EEG JNP 2008 Shell Trimble Boutros

Name /jlb_jnp201_3059019/jnp201_AI0273/Mp_7
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SPECIAL ARTICLES
Electroencephalographic
Cerebral Dysrhythmic
Abnormalities in the
Trinity of Nonepileptic
General Population,
Neuropsychiatric, and
Neurobehavioral
Disorders
Bhaskara P. Shelley, M.B., B.S., M.D., D.M.
Michael R. Trimble, M.D., F.R.C.P.,
FRCPsych
Nash N. Boutros, M.D.
Subclinical electroencephalographic epileptiform
discharges in neurobehavioral disorders are not
uncommon. The clinical signicance and behavioral, diagnostic, and therapeutic implications of
this EEG cerebral dysrhythmia have not been
fully examined. Currently the only connotation
for distinctive epileptiform electroencephalographic patterns is epileptic seizures. Given the
prevailing dogma of not treating EEGs, these potential aberrations are either disregarded as irrelevant or are misattributed to indicate epilepsy.
This article reappraises the literature on paroxysmal EEG dysrhythmia in normative studies of the
healthy nonepileptic general populations, neuropsychiatry, and in neurobehavioral disorders.
These EEG aberrations may be reective of underlying morpho-functional brain abnormalities that
underpin various neurobehavioral disturbances.
(The Journal of Neuropsychiatry and Clinical
Neurosciences 2008; 20:722)
J Neuropsychiatry Clin Neurosci 20:1, Winter 2008
ver since the introduction of the EEG by the psychiatrist Hans Berger,1 an important target of clinical neurophysiology research has been to identify the
electroencephalographic correlates of human behavioral
disorders and psychopathologies. Much of the pioneering work of Hans Berger involved schizophrenia and
other serious psychiatric disorders. The interested
reader may be referred to the earliest treatise of EEG
abnormalities in schizophrenia by Hill.2 Over the course
of the last six decades, a voluminous literature has
emerged that substantiated a high prevalence of conventional EEG ndings in the psychiatric population.
Numerous epidemiological studies of large healthy
nonepileptic populations were conducted to dene and
establish the limits of the normative EEG. Such studies
have documented a wide range of prevalence rates of
Received December 30, 2006; revised April 21, 2007; accepted May 25,
2007. Dr. Shelley is afliated with the Raymond Way Neuropsychiatry
Research Group at the Institute of Neurology at Queen Sq., London;
Dr. Trimble is afliated with the Institute of Neurology at Queen Sq.,
London; Dr. Boutros is afliated with Wayne State University School
of Medicine in Detroit, Michigan. Address correspondence to Dr. Bhaskara P. Shelley, MBBS, M.D., D.M., Head, Department of Neurology,
Father Muller Medical College, Mangalore-575 002, India; bpshelley@
yahoo.com (e-mail).
Copyright 2008 American Psychiatric Publishing, Inc.
http://neuro.psychiatryonline.org
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ELECTROENCEPHALOGRAPHIC CEREBRAL DYSRYTHMIC ABNORMALITIES

EEG dysrhythmia in the nonepileptic general population.
Although the existing EEG literature is replete with
reports of abnormalities in association with different
neuropsychiatric disorders, only a few generalizations
can be made between particular EEG patterns and disorders. The strong (and relatively straightforward) correlation that has been established between EEG abnormalities and epilepsy has overshadowed the more
complex relationship between EEG abnormalities and
psychiatric disorders. Moreover, the prevailing concept
of not treating the EEG led to further de-emphasizing
such EEG deviations. These issues prompted us to critically and systematically reappraise the extensive available literature, which spanned almost six decades, on
EEG dysrhythmia to dissect the EEG-behavior equation,
address the merits and demerits of various studies, and
examine the validity of such EEG ndings in the current
environment of evidence-based medicine. The interested reader is referred to the reviews of Hill & Parr3 on
EEG correlates of psychopathic behavior and schizophrenia, and Glaser4 on EEG correlates of human behavior for a historical perspective.
This article does not address the pearls, perils and
pitfalls in the use of EEG in epilepsy but instead reiterates that epileptiform and other paroxysmal EEG dysrhythmias unrelated to clinical seizures do occur in neuropsychiatric and behavioral disorders.
While the mainstay for use of EEG in psychiatry has
been in differentiating brain disease from primary psychiatric disorders, the recent advances in EEG and other
electrophysiology techniques have emerged as powerful
tools in the exploration of the biological substrate for
neuropsychiatric disorders. We propose that once the
clinical correlates and the underlying pathological processes of such aberrations are understood, such knowledge will signicantly contribute to our understanding
of the basic pathophysiology underlying psychiatric
symptomatology where such aberrations are evident.
Research in this area can also contribute to developing
better biopsychosocial formulations and better treatment plans for individual patients.
METHOD
An extensive search of the literature included in the
MEDLINE database for the period of 1950 to 2005 was
performed. The rst step was a general search for EEG
abnormalities in nonepileptic subjects, healthy patients,

and in the general community using multiple search
terms. Papers examining EEG in nonepileptic populations were then identied via article titles and abstracts.
The MEDLINE and textbook chapters discussing normal EEG and EEG and psychiatry were then examined for references. These two sources were the primary
sources for references. The reference lists of each paper
or book chapter were searched for older relevant papers.
For inclusion in our review, papers had to be in English.
Second, a number of narrower searches were conducted for EEG abnormalities and individual disorders
discussed in this paper. Papers not examining the conventional EEG, examining sleep, quantied EEG, or
event-related potentials were excluded. Next, searches
were performed for all studies examining the clinical
correlates of the so-called controversial EEG waveforms. Finally, a search for EEG abnormalities in pediatric neurobehavioral disorders was conducted with
similar methodology and exclusions.
In this article, EEG cerebral dysrhythmia denotes
isolated episodic paroxysmal bursts of slow activity,
controversial/anomalous spiky waveforms and/or true
non-controversial epileptiform discharges.
RESULTS
EEG Dysrhythmia in the Nonepileptic Population

Twenty-two papers were identied. Epileptiform discharges (EDs) ranged from 0.8% to 18.6% in reportedly
normal children and 0.3% to 12.3% in reportedly normal
adults. These studies have been summarized in Table 1.
Several of these investigations had attempted to determine the prevalence of such epileptiform discharges
in large healthy nonepileptic populations. In this regard, several publications have reported a wide range
of prevalence of varying EEG dysrhythmia, some of
which were in disagreement, in nonepileptic and purported normal populations. The results of such studies,
unfortunately, therefore depicted conicting EEG ndings within the healthy nonepileptic populations.
It can be seen from Table 1 that there were studies
with relatively low rates of epileptiform discharges, and
on the contrary, several studies did document a high
prevalence of epileptiform discharges. The low estimates, as in the studies of Gibbs et al. (0.4%)5 and Bennet
(0.6%),6 employed minimum EEG requirements, where
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SHELLEY et al.
only three head regions were examined, without a sleep
record, and for a limited duration of 1015 minutes. Bennetts study focused only on spike-wave abnormalities
and excluded all other epileptiform discharges. EegOlofsson et al.7 reported a high prevalence of epileptiform discharges but they considered all the EEG dysrhythmia in children during wakefulness, in addition to
studies during sleep, photic stimulation, and hyperventilation, and they included non-epileptiform activities as
well.
In other studies, factors that were incriminated in high
prevalence estimates were the inclusion of individuals
with psychiatric histories and/or history of signicant
head trauma. For instance, in a series of 6,497 nonepileptic subjects, Zivin and Marsan8 had reported the
prevalence of epileptiform discharges to be 2.2% when
careful denitions of epileptiform discharges had been
used with optimum recording standards. In this nonepileptic group, epileptiform discharges were attributable to underlying brain abnormalities (traumatic, vascular, tumor, metabolic), medications, and psychiatric
TABLE 1.
disorders. The prevalence of epileptiform discharges in

these groups was reported as 5.5% in those with mental
handicap, 9.8% with congenital or perinatal brain insults, 10.6% after cranial operations, and 8.2% in individuals with cerebral tumors.
A similar conclusion was derived from a study of patients without epilepsy in the community. In this study,
the prevalence of epileptiform discharges was reported
as 12.3%, but 73.4% of the nonepileptic patients had underlying cerebral disorders.9 This emphasized that the
presence of epileptiform discharges in subjects without
epilepsy should be inferred as electrographic markers
of underlying brain dysfunction without the vulnerability to clinical seizures. These abnormal neuronal discharges, most closely associated with seizures, do occur
in people who do not have epilepsy (subclinical epileptiform discharges), but most have been linked to underlying cerebral disorder.
After exclusion of contaminating factors, the true
prevalence of epileptiform discharges in the healthy
normal population should be extremely low. The current
Summary of Studies of EEG Epileptiform Abnormalities of Persons Without Epilepsy
Study
Study sample
Thorner, 1942
Harty et al., 1942
Gibbs et al., 1943
Williams, 1944
Buchthal & Lennox, 1953
1,100 ying cadets

Medical service candidates
1,000 adult volunteers
241 healthy aircrew
682 male Airforce applicants
EDs (prevalence)
Corbin & Bickford, 1955

Dell et al., 1958
Kitamura et al., 1958
Lennox & Buchthal, 1959
Blanc et al., 1964
OConnor, 1964
Bennet, 1967
Zivin & Marsan, 1968
71 normal children (110 years)

Commercial ying personnel
Nonepileptics
Military jet pilots
Commercial ying personnel
Air cadets
1,322 aviators
6,497 inpatients in tertiary care
5.60%
0.91.5%
4.00%
6.40%
1.00%
0.50%
0.60%
2.20%
Doose et al., 1968

Eeg-Olofsson et al., 1971
Neurologically normal children

743 normal children
0.80%
18.60%
Cavazzuti et al., 1980
3,726 Neurologically healthy children

(613 years)
3.50%
Fenton, 1982
Iida et al., 1985
Trojaborg, 1992
Gregory et al., 1993
Healthy adults
10,473 nonepileptic outpatients
5,893 jet pilot applicants
13,658 aircrew trainees (1725 years)
3.00%
8.10%
Okubo, 1993
Sam & So, 2001
1,057 healthy children (612 years)

521 nonepileptic patients
0.30%
3.00%
0.40%
0.80%
5.10%
0.50%
RemarksEEG abnormalities
Paroxysmal EEG discharges
Epileptic abnormalities
0.4%3/sec spike wave
2.6% in awake/drowsy record; 2.2% in photic
stimulation; 0.3% in hyperventilation
Spike-wave complexes
Spike discharges
Spike discharges
Spike-wave discharges
Spike-wave discharges
0.2% in photic stimulation; EDs attributable to
underlying brain abnormalities and
psychiatric disorders (55.5% of 6 Hz spikewave pattern with psychiatric disorders)
8.1% in sleep; 8.3% in photic stimulation;
nonepileptiform patterns / 14 & 6 positive
spikes were excluded
14 & 6 positive spikes/high voltage
nonepileptiform abnormalities were
excluded
EEG dysrhythmia 2.4%
6 Hz spike wave and positive spikes were
excluded
5.00%
12.30%
EDsepileptiform discharges
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estimate of EEG epileptiform dysrhythmia in the nonepileptic healthy population should be less than 1%, as
supported by the work of Gregory et al.10
Struve11 reported the prevalence of EEG abnormalities in the nonepileptic normal adult population ranging from 4% to as high as 57.5%. This wide range reected the lack of rigorous selection criteria for choosing
the normal healthy control comparison subjects. A study
by Boutros et al.12 emphasized the priority for clearly
dening the boundaries of the normative EEG, which is
critical in deriving valid generalizations for consensus
opinion on the electroencephalographic correlates of
neuropsychiatric disorders. They proposed a seven
point normality criteria for selecting healthy comparison subjects. Their search of the relevant published literature on selection methodology for normal comparison subjects from 1936 to 2005 included 38 articles. The
majority of included studies did not fulll any of their
specied normality criteria. The study conrmed the
inadequate denition for EEG normality, and also reiterated the fact that the literature concerning the prevalence or signicance of EEG correlates in neuropsychiatry remains preliminary after all these years.
EEG Dysrhythmia in Neuropsychiatric Disorders
Sixty-three papers were identied. Ten papers examined
the conventional EEG in schizophrenia populations (Table 2). Eight of the 10 papers reported varying degrees
of abnormalities and two papers reported that such deviations may be related to treatment responses. Eighteen
papers were related to mood disorders and reported
varying degrees of abnormalities. Eleven papers addressed anxiety disorders (including panic attacks),
seven addressed eating disorders, 20 addressed personality disorders (11 of those on borderline personality disorder), 12 papers addressed criminal behavior and violence, and 11 papers examined the EEGs of patients with
psychogenic nonepileptic seizures. The overwhelming
majority of papers reported varying degrees of abnormalities (Table 2).
During the last six decades there has been a large
amount of literature on electroencephalographic abnormalities in a high proportion of psychiatric patients. No
comprehensive review of this large body of psychiatrically relevant literature has been critically presented.
Our extensive search of publications on the EEG correlates of psychopathology is summarized in Table 2. The
published work of Kennard13 reviewed two decades of
pioneering literature afrming the positive correlations
10
of abnormal EEGs in psychological disorders. This section, even after six decades of psychiatric EEG research,
attempts to dissect the same behavioral/EEG equation
as it applies to our current state of EEG understanding
and evidence-based research methodology.
About two decades earlier, the work of Bridgers14
again conrmed the occurrence of epileptiform dysrhythmic abnormalities in a population of nonepileptic
hospitalized psychiatric patients. The EEG ndings
were found to correlate with conditions such as anorexia
nervosa, depression, mania, personality disorders, suicidality without depression, schizophrenia, nonpsychotic explosive behavior, and the effects of psychotropic medications. The epileptiform EEG abnormalities
were documented in 2.6%, and consisted of photoparoxysmal responses, focal temporal complexes, generalized spike-wave or polyspike-wave discharges, and
focal central/frontal complexes. This study did emphasize that EEG epileptiform dysrhythmia does occur in
nonepileptic psychiatric populations and may reect
underlying cerebral dysfunction without necessarily indicating an increased liability to seizures.
Numerous studies have documented conventional
EEG abnormalities in 20%60% of patients with schizophrenia, and have been summarized in Table 2. Abrahams and Taylor15 showed that schizophrenic patients
had twice as many left-sided temporal abnormalities
than patients with affective disorders who had more
right-sided EEG ndings. Denite EEG abnormalities
have been documented in a high proportion of schizophrenia patients, but perhaps were minor, quite nonspecic, and conjectural. EEG abnormalities were more
frequent in the cohort of schizophrenic patients who had
a positive family history suggesting that genetic factors
may be contributing to EEG traits. The EEG aberrations
possibly reected abnormalities in cortical neuronal architecture, cellular neuropathology, and neurochemical
transmitter abnormalities that underpin the schizophrenia pathophysiology, in addition to possible neuroleptic
medication effects. These EEG aberrations, along with
neuroimaging and neuropsychological abnormalities,
lend objective evidence for brain dysfunction in the genesis of schizophrenia. Furthermore, specic differences
have also been reported among subgroups of functional
mental illness. Psychotic mood disorders and atypical
psychoses are reported to have a higher frequency of
epileptiform variants, including the phantom spike and
wave, positive spikes, and small sharp spikes, as com-
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pared with nonpsychotic mood disorders and schizophrenia.16
Many previous EEG ndings in individuals with personality disorders, violent and criminal behavior, and
forensic populations have been found to suffer from
methodological problems. The EEG data were thus considered nonspecic as the results could not always be
replicated by all investigators. Therefore, the signicance of these EEG abnormalities is still a matter of debate. Abnormal EEG ndings reported in association
with personality disorders, criminal behavior, and borderline personality disorder are summarized in Table 2.
One of the interesting ndings in earlier studies was that
relatively good personality structure relates to a normal
EEG.17 The initial studies did reveal positive trends in
relating EEG dysrhythmic abnormalities to personality
traits, and a psychopathic MMPI prole.1719 These EEG
aberrations noted in personality disorders and impulsive behaviors reect the presence of cerebral dysfunction that may hamper the natural process of psychological maturation.
Hill and Watterson18 were the rst to postulate that
EEG dysrhythmia in aggressive psychopaths reected a
failure in functional cortical development (maturational
retardation hypothesis). Although some evidence supports the maturational retardation hypothesis,20,21 the
nding that many aggressive psychopaths had normal
EEGs argued against it. Other studies, however, failed
to nd a relationship between EEG abnormalities and
aggressive tendencies.2225 Ribas et al.,26 on the other
hand, found evidence of cerebral dysrhythmia in 69%
of youngsters with behavior disorders with a predominance of aggressiveness. Earlier literature did link criminal behavior and aggression to an epileptic etiology.
However, there is lack of convincing current evidence
for such a proposition of an association between violence and epileptiform EEG disturbances.27
Studies of antisocial and criminal populations have
revealed EEG abnormalities in 24%78% of individuals.
These EEG abnormalities were found to be more prevalent in subjects with violent crimes, repeated violence,
and motiveless crimes. No specic relationship had
been found between the type of EEG abnormality and
characteristics of the crime, or between EEG changes
and the degree of violence committed.28,29 Several types
of EEG abnormalities have been found in violent offenders: generalized slowing, focal slowing, and epileptiform discharges. A few studies summarized in Table 2
had established violent behavior to be linked to left-
sided temporal lateralization of EEG abnormalities.28,30

These EEG aberrations suggested an underlying brain
dysfunction in violent behavior.31 The validity of these
EEG aberrations has also been conrmed by quantitative EEG32 and neuropsychological data.33 These studies
lend support to the concept of a connection between left
hemispheric (frontal, temporal) cerebral dysfunction
and the propensity for violence. However, the presence
of EEG dysrhythmia, instead of having any specic associations with criminal behavior, may actually represent underlying comorbid factors such as multiple head
injuries, coexisting substance abuse, and associated toxic
and metabolic disorders, although a laterality effect
would not be expected.
In borderline personality disorder (BPD), the literature suggests two types of conventional EEG abnormalities: epileptiform dysrhythmia and diffuse EEG slowing. The presence of epileptiform discharges in bipolar
disorder possibly indicates cortical excitability disturbances that may be predictive of responsiveness to anticonvulsant therapy,29 whereas diffuse EEG slowing
possibly reects underlying metabolic or degenerative
etiologies. Boutros et al.34 reviewed the literature from
1966 to 2000 on the electrophysiological aberrations in
bipolar disorder. It was found that the EEG investigations of bipolar disorder were limited, as only nine articles could be retrieved. Furthermore, the majority did
not have adequate control groups or adequate evaluation of Axis I or Axis II comorbidity and controls for
medication effects.
Anorexia nervosa and other eating disorders have
also been documented to have a higher prevalence of
EEG dysrhythmia. EEG abnormalities documented include 14 and 6 positive spikes, B-mitten patterns, small
sharp spikes, paroxysmal slowing, focal slowing, minimal generalized slowing, focal & diffuse spiking, generalized fast, 6/sec spike and wave and slow with spiking. The co-occurrence of EEG abnormalities consisting
of B-mitten and small sharp spike (SSS) dysrhythmic
patterns may reect the cross relationships between anorexia nervosa, depressive disorder, and suicidality.
These are possibly related to dietary factors, neuroendocrine, and nutritional deciencies that would undoubtedly cause cerebral metabolic aberrations contributing to brain dysfunction.
As seen in Table 2, several studies have suggested a
high incidence of EEG abnormalities in patients with
anxiety disorders, panic disorders, and obsessive-compulsive disorders. Hughes35 reported that EEG parox-
11
12
Eating Disorders
Panic Disorder
Slow and generalized spike & wave; B-mitten pattern; diffuse slow paroxysmal
discharges (prevalence 28.6%)
Abnormalities (prevalence 59%); hyperventilation related abnormalities (prevalence
31%; bilateral 46/sec spike-wave complexes (prevalence 12%)
Bilateral anterio-mesial temporal spikes; 6/sec spike-wave complexes (prevalence 80%)
SSS; diffuse spike & wave; bitemporal slowing (prevalence 35%)
14 & 6 positive spikes, B-mitten patterns, SSS, paroxysmal slowing, focal slow, minimal
generalized slow, focal, and diffuse spiking, generalized fast, 6/sec spike & wave
and slow with spiking (prevalence 64.4%); paroxysmal nding of EEG
dysrhythmia (prevalence 94.7%) reported
Generalized slow; paroxysmal slow; focal spike or sharp-wave transients; generalized
spikes; B-mitten patterns; extreme spindles (prevalence 50.9%)
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Neil et al. 1980
Davis et al., 1974

Wermuth et al., 197
Rau et al., 1979
Crisp et al., 1968
Gibbs & Gibbs, 1964
Bystritsky et al., 1999
Dantendorfer et al., 1996

Gallinant & Hegerl, 1999
Weilburg et al., 1995
Slow-wave dysrhythmia (prevalence 24%)

EEG abnormalities in panic disorder reported
EEG temporal paroxysmal activity reported to be four times more common in panic
disorder patients than in depressed patients
An association between atypical panic attacks and EDs reported; focal paroxysmal
temporal abnormalities (prevalence 33%)
High incidence of EEG abnormalities (60.7%) in panic disorder patients
Correlation between EEG abnormalities in panic disorder and efcacy of valproate
therapy
Abnormal EEG (prevalence 25%); epileptiform dysrhythmia (prevalence 15%); 12 times
higher rate of EEG abnormality as compared to healthy controls
Fronto-temporal EEG abnormalities in PTSD associated with physical and sexual abuse
EEG abnormalities in anxiety, panic, and OCD documented
Ito et al., 1993

Small, 1993
Lepola et al., 1990
Abraham, Duffy, 1991
Jabourian et al., 1992; Hughes, 1996
Temporal non-specic EEG abnormalities (prevalence 33%) in OCD
SSS described in bipolar patients (prevalence 43%); familial association of SSS in rstdegree relatives of manic depressive disease
6/sec spike & wave, SSS, 14 & 6 Hz positive spikes linked to suicidal ideations and
acts
Mood disorders associated with right sided EEG abnormalities
6/sec spike & wave complexes associated with increased risk for psychopathology
Paroxysmal bitemporal EDs associated with rapid cycling bipolar affective disorder
Mood disorders associated with 6 Hz phantom spike & wave, 14 & 6 Hz positive
spike, SSS
EEG abnormalities (e.g.: TLID, TMSSA, BORTT)
EDs predicted lithium resistance in bipolar disorder
High incidence of EEG temporal slow waves in late onset depression
Abnormal EEGs found in 33% of manic-depressive patients

20%40% incidence of abnormalities-SSS, 6/sec spike & wave/phantom spike wave,
RMTD, 14 & 6 Hz positive spikes and B-mitten pattern
Jenike & Brotman, 1984
Inui et al., 2001

Ikeda et al., 2002
Motomura et al., 2002
Abrahams, Taylor, 1979; Flor-Henry, 1972, 1985

Hughes, Herman, 1984
Levy et al., 1988
Inui et al., 1998
Struve et al., 1977
Finely & Campbell, 1941; Davies, 1941

Elllingson, 1954; Small et al., 1993; Cook et al.,
1986; McElroy et al., 1998; Taylor, Abrams,
1981
Small et al., 1975
Findings
Low amplitude irregular EEG (choppy)
Generalized non-paroxysmal dysrhythmias rst reported
Left-sided temporal EEG abnormalities, two times greater proportion in comparison
with mood disorders
Temporal EEG abnormalities (prevalence 30%)
Left-sided slow-wave asymmetries, slow bursts, SSS; more pronounced over left
anterior temporal region (prevalence 20%60%)
Photic drive predicted clozapine responders
Presence of EEG abnormalities predicted favorable treatment outcome
Increased frequency of phantom spike and wave, positive spikes, and SSS (prevalence
30%33%)
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Anxiety, Panic, ObsessiveCompulsive Disorders (OCD)
Mood Disorders
Jin et al., 1995

Pillay et al., 1996
Inui et al., 1998
Stevens et al., 1979

Small, 1993; Ellingson, 1954; Small et al., 1984
Davis, 1940
Hill, 1950
Abrahams & Taylor, 1979
Study
Summary Table of Publications of EEG Cerebral Dysrhythmia in Neuropsychiatric Disorders
Schizophrenia
Disorder
TABLE 2.
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13
SSS-small sharp spikes; TLID-temporal low voltage, irregular delta wave; TMSSA-temporal minor slow and sharp activity; BORTT-bursts of rhythmical temporal theta; PTSDpost-traumatic stress disorder; MMPI-Minnesota Multiphasic Personality Inventory; RMTD-rhythmic midtemporal theta of drowsiness
Devinsky et al., 1996

Parra et al., 1999
Reuber et al., 2002
Wilkes et al., 1990; Lelliott, Fenwick, 1991

Bowman, 1993
Wilkus et al., 1984
Cohen & Suter, 1982
King et al., 1982; Luther et al., 1982
Standage et al., 1975
De la Fuente, 1998
Cornelius et al., 1986

Archer et al., 1988
Cowdry & Gardner, 1988
Messner, 1989
Schmidt et al., 1989
Ogiso et al., 1993; Hughes, 1996
Abnormal temporal theta with sharp components (unilateral/bilateral); posterior

temporal slow waves (prevalence 40%)
Unilateral/bilateral abnormal temporal theta with sharp components; nonepileptiform
EEG abnormalities (prevalence 20%25%)
Epileptiform spikes/spike-wave discharges and temporal lobe spikes (prevalence 12%);
EEG dysrhythmia (prevalence 37%)
temporal slow waves (prevalence 44%)
Dysrhythmic EEG abnormalities (prevalence 74%)
temporal slow waves (prevalence 8%37%)
EEG dysrhythmic abnormalities (prevalence 10%)
EEG epileptiform and nonepileptiform abnormalities (prevalence 49%)
EEG dysrhythmic abnormalities (prevalence 53.8%); epileptiform EEG abnormalities
(prevalence 12.3%)
Increased slow-wave activity (frequently bilateral); frontal, temporal or frontotemporal

distribution
High incidence of paroxysmal EEG activity (46%); non-focal spike, sharp wave activity;
posterior temporal spike-wave activity
Severe EEG abnormalities (prevalence 5.8%)
Bilateral spike-wave discharges (prevalence 6.3%)
Epileptiform discharges; paroxysmal posterior sharp waves
Focal temporal lobe slow-wave activity
Normal routine EEG
Positive spikes (67/sec & 14/sec) linked to impulsivity; 6/sec phantom spike wave
linked to interpersonal relationship dysfunction
Diffuse EEG slowing (incidence 40%)
Snyder & Pitts, 1984

Cowdry et al., 1986
Anticonvulsant responsiveness in BPD with EEG epileptiform discharges
High prevalence of paroxysmal EEG abnormalities (posterior temporal sharpish slowwave activity) in aggressive psychopaths, criminals and murderers (prevalence
70%)
High prevalence of EEG abnormalities in prisoners (53%)
Psychopathic crimes associated with 75% of EEG abnormalities
High prevalence of EEG abnormalities in aggressive/explosive psychopaths (73%)
Abnormal EEG (prevalence 50%) in psychotic/motiveless murderers
Low prevalence of EEG abnormalities in prisoners (30%) as compared to normal
population
Abnormal EEG (prevalence 42.7%); paroxysmal focal temporal abnormalities (slow
waves and/or sharp waves), (prevalence 20%); correlated with MMPI and CT
temporal lobe abnormalities
Low incidence of focal abnormalities (prevalence 9%); high violence rates associated
with left focal abnormalities
High frequency of atypical EEG features such as choppy, dysrhythmic with excess
theta, and dysrhythmia with paroxysmal features
Aggressive behavior associated with temporal lobe EEG focus

High amplitude paroxysmal slow-wave EEG abnormality associated with aggressive
behavior
EEG abnormalities in antisocial/psychopathic personality disorder (prevalence 53%)
EEG abnormalities in episodic violent behavior, rage attacks (prevalence 6.6%)
Poor association between EEG abnormalities and violent behavior
Monroe, 1975
Pillmann et al., 1999
Wong et al., 1994
Silverman, 1943
Silverman, 1944
Stafford-Clarke, Taylor, 1949
Hill & Pond, 1952
Levy & Kennard, 1953
Hill, 1942, 1944, 1952; Williams, 1969; StaffordClarke, Taylor, 1949
Harper et al., 1972

Riley & Neidermeyer, 1978
Driver et al., 1974; Hsu et al., 1985; Small, 1966;
Krakowski et al., 1989
Howard, 1984
Treffert, 1964
Monroe, 1970
EEG dysrhythmia in compulsive binge eaters (prevalence 64.4%); paroxysmal

dysrhythmia (prevalence 94.7%); higher prevalence of EEG abnormalities than
corresponding rates for normal controls
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Psychogenic Nonepileptic Seizures

(PNES)
Borderline Personality Disorder

(BPD)
Criminal Behavior and Violence
Personality Disorders
Struve, 1987
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SHELLEY et al.
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ysmal dysrhythmia was four times more common in
panic patients than in depressed patients. Our literature
review indicated that about 25%30% of panic attack
patients had demonstrable EEG abnormalities, especially in atypical presentations of panic attacks. Some
studies have documented an epileptic pathophysiology
to underlie atypical panic attacks.36
Our literature review (Table 2) suggests that the incidence of abnormal EEG ndings in mood disorders is
substantial, ranging from 20%40%.37,38,3941 These abnormalities were found to be higher in manic patients
than in depressed patients, in female than in male bipolar
patients, and in nonfamilial cases with late-age onset disorder. Specic patterns noted in mood-disorders include
the small sharp spikes (SSS), 6/sec spike and wave complexes (RMTD), B-mitten pattern, and positive spikes.
Abrahams and Taylor15 and Flor-Henry42,43 reported that
mood disorders particularly showed more right-sided
EEG abnormalities, in contrast to the left temporal EEG
abnormalities in schizophrenia. Further, a few reports
have demonstrated that rapid cycling bipolar affective
disorder patients had more prevalent EEG evidence of
bitemporal epileptiform paroxysmal activities than patients with nonrapid cycling mood disorders.44
Head injury with post-concussion syndromes may
have a high incidence of underlying diffuse axonal injury and have been documented to be associated with
abnormal EEGs, even in the presence of normal neurological examinations.45 Thus, as pointed out earlier in
the section EEG Dysrythmia in the Nonepileptic Population, head injury should form an exclusion criterion
in the selection of healthy comparison groups in neuropsychiatric research.
Psychogenic nonepileptic seizure (PNES) is another
area in the psychiatric EEG literature that merits a reappraisal. In our review of the literature, the only study that
specically focused on the prevalence of interictal EEG
abnormalities in psychogenic nonepileptic seizures was
that of Reuber et al.46 Other studies related to psychogenic nonepileptic seizures have been summarized in
Table 2, and relevant data extracted from these articles
pointed to a mean prevalence of interictal EEG abnormalities in psychogenic nonepileptic seizures to be estimated at 25.9%.4755 In Reubers study, the rates of
abnormal, non-specic, and epileptiform EEG abnormalities in psychogenic nonepileptic seizures were documented to be 53.8% and 12.3%, respectively. When
psychogenic nonepileptic seizures were compared with
an appropriately selected control group, nonspecic
14
EEG abnormalities were seen 1.8 times as often in psychogenic nonepileptic seizures as in healthy controls.
Such EEG abnormalities may be attributed to the complex interaction of comorbid psychiatric disorders and
various psychopathological variables, underlying brain
abnormalities, head trauma,5658 and physical and sexual abuse, which plays a pivotal role in the nal clinical
expression of psychogenic nonepileptic seizure vulnerability. It is imperative to be cognizant of the fact that
EEG dysrhythmias do occur in psychogenic nonepileptic seizures, and it is crucial to understand that the mere
presence of paroxysmal EEG dysrhythmia in psychogenic nonepileptic seizures should not lead to an epileptic connotation.
Early childhood sexual abuse, early stress, and lifetime assaultive violence have been linked to cortical
maldevelopment and increased electrophysiological abnormalities. Several studies reported that such severe
early stress and abuse have the potential to alter brain
development and cause limbic dysfunction during specic sensitive periods of cortical maturation.59 The cascade of events is mediated through stress-induced neurohormones of the glucocorticoid, noradrenergic, and
vasopressin-oxytocin stress response systems which affects neurogenesis, synaptic overproduction and pruning, and myelination. The aberrant cortical development
has been reported to involve the corpus callosum,60 left
neocortex, hippocampus, and amygdala. During the last
decade, studies have reported an emergence of EEG abnormalities in children with sexual and psychological
abuse. An increased prevalence of fronto-temporal electrophysiological abnormalities with a left-sided localization was reported in abused children.6163 Another
study reported dysrhythmic EEG abnormalities in 77%
(N22) of patients who were involved as the child or
younger member in an incestuous relationship, of which
36% had clinical seizures.64 These studies thus provide
evidence for the neurobiological underpinnings through
which early abuse increases the risk of developing various psychopathologies and its electrophysiological consequences.
Clinical Correlates of Controversial/Anomalous EEG
Patterns
Signicant literature pertaining to each of ve controversial patterns was found. Of nine papers examining
the correlates of the rhythmic mid-temporal discharges
(RMTD), six found psychiatric correlates. Similarly, six
of nine papers examining the Wicket spikes/Mu rhythm
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TABLE 3.
Clinico-Electroencephalographic Associations of Anomalous EEG Patterns
EEG patterns
Study
Correlations
RMTD
Gibbs et al., 1963

Small et al., 1968
Gibbs & Gibbs, 1964, Lipman,
Hughes, 1969; Eeg-Olofsson,
Peterson, 1982
Hughes, Olson, 1981
Variant EEG dysrhythmia in normal adults (prevalence 0.5%2%)

No association found with behavioral symptoms
Linked to behavioral symptoms (temper dyscontrol, personality disorder, and
autonomic phenomenon)
Hughes, Herman, 1984

Boutros et al., 1986
Hennessy et al., 2001
Wicket spikes/Mu
rhythm
Gastaut et al., 1954
Adult patients (prevalence 10%)
Picard et al., 1955

Beck, 1958
Doniger, Doniger, 1958
Normal healthy population (Navy personnel) (prevalence 12%)

Psychiatric patient population (prevalence 13%)
Neurosis, anxiety, aggressiveness, emotional instability, psychosomatic disorders
(prevalence 18%)
Healthy young male adults (prevalence 14.4%); psychopathic personality traits
as evidenced by the MMPI
Normal healthy population (prevalence 12%)
Not related to epilepsy; associated with nonepileptic symptoms, syncope,
headaches, vertigo
High incidence of neurovegetative symptoms (70%); presyncope/syncope (33%);
psychogenic nonepileptic events (80%); neuropsychiatric population (13%);
psychosomatic disorders; head injury (22%)
Familial occurrence of wicket spikes
Gastaut et al., 1959

Simonova et al., 1966
Reiher, Lebel, 1977
Hughes & Olson, 1981
Koshino & Isaki, 1986
14 & 6 Hz positive
spikes
Associated with signicant psychological symptoms (33%); neurovegetative

symptoms; head injury (24%)
Hypochondriasis, schizophrenia, depression, and hysteria (correlated with
MMPI scores)
Somatization disorder, anxiety related disorders (prevalence 30%50%)
Right unilateral RMTD linked with severe behavioral disturbance, episodic
aggression associated with right temporal MRI structural abnormality
Gibbs, Gibbs, 1951; Schwade, Geiger,

1953; Schawade, Otto, 1953
Schwade, Geiger, 1960
Henry, 1963; Hughes, 1965; Poser,
Ziegler, 1958
Gibbs, Gibbs, 1963
Small, Small, 1964
Andy, Jurko, 1972
Gibbs, Gibbs, 1977
Hughes, Cayaffa, 1978
Klass, Daly, 1979
Niedermeyer, 1987
DeLong et al., 1987
Hughes et al., 2000
Small sharp spikes

Reiher, Klass, 1968
(SSS)
(Benign epileptiform Small, 1970, 1975
trasients of sleep,
BETS)
Koshino, Neidermeyer, 1975
Lebel et al., 1977
Struve et al., 1977
White et al., 1977
Rau et al., 1979; Crisp et al., 1968
Hughes, Olson, 1981
Saito et al., 1983
Hughes, Gruener, 1984
Saito et al., 1987
Temporal 14 & 6 Hz positive spikes specically associated with impulsive

aggressive behavior
Behavioral episodic temper dyscontrol, irritability, and emotional lability
Strongly linked to behavioral disorders (impulsive behavior)
Variant EEG dysrhythmia in normal adults (age 2025 years of age; prevalence
1.3%)
Associated with psychiatric disorders (incidence 4%)
Neurovegetative symptoms (visceral, pain, and autonomic symptoms);
correlated with depth EEG neurovegetative symptoms (headache, dizziness,
and syncope)
Related to head trauma
Neurovegetative and psychiatric symptoms (prevalence 85% in adults)
No correlations found
No correlations found
Related to behavior disorder and aggression (prevalence 52%); also linked to
disturbances of temper, mood, attention, and learning
Related to ADHD
Related to ADHD (prevalence 34%)
No associations found; a pattern of doubtful signicance
Associated with psychiatric dysfunction, manic-depressive illness
Seizure prevalence 67.4%
No associations found
Suicidal behavior, assaultive/destructive acts
Variant EEG dysrhythmia in normal population (prevalence 24%)
Eating disorder
Associated with neurovegetative symptoms
Neurovegetative symptoms (headache, dizziness, episodic abdominal pain,
nausea, and vomiting)
Associated with moderate degree of epileptogenicity
Seizure prevalence 53%
(continued)
15
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TABLE 3.
Clinico-Electroencephalographic Associations of Anomalous EEG Patterns (continued)
6 Hz spike & slow

wave complex
(Phantom spike
wave)
Small, 1968
Associated with psychiatric disorders (incidence 4.5%)
Small, 1970
Associated with history of syncopal attacks, post-traumatic states, or psychiatric

problems, borderline personality disorder
Associated with abstinence or withdrawal phase of drug-dependent individuals
Associated with psychiatric disorders (prevalence 1.5%20.8%)
Occipital pattern linked to drug dependence (barbiturates) and withdrawal
Frontal pattern associated with seizures and occipital pattern linked to
neurovegetative/psychological complaints
Kocher et al., 1975

Gibbs & Novick, 1977; Struve, 1977
Hecker et al., 1979
Hughes, 1980
MMPIMinnesota Multiphasic Personality Inventory
found psychiatric correlates. The pattern with most attention is the 14 and 6 positive spikes. Of 17 papers examining this pattern 10 reported psychiatric correlates.
Seven of 13 papers examining small sharp spikes reported clinical correlates while all six papers examining
the 6/second spike and wave pattern reported clinical
psychiatric associations.
Our literature review on controversial/anomalous
patterns revealed numerous reports of a high prevalence
of these patterns associated with various neuropsychiatric disorders. Some of these patterns have been reported to occur in normal individuals, and hence have
been referred to as benign epileptiform variants. Such
attributes of the various patterns have been summarized
in Table 3. Despite the repeated demonstration of a
higher prevalence in psychiatric populations, these EEG
patterns were deemed normal variants or considered
controversial and have been the subject of well-designed
investigations. Notwithstanding the increased prevalence of these EEG patterns in neuropsychiatric disorders, their neurobiological and genetic basis, and neural
source generators have not been clearly elucidated.
There have also been no studies over the last few decades specically addressing these controversial patterns and their psychiatric relevance.
EEG Dysrhythmia in Pediatric Neurobehavioral
Disorders
Twelve papers were identied addressing autistic spectrum disorders. All papers reported increased prevalence of EEG abnormalities ranging from 5.7%60.7%
(Table 4). Five of the six papers examining the EEGs of
patients with Gilles de la Tourette syndrome reported
abnormal EEGs, as well as the six papers investigating
attention decit hyperactivity disorder (ADHD).
Two of the common neurobehavioral disorders of
childhood are autistic spectrum disorders (autism, per-
16
vasive developmental disorder not otherwise specied,

Aspergers syndrome, Retts syndrome, and disintegrative disorder) and attention decit disorders with or
without hyperactivity (ADHD or attention decit disorder). Autistic spectrum disorders, Landau-Kleffner
syndrome, electrical status in slow wave sleep, developmental dysphasia, and benign rolandic epilepsy have
overlapping features, and from our review, the high incidence of epilepsy and/or subclinical or infraclinical
epileptiform EEG dysrhythmia does seem to be the interesting common thread that exists among these conditions. The studies that have linked the various pediatric neurobehavioral disorders without overt clinical
seizures to EEG abnormalities have been summarized
in Table 4.
The earliest review of studies on autism was contributed by Small et al.65 who, from 14 pooled studies, reported a wide range of prevalence of EEG dysrhythmia.
This large range undoubtedly arose from differences
both in the populations under study and, more importantly, the diagnostic criteria used for the abnormality.
Kim et al.66 reported 59% prevalence of interictal epileptiform EEG abnormalities that included focal sharp
waves, multifocal sharp waves, generalized spike-wave
complexes, and generalized paroxysmal fast activity/
polyspikes in nonepileptic autistic children. These EEG
dysrhythmias probably represent an age-dependent epiphenomenon of impaired brain maturation, with cumulative effects of these EEG discharges contributing to
cognitive abnormalities.
Several studies summarized in Table 4 have documented positive correlations between subclinical paroxysmal EEG dysrhythmia in nonepileptic autism6774
and nonepileptic ADHD,7578 and have also brought to
light the clinical overlap between nonepileptic ADHD
and typical benign rolandic epilepsy as evidenced by the
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increased frequency of EEG subclinical rolandic spikes
in these nonepileptic groups.79
The electrographic dysrhythmia in these pediatric
neurobehavioral disorders may represent an epiphe-
TABLE 4.
nomenon of cerebral dysfunction or underlying cortical

morpho-functional abnormalities, and/or reect a brain
neurophysiological disorder which is not sufcient to be
expressed as epilepsy. This may be due to the lack of
Summary Table of Publications of EEG Cerebral Dysrhythmia in Pediatric Neurobehavioral Disorders
Disorder
Study
Autism
Small et al., 1977
EEG abnormalities prevalence: range from 10% to 83%, with an average

of 48.6% (review of 12 studies; total of 800 autistic children) (1964
1975)
Tuchman et al., 1991; Villalobos et EEG (subclinical) epileptiform dysrhythmia in nonepileptic autistic
al., 1996
children (prevalence 13%83%)
Rossi et al., 1995
CTS (prevalence 45%) typical of Benign rolandic epilepsy reported
Beaumanoir et al., 1995
Paroxysmal EEG dysrhythmia (prevalence 10%); similar to LKS, or ESES
Tuchman et al., 1997
Subclinical EDs (prevalence 13%83%)
Tuchman, Rapin, 1997
EDs without regression/epilepsy (prevalence 6%); EDs in autistic
regression without epilepsy (prevalence 14%); CTS associated with
autism without regression/epilepsy; CTS also linked to BECTS/BRE
and LKS
Gabis et al., 2005
EDs not associated with clinical seizures or regression (prevalence 5.7%)
Hughes, Melyn, 2005
EDs in nonepileptic autistics (prevalence 20%)
Canitano et al., 2005
Paroxysmal EEG dysrhythmia in nonepileptic autistics (prevalence 22%)
Kim et al., 2006
EDs (prevalence 59%); focal sharp waves, multifocal sharp wave,
generalized spike-wave complexes, and generalized paroxysmal fast
activity/polyspikes
Chez et al., 2006
EDs (in sleep) (prevalence 60.7%); right temporal localization
Retts Disorder
Niedermeyer, Naidu, 1998; Cooper EDs (central spikes) without clinical seizures; rhythmic frontal-central
et al.,1998
slow (theta) activity (British Rett Survey,1998)
Hellers Childhood
Disintegrative Disorder
Corbett et al., 1977; Volkmar &

Cohen, 1989
EEG abnormalities reported
Tourettes Syndrome
Bergen et al., 1982

Krumholz et al., 1983
Dysrhythmia (prevalence 34%)

Dysrhythmia: central spikes, generalized and paroxysmal slow activity,
and background slowing (prevalence 12.5%)
Dysrhythmia (prevalence 6.6%); EDs (prevalence 13.4%)
No EEG associations found
Lees et al., 1984

Verma et al., 1986
Neufeld et al., 1990
Semerci et al., 2000
Attention Decit Hyperactivity
Disorder
Small et al., 1978

Hughes et al., 2000
Hemmer et al., 2001

Richer et al., 2002
Holtmann et al., 2003
Benign Rolandic Epilepsy
Massa et al., 2001
Findings
Diffuse generalized and/or intermittent slow wave dysrhythmia

(prevalence 30%60%)
14/second and 6/second positive spike patterns (prevalence 24.5%); EDs
(prevalence 28%); slow wave dysrhythmia (prevalence 22%)
Abnormal EEGs (prevalence 53.4%); focal EDs- occipital/frontal
(prevalence 30.1%; generalised spike-wave EDs 6.3%/focal EDs 23.9%:
temporal 37.5%, central, frontal, occipital 43.8%); controversial 67/
second and 14/second positive spike patterns (prevalence 34%); and
abnormal frontal/temporal slow waves (prevalence 18.8%); Frontal
arousal rhythm (prevalence 12.5%); extreme spindles prevalence 6.8%)
EDs (prevalence 15.4%); rolandic spikes (40%); focal abnormalities (60%)
EDs (prevalence 6%); generalized 3 Hz spike slow wave (9.5%),
generalized spike/multispike-slow wave (28.6%), midtemporal spikes
(19%), rolandic spikes (14.3%), bilateral midtemporal and/or rolandic
spikes (9.5%), occipital spikes (19%)
Rolandic spikes in nonepileptic ADHD (prevalence 5.6%); right sided
lateralization (51%) and bilateral localization (30%); overlap between
ADHD and BRE
intermittent slow wave focus; multiple asynchronous spike-wave foci;
long spike-wave clusters; generalized 3 Hz absence-like spike-wave
patterns; abundant wake interictal abnormalities linked to a
complicated evolution
EDs-epileptiform discharges; BRE-benign rolandic epilepsy; CTS-centrotemporal spikes
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properly functioning corticocortical bers which restricts the spread of epileptiform activity from one brain
area to another and prevents its evolution to a clinical
seizure. The subclinical epileptogenesis in the developing brain may also directly impair cognitive behavior
functioning by way of transient cognitive impairment
mechanisms, well described by Binnie and his colleagues.8082 A complicated evolution in benign rolandic
epilepsy had been reported to occur in a proportion of
benign rolandic epilepsy patients. This benign rolandic
epilepsy subset developed behavioral, cognitive, and
learning problems independent of their clinical seizures
or treatment. The complicated evolutions were found to
be correlated with certain interictal EEG variables: intermittent slow-wave focus, multiple asynchronous
spike-wave foci, long spike-wave clusters, and generalized 3 Hz absence-like spike-wave discharges.83
Complicated benign rolandic epilepsy does further implicate the role of subclinical interictal EEG discharges
in the etiology of behavioral and cognitive problems unrelated to any seizure characteristics.
The studies summarized in Table 4 put forward arguments for an association between subclinical epileptiform discharges and neurobehavioral disorders as well
as about causality. Given the established link between
EEG epileptiform abnormalities and neuropsychiatric
symptoms in these overlapping disorders, EEG evaluation seems to be justied in children with cognitive and
behavioral problems, even in the absence of overt clinical seizures. In this context, Engler et al.84 showed benecial effects of sulthiame on EEG features, neuropsychological decits, and speech decits in seizure-free
children with rolandic spikes. Duane et al.85 reported
similar ndings in their study demonstrating benecial
effects on cognitive, behavioral, and EEG indices using
levetiracetam in those with learning and attention problems. In a recent study, Chez et al.74 reported a frequency
of 60.7% abnormal EEG epileptiform activity in autism
spectrum disorder patients with no known genetic
conditions, brain malformations, prior medications, or
clinical seizures. In the valproate treated group, 45%
normalized on EEG and about 20% showed EEG improvement when compared with the rst EEG.
At the end of this section, we opine that the maxim
treat the patient, not the EEG may perhaps be an oversimplied clinical standpoint as evidence is mounting
that some of the disorders reviewed (autism spectrum
disorder, ADHD associated with subclinical rolandic
epileptiform EEG discharges) with coincident subclini-
18
cal epileptiform discharges might benet from antiepileptic therapy even in the absence of overt clinical seizures.86,87
DISCUSSION
During the 60 years in which electroencephalography
has been studied, it has become evident that EEG cerebral dysrhythmia does exist in behavioral and psychiatric disorders, as shown by this review. At the end of
this article, keeping in mind the extensive EEG data
summarized in the various tables, a few pertinent questions emerge as to the signicance and relevance of this
large body of literature: Is there truly a high prevalence
of abnormal EEG ndings in nonepileptic individuals
with behavioral disorders and psychopathology? What
could be the underlying contributory factors that led
to these EEG dysrhythmic aberrations? What are the
practical/research implications of these EEG abnormalities?
We will now attempt to address these questions.
From our review, there is a broad consensus that conventional EEG does reveal abnormalities in neuropsychiatric disorders. Although such results could not always be replicated by a few investigators, the vast
majority of studies were in favor of a positive correlation. EEG aberrations reected biological vulnerabilities
to various psychiatric disorders and psychopathologies
and are electrographically represented by EEG dysrhythmias. However, unlike the linear relationship observed between EEG abnormalities and some neurological disorders, the agreement is limited in terms of
conventional EEG data in neuropsychiatric disorders.
The lack of valid generalizations for conventional EEG
abnormalities in neuropsychiatric populations could be
attributed to several factors. Several studies were
plagued by methodological defects, lack of controls,
small sample size, differences in EEG interpretative criteria, lack of denitive psychiatric diagnostic criteria applied, and by the inadequate selection criteria for a
healthy EEG control comparison group, which is a crucial element in neuropsychiatric EEG research. The majority of initial studies were performed prior to the publication of the DSM-III and IV criteria. At this point in
time, our reappraisal of EEG associations in neuropsychiatric disorders is one of statistical and inferential
value, and perhaps the existing literature still reects a
preliminary stage of the area.
From our search, a number of additional factors that
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contributed to the poor denition of the boundaries of
normative EEGs have emerged. These factors include
considerable variability and lack of homogeneity in the
types of subjects examined, the small sample sizes in a
number of studies, nonuniformity, and lack of technical
standardization of the EEG methodology used in many
of the earlier studies, lack of accurate EEG classication
criteria for epileptiform discharges, and the lack of semi
quantitative grading systems for EEG abnormalities.
Many studies used observations made before strict criteria for noncontroversial epileptiform discharges were
recognized, and therefore included the benign nonepileptogenic epileptiform or other controversial anomalous EEG patterns.
The heterogeneity of conventional EEG abnormalities
in schizophrenia and mood disorders perhaps can be, to
a large extent, attributed to medication effects. While
many studies that we reviewed here were comprised of
unmedicated subjects, several studies had not examined
the effects of psychotropic medications on EEG. These
factors do not, however, sufciently explain the observed laterality differences in schizophrenia and mood
disorders. We are cognizant of the fact that there is a
widespread clinical use of antiepileptic drugs in such
psychiatric patients. Pharmaco-EEG is a potential application in the future that will provide sensitive methods to monitor psychotropic drug therapy, and would
have a role in the prediction of clinical response to treatment with psychotropic drugs.88
The EEG abnormalities that are seen to underlie neuropsychiatric disorders reect unequivocal evidence of
underlying brain dysfunction at the cortical, neuronal architectural level, as well as neurochemical perturbations
that underpin several psychiatric pathophysiologies. In
addition, EEG abnormalities represent the phenotypic expression of cellular and biochemical dysfunction, and are
also indicative of maturational retardation factors, possibly genetically determined, underlying subclinical earlier organic brain damage, neurotransmitter imbalance,
or morpho-functional disturbances that may be present
in neuropsychiatric disorders. The EEG is indeed a powerful tool in the exploration of the biological substrate for
neuropsychiatric disorders. Currently, an increasing body
of knowledge from brain imaging research has implicated brain abnormalities in the etiology of psychopathic
and antisocial behavior. Functional brain imaging techniques such as fMRI and PET are certainly tools to further
explore the existing relationship between the EEG, brain
dysfunction, and deviant personality traits.
As far as pediatric neurobehavioral disorders discussed in the section EEG Dysrythmia in Pediatric Neurobehavioral Disorders, are concerned, further research
is needed to explore and ascertain whether these electrophysiological aberrations are a cause, consequence, epiphenomenon, or a coincidence. The clinical overlaps between autism, ADHD, benign rolandic epilepsy, and
Landau-Kleffner syndrome have received relatively little
attention, and future studies need to focus on this EEGbehavior relationship. There is also no current consensus
on whether treatment of EEG abnormalities in these
disorders does improve behavior. The benet of antiepileptic pharmacotherapy for non-epileptic children
with behavioral problems and EEG epileptic discharges must be claried.89 Randomized studies involving blinded pre- and post-treatment assessments
of behavioral, cognitive, and neuropsychological domains as outcome measures will be needed to answer
this question. Therefore, from an evidence-based research perspective, well-designed larger studies with
adequately selected control comparison group, adequate diagnostic construct, and blinded EEG interpretations are needed in the future to reevaluate and conrm the precise relationship of the behavioral/EEG
equation as outlined in Table 5.
CONCLUSIONS
This review has critically and systematically reappraised the published electroencephalographic correlates of
human behavioral disorders, and placed this subject
into the current perspective. Despite the difculty in
drawing direct inferences from the vast volume of EEG
literature, the reported EEG dysrhythmias suggest underlying brain dysfunction to be common among behavioral and neuropsychiatric disorders. It is important
for both the neurologists and psychiatrists to recognize
that paroxysmal EEG dysrhythmias do occur in the various disorders at the brain-mind interface that are not
associated with overt clinical epileptic seizures. Emphasis has been placed on the need for future prospective
evidence-based research to further revalidate the existing relationship between EEG and behavior/psychopathology. Electrophysiological investigations in neuropsychiatric disorders have the potential to contribute to
our understanding of the different pathophysiological
processes that may be aberrant in these disorders.
We would conclude that neuropsychiatric and/or
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neurobehavioral electrophysiology holds an exciting future promise by striving to combine different complimentary electrophysiological test modalities such as
sleep EEG; quantitative EEG; magnetoencephalography; transcranial magnetic stimulation; evoked potentials; and EEG neurofeedback. The neurobehavioral
electrophysiology data can be further veried with the
current functional neuroimaging techniques: functional
MRI and PET. Dissecting the behavioral phenotypes and
their EEG associations will certainly help in further explicating the broader relationship between brain and beTABLE 5.
havior: the domain of neurobehavioral electrophysiology. The quotation by Stevens90 that all that spikes is
not ts is still relevant, and particularly true in the eld
of neuropsychiatry and behavioral neurology as illustrated in this review.
Dr. Shelley was a Visiting Research Fellow in Behavioral
Neurology, and Professor Trimble was funded by the Raymond Way Neuropsychiatry Research Group, Institute of
Neurology, Queen Sq., London. There are no conicts of interest.
Future Areas for Brain-Behaviour EEG Research
(i) Standardization of the testing procedure (length of recording, activation protocols, inclusion of sleep study, serial EEGs when initial
study is normal)
(ii) Standardization of interpretation criteria for both conventional EEG abnormalities and for controversial abnormalities
(iii) Re-evaluation of the prevalence of EEG abnormalities in healthy non-epileptic population using (i) and (ii)
(iv) Evaluation of the prevalence of EEG abnormalities in psychopathological states, with and without psychoactive medications
(v) Examination of the predictive ability of EEG abnormalities for response to treatment, particularly anticonvulsant medications
(vi) Re-examination of the controversial EEG patterns using healthy comparison controls and their relevance
(vii) Randomized studies on the benet of anti-epileptic pharmacotherapy in non-epileptic neurobehavioral disorders
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J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

ELECTROENCEPHALOGRAPHIC CEREBRAL DYSRYTHMIC ABNORMALITIES

abnormalities in nonepileptic subjects, healthy patients,

EEG Dysrhythmia in the Nonepileptic Population

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

disorders. The prevalence of epileptiform discharges in

Summary of Studies of EEG Epileptiform Abnormalities of Persons Without Epilepsy

1,100 ying cadets

Corbin & Bickford, 1955

71 normal children (110 years)

Doose et al., 1968

Neurologically normal children

Cavazzuti et al., 1980

3,726 Neurologically healthy children

1,057 healthy children (612 years)

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

ELECTROENCEPHALOGRAPHIC CEREBRAL DYSRYTHMIC ABNORMALITIES

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

sided temporal lateralization of EEG abnormalities.28,30

Neil et al. 1980

Davis et al., 1974

Crisp et al., 1968

Gibbs & Gibbs, 1964

Bystritsky et al., 1999

Dantendorfer et al., 1996

Weilburg et al., 1995

Slow-wave dysrhythmia (prevalence 24%)

Ito et al., 1993

Temporal non-specic EEG abnormalities (prevalence 33%) in OCD

Abnormal EEGs found in 33% of manic-depressive patients

Jenike & Brotman, 1984

Inui et al., 2001

Abrahams, Taylor, 1979; Flor-Henry, 1972, 1985

Struve et al., 1977

Finely & Campbell, 1941; Davies, 1941

Anxiety, Panic, ObsessiveCompulsive Disorders (OCD)

Jin et al., 1995

Stevens et al., 1979

Summary Table of Publications of EEG Cerebral Dysrhythmia in Neuropsychiatric Disorders

ELECTROENCEPHALOGRAPHIC CEREBRAL DYSRYTHMIC ABNORMALITIES

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

J Neuropsychiatry Clin Neurosci 20:1, Winter 2008

Devinsky et al., 1996

Wilkes et al., 1990; Lelliott, Fenwick, 1991

Wilkus et al., 1984

Cohen & Suter, 1982

King et al., 1982; Luther et al., 1982

Standage et al., 1975

Cornelius et al., 1986

Abnormal temporal theta with sharp components (unilateral/bilateral); posterior

Increased slow-wave activity (frequently bilateral); frontal, temporal or frontotemporal

Snyder & Pitts, 1984

Anticonvulsant responsiveness in BPD with EEG epileptiform discharges

Aggressive behavior associated with temporal lobe EEG focus

Pillmann et al., 1999

Wong et al., 1994

Hill, 1942, 1944, 1952; Williams, 1969; StaffordClarke, Taylor, 1949

Harper et al., 1972

EEG dysrhythmia in compulsive binge eaters (prevalence 64.4%); paroxysmal

Psychogenic Nonepileptic Seizures

Borderline Personality Disorder

Criminal Behavior and Violence