THE NORMAL EEG 1005 - USF Healthhsc.usf.edu/com/epilepsy/EEG introduction (Lee Chiong) part...

Figure 130.21 Hypnagogic hypersynchrony. This less common but well recognized normal variant of drowsiness is seen in children aged 3

months to 13 years. It consists of paroxysmal bursts (3–5 Hz) of high-voltage (as high as 350 mV) rhythmic waves. Note the normal alpha

rhythm in the first two-thirds of the sample, which precedes drowsiness.

Figure 130.22 Stage 2: sleep spindles. This segment depicts typical short bursts (1–3 seconds) of sinusoidal 12–16 Hz central activity that

waxes and wanes.

THE NORMAL EEG 1005

By strict sleep staging criteria on polysomnography,

REM sleep is defined by (1) rapid eye movements, (2) muscle

atonia, and (3) EEG ‘‘desynchronization’’ (compared to

slow-wave sleep). Thus two of the three defining character-

istics are not cerebral waves and theoretically require

monitoring of eye movements (electro-oculogram (EOG))

and muscle tone (electromyogram (EMG)). Fortunately,

muscle activity and eye movements can be evaluated

on EEG; thus REM sleep is usually not difficult to

identify (Figure 130.25). In addition to the three features

already named, ‘‘sawtooth’’ waves also are seen in REM

sleep.

� EEG Desynchronization. The EEG background activ-

ity changes from that seen in slow-wave sleep (stage 3

or 4) to faster and lower voltage activity (theta and

beta), resembling wakefulness.

� Rapid Eye Movements. These are saccadic,

predominantly horizontal, and occur in repetitive

bursts.

� Despite the lack of a dedicated EMG channel, the

muscle atonia that characterizes REM sleep is usually

apparent as a general sense of ‘‘quiet’’ muscle activity

compared to wakefulness.

� Sawtooth waves are a special type of central theta

activity that has a notched morphology, resembling

the blade of a saw, and usually occurs close to rapid

eye movements (i.e., phasic REM). They are only

rarely identifiable on EEG.

The duration of REM sleep increases progressively with

each cycle and tends to predominate late in the sleep period

into early morning.

Figure 130.23 Stage 2: K-complexes. This sample shows the typical long-duration (�1 second) diphasic waveform. Note the widespread

distribution on this double banana montage, but on a transverse montage one would typically see a maximum (phase reversal) at the midline

(Cz, Fz).

1006 INTRODUCTION TO SLEEP ELECTROENCEPHALOGRAPHY

Less Common Patterns and Normal Variants

Just like human anatomy, sizes and shapes vary somewhat

among individuals, so too do brain waves. There is a wide

range of variability, and it is important to read EEG ‘‘con-

servatively’’ and avoid overreading normal variants [9].

There are many normal variants that have been well

described as benign and have no association with epilepsy.

These include small sharp spikes (also called benign epilep-

tiform transients of sleep, Figure 130.26), wicket spikes

(Figure 130.27), 14 and 6 Hz positive spikes, phantom

spike waves, rhythmic midtemporal theta of drowsiness

(also called psychomotor variant), and subclinical rhythmic

epileptiform discharges of adults. These can be overread as

abnormal. Lambda waves (Figure 130.28) are occipital

sharp transients that resemble POSTS but occur in wake-

fulness when subjects (especially children) scan the envir-

onment. Despite these, the most commonly overread

patterns are ‘‘nameless’’ fluctuations of background

activity [9].

THE ABNORMAL EEG

Like most neurophysiologic tests, EEG is a test of cerebral

function, and as such is for the most part nonspecific as to

etiology. Although earlier investigators have attempted to

identify the reliability of EEG in differentiating types of

lesions, this has clearly become a senseless and futile exer-

Figure 130.24 Slow-wave sleep. This is the same sample at an EEG time-base (left) and at a PSG time-base (right). There is widespread

delta (2 Hz) activity.

THE ABNORMAL EEG 1007

cise in the modern era of neuroimaging [10]. The exercise

to describe EEG abnormalities by pathology (stroke,

abscess, tumor, etc.), which was common in old EEG

texts [11], is clearly obsolete and will not be followed

here.

There are many different ways to classify EEG abnorm-

alities. This chapter will use a very practical classification

developed at the Cleveland Clinic Foundation [12] and used

at many centers. The outline of the classification is shown

in Table 130.1.

Epileptiform Abnormalities

Types of Epileptiform Abnormalities EEG is useful in

epilepsy because it is the only test that gives direct evidence

for epileptogenicity. Most commonly, clinicians have to

rely on interictal abnormalities. Interictal epileptiform

abnormalities include spikes, sharp waves, and spike–

wave complexes. In addition to type and morphology, loca-

tion is very important and is typically either focal or gener-

alized. Generalized epileptiform discharges (i.e., spikes,

sharp waves, polyspikes, spike–wave complexes), as seen

in the primary generalized epilepsies, are usually maximal

in the frontal regions, with typical ‘‘phase reversals’’ at the

F3 and F4 electrodes or less commonly at F7 and F8.

� Spikes and sharp waves are sharp transients that have a

very strong association with epilepsy. The two are

distinguished only by their duration (spikes <70 ms,

sharp waves 70–200 ms), but they have no differences

in terms of clinical significance. Several characteris-

tics help distinguish these from benign epileptiform

variants but this distinction can at times be difficult.

Helpful features that indicate pathologic discharges

include high amplitude, which makes them ‘‘stand

out’’ from ongoing background activity, and after-

going slow waves, which indicate ‘‘disruption’’ of

background activity (Figures 130.29 and 130.30).

The terms ‘‘spikes’’ and ‘‘sharp waves’’ should be

reserved for these abnormalities thought to be patholo-

gical and indicative of epileptogenicity. If one wants to

use purely descriptive (uncommitted) terms, then

‘‘generic’’ phrases should be used, such as ‘‘sharp

transients’’ or ‘‘sharply contoured waveforms.’’

Figure 130.25 REM sleep. This segment shows rapid eye movements (3rd and 10th seconds). Note also the sawtooth waves: notched theta

(�5 Hz) transients in the central regions.


Figure 130.26 Small sharp spikes (SSS) or benign epileptiform transients of sleep (BETS). Typical brief (<50 ms) and low-amplitude (<50

mV) sharp transients in the temporal region, typically in stage 1 or 2 sleep.

Figure 130.27 Wicket spikes. These are typically sharp transients seen in the temporal regions during wakefulness or stage 1 sleep. They

have a symmetric upgoing and downgoing phase, typically arise from an ongoing background activity, and do not disrupt the background

(i.e., no after-going slow wave). They are basically fluctuations of background activity.


TABLE 130.1 Cleveland Clinic EEG Classification

Slow activity

Background slow (BS)

Intermittent slow (IS)a

Intermittent rhythmic slow (IRS)a

Continuous slow (CS)a

Epileptiform patternsa

Spikes

Sharp waves

Benign epileptiform discharges of childhood (BEDC)

Spike–wave complexes (SWCs)

Slow spike–wave complexes (SSWCs)

3 Hz spike–wave complexes (3 Hz SWCs)

Polyspikes

Hypsarrhythmia

Photoparoxysmal response (PPR)

EEG seizure pattern

Artifact obscured EEG

Special patterns

Asymmetry

Excessive fast

Sleep-onset REM

Periodic pattern

Triphasic waves

PLEDsa

Background suppressiona

Special patterns used only in coma

Alpha coma

Spindle coma

Beta coma

Theta coma

Delta coma

ECI

a Abnormalities that require localization:

� Generalized

� Lateralized

� Multiregional

� Regional

� Multifocal

� Focal

Source: From [12].

Figure 130.28 Lambda waves. This sample shows the typical occipital sharp transients that resemble POSTS but occur in wakefulness

when subjects (especially children) scan the environment.


� Polyspikes are usually generalized (rarely focal),

although focal spikes can at times have a multiphasic

‘‘polyspike-like’’ morphology. Polyspikes are multi-

ple repetitive spikes occurring at about 20 Hz and

are typically seen in the primary generalized epilepsy

with myoclonic seizures (Figure 130.31).

� Spike–wave complexes (SWCs) are the repetitive

occurrence of a spike followed by a slow-wave. Since

any significant spike or sharp wave usually is followed

by a slow wave (see earlier), a run of 3 seconds is

required to classify a record as SWC, as opposed to

the categories already mentioned (spike or sharp

wave). SWCs can be divided further into two more

specific types, as follows:

3 Hz SWC. This pattern is characterized by a

frequency of 2.5–4 Hz and a very monomorphic

(‘‘perfectly regular’’) morphology (Figure 130.32).

It occurs in very discrete bursts, and between

bursts the EEG is normal.

Slow SWC. This pattern is not only slower (<2.5

Hz) but also more irregular (less monomorphic)

than the 3 Hz SWC. Bursts are less discrete than

the 3 Hz SWC, and between bursts other abnorm-

alities are seen in symptomatic/cryptogenic epi-

lepsies of the Lennox–Gastaut type.

Hypsarrhythmia. This is characterized by continuous

(during wakefulness) high-amplitude >200 mV

(microvolts) generalized and polymorphic slow-

ing with no organized background, and multifocal

spikes (Figure 130.33). During NREM sleep, the

pattern becomes discontinuous and fragmented,

resembling a burst-suppression or pseudoperiodic

pattern, while it tends to disappear in REM sleep.

� Electrographic Seizures (Ictal Patterns)

Figure 130.29 Typical left anterior temporal sharp wave. The maximum (negativity) is at F7 and T1 (phase reversal). Note the after-going

slow wave. Classification: sharp wave, regional, left frontotemporal.


Focal seizures are discharges characterized by rhyth-

micity and evolution (‘‘buildup’’) in frequency,

amplitude, and distribution. The discharge can

consist of rhythmic theta or delta activity, or

repetitive spikes or sharp waves, but the most

characteristic features of electrographic focal sei-

zures are rhythmicity and evolution (Figure 130.34).

Generalized seizures are also characterized by rhyth-

mic discharges that evolve. They can be variable

and there are rhythmic or periodic abnormalities

that are not ictal (see later under status epilepticus).

Spike–wave complexes are both an interictal and an

ictal pattern. The distinction is arbitrary and based

on duration and the presence of detectable clinical

symptoms (i.e., alteration of awareness).

Electrodecrement consists of abrupt attenua-

tion (‘‘flattening’’) of background activity, often

preceded by a high-amplitude transient, which

can be sharply contoured or broad, or generalized

paroxysmal fast activity (GPFA). This typically is

associated with infantile spasms and tonic or ato-

nic seizures (Figure 130.35).

Figure 130.30 This sample shows a left frontal spike in a patient with left frontal lobe epilepsy. The left panel is a double banana, the right

is a referential montage showing the same sample. Note that there are two different spikes: the first is maximum at F7, the second at Fp1.

Classification: spike, regional left frontal.


Epileptiform discharges have to be differentiated from

normal patterns and normal variants that can look like

epileptiform, and this can at times be difficult. The overin-

terpretation of EEG is a common and underreported pro-

blem [9, 13, 14] and a major cause for the misdiagnosis

of epilepsy. If read conservatively (being careful not to

overinterpret normals), the specificity of EEG for epilepsy

is very high, that is, greater than 90%. It is generally

accepted that <3% of the general population has interictal

epileptiform abnormalities, with a slightly higher percen-

tage in children [15] (largely because of benign focal

epilepsies in that age group, see later) Because of the rela-

tively frequent misinterpretation (overreading) of benign

EEG recordings, it is unfortunately true that ‘‘routine inter-

ictal EEG is one of the most abused investigations in clin-

ical medicine and is unquestionably responsible for great

human suffering’’ [16]. One of the important remedies to

this pitfall is that when in doubt, one should err on the

side of underreading. Clinical experience strongly supports

the view that less harm will be done by underinterpreting an

abnormality than by overinterpreting a normal pattern.

Electrographic Status Epilepticus Status epilepticus (SE)

is typically an obvious clinical diagnosis, but in some situa-

tions an EEG is required to diagnose ‘‘nonobvious’’ SE.

Electrographically, SE can take the form of either repetitive

discrete seizures or, more commonly, a continued pattern of

rhythmic or periodic discharges such as generalized peri-

odic epileptiform discharges (GPEDs) [17, 18]. Unfortu-

nately this pattern (Figure 130.36) is not specific for

electrographic SE and can be seen in severe metabolic

encephalopathies such as anoxic, uremic, or hepatic distur-

bances [19, 20, 21]. Thus the final answer as to whether it

does or does not represent SE in a given patient often will

depend on the clinical circumstances and the response to

treatment [21].

Figure 130.31 Polyspike. This is a typical generalized polyspike in a patient with an idiopathic (‘‘primary’’) generalized epilepsy. Note that

the discharge is followed by about 2 seconds of delta activity. This after-going slow activity indicates substantial disruption of the background

and is a significant argument to consider this discharge pathological and not a normal variant. Classification: polyspike, generalized.


Figure 130.32 3 Hz spike–wave complexes. This shows typical 3 Hz spike–wave complexes in a patient with an idiopathic (‘‘primary’’)

generalized epilepsy. This patient likely has absence seizures. If tested with a clicker, a discharge of this duration (�4.5 seconds) is likely

associated with a brief impairment of awareness. Classification: 3 Hz spike–wave complexes, generalized.

Figure 130.33 Hyparrhythmia. These recordings are from two different patients. Note on both the lack of any reactive background, the very

high-amplitude polymorphic delta activity, and the multifocal spikes. Classification: hypsarrhythmia.


Figure 130.34 Focal seizure. Left temporal seizure (singular), showing the typical rhythmic activity that evolves (build up). Classification:

EEG seizure, regional left temporal.

Figure 130.35 Generalized paroxysmal fast activity followed by attenuation (electrodecrement) in a patient with a symptomatic general-

ized epilepsy of the Lennox–Gastaut type. This could be an interictal (asymptomatic) discharge but could also be an ictal pattern associated

with a tonic or atonic seizure. Classification: EEG seizure, generalized.


EEG-Video Monitoring and the Differential Diagnosis ofEpilepsy Prolonged EEG-video monitoring is indicated

when seizures do not respond to medications [4]. About

20–30% of patients referred for refractory seizures do not

have epilepsy but have psychogenic nonepileptic seizures

(PNESs) instead [3, 13]. A small percentage have syncope

[14, 22]. Occasionally other paroxysmal conditions can be

misdiagnosed as epilepsy, but PNESs are by far the most

common condition, followed by syncope. Unfortunately,

the current average delay in the diagnosis of PNESs is

over 7–9 years and 80% of patients with PNESs have

received antiepileptic drugs [23]. This means that EEG-

video monitoring is probably underutilized and the ‘‘estab-

lished’’ diagnosis of seizures is not verified often enough.

Once the diagnosis of PNESs is suspected clinically [7],

it is usually easily confirmed by EEG-video monitoring,

which can even be performed as an outpatient. In the

hands of experienced epileptologists, the combined electro-

clinical analysis of both the clinical semiology of the

‘‘ictus’’ and the ictal EEG findings allows a definitive diag-

nosis in nearly all cases. The second reason why medica-

tions may fail is that 30% of epilepsies are intractable

and require nonpharmacologic treatments [4].

Encephalopathic Patterns

These patterns are associated with diffuse (generalized)

brain dysfunction, that is, diffuse encephalopathies. Again,

in general, they are completely nonspecific in terms of

etiology. In order of increasing severity, they include:

� Background Slowing (Classification as ‘‘Background

slow’’). There is a posterior dominant background

that is reactive, but the frequency is too slow for age

(<8 Hz after the age of 8) (Figure 130.37).

� Intermittent Generalized Slowing (Classification as

‘‘Intermittent Slow, Generalized’’). There are intermit-

tent bursts of generalized slowing, in the theta or

(more commonly) delta range (Figure 130.38), which

are not attributable to normal circumstances such as

hyperventilation or sleep. A subtype of intermittent

generalized slowing is intermittent rhythmic slowing,

which is usually frontally predominant and thus often

referred as ‘‘FIRDA.’’

� Continuous Generalized Slowing (Classification as

‘‘Continuous Slow, Generalized’’). Here the slowing

is continuous or nearly continuous (>80% of the

Figure 130.36 Periodic pattern, periodic complexes, or generalized periodic epileptiform discharges (GPEDs). This pattern is equally com-

patible with some severe metabolic encephalopathies (e.g., anoxic, uremic, or hepatic) or nonconvulsive status epilepticus. Only the clinical

situation can distinguish among these possibilities, and when in doubt patients with this pattern should be treated for status epilepticus and

monitored for clinical improvement. Classification: periodic pattern, generalized.


Figure 130.37 Background slowing. Note that there is a posterior dominant background, which is even normally reactive (attenuation with

eye opening in the last 2 seconds). However, the frequency is only 6 Hz, which is too slow (for a subject older than 3 years) and thus is

evidence for a mild diffuse encephalopathy. Classification: background slow.

Figure 130.38 Intermittent generalized slowing. Note the brief (�4 sec) burst of polymorphic delta (�2 Hz) activity. When this is

intermittent or reactive, it is indicative of a mild to moderate diffuse encephalopathy. Classification: intermittent slow, generalized.


record) and is unreactive. Unreactive means that

it does not change with external stimulation, and

that there are no state changes such as evidence

for drowsiness, sleep, or alerting responses (Fig-

ure 130.39).

� Periodic patterns are generalized discharges that occur

with periodicity (i.e., at regular intervals) and are often

referred to as generalized periodic epileptiform dis-

charges (GPEDs) (Figure 130.35). The discharges

are often sharply contoured, and the periodicity is

most often 1–3 seconds. The etiology is diverse and

includes nonconvulsive status epilepticus [17, 18] as

well as severe metabolic encephalopathies such as

anoxic, uremic, or hepatic disturbances [19, 20, 21].

Another cause of generalized periodic pattern is

Creutzfeldt–Jakob disease.

Burst-suppression (Figure 130.40) is a subtype of

periodic patterns where the activity between

complexes is suppressed (i.e., <10 mV). This is

indicative of an extremely severe degree of ence-

phalopathy, which in fact immediately precedes

eletrocerebral inactivity. It is typically caused by

either drugs (e.g., anesthetic agents), in which

case it is reversible, or anoxia.

Triphasic waves (Figure 130.41) can also be viewed

as a subtype of periodic patterns. These are high-

amplitude surface-positive sharp transients pre-

ceded and followed by lower amplitude negative

components (thus ‘‘triphasic’’) and occur semi-

periodically at 1–3 seconds. They are typically

seen in metabolic encephalopathies, especially

hepatic or renal.

� Background suppression is the absence of any cerebral

activity greater than 10 mV, including with attempts

at activating/stimulating the patient (unreactive).

This is often used for severely ‘‘flat’’ EEG recordings

that do not meet the criteria for electrocerebral

inactivity (see later).

� Electrocerebral inactivity (ECI) (Figure 130.42) is the

EEG pattern of brain death. The criteria are precisely

defined [24], but it should be remembered that, at least

in the United States, brain death is a clinical diagnosis

and EEG is a supportive test (i.e., not required) for

the diagnosis. The main criteria for ECI include no

Figure 130.39 Continuous generalized slowing. Note the polymorphic delta (�2 Hz) activity. When this is continuous (>80% of the

record) and unreactive, it is indicative of a severe diffuse encephalopathy. Classification: continuous slow, generalized.


Figure 130.41 Triphasic waves. Note the quasiperiodicity, triphasic morphology with a prominent frontal (anterior) positivity, and the

(mild) anteroposterior lag shown by the vertical bold line. Classification: triphasic waves.

Figure 130.40 Burst-suppression. This sample depicts the typical periods of suppression (activity < 10 mV), which in this example last 3–5

seconds, interrupted by ‘‘bursts’’ of activity. Classification: burst-suppression.


activity greater than 2 mV with double interelectrode

distances, complete lack of reactivity, and exclusion

of confounding factors such as sedative drugs and

hypothermia.

Patterns of Focal Abnormalities

Slow Activity Abnormal slow activity is by far the most

common EEG manifestation of focal brain dysfunction.

Like generalized slow activity, focal slow activity can be

either intermittent (classification as ‘‘Intermittent slow,

regional ___’’) or continuous (classification as ‘‘Continuous

slow, regional___’’). Continuous focal slowing is typically

in the delta range and polymorphic and is also known as

polymorphic delta activity (Figure 130.43). This is a very

strong finding, highly associated with the presence of a

structural lesion (but completely nonspecific as to the nat-

ure of the lesion). Continuous focal slow activity is the only

nonepileptiform abnormality that can unequivocally be

interpreted as abnormal as an isolated finding. By contrast,

intermittent focal slowing (Figure 130.44) is a weak and

nonspecific finding, which can even be normal (e.g., ‘‘tem-

poral slowing of the elderly’’).

As outlined above, focal slowing is completely non-

specific as to etiology, and in the era of imaging the EEG

has no role in diagnosing the nature of a lesion. Focal slow-

ing is the most common abnormality associated with focal

lesions of any type, including (but not limited to) neoplastic,

vascular, subdural collections, traumatic, and infectious [10].

Amplitude Asymmetry In this discussion, the term asym-

metry refers to an asymmetry of amplitude and refers to

normal rhythms. By contrast, a focal frequency asymmetry

would be classified as focal slow.

Destructive lesions can attenuate normal rhythms. How-

ever, normal rhythms are never perfectly symmetric in

amplitude, so when to consider asymmetries significant is

not always clear. A good rule of thumb is that, with very

few exceptions, significant focal asymmetries will be asso-

ciated with slowing. In general, as with other types of focal

EEG abnormalities such as slowing, asymmetry is nonspe-

cific as to etiology.

Although asymmetry in amplitude is usually indicative

of dysfunction on the side of depressed amplitude, one

very common exception to this rule is the so-called breach

rhythm [25] (Figure 130.45). This is caused by a skull

Figure 130.42 Electrocerebral inactivity. There is no cerebral activity greater than 2 mV. Because this is recorded at a sensitivity of 2 mV/mm,

there is prominent EKG and 60 Hz artifact. Classification: electrocerebral inactivity.


Figure 130.44 Intermittent lateralized slowing in the left hemisphere. Note the brief (�2 second) burst of delta (�2 Hz) activity over the left

hemisphere. This type of focal slowing, unlike that showed in Figure 130.42, is indicative of mild dysfunction and is a ‘‘weak’’ (nonspecific)

abnormality. Classification: intermittent slow, lateralized left hemisphere.

Figure 130.43 Continuous lateralized slowing in the right hemisphere. Note the clear polymorphic delta (�3 Hz) activity over the right

hemisphere. Such focal slow activity, when persistent (>80% of the record), is strongly associated with a structural lesion. Classification:

continuous slow, lateralized right hemisphere.


Figure 130.45 Breach rhythm. These are two different examples in two patients who are status post craniotomy. Left sample: Note the

increase in amplitude very focally at C3, of what is likely a mu rhythm. Classification: asymmetry, increased mu, left central. Right sample:

Here the increase is in fast (beta) activity at C4. Classification: asymmetry, increased beta, right central. The increased amplitude should not

be mistaken for sharp waves.

Figure 130.46 PLEDs—periodic lateralized epileptiform discharges. These discharges occur periodically, here with a periodicity of 1–1.5

seconds, and are lateralized (here in the right hemisphere). Note that the discharges look to be of low amplitude but in reality are �100 mV

(see scale). Classification: PLEDs, lateralized right hemisphere.


defect, which attenuates the high-frequency filter function

of the intact skull. As a result, faster frequencies (alpha,

spindles, beta) are of higher amplitude on the side of the

defect. Since morphology is often sharply contoured, deter-

mining the epileptogenicity of these discharges can be

extremely difficult, and in this situation one should prob-

ably err on the conservative side by not interpreting them

as epileptiform. Finally, it should be kept in mind that

amplitude asymmetries are best interpreted on referential

montages, since amplitude is highly dependent on interelec-

trode distances.

PLEDs Periodic lateralized epileptiform discharges

(PLEDs) (Figure 130.46) are a special type of focal

abnormality. As implied by their name, they are periodic,

lateralized, and often epileptiform in morphology. Periodi-

city is the most characteristic feature, and the one that sets

PLEDs apart from other focal abnormalities. Periodicity

refers to a relatively constant interval between two dis-

charges and varies between 0.5 and 3 seconds, most often

around 1 second. The epileptiform morphology of the dis-

charges is not invariable, as PLEDs are often closer to slow

waves than to sharp waves in morphology.

PLEDs are caused by acute destructive focal lesions and

are a transitory phenomenon: they tend to disappear in

weeks, even if the causal lesion persists. With time, periodi-

city and duration increase, and the record takes on a less

specific focal slow appearance that is more likely to persist.

By far the most common etiology is an acute cerebrovascu-

lar event, followed by focal encephalitis such as herpes

[26–28]. Although the periodic patterns of Creutzfeldt–

Jakob disease are usually generalized and bisynchronous,

occasionally, especially early in the course, they may be

unilateral or markedly asymmetric and thus take on the

appearance of PLEDs [29].

As implied by their name, PLEDs have a high associa-

tion with clinical seizures, and on average about 80%

of patients with PLEDs will have clinical seizures. In

clinical practice, PLEDs are usually managed as interictal

discharges (spikes or sharp waves). They indicate a

high risk of focal seizures but are usually not treated with

antiepileptic drugs unless there is clinical evidence for sei-

zures, although there is some controversy about this [10].

REFERENCES

1. Ajmone-Masan C, Zivin LS. Factors related to the occurrence

of typical paroxysmal abnormalities in the EEG records of

epileptic patients. Epilepsia 11:361–381(1970).

2. Tatum WO IV, Winters L, Gieron M, Passaro EA, Benbadis S,

Ferreira J, Liporace J. Outpatient seizure identification: results

of 502 patients using computer-assisted ambulatory EEG.

J Clin Neurophysiol 18:14–19(2001).

3. Benbadis SR, O’Neill E, Tatum WO, Heriaud L. Outcome of

prolonged EEG-video monitoring at a typical referral epilepsy

center. Epilepsia 45:1150–1153(2004).

4. Benbadis SR, Tatum WO IV, Vale FL. When drugs don’t work:

An algorithmic approach to medically intractable epilepsy.

Neurology 55:1780–1784(2000).

5. Anonymous. Patient referral to specialty epilepsy care. Epilep-

sia 31:S10–S11(1990).

6. Benbadis SR, Wyllie E, Bingaman W. Intracranial EEG and

localization studies. In: Wyllie E (Ed), The Treatment of Epi-

lepsy: Principles and Practice, 3rd ed. Lippincott, Williams &

Wilkins, Philadelphia, 2001, pp 1067–1075.

7. Benbadis SR. Psychogenic non-epileptic seizures. In: Wyllie E

(Ed), The Treatment of Epilepsy: Principles and Practice. 4th

ed. Lippincott, Williams & Wilkins, Philadelphia, in press.

8. Lesser RP, Luders H, Dinner DS, Morris H. An introduction

to the basic concepts of polarity and localization. J Clin

Neurophysiol 2:45–61(1985).

9. Benbadis SR, Tatum WO. Over-intepretation of EEGs

and misdiagnosis of epilepsy. J Clin Neurophysiol 20:42–

44(2003).

10. Benbadis SR. Focal disturbances of brain function. In: Levin

KH, Luders HO (Eds), Comprehensive Clinical Neurophysiol-

ogy. Saunders, Philadelphia, 2000, pp 457–467.

11. Niedermeyer E, Lopes da Silva F. Electroencephalography:

Basic Principles, Clinical Applications, and Related Fields,

3rd ed. Williams & Williams, Baltimore, 1993.

12. Luders H, Noachtar S (Eds.) Atlas and Classification of

Electroencephalography. Saunders, Philadelphia, 2000.

13. Smith D, Defalla BA, Chadwick DW. The misdiagnosis of epi-

lepsy and the management of refractory epilepsy in a specialist

clinic. QJM 92:15–23(1999).

14. Eiris-Punal J, Rodriguez-Nunez A, Fernandez-Martinez N,

Fuster M, Castro-Gago M, Martinon JM. Usefulness of the

head-upright tilt test for distinguishing syncope and epilepsy

in children. Epilepsia 42:709–713(2001).

15. Cavazzuti GB, Capella L, Nalin A. Longitudinal study of epi-

leptiform EEG patterns in normal children. Epilepsia 21:43–

55(1980).

16. Chadwick D. Diagnosis of epilepsy. Lancet 336:291–295(1990).

17. Towne AR, Waterhouse EJ, Boggs JG, Garnett LK, Brown AJ,

Smith JR Jr, DeLorenzo, RJ. Prevalence of nonconvulsive

status epilepticus in comatose patients. Neurology 54:340–

345(2000).

18. Treiman DM. Electroclinical features of status epilepticus.

J Clin Neurophysiol 12:343–362(1995).

19. Brenner RP, Schaul N. Periodic EEG patterns: classification,

clinical correlation, and pathophysiology. J Clin Neurophysiol

7:249–267(1990).

20. Husain AM, Mebust KA, Radtke RA. Generalized periodic

epileptiform discharges: etiologies, relationship to status epi-

lepticus, and prognosis. J Clin Neurophysiol 16:51–58(1999).

21. Benbadis SR, Tatum, WO IV. Prevalence of nonconvulsive

status epilepticus in comatose patients (letter). Neurology

55:1421–1423(2000).

REFERENCES 1023

22. Zaidi A, Clough P, Cooper P, Scheepers B, Fitzpatrick

AP. Misdiagnosis of epilepsy: many seizure-like attacks

have a cardiovascular cause. J Am Coll Cardiol 36:181–

184(2000).

23. Benbadis SR. How many patients with pseudoseizures receive

antiepileptic drugs prior to diagnosis? Eur Neurol 41:114–

115(1999).

24. American Electroencephalographic Society. Guideline three:

minimum technical standards for EEG recording in suspected

cerebral death. J Clin Neurophysiol 11:10–13(1994).

25. Cobb WA, Guillof R, Cast J. Breach rhythm: the EEG related

to skull defects. Electroencephalogr Clin Neurophysiol

47:251–271(1979).

26. Schaul N, Green L, Peyster R, Gotman J. Structural determi-

nants of elctroencephalographic findings in acute hemispheric

lesions. Ann Neurol 20:703–711(1985).

27. Schwartz MS, Prior PF, Scott DF. The occurrence and evolu-

tion in the EEG of a lateralized periodic phenomenon. Brain

96:613–622(1973).

28. Snodgrass SM, Tsuburaya K, Ajmone-Marsan C. Clinical signif-

icance of periodic lateralized epileptiform discharges: relation-

ship to status epilepticus. J Clin Neurophysiol 6:159–172(1989).

29. Heye N, Cervos-Navarro J. Focal involvement and lateraliza-

tion in Creutzfeldt–Jakob disease: correlation of clinical,

electroencephalographic and neuropathological findings. Eur

Neurol 32:289–292(1992).


THE NORMAL EEG 1005 - USF Healthhsc.usf.edu/com/epilepsy/EEG introduction (Lee Chiong) part...

Documents

Transcript of THE NORMAL EEG 1005 - USF Healthhsc.usf.edu/com/epilepsy/EEG introduction (Lee Chiong) part...