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Henri Gastaut observed that PMR occurs in 0.3 percent of normal subjects, 3 percent of
epileptic patients, and 17 percent of patients with psychiatric disorders. The PMR is also
enhanced in early stages of alcohol withdrawal in chronic alcoholics and after a sudden
withdrawal from barbiturates and other sedatives. The clinical relevance of PMR is yet to be
fully explored in systematic research.
In terms of activating EEG abnormalities, one looks for a photoconvulsive response that
consists of bilaterally synchronous, usually diffuse, spike-and-wave discharges of various
frequencies or diffuse, multiple spike-wave complexes. When the resting EEG is normal, and
a seizure disorder or behavior that is suspected to be a manifestation of a paroxysmal EEG
dysrhythmia is suspected, PS can be a valuable activation to use. Its primary limitation,
especially as a routine procedure, is the not insignificant false positive incidence of
photoconvulsive EEG responses in individuals with no history of seizure disorder and no
current symptoms suggestive of such. The persistence of the spike-wave discharges after the
cessation of the PS may also be indicative of a photoconvulsive response. Moreover, the
spread of the spike-wave activity to other leads besides the occipital leads may also be
indicative of a pathological process.
Sleep
Largely because of the pioneering studies and perseverance of Fred and Erna Gibbs, EEG
recording during sleep, natural or sedated, is now widely accepted as an essential technique
for eliciting a variety of paroxysmal discharges, when the wake tracing is normal, or for
increasing the number of abnormal discharges to permit a more definitive interpretation to be
made. A variety of focal and diffuse spike and spike-wave discharges, as well as several
minor or controversial paroxysmal patterns, occurs much more often during drowsiness and
light sleep than during the wake recording, and some of them are seen almost exclusively
during the sleep recording. Paroxysmal patterns differ substantially among themselves in the
degree to which their appearance in the tracing is sleep activation dependent (Fig. 1.14-13).
Although most clinical EEGs should contain a drowsy- and light-sleep tracing to be
complete, deep stages III and IV sleep with generalized high-voltage delta slowing has almost
no activating property and is not clinically useful.
Gambar:
FIGURE 1.14-13 Percent of various electroencephalography patterns detected only during
drowsiness or sleep, or both. To be read as follows: Of all cases of multiple spike foci, 30
percent required a drowsy or sleep, or both, recording for their detection, and 70 percent were
detected during a wake recording. RMTD, rhythmic mid-temporal discharges. (Data abridged
from Gibbs FA, Gibbs EL: How much do sleep recordings contribute to the detection of
seizure activity? Clin Electroencephalogr. 1971;2:169; and Struve FA, Pike LE: Routine
admission electroencephalograms of adolescent and adult psychiatric patients awake and
asleep. Clin Electroencephalogr. 1974;5:67. A greatly expanded graph with 27
electroencephalography patterns can be found in Struve FA. Clinical electroencephalography
as an assessment method in psychiatric practice. In: Hall RCW, Beresford TP, eds. Handbook
of Psychiatric Diagnostic Procedures. Vol 2. New York: Spectrum Publications, 1985.)
Sleep Deprivation
It has been shown that the CNS stress produced by 24 hours of sleep deprivation alone can
lead to the activation of paroxysmal EEG discharges in some cases. This effect is presumably
independent of the known activating properties of natural or sedated sleep itself. Sleep
deprivation is without risk for the healthy patient but may be contraindicated for patients

medically or physically compromised. The primary disadvantage is the tendency for sleep
deprived individuals to enter into deep sleep (stages III and IV) immediately at the start of the
recording, thus reducing the chances of detecting spike activity. The optimal method is to
ensure that the subject stays awake until the recording begins and remains so for the initial
recording period, after which a gradual transition into drowsy sleep can be observed.
Miscellaneous Special Activations
It has long been recognized that seizure manifestations or aberrant behaviors that might rest
on a seizure basis can be triggered by specific stimuli. In this regard, cases of audiogenic,
musicogenic, photogenic, and reading epilepsy readily come to mind, even though such cases
are rare, and most practitioners have never encountered them. Seizure phenomena related to
other sensory system input (e.g., somatosensory and gustatory) are even more rare.
Sometimes, it may be possible for laboratory personnel to duplicate or approximate sensory
triggers in various modalities to determine if they activate EEG seizure discharges combined
with overt symptoms. Psychiatrists evaluating a patient with an atypical behavioral reaction
to a drug (for example, an unusually explosive reaction after a small amount of alcohol or
other abused drug or some other highly idiosyncratic response) may want to consider a drugactivated EEG to determine if ingestion of the drug activates any type of seizure or other
paroxysmal abnormality in the tracing that might have explanatory clinical value.
NORMAL ANALOG EEG TRACING
Although the appearance of the EEG tracing may vary somewhat between individuals, the
range of frequencies, voltages, and waveforms that characterize the normal EEG during wake
and sleep has been well established. Nonetheless, there are certain waveforms that continue
to engender disagreements regarding their place on the normal-abnormal continuum, and
several of these controversial waveforms may have significant importance to psychiatry.
Stated somewhat differently, the normal boundaries of the EEG, although well established for
evaluating neurological or medical disorders, are not nearly as well established for
psychiatric disorders. Furthermore, the dynamic nature of many psychiatric disorders,
combined with the fact that many EEG findings and their associated symptoms are known to
cut across specific psychiatric diagnostic categories, makes the electroclinical relationships
between psychiatric syndromes and EEG more complex. Nonetheless, normative patterns that
are not controversial are discussed in this section.
Normal Intrinsic Frequencies
The normal EEG tracing is composed of a complex mixture of many different frequencies.
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Furthermore, some frequency bands are expressed more strongly over some cortical regions
than others, and, in addition, the frequency profile varies considerably as the recording moves
from alert wakefulness into sleep. Following the lead of Berger, discrete frequency bands
within the broad EEG frequency spectrum are designated with Greek letters.
Alpha
Highly rhythmic alpha waves with a frequency range of 8 to 13 Hz constitute the dominant
brain wave frequency of the normal eyes-closed wake EEG. Through middle age, the vast
majority of normal adults have an alpha frequency at, or close to, 10 Hz, whereas, with
normal geriatric populations, a slower alpha frequency of 8 to 9 Hz is not uncommon. Alpha
activity is also most prominent over the posterior cortex, particularly the parietal, posterior
temporal, and occipital cortex, with the occipital region being best suited to show this
activity. The registration of alpha activity diminishes as one records from more anterior
locations, and this frequency is rare at prefrontal electrode sites. Alpha activity is abolished,
or at least severely attenuated, by eye opening, and alpha activity also disappears with
drowsiness and sleep. It is often not appreciated that alpha activity can be highly responsive

to cognitive activity, such as focused attention or concentration. For example, under eyesclosed recording conditions, alpha can be blocked or attenuated by engaging in visual
imagery, numeric calculation, or almost anything requiring significant concentration (Fig.
1.14-14). Alpha frequency can be increased or decreased by a wide variety of
pharmacological, metabolic, or endocrine variables
Gambar..
FIGURE 1.14-14 Resting, eyes-closed, awake electroencephalography recording. Effect of
mental concentration on alpha activity. While instructed to keep the eyes closed, at the heavy
vertical line, the patient is asked to divide 389 by 7. Note the immediate blocking of alpha
activity.
Theta
Waves with a frequency of 4.0 to 7.5 Hz are collectively referred to as theta activity. A small
amount of sporadic, arrhythmic, and isolated theta activity can be seen in many normal
waking EEGs, particularly in frontal-temporal regions. Although theta activity is limited in
the waking EEG, it is a prominent feature of the drowsy and sleep tracing. Excessive theta in
wake, generalized or focal in nature, suggests the operation of a pathological process.
Delta
Delta activity (equal to or less than 3.5 Hz) is not present in the normal waking EEG but is a
prominent feature of deeper stages of sleep. The presence of significant generalized or focal
delta in the wake EEG is strongly indicative of a pathophysiological process.
Beta
Frequencies that are faster than the upper 13 Hz limit of the alpha rhythm are termed beta
waves, and they are not uncommon in normal adult waking EEGs, particularly over frontalcentral regions. It is also not uncommon for beta to appear as runs of rhythmic activity as
opposed to sporadic isolated waves. Although there is no real upper limit designation for beta
activity, the practical constraints of recording apparatus and filtering requirements tend to
restrict beta activity to less than 40 or 50 Hz. The voltage of beta activity is also almost
always lower than that of activity in the other frequency bands described previously.
Researchers sometimes divide beta activity into low and high beta frequencies, and some
have even specified the higher frequencies by using designations, such as gamma 1 (25 to 35
Hz), gamma 2 (35 to 50 Hz), and gamma 3 (50 to 100 Hz).
Changes with Age
The appearance of the EEG tracing changes dramatically from birth to advanced age. From a
preponderance of irregular medium- to high-voltage delta activity in the tracing of the infant,
EEG activity gradually increases in frequency and becomes more rhythmic with increasing
age. Rhythmic activity in the upper thetalower alpha range (7 to 8 Hz) can be seen in
posterior areas by early childhood, and, by the time mid-adolescence is reached, the EEG
essentially has the appearance of an adult tracing. The interpretation of EEGs secured from
children demands a solid grounding in the age-related changes during this period and is best
performed by one specializing in pediatric EEG.
Sleep Patterns
The EEG patterns that characterize drowsy and sleep states are different from the patterns
seen during wake state. A detailed accounting of the nuances of sleep patterns would exceed
the scope of this chapter. In simplistic terms, the rhythmic posterior alpha activity of the
waking state subsides during drowsiness and is replaced by irregular low-voltage theta
activity. As drowsiness deepens, slower frequencies emerge, and sporadic vertex
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sharp waves may appear at central electrode sites, particularly among younger persons.
Finally, the progression into sleep is marked by the appearance of 14-Hz sleep spindles (also
called sigma waves), which, in turn, gradually become replaced by high-voltage delta waves
as deep sleep stages are reached.
Artifacts
Artifacts are electric potentials of nonbrain origin that are in the frequency and voltage range
of EEG signals and that are detected by scalp electrodes. Most EEGs contain some artifacts,
and the electroencephalographer must identify them, particularly those that can closely mimic
real brain waves, before making an interpretation. Common artifacts include eye blinks,
vertical or lateral eye movements, frontalis EMG, muscle potentials from jaw clenching,
perspiration artifact (galvanic skin response), and head movement. Less frequently seen are
artifacts from electrocardiogram (ECG) (especially in heavy barrel-chested subjects
recorded with a monopolar EEG montage), lateral rectus eye muscle spikes, lingual
movements, and a variety of electrode and amplifier problems. The competent technologist is
capable of modifying recording conditions and patient instructions to distinguish artifact from
brain waves when necessary, and, when this competence is not available, the quality of the
EEG may become compromised. Automatic artifact rejection programs exist for some
computerized research applications, but they have not strongly entered the clinical arena.
EEG ALTERATIONS FROM MEDICATIONS AND DRUGS
A great many medications, as well as substances consumed for recreational or abuse
purposes, can produce some degree of alteration in the EEG. This section attempts to
highlight those compounds most relevant to clinical and research psychiatry.
Psychotrophic Medications (General Considerations)
It is well known that psychotropic agents can affect the EEG. For the routine EEG, with the
exception of the benzodiazepines and some compounds with a propensity to induce
paroxysmal EEG discharges, there is little, if any, clinically relevant effect when the
medication is not causing any toxicity. Benzodiazepines, even in small doses, always
generate a significant amount of beta activity that is seen diffusely. This response is so
universal that it has been suggested that, if a particular brain region fails to exhibit the
expected benzodiazepine-induced beta activity, that area may be dysfunctional.
Psychotropic Medications (Toxic Effects)
For a long time, it has been accepted that the EEG is sensitive to the neurotoxic effects of
psychotropic medications, and clinical vignettes illustrating the value of EEG in detecting a
neurotoxic reaction to medications when a clinical deterioration was evident have been
reported. It is
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often specifically stressed that such a scenario could occur at any time during the course of
treatment, because many factors impact the patient, and the symptoms could be subtle. An
EEG investigation may be useful when patients undergoing long-term therapy present with
clinical deterioration, particularly if the patient is known to be taking the medication, and the
serum plasma levels are within the therapeutic range. Such clinical situations may also
highlight the need for having baseline EEGs available for comparison when a patient presents
with clinical exacerbation. EEG norms currently available are based on cross sectional
evaluations and do not take into account the dynamic nature of psychiatric disorders or the
constantly changing medication status. Thus, in terms of possible toxicity, the effects of
medications on the routine (visually inspected) EEG remain of immediate significance and of
relevance to the everyday management of patients. The appearance of significant diffuse EEG
slowing in a patient who is receiving psychotropic medications and whose clinical condition

is not stable (particularly the elderly) should prompt the clinician to consider medication
toxicity, as well as other causes of encephalopathy (e.g., electrolyte imbalance and thyroid
problems, to name only two).
Psychotropic DrugInduced EEG Abnormality (Nonparoxysmal and Paroxysmal)
Almost from the time psychotropic medications were introduced, it was known that some of
these compounds could precipitate EEG abnormalities, including paroxysmal EEG discharges
(spike and spike-wave activity) in some individuals. Usually, medication-induced paroxysmal
EEG activity remains behaviorally silent and is not accompanied by iatrogenic overt seizure
manifestations. A little more than 20 years ago, a team of investigators from the Psychiatry
Department at the University of Munich led by J. Kuglar conducted an exceptionally large
retrospective study (680 EEGs obtained from 593 patients) of the effects of psychotropic
agents on the EEG and reported that the highest proportion of abnormal EEGs occurred in
clozapine (Clozaril)treated patients (59 percent), followed by lithium (Eskalith, Lithobid)
(50 percent). The overall proportion of paroxysmal EEG discharges was 13 percent, and
actual seizures were witnessed with treatment with clozapine, lithium, and maprotiline
(Ludiomil). Lithium continues to be widely used in the treatment of bipolar disorder, as well
as other episodic behavioral syndromes, including aggressive tendencies. This compound is
capable of causing abnormal generalized slowing or paroxysmal activity, or both, including a
10 percent incidence of toxic delirium, in normal research volunteers and patients undergoing
lithium treatment.
Recent times have seen the emergence of several new atypical antipsychotic compounds.
Although clozapine has received extensive EEG study and is now recognized as a compound
highly associated with risk of induced EEG abnormality, information regarding the other new
compounds remains sparse. A research team led by Franca Centorrino recently made a
substantial effort to fill this knowledge gap. In their study, the effects of typical and atypical
antipsychotic medications were compared using EEG recordings from 323 hospitalized
psychiatric patients (293 on antipsychotic medications and 30 not receiving antipsychotic
drugs) who were graded blind to diagnosis and treatment for type and severity of EEG
abnormalities. Abnormal EEGs occurred in 19 percent of treated patients and 4 percent of
untreated patients; however, the risk for EEG abnormality varied widely among the different
types of medication (Fig. 1.14-15). The highest incidence of EEG abnormalities was
associated with clozapine (47 percent) and was somewhat lower with olanzapine (Zyprexa)
(38.5 percent) and risperidone (Risperdal) (28 percent). There were no EEG abnormalities
seen in association with quetiapine (Seroquel). The incidence of EEG abnormalities in
association with typical neuroleptics was lower, in general, than with atypical antipsychotics.
The clinical significance of EEG abnormalities associated with the therapeutic use of
antipsychotic agents, particularly in the absence of any indications of seizures or
encephalopathic effects, remains an open research question.

Gamabar 3
FIGURE 1.14-15 Risk of electroencephalography (EEG) abnormalities with specific
antipsychotic agents among 293 hospitalized psychiatric patients. (From Centorrino F et al.:
EEG abnormalities during treatment with typical and atypical antipsychotics. Am J
Psychiatry. 2002;159:109, with permission.)
Pharmaco-EEG
The effects of psychotropic drugs on the frequency and power distribution of the different
EEG spectra, using topographic QEEG methods, is the subject of a vast and growing field

entitled pharmacoelectroencephalography (pharmaco-EEG). The focus of this field is to be

able to predict the likely psychotropic effect of newly developed agents (i.e., antipsychotic vs.
antidepressant vs. anxiolytic). Researchers in this field are also developing methods to predict
the responsiveness of a particular patient to a particular compound by using test doses with
the hopes of avoiding having to subject patients to 3 to 6 weeks of a medication trial before
realizing that this agent is not helpful.
Drugs of Abuse
Recreational and addictive involvement with abuse drugs is a significant phenomenon in
society today, and it is becoming of increasing concern for those involved in the assessment
and treatment of psychiatric disorders. Nearly all abuse drugs are capable of altering the
frequency spectrum of the EEG, and the degree of alteration varies with recreational versus
heavy use and whether the EEG was secured during or close to acute exposure (intoxication),
during intervening nonintoxication states, or during clinical withdrawal in the addicted
individual.
With only infrequent exceptions, the use of an abuse drug does not introduce frank clinical
abnormalities into the visually analyzed EEG tracing. This is especially true for recreational
drug use and is even largely true for dependent and addictive use, as well, and, for this
reason, drug abuse alone is not a sufficient reason for EEG referral. Although the alterations
of EEG frequency and voltage in the visually analyzed EEG produced by many abuse drugs
are often unimpressive, topographic QEEG analyses often reveal marked alterations of the
EEG
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spectrum that constitute significant deviations from population norms, even though the
clinical implications may not be clear. Because of this, they constitute significant problems
for researchers using topographic QEEG measures in their work. For example, if one wants to
establish a QEEG profile for a particular diagnostic group or a particular psychotropic
medication (i.e., as in pharmaco-EEG research), the QEEG effects of certain abuse drugs may
constitute serious methodological confounds, rendering any results scientifically
uninterpretable.
Alcohol
There is considerable consensus that an increase in the amount of alpha activity and a slight
slowing of alpha frequency typically accompany alcohol consumption and that higher blood
alcohol levels increase the amount of theta in the tracing. Some reports have indicated that
chronic alcohol consumption may be associated with a lower voltage and slightly faster
resting EEG, although the clinical relevance of this remains obscure. Higher-frequency beta
activity may be substantially increased in the addicted alcoholic undergoing withdrawal, and,
if delirium tremens complicates the clinical picture, excessive fast activity may dominate the
EEG tracing (whereas delirium from other causes is associated with generalized slowing).
Opiates
Opiate effects on the EEG are similar to those of alcohol and involve slight reductions in
alpha frequency. They may also increase the voltage of the EEG, particularly the power of
theta and delta activity. However, when an opiate overdose produces a comatose clinical
presentation, the EEG usually consists of clinically abnormal diffuse slowing.
Barbiturates
When barbiturates are taken for medical purposes or for recreational or habitual abuse, beta
activity is introduced into the EEG, particularly over frontal regions. The barbiturate effect on
the EEG is thus opposite to that of alcohol. However, sudden, abrupt withdrawal from
barbiturates after long-term dependence can produce EEGs containing generalized

paroxysmal activity and spike discharges, which are often not associated with overt motor
seizure manifestations, and these effects may be seen for days or even a few weeks after last
drug exposure.
Marijuana
Use of marijuana (tetrahydrocannabinol [THC]) is widespread in society and not infrequently
constitutes a comorbid feature of psychiatric conditions. Exposure to THC produces highly
characteristic alterations of the waking EEG that can be appreciated visually but are best
documented through use of topographic QEEG study. The EEG response to smoking THC is
rapid. The voltage, amount, and interhemispheric coherence of alpha activity increases
dramatically over the bilateral frontal cortex (areas in which alpha activity normally is only
rarely seen) within 2 minutes of the first THC inhalation. The frequency of the alpha activity
also slows by as much as 0.5 Hz. Some studies have shown that increases in frontal alpha are
accompanied by subjective feelings of euphoria. With the chronic user, the EEG always
shows increased frontal alpha and slowed alpha frequency, even when THC urine levels are
absent, to the degree that a suspicion of THC use from mere inspection of the tracing would
not be unreasonable.
Cocaine
Chronic cocaine exposure produces topographic QEEG changes similar (but not identical) to
those seen with marijuana abuse, and the EEG effects can last throughout 6 or more months
of abstinence. Primary effects are reported to consist of increased relative power (i.e.,
amount, abundance) of alpha activity seen maximally over the frontal cortex combined with a
deficit of the amount and voltage of theta and delta frequencies.
Inhalants
Inhalation abuse of volatile substances (e.g., airplane glue, cleaning fluid, paint thinner, and
gasoline) can produce a nearly instantaneous sensation of euphoria, and, in the early period of
use, there may be no obvious residuals after the acute response subsides. However, with
continued inhalant abuse, neurological and neurocognitive deficits, which are often quite
serious, can emerge, and they are not always completely reversible with abstinence. The
immediate effects of inhalation of volatiles on the human EEG appear not to have been well
studied. Where persistent neurological or neurocognitive sequelae follow chronic inhalant
abuse, clinically abnormal diffuse EEG slowing in the lower theta to upper delta range may
be seen.
Hallucinogens
Drugs, such as lysergic acid diethylamide (LSD) and mescaline, appear to have only minor
effects on the visualized EEG and do not produce clinically relevant changes.
Tobacco
Like many of the drugs reviewed previously, tobacco does not appear to produce dramatic
alterations in the analog EEG. However, topographic QEEG analyses reveal striking EEG
changes with acute exposure to, as well as withdrawal from, tobacco. The immediate effects
of smoking include a decrease in slower frequencies (especially theta), increased power of
frequencies in the upper one-half of the alpha frequency band, and beta activity. Twenty-four
hours of tobacco deprivation produce a marked decrease in alpha frequency, with a
corresponding marked increase in the relative power (amount) of theta activity. The effects of
acute smoking and abstinence are essentially opposite to one another.
Caffeine
Coffee and products containing caffeine are also ubiquitous in this culture. The use of
caffeine is of little concern to the electroencephalographer interpreting the visually analyzed
EEG. Withdrawal from caffeine in the caffeine-dependent individual, however, produces a
markedly significant increase in the amplitude, or voltage, of theta activityan effect that is
reversible within 15 minutes of consuming one cup of coffee.

CLINICAL INTERPRETATION OF THE EEG

The interpretation of the standard or analog EEG tracing is essentially a problem of learning
to recognize all of the myriad intrinsic waveforms, their expected distributions over the
various cortical regions, and their range of variation in amplitude and degree of symmetry.
Although there is little doubt that 16, 32, or even 64 channels of oscillating waves appear
quite confusing to the beginner, there is an inherent regularity to the brain's electrical output
that the experienced electroencephalographer comes to recognize. Because of this inherent
regularity, the intrinsic EEG rhythms and their range of variation that characterizes the wake,
drowsy, and various sleep states become easily recognized through practice and experience.
Furthermore, various artifacts (electrical potentials of nonbrain origin) produce localized or
regional waveforms of distinctive shapes, allowing for their identification. The primary job of
the interpreter is to identify those EEG waveforms that appear to fall outside of what one
might call the normal range of variation of the intrinsic background activity and that are
therefore (1) frankly abnormal with known pathophysiological correlates or (2) controversial
abnormal waveforms of potential clinical relevance, pending the results of further continuing
clinical investigation. The number of accepted and still controversial EEG abnormalities is
quite large and well beyond the scope of this chapter. For the purpose of illustration only, four
classic abnormal EEG patterns are shown (Figs. 1.14-16, 1.14-17, 1.14-18, and 1.14-19).
Gambar 4
FIGURE 1.14-16 Diffuse three-per-second spike-and-wave discharge of the petit mal type
with a multiple spike component. Female patient, 16 years of age. Previous history of petit
mal seizures and rare grand mal attacks. At a previous psychiatric facility, the diagnosis was
changed to hysterical seizures after a psychological evaluation.
Gambar 5
FIGURE 1.14-17 Focal slow (delta), right prefrontal spreading with reduced voltage to right
anterior and mid-temporal and right central. During the sleep recording (not shown), sleep
spindles were absent in the right hemisphere. Female patient, 49 years of age. No prior
psychiatric history. Recent emergence (over 6 months) of depression, mild episodic
confusion, symptoms of hyperthyroidism, and pathological crying. Glioblastoma found at
surgery.
Gambar 6
FIGURE 1.14-18 Focal negative spike and spike-wave discharges in the right anterior
temporal cortex and often spreading with reduced voltage throughout the right hemisphere.
Adult male patient. Complex partial seizures (psychomotor). Psychiatric outpatient with
infrequent periods of sudden unresponsiveness during which time he would make grunting
and guttural sounds and speak with incoherent words and syllables with amnesia for these
events. (His girlfriend, who was involved in New Age phenomena, was convinced that he
was communicating with spirits during these unresponsive spells and did not want him to be
medicated.)
Gamabr 7
FIGURE 1.14-19 Diffuse spike-and-wave discharges during the sleep recording. The waking
electroencephalography (EEG) was within normal limits. Female patient, 15 years of age.
Admitted to inpatient adolescent psychiatric unit with the complaint of serious temper
dyscontrol and episodic dizzy spells.
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Interpreter Reliability
Because the EEG record is obtained by precisely measuring the microvolt fluctuations of
electrical potentials over the scalp, a misconception often emerges that EEG interpretation is
purely objective in the sense that measurements of temperature, weight, length, and volume
are objective. In truth, there is a large, subjective element of judgment in EEG interpretation,
and the achievement of skill in this area only follows a period of thorough training and the
guiding hand of clinical experience. Accepted EEG abnormalities do not always appear in the
EEG tracing in clear-cut textbook form, and there is always a gray area in which EEG activity
that is clearly normal becomes blurred and shades off into waveforms that are unequivocally
abnormal.
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Although the important area of reliability of clinical EEG interpretation has not enjoyed
extensive study over the years, the balance of available evidence suggests that high levels of
statistically (and clinically) significant interpretation reliability can be obtained. The two
methods for assessing reliability involve comparing the independent readings of two or more
EEG interpreters (interjudge reliability) and asking one electroencephalographer to blindly
reinterpret a sample of EEGs after an elapsed time (intrajudge reliability). A review of
interjudge and intrajudge interpretative comparisons involving 1,567 clinical standard EEGs
revealed a weighted average of 91 percent interpretive agreement over 11 separate studies
(see the 1985 article by Frederick Struve). It should be noted that interpretive differences
usually involve disagreements over gray areas in which alterations in the frequency,
symmetry, or amplitude of the intrinsic EEG activity begin to shade off into what, by
consensus, would be considered outside of normal limits. In such transition areas in which the
dividing line is not sharply precise, statements such as borderline slowing are sometimes used
to denote the understandable uncertainty that is involved. When disagreements in this
borderline region are removed from consideration, interpretive agreements ranging from 95
to 98 percent are not uncommon.
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Normal versus Abnormal: General Considerations
One of the factors that may have limited the perception of clinical EEG as a useful
assessment tool in psychiatry is the simplistic attempt to conceptualize EEG findings as a
normal-versus-abnormal dichotomy. Psychiatric practitioners commonly ask if their patient's
EEG is abnormal and seem content with an affirmative or negative answer. Furthermore,
much of the published research literature reports the percentage of abnormal EEGs in this or
that study population without much in the way of clarifying discussion. In actuality, the
simple normalabnormal dichotomy has little to recommend it, and, for the practicing
psychiatrist, it may lead to conceptual confusion. Rather than being considered as a
dichotomy, the range of EEG findings exists on a broad continuum anchored on one end by
unequivocally normal EEGs and extending in the other direction through a long parade of
findings from those with unclear yet potential clinical relevance all the way to findings that
correlate with life-threatening pathology. Some EEG patterns that are correctly classified as
abnormal are on the low end of the continuum of clinical expressivity and may not always
contribute strongly to diagnostic decisions. The psychiatrist receiving a report (without
clarification) of a minor finding of limited clinical relevance may understandably begin to
question the value of EEG when no current or past history organic signs are detected. The

bottom line is that one should not ask simply if an EEG is abnormal, as if it were one side of
a dichotomy, but instead should ask what specific kind of finding was present and what is the
range of possible clinical correlates associated with it.
An additional confusion caused by unwise reliance on the normal-abnormal dichotomy
involves reports in review articles and book chapters stating that 10 percent, 15 percent, or
even 20 percent of the normal population have abnormal EEGs. Because such statements are
almost never properly clarified, they tend to be terribly misleading. Clearly, there can be an
understandable reluctance to follow up an abnormal EEG report if one has read in a
presumably authoritative source that 20 percent of the normal population have abnormal
EEGs. More importantly, there may also be an equally understandable reluctance to refer a
patient for EEG study for the same reason. To place the issue in proper perspective, the
reports of substantial percentages of abnormal EEGs within the normal population are heavily
skewed by the inclusion of minor EEG findings which often have low levels of clinical or
diagnostic relevance. Furthermore, Nashaat Boutros, Hugh Mirolo, and Struve provided a
comprehensive review of the literature on EEG findings in normal control populations that
highlights the fact that most control studies have been seriously compromised by failure to
screen subjects for a variety of medical and psychiatric variables that can impact on the EEG
results. One of the authors (see the 1985 article by Struve) previously reanalyzed data from
numerous published EEG-control population studies. When borderline EEG findings were
removed from the data, the incidence of EEG abnormality dropped to 3.2 percent of 6,182
adult control subjects and 3.5 percent of 1,450 children control subjects, and the prevalence
of accepted paroxysmal EEG abnormalities dropped to only 1.14 percent of a sample of
11,560 mixed-age control subjects.
Topographic Quantitative Electroencephalography (QEEG)
In QEEG analyses, raw analog waveforms are replaced by quantitative estimates of absolute
power (V2), the percentage of relative power and mean frequency at all electrode locations
for all four standard EEG frequency bands (alpha, theta, delta, and beta). In addition,
estimates of power asymmetry and interhemispheric coherence between homologous regions
can be obtained, and some systems permit estimates of intrahemispheric coherence values as
well. It has been demonstrated that many QEEG measures show considerable variation with
age or are not distributed normally, or both. Recognizing these constraints, E. Roy John has
developed a sophisticated topographic QEEG method of analyses (termed neurometrics) in
which raw quantitative measures extracted from the artifact-free analog EEG are age
regressed and transformed to achieve a gaussian curve (e.g., a normal, bell-shaped curve).
The neurometric normative database spans the age range and is comprised of large numbers
of well-screened subjects free of significant medical or psychiatric complaint. Because all of
the QEEG variables are z-transformed, it becomes possible to express, in standard deviation
units, the degree to which any of a given patient's QEEG values deviate above or below the
mean for the normal population for their age. Thus, unlike standard EEG interpretation,
which relies on waveform recognition, interpretation of the QEEG involves an assessment of
the statistical degree of congruence or lack of congruence between a patient and the normal
population or the degree of similarity between a given patient and a QEEG profile that may
be characteristic of some defined clinical group. Typically, the interpretive results can be
displayed numerically or with topographic color-graphic brain maps. Among many other
things, the quantitative approach can display variations in QEEG profiles (which presumably
reflect variations in neurophysiological function) across primary diagnostic groups (Fig. 1.1420). It can also display progressive change in neurophysiological function over time.
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FIGURE 1.14-20 Baseline group average topographic images of z scores for selected
quantitative electroencephalography (QEEG) features in different Diagnostic and Statistical
Manual of Mental Disorders, 4th edition, text revision, psychiatric populations. Successive
columns in the left and right panels include absolute (Abs.) power delta, relative (Rel.) power
theta, interhemispheric coherence (Coh.) alpha, interhemispheric power asymmetry (Asy.)
beta, and total power mean frequency (Freq.). Populations include normal adults; unipolar
depressions; bipolar depressions; alcoholics (in withdrawal); cocaine-dependent subjects (5 to
14 days after last drug use); obsessive-compulsive disorder (OCD); global deterioration scale
(GDS) 2, which are normal elderly with only subjective cognitive complaints; GDS 3, which
meet criteria for mild cognitive impairment; GDS 4 through 6, which meet criteria for
dementia; first-break schizophrenics (Sz FB); schizophrenics off medication (Sz NoMed);
and schizophrenics on medication (Sz Med). The color scale of each z image is in standard
deviation units, with a range of +0.75, indicated with a diamond, or +1.25, indicated with a
club. To estimate the significance of any regional z score for this group average data, the z
score should be multiplied by the square root of the number of patients in the group. For a
group with 100 subjects, the z value imaged should be multiplied by 10 to get the estimate of
the significance of that z. (See Color Plate.) (Courtesy of Dr. E. Roy John, Director, Brain
Research Laboratories, Department of Psychiatry, New York University School of Medicine,
New York, NY and Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY.)
Recent years have seen a substantial growth in research and attempted clinical applications
involving topographic QEEG. Such methods hold considerable promise for psychiatry,
particularly in terms of possibly establishing neurophysiological subtypes of certain
psychiatric disorders and in seeking electrophysiological indicators of clinical outcome. For
example, in papers published in 1999 and 2002, Leslie Prichep, Kenneth Alper, and their
colleagues successfully used topographic QEEG methods to derive three distinct
electrophysiological subtypes of cocaine dependence. They were able to show that
electrophysiological subtype membership significantly predicted outcome retention in
treatment, defined as ability to maintain abstinence for 6 months or longer. In 2003, this same
team also demonstrated distinct topographic quantitative QEEG correlates of cue-induced
cocaine craving. Beginning in 1993, a team led by Prichep developed a topographic QEEG
electrophysiological subtyping of obsessive-compulsive disorder (OCD) that predicted
clinical responsiveness versus lack of responsiveness to treatment with selective serotonin
uptake inhibitors (SSRIs), and Elsebet Hanson, Prichep, and associates confirmed those
results in 2003. Topographic QEEG also appears to be superior to standard visually analyzed
EEG in documenting electrophysiological sequelae of both chronic and acute exposure to
abuse drugs.
Because the waveforms of artifacts of nonbrain origin are quantified by the computer
program as if they were real brain waves, it is extremely important to remove artifacts from
the analog EEG signals one is submitting for quantification. Furthermore, QEEG is usually
based on the waking EEG, and, if drowsy or sleep segments are allowed to inadvertently
enter the quantification process, serious distortions of the QEEG profile or topographic brain
map, or both, occur, and the distortions may not be easily recognized as such. On numerous
occasions, the authors have seen color graphic topographic displays of pronounced frontal
delta activity that probably represented vertical eye movement, as well as maps showing
widespread theta that may have been based on drowsy segments entered into quantification in
error. The identification and rejection of artifacts is an involved task and can only be done
with visual inspection of the analog tracing by experienced electroencephalographers or
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technologists skilled in EEG interpretation. When the issue of artifact contamination of the

QEEG is not properly addressed, one has a situation described a generation ago by computer
programmers, namely, garbage ingarbage out. Several commercial QEEG instruments also
have programs for automatic artifact rejection. Although some of these may be useful to some
degree for major high-voltage artifacts, such as vertical eye blinks, seldom are they
completely effective with all sources of contamination.
CLINICAL FINDINGS (GENERAL OVERVIEW)
The routine EEG is a completely noninvasive test that is even available in out-of-the-way
rural areas. It is a relatively inexpensive test, with charges of $200 for the test and $100 for
the interpretation being common (in some instances a range of $500 to $600). Furthermore,
any psychiatrist can be fully trained to interpret EEGs, and, with skill, useful EEG data can
often be obtained from agitated and psychotic patients.
Brief Synopsis of EEG Findings in Organic Pathophysiology
The standard clinical EEG has a high degree of sensitivity to a wide variety of medical
conditions and events that impinge on CNS function. For this reason, EEGs have sometimes
contributed to the detection of unsuspected organic pathophysiologies influencing the
psychiatric presentation. However, the range of EEG findings in medical disease is enormous
and far beyond the scope of this chapter. The reader is referred to the large edited volume by
Ernst Niedermeyer and Fernando Lopes da Silva for more in-depth coverage.
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Findings with Seizures
The hallmark EEG finding for a seizure disorder is the generalized, hemispheric, or focal
spike or spike-wave discharge, or both (Figs. 1.14-16, 1.14-18, and 1.14-19). However, this
statement constitutes a large oversimplification, because many types of EEG abnormalities
have been associated with seizures at one time or another, and some patients with a bona fide
seizure disorder have been known to have normal interictal EEG tracings. Furthermore,
seizure disorders can be associated with an extremely wide range of etiologies (idiopathic or
genetic, closed or open head trauma, cerebrovascular pathophysiology, metabolic disorders,
structural brain lesions, infectious or toxic encephalopathies, certain drug-abuse withdrawal
states, iatrogenic causes, to name only a few), and these considerations may modify the
nature of the EEG-seizure disorder association.
The classification of seizure types is also wide, and the majority of specific seizure
manifestations may be of little concern to the practicing psychiatrist. One of the exceptions
may be petit mal status, which can last from less than 1 hour to longer than 1 day, during
which time the patient presents with grossly impaired consciousness marked by pronounced
confusion, greatly slowed mental processes, or stuporous or somnolent behavior, or both. The
psychiatrist is most likely to encounter this clinical presentation in the emergency room,
where it is often confused with other functional or organic syndromes or intoxicant states. If
suspected, the status can be confirmed quickly by an EEG demonstration of continuous,
diffuse spike-wave activity. Typical petit mal seizures (i.e., nonstatus) may also be of
relevance to the child psychiatrist, because this type of epilepsy has a peak age distribution
during childhood and early adolescence, and, in some cases, the absence attack may be
mistaken for inattention or other functional behavioral reactions. Spike foci, usually anterior
temporal, associated with CPSs (psychomotor) should also interest the psychiatrist, because
the wide range of possible seizure manifestations is truly amazing, and almost any
combination of automatic motor movements, sensory disturbances, seemingly psychiatric
symptoms, or autonomic signs may be seen. The symptom cluster almost always remains the
same from one attack to another, and the automatic behavior during the ictal event may, at
times, be bizarre, with the patient undressing, picking at clothing and lip smacking, walking

in circles and yelling, trying to climb on a table while making guttural noises, experiencing
hallucinatory symptoms, or almost any other action. When continuous or closely spaced CPS
attacks (complex partial status) lasting hours or longer than a day occur, they may mimic
hysterical dissociative states.
Spike activity of various kinds and locations is sometimes found in the EEGs of psychiatric
patients with no obvious seizure manifestations. In such cases, one might consider possible
relationships to episodic aberrant behavior (particularly explosive aggressiveness), if present,
followed by an empirical trial with an anticonvulsant. Sometimes, such spike discharges in
the nonseizure psychiatric patient may indicate an elevated risk for iatrogenic seizures after
treatment with neuroleptic medication (Fig. 1.14-21).
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FIGURE 1.14-21 Routine admission electroencephalography (EEG). Diffuse spike and wave
with multiple spike component during drowsy recording (the wake EEG was normal). Male
patient, 16 years of age. No present or past history of seizures. No history of head trauma,
encephalitis, or other plausible cause for the spiking. Patient later developed iatrogenic grand
mal seizures during treatment with neuroleptics.