials do not contribute directly to EEG activity. A conventional EEG recording is a continuous graph, over time, of the spatial distribution of changing voltage fields at the scalp surface that result from ongoing synaptic activity in the underlying cortex.

EEG rhythms appear to be part of a complex hierarchy of cortical oscillations that are fundamental to the brain’s information processing mechanisms, including input selection and transient “binding” of distributed neuronal assemblies ( ). In addition to reflecting the spontaneous intrinsic activities of cortical neurons, the EEG depends on important afferent inputs from subcortical structures including the thalamus and brainstem reticular formation. Thalamic afferents, for example, are probably responsible for entraining cortical neurons to produce the rhythmic oscillations that characterize normal patterns like alpha rhythm and sleep spindles. An EEG abnormality may occur directly from disruption of cortical neural networks or indirectly from modification of subcortical inputs onto cortical neurons.

A scalp-recorded EEG represents only a limited, low-resolution view of the electrical activity of the brain. This is due in part to the pronounced voltage attenuation and “blurring” that occurs from overlying cerebrospinal fluid (CSF) and tissue layers. Relatively large areas of cortex have to be involved in similar synchronized activity for a discharge to appear on the scalp EEG. For example, recordings obtained from arrays of microelectrodes penetrating into the cerebral cortex reveal a complex architecture of seizure initiation and propagation invisible to recordings from the scalp or even the cortical surface, with seizure-like discharges occurring in areas as small as a single cortical column ( ). Furthermore, potentials involving surfaces of gyri are more readily recorded than potentials arising in the walls and depths of sulci. Activity generated over the lateral convexities of the hemispheres records more accurately than does activity coming from interhemispherical, mesial, or basal areas. In the case of epileptiform activity, estimates are that 20%–70% of cortical spikes do not appear on the EEG, depending on the region of cortex involved. Additionally, although the scalp-recorded EEG consists almost entirely of signals slower than approximately 40 Hz, intracranial oscillations of several hundred hertz may be recorded and, of clinical importance, have been associated with both normal physiological processes and seizure initiation ( ).

Such considerations limit the usefulness of the EEG. First, surface recordings are not useful for unambiguously determining the nature of synaptic events contributing to a particular EEG wave. Second, the EEG is rarely specific as to cause because different diseases and conditions produce similar EEG changes. In this regard, the EEG is analogous to findings on the neurological examination—hemiplegia caused by a stroke cannot be distinguished from that caused by a brain tumor. Third, many potentials occurring at the brain surface involve such a small area or are of such low voltage that they cannot be detected at the scalp. The EEG results may then be normal despite clear indications from other data of focal brain dysfunction. Finally, abnormalities in brain areas inaccessible to EEG recording electrodes (some cortical areas and virtually all subcortical and brainstem regions) do not affect the EEG directly but may exert remote effects on patterns of cortical activity.

Normal Electroencephalographic Activities

Spontaneous fluctuations of voltage potential at the cortical surface are in the range of 100–1000 mV, but at the scalp are only 10–100 mV. Different parts of the cortex generate relatively distinct potential fluctuations, which also differ in the waking and sleep states.

In most normal adults and children aged 3 years and older, the waking pattern of EEG activity consists mainly of sinusoidal oscillations occurring at 8–12 Hz, which are most prominent over the occipital area—the alpha rhythm ( Fig. 35.1 , A ). Eye opening, mental activity, and drowsiness attenuate (block) the alpha rhythm. Activity faster than 12 Hz beta activity is normally present over the frontal areas and may be especially prominent in patients receiving barbiturate or benzodiazepine drugs. Activity slower than 8 Hz is divisible into delta activity (1–3 Hz) and theta activity (4–7 Hz). Adults may normally show a small amount of theta activity over the temporal regions; the percentage of intermixed theta frequencies increases after the age of 60 years. Delta activity is not normally present in adults when they are awake but appears when they fall asleep (see Fig. 35.1 , B ). The amount and amplitude of slow activity (theta and delta) correlate closely with the depth of sleep. Slow frequencies are abundant in the EEGs of newborns and young children, but these disappear progressively with maturation. A posterior dominant rhythm in the theta frequency range is apparent from about 3 months of age, which gradually increases in frequency to reach at least 8 Hz by 3 years.

Fig. 35.1, Samples of Normal Electroencephalographic Recordings from Two Patients.

An EEG undergoes characteristic changes during sleep. During stage I sleep, or drowsiness, the alpha rhythm becomes less regular, may slow slightly, and then disappears; theta activity becomes more prominent. During stage II sleep, sleep spindles, brief (1- to 2-second) runs of 12- to 14-Hz rhythmic waves, are seen synchronously over the central head regions. Vertex sharp waves are seen during stage II sleep and may also be present during stage I. With slow-wave sleep, diffuse delta activity dominates the EEG. During rapid-eye-movement (REM) sleep, which is associated with dreaming, the EEG demonstrates a low-voltage mixed-frequency pattern.

Common Types of Electroencephalographic Abnormalities

Focal Polymorphic Slow Activity

Polymorphic slow activity is irregular activity in the delta (1–4 Hz) or theta (4–7 Hz) range, which, when continuous, has a strong correlation with a localized cerebral lesion such as infarction, hemorrhage, tumor, or abscess. Intermittent focal slow activity may also indicate localized parenchymal dysfunction but is less predictive than continuous polymorphic slow activity.

Generalized Polymorphic Slow Activity

Diffuse disturbances in background rhythms marked by excessive slow activity and disorganization of waking EEG patterns arise in encephalopathies of metabolic, toxic, or infectious origin and with brain damage caused by a static encephalopathy.

Intermittent Monomorphic Slow Activity

Paroxysmal bursts of generalized bisynchronous rhythmic theta or delta waves usually indicate thalamocortical dysfunction and may be seen with metabolic or toxic disorders, obstructive hydrocephalus, deep midline or posterior fossa lesions, and also as a nonspecific functional disturbance in patients with generalized epilepsy. Focal bursts of rhythmic waves lateralized to one hemisphere usually indicate deep (typically thalamic or periventricular) abnormalities, often of a structural nature.

Voltage Attenuation

Cortical disease causes voltage attenuation. Generalized voltage attenuation is usually associated with diffuse depression of function such as after anoxia or with certain degenerative diseases (e.g., Huntington disease). The most severe form of generalized voltage attenuation is electrocerebral inactivity, which is corroborative evidence of brain death in the appropriate clinical setting. Focal voltage attenuation reliably indicates localized cortical disease such as porencephaly, atrophy, or contusion, or an extra-axial lesion such as a meningioma or subdural hematoma.

Epileptiform Discharges

Epileptiform discharges are spikes or sharp waves that occur interictally (between seizures) in patients with epilepsy and sometimes in persons who do not experience seizures but have a genetic predisposition to epilepsy. Epileptiform discharges may be focal or generalized, depending on the seizure type.

Recording Techniques

The EEG recording methods in common use are summarized in the following discussion. Details can be found in guidelines of the .

A series of small gold, silver, or silver–silver chloride disks is symmetrically positioned over the scalp on both sides of the head in standard locations (the International 10–20 system). In practice, 20 or more channels of EEG activity are recorded simultaneously, each channel displaying the potential difference between two electrodes. Electrode pairs are interconnected in different arrangements called montages to permit a comprehensive survey of the brain’s electrical activity. Typically, the design of montages is to compare symmetrical areas of the two hemispheres—anterior versus posterior regions or parasagittal versus temporal areas in the same hemisphere.

A typical study is about 30 to 45 minutes in duration and includes two types of “activating procedures”: hyperventilation and photic stimulation. In some patients, these techniques provoke abnormal focal or generalized alterations in activity that are of diagnostic importance and would otherwise go undetected ( Fig. 35.2 ). Recording during sleep and after sleep deprivation and placement of additional electrodes at other recording sites are useful in detecting specific kinds of epileptiform potentials. The use of other maneuvers depends on the clinical question posed. For example, epileptiform activity may occasionally activate only by movement or specific sensory stimuli. Vasovagal stimulation may be important in some types of syncope.

Fig. 35.2, Intermittent stroboscopic light stimulation at 13 flashes per second elicited generalized bursts of 4- to 5-Hz spike-wave activity, termed a photoparoxysmal (photoconvulsive) response . The spike-wave paroxysm was associated with a brief absence, as documented by the patient’s (P) inability to respond to a tone given by the technologist (T) . Normal responsiveness returned immediately on cessation of the spike-wave activity. The remainder of the electroencephalogram was normal.

In the past, EEG recording instruments were simple analog devices with banks of amplifiers and pen writers. In contrast, modern EEG machines make use of digital processing and storage, and the electroencephalographer interprets the EEG from a computer display rather than from paper. Technological advances have not fundamentally changed the principles of EEG interpretation, but they have facilitated EEG reading. Early paper-based EEG systems required that all recording parameters—display gain, filter settings, and the manner in which scalp-recorded signals were combined and displayed (montages)—be fixed by the technologist at the time of recording. In contrast, digital EEG systems permit the electroencephalographer to adjust these settings at the time of interpretation. A given EEG waveform or pattern can be examined using a number of different instrument settings, including sophisticated montages (e.g., common average reference, Laplacian reference) that were unavailable using traditional analog recording systems. Although this flexibility does not change the interpretive strategies used to read an EEG, it does allow the electroencephalographer to apply them more effectively.

In addition to facilitating the standard interpretation of EEGs, mathematical techniques can also be used to reveal features that may not be apparent to visual inspection of raw EEG waveforms. For example, averaging techniques, useful in improving the signal-to-noise ratios of spikes and sharp waves, can reveal field distributions and timing relationships that are not otherwise appreciable. Dipole source localization methods have been used to characterize both interictal spikes and ictal discharges in patients with epilepsy and may contribute to localization of the seizure focus ( ). Such methods are based on a number of critical assumptions that, if applied without recognition of their limitations, can result in anatomically and physiologically erroneous conclusions ( ). Therefore caution is warranted in their use.

For patients undergoing long-term EEG recordings as part of the diagnosis or management of epilepsy, a time-locked digital video image of the patient is recorded simultaneously with the EEG. EEG data are often processed by software that can automatically detect most seizure activity. Similar systems are finding increased use in intensive care units (ICUs), where EEG monitoring has become increasingly important in the management of patients with nonconvulsive seizure (NCS) activity, threatened or impending cerebral ischemia, severe head trauma, and metabolic coma ( ).

Clinical Uses of Electroencephalography

The EEG assesses physiological alterations in brain activity. Many changes are nonspecific, but some are highly suggestive of specific entities (epilepsy, herpes encephalitis, metabolic encephalopathy). The EEG is also useful in following the course of patients with altered states of consciousness and may, in certain circumstances, provide prognostic information. EEG can be used as an ancillary test in the determination of brain death.

EEG is not a screening test. It serves to answer a particular question posed by the patient’s condition; therefore the provision of sufficient clinical information helps in designing an appropriate test with meaningful clinical correlation. The request for this study should specifically state the question addressed by the EEG.

EEG interpretation should be based on a systematic analysis using consistent parameters that permit comparisons with findings expected from the patient’s age and circumstances of recording. Accurate interpretation requires high-quality recording. This depends on trained technologists who understand the importance of meticulous electrode application, proper use of instrument controls, recognition and (where possible) elimination of artifacts, and appropriate selection of recording montages to allow optimal display of cerebral electrical activity.

Epilepsy

The EEG is usually the most helpful laboratory test when a diagnosis of epilepsy is being considered. Because the onset of seizures is unpredictable, and their occurrence is relatively infrequent in most patients, EEG recordings are usually obtained when the patient is not having a seizure (interictal recordings). Fortunately, electrical abnormalities in the EEG occur in most patients with epilepsy even between attacks.

The only EEG finding that has a strong correlation with epilepsy is epileptiform activity , a term used to describe spikes and sharp waves that are clearly distinct from ongoing background activity. Clinical and experimental evidence supports a specific association between epileptiform discharges and seizure susceptibility. Only about 2% of patients without epilepsy have epileptiform discharges on EEG, whereas as many as 90% of patients with epilepsy demonstrate epileptiform discharges, depending on the circumstances of the recording and the number of studies obtained.

Nonetheless, interpretation of interictal findings always requires caution. There is poor correlation between most epileptiform discharges and the frequency and likelihood of recurrence of epileptic seizures ( ). Furthermore, a substantial number of patients with unquestionable epilepsy have consistently normal interictal EEGs. The most convincing proof that a patient’s episodic symptoms are epileptic is obtained by recording an electrographic seizure discharge during a typical behavioral attack.

Videos showing actual EEG recordings obtained during seizures ( , , ) are available at http://www.expertconsult.com .

Seizure 1. Generalized tonic-clonic seizure in a 17-year-old patient with primary generalized epilepsy. The recording shows several brief bursts of generalized spike- and polyspike-wave activity followed by a generalized seizure lasting approximately 1 1/2 minutes. The seizure is followed by generalized voltage attenuation and then by diffuse background slowing. Playback speed is approximately 10 times real time; vertical lines represent 1 second.

Seizure 2.Complex partial seizure in a 22-year-old patient. The recording shows a 1-minute episode of right temporal rhythmic delta and theta activity during which the patient was confused but able to converse.

Seizure 3.Complex partial seizure with secondary generalization in a 17-year-old patient. The seizure begins focally in the right posterior temporal area and spreads to involve right central as well as temporal regions. For about 3 1/2 minutes, the seizure remains confined to the right hemisphere; the patient complains of not feeling well and is observed to have automatisms involving the left hand and mouth. The seizure then spreads to involve the left hemisphere and the patient has a generalized tonic-clonic convulsion.

In addition to epileptiform patterns, EEGs in patients with epilepsy often show excessive focal or generalized slow-wave activity. Less often, asymmetries of frequency or voltage may be noted. These findings are not unique to epilepsy and are present in other conditions such as static encephalopathies, brain tumors, migraine, and trauma. In patients with unusual spells, nonspecific changes on EEG should be weighed cautiously and are not to be considered direct evidence for a diagnosis of epilepsy. On the other hand, when clinical data are unequivocal or when epileptiform discharges occur as well, the degree and extent of background EEG changes may provide information that is important for judging the likelihood of an underlying focal cerebral lesion, a more diffuse encephalopathy, or a progressive neurological syndrome. Additionally, EEG findings may help determine prognosis and aid in the decision to discontinue antiepileptic medication.

The type of epileptiform activity on EEG is helpful in classifying a patient’s epilepsy correctly and sometimes in identifying a specific epilepsy syndrome (see Chapter 100 ). Clinically, generalized tonic-clonic seizures may be generalized from the onset (primary generalized seizures) or may begin focally and then spread to become generalized (secondary generalized seizures). Impairment of consciousness, with or without automatisms, may be a manifestation of either a generalized nonconvulsive epilepsy (e.g., absence seizures) or a focal epilepsy (e.g., temporal lobe epilepsy). The initial clinical features of a seizure may be uncertain because of postictal amnesia or nocturnal occurrence. In these and similar situations, the EEG can provide information crucial to the correct diagnosis and appropriate therapy.

In generalized seizures, the EEG typically shows bilateral synchronous diffuse bursts of spikes and spike-and-wave discharges ( Fig. 35.3 ). All generalized EEG epileptiform patterns share certain common features, although the exact expression of the spike-wave activity varies depending on whether the patient has pure absence, tonic-clonic, myoclonic, or atonic-astatic seizures. The EEG also may help to distinguish between idiopathic and symptomatic generalized epilepsy. In idiopathic generalized epilepsy, no cerebral disease is demonstrable and EEG background rhythms are normal or near normal. In symptomatic generalized epilepsy, evidence can be found for diffuse brain damage and the EEG typically demonstrates some degree of generalized slow-wave activity.

Fig. 35.3, Example of generalized spike-wave patterns with primary generalized (idiopathic) epilepsy. The patient had mainly tonic-clonic seizures with occasional absence attacks.

Consistently focal epileptiform activity is the signature of focal-onset (partial) epilepsy ( Fig. 35.4 ). With the exception of the benign focal epilepsies of childhood, focal epileptiform activity results from neuronal dysfunction caused by demonstrable brain disease. A reasonable correlation exists between spike location and the type of ictal behavior. Anterior temporal spikes are usually associated with complex partial seizures, rolandic spikes with simple motor or sensory seizures, and occipital spikes with primitive visual hallucinations or diminished visual function as an initial feature.

Fig. 35.4, Focal right anterior temporal spikes occurring on the electroencephalogram of a 69-year-old woman with complex partial seizures after a stroke involving branches of the right middle cerebral artery.

In addition to distinguishing epileptiform from nonepileptiform abnormalities, EEG analysis sometimes permits the identification of specific epilepsy syndromes. Such electroclinical syndromes include hypsarrhythmia associated with infantile spasms (West syndrome; Fig. 35.5 ); 3-Hz spike-and-wave activity associated with typical absence attacks (childhood or juvenile absence epilepsy; Fig. 35.6 ); generalized multiple spikes and waves (polyspike-wave pattern) associated with myoclonic epilepsy, including so-called juvenile myoclonic epilepsy of Janz ( Fig. 35.7 ); generalized sharp and slow waves (slow spike-and-wave pattern) associated with Lennox-Gastaut syndrome ( Fig. 35.8 ); and central-midtemporal spikes associated with benign rolandic epilepsy ( Fig. 35.9 ).

Fig. 35.5, Electroencephalographic pattern, termed hypsarrhythmia , in a recording obtained in an 8-month-old boy with infantile spasms. Background activity is high-voltage and unorganized, with abundant multifocal spikes.

Fig. 35.6, A 3-Hz spike-and-wave paroxysm on the electroencephalogram of a 9-year-old boy with absence seizures (petit mal epilepsy). During this 12-second discharge, the child was unresponsive and demonstrated rhythmic eye blinking.

Fig. 35.7, Example of generalized spike-wave patterns with primary generalized (idiopathic) epilepsy. The patient had juvenile myoclonic epilepsy.

Fig. 35.8, Generalized sharp- and slow-wave discharges on the electroencephalogram (EEG) of a 9-year-old child with intellectual disability and uncontrolled typical absence, tonic, and atonic generalized seizures. This constellation of clinical and EEG features constitutes the Lennox-Gastaut syndrome.

Fig. 35.9, Electroencephalogram obtained during drowsiness in a 10-year-old boy with benign rolandic epilepsy. Stereotypical diphasic or triphasic sharp waves occur in the right central-parietal and midtemporal regions.

The increased availability of special monitoring facilities for simultaneous video and EEG recording and of ambulatory EEG recorders has improved diagnostic accuracy and the reliability of seizure classification. Prolonged continuous recordings through one or more complete sleep/wake cycles constitute the best way to document ictal episodes and should be considered in patients whose interictal EEGs are normal or nondiagnostic and in clinical dilemmas that are resolvable only by recording actual behavioral events. Although EEG documentation of an ictal discharge establishes the epileptic nature of a corresponding behavioral change, the converse is not necessarily true. Sometimes muscle or movement artifacts so obscure the EEG recording that it is impossible to know whether any EEG change has occurred. In these circumstances, postictal slowing is usually indicative of an epileptic event if similar slow waves are not present elsewhere in the recording and if the EEG recording subsequently returns to baseline. In addition, focal seizures not accompanied by alteration in consciousness occasionally have no detectable scalp correlate. On the other hand, the persistence of alpha activity and absence of slowing during and after an apparent convulsive episode are inconsistent with an epileptic generalized tonic-clonic seizure.

Focal Cerebral Lesions

The use of EEG to detect focal cerebral disturbances has declined because of the development and widespread availability of modern neuroimaging techniques. Nonetheless, the EEG has a role in documenting focal physiological dysfunction in the absence of discernible structural pathology and in evaluating the functional disturbance produced by known lesions.

Focal slow-wave activity (delta, theta) is the usual EEG sign of a focal disturbance. A structural lesion is likely if the slowing is (1) present continuously; (2) shows variability in waveform, amplitude, duration, and morphology (so-called arrhythmic or polymorphic activity); and (3) persists during changes in wake/sleep states ( Fig. 35.10, A and B ). The localizing value of focal slowing increases when it is topographically discrete or associated with depression or loss of superimposed faster background frequencies. The character and distribution of the EEG changes caused by a focal lesion depend on the lesion’s size, its distance from the cortical surface, the specific structures involved, and its acuity. Superficial lesions tend to produce more focal EEG changes, whereas deep cerebral lesions produce hemispheric or even bilateral slowing. For example, a small stroke located in the thalamus may produce widespread hemispheric slowing and alteration in sleep spindles and alpha rhythm regulation, whereas a lesion of the same size located at the cortical surface may produce few if any EEG findings.

Fig. 35.10, The patient was a 46-year-old man with a glioblastoma involving the right temporal and parietal lobes. A, Lesion is well demonstrated on this computed tomography scan of the brain. B, Electroencephalogram demonstrates continuous arrhythmic slowing over the right temporal and parieto-occipital areas. In addition, loss of the alpha rhythm and overriding faster frequencies are seen in corresponding areas of the left cerebral hemisphere.

Bilateral paroxysmal bursts of rhythmic delta waves ( Fig. 35.11 ) with frontal predominance—once attributed to subfrontal, deep midline, or posterior fossa lesions—are actually nonspecific and seen more often with diffuse encephalopathies. Focal or lateralized intermittent bursts of rhythmic delta waves as the prominent EEG abnormality suggest a deep supratentorial (periventricular or diencephalic) lesion.

Fig. 35.11, Bursts of intermittent rhythmic delta waves on the electroencephalogram (EEG) of a 36-year-old patient with primary generalized epilepsy and tonic-clonic seizures. Generalized spike-wave activity occurred elsewhere in the EEG. Intermittent rhythmic delta waves are a nonspecific manifestation of the patient’s generalized epileptic disorder.

Single lacunae usually produce little or no change in the EEG. Similarly, transient ischemic attacks not associated with chronic cerebral hypoperfusion or imminent occlusion of a major vessel do not significantly affect the EEG outside the symptomatic period. Superficial cortical or large, deep hemispheric infarctions are usually associated with localized EEG abnormalities.

EEG is generally not indicated for the diagnosis of headache. That being said, focal EEG changes (and other nonepileptiform abnormalities) may be seen during migraine. The likelihood of an abnormal EEG and the severity of the abnormality relate to the timing and character of the migraine attack. EEGs are more likely to be focally abnormal with complicated rather than common migraine and during rather than between headaches.

EEG changes seen with brain tumors are caused by disturbances in bordering brain parenchyma, as most tumor tissue is electrically silent. Focal EEG changes are caused by interference with patterns of normal neuronal synaptic activity; by destruction or alteration of the cortical neurons; and by metabolic effects caused by changes in blood flow, cellular metabolism, or the neuronal environment. Diffuse EEG changes are the consequence of increased intracranial pressure, shift of midline structures, or hydrocephalus. EEG is especially helpful in following the extent of cerebral dysfunction over time; in distinguishing between direct effects of the neoplasm and superimposed metabolic or toxic encephalopathies; and in differentiating among epileptic, ischemic, and noncerebral causes for episodic symptoms.

The role of EEG in the management of patients with head injuries is limited. Transient generalized slowing is common after concussion. A persistent area of continuous localized slow-wave activity suggests cerebral contusion even in the absence of a focal clinical or CT abnormality, and unilateral voltage depression suggests subdural hematoma. EEG performed in the first 3 months after injury does not predict posttraumatic epilepsy.

Altered States of Consciousness

The EEG has a major role in evaluating patients with altered levels of consciousness. Because EEG permits a reasonable assessment of supratentorial brain function, it complements the clinical examination in patients with significant depression of consciousness. Abnormalities are typically nonspecific with regard to etiology. In general, however, correlation with the clinical state is good. Some findings are more suggestive of particular causes than of others and are occasionally prognostically useful as well. Specific questions the EEG may help to answer (depending on the clinical presentation) are the following:

Are psychogenic factors playing a major role?
Is the process diffuse, focal, or multifocal?
Is depressed consciousness due to unrecognized epileptic activity (nonconvulsive status epilepticus)?
What evidence, if any, points to improvement, despite relatively little change in the clinical picture?
What findings, if any, assist in assessing prognosis?

Metabolic Encephalopathies

Metabolic derangements affecting the brain diffusely are among the most common causes of altered mental function in a general hospital. Generalized slow-wave activity is the main indication of decreased consciousness. The degree of EEG slowing closely parallels the patient’s mental status and ranges from only minor slowing of alpha-rhythm frequency (slight inattentiveness and decreased alertness) to continuous delta activity (coma). Slow-wave activity sometimes becomes bisynchronous and assumes a high-voltage, sharply contoured triphasic morphology, especially over the frontal head regions ( Fig. 35.12 ). These generalized periodic discharges (PDs) with triphasic morphology, originally considered diagnostic of hepatic failure, occur with equal frequency in other metabolic disorders, such as uremia, hyponatremia, hyperthyroidism, anoxia, and hyperosmolarity. The value of these so-called triphasic waves is that they suggest a metabolic cause in an unresponsive patient ( ).

Fig. 35.12, Triphasic waves on the electroencephalogram of a 61-year-old man with hepatic failure.

Some EEG features increase the likelihood of a specific metabolic disorder. Prominent generalized rhythmic beta activity raises the suspicion of drug intoxication in a comatose patient. Severe generalized voltage depression indicates impaired energy metabolism and suggests hypothyroidism if anoxia and hypothermia can be excluded. A photoconvulsive response is seen more often with uremia than with other causes of metabolic encephalopathy. Focal seizure activity is common in patients with hyperosmolar coma.

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