Electroencephalography and Evoked Potentials
351
87–0070
Fp1–F3
F3–C3
C3–P3
P3–O1
Fp2–F4
F4–C4
C4–P4
P4–O2
Flash 13/sec
Stimulus
T T
Fig. 34.2  Intermittent stroboscopic light stimulation at 13 flashes per second elicited generalized bursts of 4- to 5-Hz spike-wave activ-
ity, 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.
Fig. 34.3  Frequency-domain topographical brain map obtained
from a 32-channel bipolar electroencephalographic (EEG) record-
ing. The patient was a 53-year-old man with hemodynamically signifi-
cant left carotid stenosis. This map demonstrates an asymmetry over
the occipital regions during eye opening, reflecting relative failure of
left hemisphere alpha activity to attenuate normally. The color scale at
the right reflects percentage change in EEG activity on going from the
eyes-closed to the eyes-open state. (Courtesy Dr. Bruce J. Fisch.)
localization of the seizure focus (Ebersole, 2000). 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
(Emerson et al., 1995), so caution is warranted in their use.
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31 F
34
75 µV
1 sec
P
T
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 (ICU), where
EEG monitoring has become increasingly important in the
management of patients with nonconvulsive seizure activity,
threatened or impending cerebral ischemia, severe head
trauma, and metabolic coma (Drislane et al., 2008; Friedman
et al., 2009).
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 also is useful in following the
course of patients with altered states of consciousness and
may, in certain circumstances, provide prognostic informa-
tion. EEG can be used as an ancillary test in the determination
of brain death.
Electroencephalography is not a screening test. It serves to
answer a particular question posed by the patient’s condition,
so providing sufficient clinical information helps design 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 analy-
sis that uses consistent parameters that permit comparisons
with findings expected from the patient’s age and circum-
stances of recording. Accurate interpretation requires high-
quality recording. This depends on trained technologists who
understand the importance of meticulous electrode applica-
tion, 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.
352 PART II  Neurological Investigations and Related Clinical Neurosciences
Epilepsy
The EEG usually is 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 usually are
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 back-
ground activity. Clinical and experimental evidence supports
a specific association between epileptiform discharges and
seizure susceptibility. Only about 2% of patients without epi-
lepsy 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 epi-
leptiform discharges and the frequency and likelihood of
recurrence of epileptic seizures (Selvitelli et al., 2010). Further-
more, a substantial number of patients with unquestionable
epilepsy have consistently normal interictal EEGs. The most
convincing proof that a patient’s episodic symptoms are epi-
leptic is obtained by recording an electrographical seizure dis-
charge during a typical behavioral attack.
Videos showing actual EEG recordings obtained during
seizures (Videos 34.1 to 34.3) are available at http://www
.expertconsult.com.
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 cau-
tiously 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 important for judging the likelihood of
an underlying focal cerebral lesion, a more diffuse encepha-
lopathy, 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 clas-
sifying a patient’s epilepsy correctly and sometimes in identi-
fying a specific epilepsy syndrome (see Chapter 101). Clinically,
generalized tonic-clonic seizures may be generalized from the
onset (primary generalized seizures), or may begin focally and
then spread to become generalized (secondarily 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 epi-
lepsy (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 bilaterally
synchronous diffuse bursts of spikes and spike-and-wave dis-
charges (Fig. 34.4). 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
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Fp1–F3
F3–C3
C3–P3
P3–O1
Fp2–F4
F4–C4
C4–P4
P4–O2
75 µV
A 1 sec
B
Fig. 34.4  Examples of generalized spike-wave patterns from dif-
ferent patients with primary generalized (idiopathic) epilepsy. The
patient in A had mainly tonic-clonic seizures, with occasional absence
attacks. The patient in B had juvenile myoclonic epilepsy.
idiopathic and symptomatic generalized epilepsy. In idio-
pathic generalized epilepsy, no cerebral disease is demonstra-
ble 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.
Consistently focal epileptiform activity is the signature of
focal-onset (partial) epilepsy (Fig. 34.5). With the exception
of the benign focal epilepsies of childhood, focal epileptiform
activity results from neuronal dysfunction caused by demon-
strable brain disease. A reasonable correlation exists between
spike location and the type of ictal behavior. Anterior tempo-
ral spikes usually are associated with complex partial seizures,
rolandic spikes with simple motor or sensory seizures, and
occipital spikes with primitive visual hallucinations or dimin-
ished visual function as an initial feature.
In addition to distinguishing epileptiform from nonepilep-
tiform abnormalities, EEG analysis sometimes permits the
identification of specific epilepsy syndromes. Such electro-
clinical syndromes include hypsarrhythmia associated with
infantile spasms (West syndrome) (Fig. 34.6); 3-Hz spike-and-
wave activity associated with typical absence attacks (child-
hood or juvenile absence epilepsy) (Fig. 34.7); generalized
multiple spikes and waves (polyspike-wave pattern) associated
with myoclonic epilepsy, including so-called juvenile myo-
clonic epilepsy of Janz (see Fig. 34.4, B); generalized sharp and
slow waves (slow spike-and-wave pattern) associated with
Lennox–Gastaut syndrome (Fig. 34.8); central-midtemporal
spikes associated with benign rolandic epilepsy (Fig. 34.9).
The increased availability of special monitoring facilities
for simultaneous video and EEG recording and of ambulatory
 Electroencephalography and Evoked Potentials 353

87–0233 69 F
Fp1–F7 34
F7–T3
T3–T5
T5–O1
Fp2–F8
F8–T4
50 µV
1 sec
T4–T6
T6–O2

Fig. 34.5  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.

JV 399–30–53 8 moM
Fp1–F3
F3–C3
C3–P3
P3–O1
Fp2–F4
F4–C4
C4–P4
P4–O2
Fp1–F7
F7–T3
T3–T5
T5–O1
Fp2–F8
F8–T4
T4–T6
T6–O2
150 µV
1 sec

Fig. 34.6  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.

87–1178
9M
Fp1–F3
F3–C3
C3–P3
P3–O1
Fp2–F4
F4–C4
C4–P4
P4–O2
100 µV
1 sec

Fig. 34.7  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.

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 usually is indicative of an epileptic event if
similar slow waves are not present elsewhere in the recording

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354 PART II  Neurological Investigations and Related Clinical Neurosciences

9 y/o
1
Fp2–F4

F4–C4 2

C4–P4 3

4
P4–O2

5
Fp1–F3

6
F3–C3
50 µV
1 sec
C3–P3 7

8
P3–O1

Fig. 34.8  Generalized sharp-wave 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.

587
Fp1–F3

F3–C3

C3–P3

P3–O1

Fp2–F4

F4–C4

C4–P4

P4–O2

Fp1–F7

F7–T3 50µV
1 sec
T3–T5

T5–O1

Fp2–F8

F8–T4

T4–T6

T6–O2

Fig. 34.9  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.

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 Electroencephalography and Evoked Potentials 355

and if the EEG recording subsequently returns to baseline. In
addition, focal seizures not accompanied by alteration in con-
sciousness occasionally have no detectable scalp correlate. On
the other hand, 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 electroencephalography 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 physi-
ological dysfunction in the absence of discernible structural 34
pathology and in evaluating the functional disturbance pro-
duced 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. 34.10). The localizing value of
focal slowing increases when it is topographically discrete or
associated with depression or loss of superimposed faster

A
87–0624 46 M
Fp1–F3
F3–C3
C3–P3
P3–O1

Fp2–F4

F4–C4
C4–P4

P4–O2
Fp1–F7
F7–T3
T3–T5
T5–O1
Fp2–F8
F8–T4
T4–T6

T6–O2

50 µV
B 1 sec

Fig. 34.10  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.

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356 PART II  Neurological Investigations and Related Clinical Neurosciences

background frequencies. The character and distribution of the
EEG changes caused by a focal lesion depend on its 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 wide-
spread 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.
Bilateral paroxysmal bursts of rhythmic delta waves (Fig.
34.11) with frontal predominance—once attributed to sub-
frontal, deep midline, or posterior fossa lesions—are actually
nonspecific and seen more often with diffuse encephalopa-
thies. Focal or lateralized intermittent bursts of rhythmic delta
waves as the prominent EEG abnormality suggest a deep
supratentorial (periventricular or diencephalic) lesion.
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 hemi-
spheric infarctions are usually associated with localized EEG
abnormalities.
EEG is generally not indicated for the diagnosis of head-
ache. That being said, focal EEG changes (and other nonepi-
leptiform abnormalities) may be seen during migraine. The
likelihood of an abnormal EEG and the severity of the abnor-
mality relate to the timing and character of the migraine
attack. EEGs are more likely to be focally abnormal with com-
plicated rather than common migraine, and during rather
than between headaches.
EEG changes seen with brain tumors are caused by distur-
bances in bordering brain parenchyma, as most tumor tissue
is electrically silent. Focal EEG changes are caused by inter-
ference 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 pres-
sure, shift of midline structures, or hydrocephalus. Electroen-
cephalography 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 electroencephalography in the management of
patients with head injuries is limited. Transient generalized
slowing is common after concussion. A persistent area of con-
tinuous localized slow-wave activity suggests cerebral contu-
sion even in the absence of a focal clinical or CT abnormality,
and unilateral voltage depression suggests subdural hematoma.
Electroencephalography performed in the first 3 months after
injury does not predict post-traumatic 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 depres-
sion of consciousness. Abnormalities typically are nonspecific
with regard to etiology. In general, however, a correlation with
the clinical state is good. Some findings are more suggestive
of particular causes than of others and occasionally are prog-
nostically 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)?

36 y/o H963916

Fp1–F3

F3–C3

C3–P3

P3–O1

Fp2–F4

F4–C4

C4–P4

P4–O2

75 µV
1 sec

Fig. 34.11  Bursts of intermittent rhythmic delta waves on the electroencephalogram (EEG) of a 36-year-old man with primary general-
ized 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. (Courtesy Dr. Bruce J. Fisch.)

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79–1019
F3–C3
F4–C4
C3–P3
C4–P4
P3–O1
P4–O2
Fig. 34.12  Triphasic waves on the electroencephalogram of a 61-year-old man with hepatic failure. (Courtesy Dr. Bruce J. Fisch.)
• What evidence, if any, points to improvement, despite rela-
tively little change in the clinical picture?
• What findings, if any, assist in assessing prognosis?
Metabolic Encephalopathies
Metabolic derangements affecting the brain diffusely consti-
tute one of the most common causes of altered mental func-
tion 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. 34.12). These triphasic waves, originally considered diag-
nostic of hepatic failure, occur with equal frequency in other
metabolic disorders such as uremia, hyponatremia, hyperthy-
roidism, anoxia, and hyperosmolarity. The value of triphasic
waves is that they suggest a metabolic cause in an unrespon-
sive patient.
Some EEG features increase the likelihood of a specific
metabolic disorder. Prominent generalized rhythmic beta
activity raises the suspicion of drug intoxication in a coma-
tose 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.
Hypoxia
Hypoxia, with or without circulatory arrest, produces a wide
range of EEG abnormalities depending on the severity and
reversibility of the brain damage. EEGs obtained 6 hours or
more after the hypoxic insult may show patterns that have
prognostic value (see Chapter 5). Sequential EEGs strengthen
the validity of such findings. EEG abnormalities associated
with poor neurological outcome are alpha coma, burst sup-
pression, and periodic patterns.
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Electroencephalography and Evoked Potentials 357
61 M
34
50 µV
1 sec
The term alpha coma refers to the apparent paradoxical
appearance of monorhythmic alpha frequency activity in the
EEG of a comatose patient; the EEG recording may appear
normal to the inexperienced observer (Fig. 34.13). In contrast
with normal alpha activity, that seen with alpha coma is gen-
eralized, often maximal frontally, and unreactive to external
stimuli.
The burst suppression pattern consists of occasional general-
ized bursts of medium- to high-voltage, mixed-frequency,
slow-wave activity, sometimes with intermixed spikes, with
intervening periods of severe voltage depression or cerebral
inactivity (Fig. 34.14). Massive myoclonic body jerks may
accompany the bursts.
The periodic pattern consists of generalized spikes or sharp
waves that recur with a relatively fixed interval, typically 1 or
2 per second (Fig. 34.15). Sometimes the periodic sharp waves
occur independently over each hemisphere. Myoclonic jerks
of the limbs or whole body usually accompany a postanoxic
periodic pattern.
The prognostic value of these patterns relates exclusively to
the cause. Similar features are recognized with potentially
reversible causes of coma including deep anesthesia, drug
overdose, and severe liver or kidney failure.
Infectious Diseases
Of all infectious diseases affecting the brain, herpes simplex
encephalitis is the one for which electroencephalography is
most useful in initial assessment. Early and accurate diagnosis
is important because the response to acyclovir is best when
treatment is started early. Characteristic EEG changes in the
clinical setting of encephalitis are helpful in selecting patients
for early antiviral treatment, as the EEG is usually abnormal
and suggestive of herpes infection before abnormalities are
apparent on CT.
Viral encephalitis is expected to cause diffuse polymorphic
slow-wave activity, and a normal EEG result raises doubt about
the diagnosis. With herpes simplex encephalitis, a majority of
patients show focal temporal or frontotemporal slowing that
may be unilateral or, if bilateral, asymmetrical. Periodic sharp-
wave complexes over one or both frontotemporal regions
(occasionally in other locations and sometimes generalized)
358 PART II  Neurological Investigations and Related Clinical Neurosciences

34 M
Fp1–A1
Fp2–A2
F3–A1
F4–A2
C3–A1
C4–A2
P3–A1
P4–A2
50 µV
O1–A1 1 sec

O2–A2

Fig. 34.13  Alpha coma in a 34-year-old man with severe hypoxic-ischemic brain damage from subarachnoid hemorrhage with diffuse
prolonged cerebral vasospasm. Unlike the normal alpha rhythm, the alpha range activity on the electroencephalogram of this comatose patient
is widespread but maximal frontally, unreactive, and superimposed on low-voltage arrhythmic delta frequencies.

068–22–91 53 F
Fp1–F3
F3–C3
C3–P3
P3–O1
Fp2–F4
F4–C4
C4–P4
P4–O2
F7–T3
T3–T5 75 µV
F8–T4 1 sec
T4–T6

Fig. 34.14  Burst suppression pattern on the electroencephalogram of a 53-year-old woman with anoxic encephalopathy following
cardiorespiratory arrest. The patient died several days later. (Courtesy Dr. Barbara S. Koppel.)

75M #88–1931
Fp1–F7
F7–T3
T3–T5
T5–O1
Fp1–F3
F3–C3
C3–P3
P3–O1
FZ–CZ
CZ–PZ
Fp2–F8
F8–T4
T4–T6
50 µV 1 sec
T6–O2
Fp2–F4
F4–C4
C4–P4
P4–O2

Fig. 34.15  Periodic pattern on the electroencephalogram of a patient with anoxic encephalopathy following cardiorespiratory arrest.
The patient was paralyzed with pancuronium because of bilateral myoclonus.

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add additional specificity to the EEG findings. These diagnos-
tic features usually appear between days 2 and 15 of illness
and sometimes are detectable only with serial tracings.
Bacterial meningitis causes severe and widespread EEG
abnormalities, typically profound slowing and voltage depres-
sion, but viral meningitis produces little in the way of
significant changes. Although CT and MRI have replaced elec-
troencephalography in evaluating patients with suspected
brain abscess, focal EEG changes may occur in the early stage
of cerebritis before an encapsulated lesion is demonstrable on
CT or MRI.
EEG abnormalities usually resolve as the patient recovers,
but the rate of resolution of clinical deficits and that of the
electrographical findings may be different. It is not possible to
predict either residual neurological morbidity or postencepha-
litic seizures by EEG criteria. An early return of normal EEG
activity does not exclude the possibility of persistent neuro-
logical impairment.
Brain Death
The diagnosis of brain death rests on strict clinical criteria that,
when satisfied unambiguously, permit a conclusive determi-
nation of irreversible loss of brain function. In the United
States, the usual definition of brain death is irreversible cessa-
tion of all functions of the entire brain, including the brain-
stem. Because the EEG is a measure of cerebral—especially
cortical—function, it has been widely used in association with
clinical evaluation to provide objective evidence that brain
function is lost. Several studies have demonstrated that endur-
ing loss of cerebral electrical activity, termed electrocerebral
inactivity or electrocerebral silence, accompanies clinical brain
death and is never associated with recovery of neurological
function. The determination of electrocerebral inactivity is
technically demanding, requiring a special recording protocol.
Minimum technical standards for EEG recording in suspected
cerebral death have been established by the American Clinical
Neurophysiology Society (American Clinical Neurophysiol-
ogy Society, 2014).
Temporary and reversible loss of cerebral electrical activity
is observable immediately after cardiorespiratory resuscitation,
drug overdose from CNS depressants, and severe hypothermia.
Therefore, accurate interpretation of an EEG demonstrating
electrocerebral inactivity must take into account these excep-
tional circumstances. Chapter 57 summarizes the clinical cri-
teria for establishing the diagnosis of brain death.
Aging and Dementia
Because the EEG is a measure of cortical function, theoretically
it should be useful in the diagnosis and classification of
dementia. The utility of single EEG examinations in evaluating
patients with known or suspected cognitive impairment,
however, is often disappointing. Two important reasons for
this limitation are (1) problems in distinguishing the effects
on cerebral electrical activity of normal aging from those
caused by disease processes and (2) the absence of generally
accepted quantifiable methods of analysis and statistically
valid comparison measures.
With increasing age beyond 65 years, a slight reduction in
alpha rhythm frequency and in the total amount of alpha
activity is normal. Normal elderly persons also show slightly
increased amounts of theta and delta activity, especially over
the temporal and frontotemporal regions, as well as changes
in sleep patterns. Early in the course of some dementing
illnesses, no EEG abnormality may be apparent (this is the
rule with Alzheimer disease), or the normal age-related
changes may become exaggerated, differing more in degree
than in kind.
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Electroencephalography and Evoked Potentials 359
In practice, the EEG can assist in the evaluation of sus-
pected dementia by confirming abnormal cerebral function in 34
patients with a possible psychogenic disorder and by delineat-
ing whether the process is focal or diffuse. Sequential EEGs
usually are more helpful than a single tracing, and a test early
in the course of the illness may provide more specific informa-
tion than can be obtained later on. Overall, the degree of
EEG abnormality shows good correlation with the degree of
dementia.
EEG findings in Alzheimer disease are highly dependent on
timing. The EEG initially is normal or shows an alpha rhythm
at or just below the lower limits of normal. Generalized
slowing ensues as the disease progresses. In patients with focal
cognitive deficits, accentuation of slow frequency activity over
the corresponding brain area may be a feature. Continuous
focal slowing is sufficiently unusual to suggest the possibility
of another diagnosis. Prominent focal or bilateral independ-
ent slow-wave activity, especially if seen in company with a
normal alpha rhythm, favors multifocal disease such as mul-
tiple cerebral infarcts. Sometimes a specific cause may be sug-
gested. For example, an EEG showing generalized typical
periodic sharp-wave complexes in a patient with dementia is
virtually diagnostic of Creutzfeldt–Jakob disease (Fig. 34.16).
Event-related evoked potentials have application in the
study of dementia. These long-latency events (i.e., potentials
occurring more than 150 milliseconds after the stimulus) are
heavily dependent on psychic and cognitive factors. Ideally,
they measure the brain’s intrinsic mechanisms for processing
certain types of information and are potentially valuable in
the electrophysiological assessment of dementia. The best
known of the event-related potentials is the P300, or P3,
wave. The place of these long-latency evoked potentials
in the evaluation of dementia is still under investigation,
but the pattern of electrophysiological abnormality may be
helpful in distinguishing among types of dementia (Comi
and Leocani, 2000).
Continuous EEG Monitoring in the Intensive
Care Unit
Recent technological advances have brought continuous EEG
monitoring (cEEG) to the ICU bedside to assist in the evalu-
ation of brain function in critically ill patients. As a real-time
monitor of brain function, cEEG has the advantages that it is
86–1699 67F
Fp1
F3
C3
P3
O1
Fp2
F4
C4
P4
O2
AVE REF 50 µV
1 sec
Fig. 34.16  Periodic sharp-wave pattern on the electroencephalo-
gram of a 67-year-old woman with Creutzfeldt–Jakob disease.
Generalized bisynchronous diphasic sharp waves occur approximately
1.5 to 2.0 per second.