Talking psychiatry...The role of EEG in the management of psychiatric disorders

1. INDEX
 INTRODUCTION
 CURRENT APPLICATIONS OF
ELECTROENCEPHALOGRAPHY
EEG IN THE PSYCHIATRY OF PATIENTS WITH MEDICAL ILLNESS
This article's objectives are to guide psychiatrists caring for the medically ill in deciding when to request
an electroencephalogram (EEG), in choosing what to do to maximize the possibility of eliciting positive
findings, and in determining how to apply information in the EEG report. Although major advances in
imaging techniques have eclipsed the EEG's importance as a tool for studying brain structure in recent
decades, it continues to have a significant role in clarifying psychiatric presentations in the medical-
surgical setting. EEG remains the pre-eminent cost-effective and readily available method for identifying
brain dysfunctions such as delirium and seizure disorders, which often masquerade as purely psychiatric
conditions whose organic bases go undetected. This article emphasizes the EEG's role as a correlational
rather than a screening tool. A series of case reports illustrate how the EEG can be used to tease apart a
diagnostic differential that can include entities as diverse as acute brain dysfunction, longstanding
personality structure, and intermittent seizure discharge. The thoughtful integration of EEG data with
material from clinical history and examination is fundamental to the EEG remaining a useful component
in a psychiatric diagnostic armamentarium.
The electroencephalogram (EEG) is one of the oldest tools in clinical psychiatry. As the new millennium
dawns, however, it is worth considering whether the EEG is also one of the most irrelevant. Although
focal electrical abnormalities can point to localized lesions, particularly when acute, the advent of CT
scanning in the 1970s and MR imaging in the 1980s has rendered EEG essentially obsolete as a
diagnostic tool for assessing structural damage.1 EEG still has significant merit in the medical-surgical
setting, however, even as the medical psychiatry literature remains largely silent about it. This article
offers guidelines to help psychiatrists determine appropriate situations in which to request EEGs and
provides some ideas about how to understand and apply the information that comes back in the EEG
report. It is not a primer on interpreting EEG tracings. In the authors' opinion, the busy medical
psychiatrist best leaves that to the EEG technician.

2. Developed in the early twentieth century as a noninvasive method for investigating both cerebral
function and structure, the EEG was, for decades, standard in the workup of brain disease.1 Despite
poor sensitivity and specificity for identifying particular clinical conditions, it was the only tool short of
surgery and direct visualization of the brain that reliably delivered information on the cerebral
parenchyma. As a result, a large body of literature exists, attempting to make pathognomonic sense of
the electrical tracings gathered from many clinical conditions.
EEG failed as a diagnostic tool of functional alteration on many grounds, however. Multiple studies of
general psychiatric and healthy populations debunked its value as a screening tool.2, 5, 8, 13 Not only do
most psychiatric conditions not have specific electrical patterns associated with them, but also
nonspecific abnormalities appear on tracings from both the psychiatrically ill and the well. Among
healthy subjects, 10% to 15% have some EEG abnormalities.4, 9 In one study, 20% of patients with
bipolar disorder had marginally abnormal EEGs. One fourth of patients with schizophrenia, and half of
individuals with sociopathy, had tracings with nonspecific abnormalities.9 Moreover, in most general
psychiatry cases, EEG adds nothing to the diagnostic impression. In a review of 190 inpatient psychiatric
charts of patients who have had screening EEGs, Warner et al13 found that 36 of the screening tracings
contained abnormalities, but that only 2 of 36 provided additional information that resulted in a
different diagnosis from that based on non-EEG data alone.
 To appreciate the value of EEG, it is necessary to understand its limitations. Neylan et al10
summed them up as follows:
quot;The EEG is a nonspecific indicator of cerebral function. Any pathophysiological insult to the central
nervous system can result in alterations in electrophysiology. Thus, with few exceptions, the EEG does
little in providing a precise diagnosis. EEG abnormalities are most pronounced with acute injuries of the
outer cortex. Disorders that affect deep brain structure or result in a chronic, indolent loss of neurons
may show little or no EEG changes.quot;
Their words point out the tendency of any brain injury to result in electrical alteration, a concept that
makes intuitive sense if the brain is understood as an electrical organ. They remind us that, because
electrical signals attenuate in proportion to the distance they must travel from deep structures, EEG
surface leads primarily survey only shallow cortical layers. Signals originating in the brainstem or in
orbitofrontal, mesial, or deep temporal structures are for this reason notoriously difficult to capture.
Finally, slow, degenerative changes may not even register as deranged electrical signals because dead-
brain tissue sends no signal at all.10
CURRENT APPLICATIONS OF ELECTROENCEPHALOGRAPHY
The nonspecificity of EEG signal abnormalities helps to explain why its promise as a screening tool for
particular conditions affecting function has not been realized. But Neylan's observations, read in reverse,
tell us how EEG can be useful. When a patient has experienced a known insult acutely that could have
affected the neocortex, the nonspecific findings on EEG have a high likelihood of correlating with the
insult's effect.
 Case 1: Postoperative Delirium Versus Problematic Personality
Mr. G. was a 62-year-old man who had undergone hip-replacement surgery 2 days prior. Before surgery,
he was irascible and demanding. Since surgery, he had demonstrated more of the same behavior, with
the addition of the following symptoms: instructed to remain in bed, he was found, on several occasions,
hobbling around his room despite his unstable hip; and, when interviewed about his rehabilitation plans,
he failed to pay attention, finally answering a question about whether he would need a hospital bed after
discharge with, “the skew of the angle interferes with the formation of the committee.” The orthopedics
team asked the psychiatrist whether Mr. G. was “crazy.” The psychiatrist opined that Mr. G. probably

3. had a challenging premorbid personality, and his problem now was likely delirium in the context of
general surgery and anesthesia. An EEG showed a grade 2 generalized dysrhythmia consistent with
toxic-metabolic encephalopathy.
For the psychiatrist working in the medical-surgical setting, the EEG remains an economic and generally
available tool for assessing brain activity.9 An abnormal EEG tracing in conjunction with a negative MR
imaging or CT study illustrates a truism often forgotten in this age of exquisitely detailed imaging
studies: All cerebral abnormalities cannot be “seen” in the conventional sense. Even when an
abnormality is visible, it must be correlated with a functional measure, either from history or clinical
examination or another study. His words still true 2 decades after he wrote them, Itil6 reminds us that,
“the EEG is still the only method able to provide information on cerebral function in a continuous and
noninvasive way that is also cost-efficient.”
Medical psychiatrists work in situations in which many of their patients have psychiatric presentations
or acute mental status changes secondary to brain dysfunction induced by a primary medical or surgical
condition. Fenton4 notes the value of the EEG as “a noninvasive tool for the investigation of organic
mental syndromes and epilepsy.” Lam et al8 broaden its applicability to include exploration of
“symptoms that mimic psychiatric disorders but actually result from iatrogenic, metabolic, or
nonconvulsive seizure disorders.” EEG is ideally suited to detect encephalitides, particularly herpes
simplex encephalitis, with its pathognomonic periodic high-voltage, sharp waves and slow-wave
complexes at two to three per second in the temporal regions, and rapidly progressive dementias, such as
subacute sclerosing panencephalitis and Creutzfeldt-Jakob disease, with their characteristic periodic,
high-amplitude bursts. While causing localized slowing detectable on EEG, cerebrovascular accidents
and space-occupying lesions, such as tumors, typically are identified these days on CT or MR imaging.
As time passes from the stroke, the EEG tends to normalize. Deep lacunar infarcts may never register at
all on a scalp tracing. If a tumor grows slowly or degenerates insidiously, as in Alzheimer's disease, the
EEG may show little, if any, change.2
Until specific anatomic or physiologic causes have been ruled out, the “depression,” “anxiety,”
“psychosis,” or “conversion disorder” that commonly earns the medical-surgical patient a psychiatry
consultation initially should be regarded only as a phenotype consistent with mental illness. Medical
psychiatrists must convince themselves that there is no cause for the abnormality other than the
psychiatric condition.
 Case 2: Iatrogenic Seizures versus Conversion Disorder
Ms. W was a 33-year-old woman with a complex medical history that included congenital connective
tissue disease, pheochromocytoma, and frontal meningioma, the latter two in the context of von Hippel-
Lindau syndrome. She was admitted to a general neurology service for evaluation of multiple seizure-
like events and was behaviorally polymorphous in presentation since having gamma knife surgery for
the meningioma 1 year ago.
Ms. W's initial EEG failed to show epileptic activity, and her spells were neither stereotypic nor classic in
their description. In terms of her psychosocial history, moreover, she and her estranged husband were
engaged in an emotion-laden custody battle, and she had multiple blood relatives with diverse
psychiatric diagnoses. Given all of these factors, the neurology service consulted the psychiatry
department to rule out conversion disorder with pseudoseizures as its manifestation. After ascertaining
that Ms. W herself had no previous psychiatric history and no characteristics of the typical conversion-
disordered patient, the psychiatrist encouraged the neurology team to pursue extended observation.
After several days off antiepileptic medication, while on continuous EEG monitoring, Ms. W had a grand
mal seizure that resembled her presenting spells and originated from the gamma radiation scar at the
meningioma site.

4. For the EEG to be useful despite its anemic sensitivity and specificity, the importance of the psychiatrist
gathering history from chart data, patient interview, and collateral sources cannot be overemphasized.
This case illustrates this well. “Each EEG must be read in its proper context in relation to a particular
problem of an individual patient,” Kiloh7 writes, and “full clinical details should be available, including
the results of other investigations.” EEG is first and foremost a correlational tool, powerful when
deployed to clarify a drug-induced, metabolic, or convulsive state. Indications from history for ordering
an EEG cluster around the sudden, recent, discrete, or episodic mental status change. Indications for
ordering an EEG include the following:
Helpful
 Seizure disorder
 Encephalitis
 Delirium
 Rapidly progressive dementia
 Profound coma
Often abnormal, but unhelpful
 Space-occupying lesions
 Dementia
Variable findings, therefore, unhelpful
 Cerebral infarctions
 Head injury
Acute psychiatric symptoms in a patient with a known neurologic diagnosis, such as epilepsy or multiple
sclerosis, especially call for an EEG investigation. New-onset mental status abnormalities or localizing
neurologic signs also point to conditions that should be considered “functional” only after the organic
workup, including EEG, is negative.
An abnormal EEG may raise suspicion of a previously unsuspected abnormality. Paradoxically, the key
to clarifying the following case turned on the EEG finding demonstrating why the psychiatrist could not
induce a desired seizure. The EEG findings also led to additional investigations that revealed heretofore
undiagnosed pancreatic and hepatic disease.
 Case 3: Hepatic Encephalopathy Versus Recurrent Major Depression
Mrs. A, an 80-year-old woman with a history of diabetes mellitus, recurrent major depression, and
remote ovarian cancer, was admitted to a medical psychiatry unit after failure to respond to adequate
antidepressant trials. Having responded to electroconvulsive therapy (ECT) in the past, she consented to
receive ECT once again; however, a seizure could not be induced on several successive days, even with
the deployment of maximum energy, hyperventilation, an extender, and a change in anesthetic agents.
Meanwhile, she became increasingly withdrawn, mute, and disinterested in oral intake. Hoping to clarify
whether she had slipped into an apathetic, hypoactive delirium versus nihilistic progression of

5. depression, an EEG was performed and demonstrated diffuse, generalized slowing consistent with
metabolic encephalopathy. Additional laboratory studies yielded elevated liver function tests. A liver
sonogram revealed a large pancreatic mass with metastases to the liver.
In ordering the EEG, medical psychiatrists must keep in mind certain recommendations and caveats. In
the setting of delirium, the EEG is almost always abnormal if the patient has an altered level of
consciousness. Not only does the degree of EEG change correlate with the severity of the encephalopathy,
but also EEG changes reverse as the causative condition resolves, thus permitting serial EEGs to track
response to therapy.3 Complicating matters, however, is that an EEG may be read as normal, relative to
general parameters, when it actually represents a change for that particular patient. Although an
individual's rhythm is consistent at one frequency, normal ? value can range from 8 to 13 Hz. Thus, a
normal ? value for one patient may represent significant slowing for another. As a result, the presence of
slowing as the result of a syndrome such as delirium cannot be definitively inferred without a baseline
EEG for comparison to health.1, 11
Events such as seizures are typically sporadic, with the EEG tracing normal between events. “A normal
EEG never excludes any clinical condition, but can merely serve to diminish the probability of its
existence,” Kiloh7 warns. Serial EEGs days apart can help to resolve the dilemma as the EEG changes
with the resolution or worsening of the delirium. In emphasizing the evanescent nature of some EEG
findings, Adams et al1 caution that an EEG is ordinarily “recorded under restricted circumstances . . .
from several parts of the cerebral convexities (only) during an infinitesimal part of a person's life.” It is
this concern that leads to recommendations for serial tracings, up to months apart, or for extended EEG
observation in a video-monitoring unit in an attempt to capture an event. While multiple investigators
report what intuitively makes sense—that serial tracings increase yield—specific guidelines for the
appropriate intervals do not exist.2, 5, 8
 Case 4: Partial Complex Seizures Versus Behavioral Dyscontrol
Mr. R. was a 49-year-old man whose history of refractory seizures had culminated in a right temporal
lobectomy 1 year before his present psychiatric admission. Postoperatively, his seizures had been well-
controlled with carbamazepine and phenytoin, but he had begun experiencing vexing bouts of intense
anxiety associated with despondent mood. He was admitted to a medical psychiatry unit after
antidepressants proved ineffective. He received bilateral electroconvulsive treatments nine times without
benefit. In addition to his profound anxiety and depression, he had periodic outbursts, sudden
paroxysms of suicidality, and intermittent sexual impropriety. Staff became increasingly convinced that
these behavioral perturbations were consonant with a personality disorder. He was referred to the
epilepsy monitoring unit, however, where he was found to have frequent partial complex seizures
originating in the right frontal region and frequently generalizing to the left frontal and right temporal
regions. They lasted 5 to 60 seconds, provoked significant sleep disruption, and correlated with a variety
of behavioral and cognitive abnormalities. After a more complex anticonvulsant regimen had been
instituted, the behavioral dyscontrol resolved. Venlafaxine effectively treated remaining depressive and
anxiety symptoms.
Detecting seizure disorders often requires technical adjustments as well. Activating procedures and
yield-enhancing techniques include the following:
Activating Procedures
 Hyperventilation
 Photic stimulation
 Sleep

6.  Drug administration
Yield-enhancing Techniques
 Alternate electrode placement
 Replication of patient-specific provocations
 Minimization of confounding variables (e.g., medications)
A single interictal tracing is normal in 20% of patients with absence seizures and 40% with grand mal
seizures.1 Serial tracings eventually may show the suspected seizure, but the patient can be prepared
both before and during the study to maximize the likelihood inducing seizure activity at the time that the
tracing is made. These activating procedures lower the seizure threshold in susceptible individuals. Sleep
deprivation for the night before a study can help to ensure that a patient will fall asleep during the study.
A patient with partial complex seizures, for example, may have a normal tracing until asleep. Epileptic
abnormalities appear on 10% to 30% more EEGs in patients who sleep during the examination.12
In addition to sleep, many activating procedures are used to bring out abnormality on the EEG tracing,
particularly when convulsive phenomena are suspected. Hyperventilation, typically at a rate of 20 times
a minute for 2 to 3 minutes, is especially helpful in elucidating petit mal activity.2 A strobe light for
photic stimulation, placed 37.5 cm (15 inches) from a patient's eyes and flashed at frequencies ranging
from 1 to 20 times per second may bring on seizure activity. When it does not occur spontaneously
during a tracing, sedatives, such as barbiturates, or antipsychotics, such as chlorpromazine, may be
administered to suppress ascending reticular activity and help unmask abnormalities not present on the
EEG tracing in the awake subject.9 If patients report that a particular stimulus (e.g., music) induces a
seizure, exposure to that stimulus during monitoring is recommended. Potentially confounding
medications, such as anticonvulsants or benzodiazepines, may need to be discontinued in anticipation of
the study.
Given the shallow surveillance depth of surface leads, alternative lead placements can put the electrode
closer to the source in cases in which temporal lobe seizures are suspected. Nasopharyngeal leads,
inserted into the nose, rest on the mucosa of the pharyngeal roof, several centimeters closer to the
temporal tissue inferiorly. Sphenoidal leads, ensheathed in a lumbar puncture needle, can be angled into
the cheeks inferior to the zygomatic arches to the neighborhood of the foramen ovale. These lead
manipulations capture up to one third of patients with partial complex seizures who have normal scalp
tracings.12
Beyond these measures to enhance yield, it is also useful to minimize confounding factors that may
attenuate the useful information that can be gleaned from a tracing. Ideally, a patient should not fast
before an EEG because hypoglycemia can influence a tracing. Similarly, an overly anxious or frankly
uncooperative patient can introduce a variety of motion artifacts. Recent electroconvulsive therapy or
psychoactive medications (e.g. sedatives, neuroleptics, tricyclics, or lithium carbonate) also can influence
the EEG tracing. The EEG technician should take such details into consideration when attempting to
extract relevant information from a compromised tracing.2
Once the EEG technician has read the EEG tracing and provided a narrative report, the psychiatrist
must interpret the findings. This process of putting them in context is best accomplished by asking a
series of questions that confirm the adequacy of the tracing while translating the findings into the
psychiatric context.
Is the tracing adequate, that is, was the patient monitored for a sufficient time period without artifact or
confounding factors present? Does the report note that tracings were obtained with the patient asleep as

7. well as awake? If abnormalities are mentioned, are they generalized and symmetric, indicating global
dysfunction, or focal and asymmetric, suggesting a specific site of injury? Are there general patterns of
either slowing, suggestive of encephalopathy, or acceleration, typically associated with sedative-hypnotic
or alcohol withdrawal? Are there focal abnormalities, such as the spikes characteristic of seizures, or
patterns pathognomonic for particular encephalitides? Did the EEG technician correlate any electrical
aberrations with clinical history?
The EEG, finally, serves a useful purpose in resolving debates that occur with unfortunate frequency in a
medical environment that, nearly 400 years later, has still not bridged Descartes' mind-brain split. When
Miss X suddenly began to exhibit bizarre behavior, as described in the following case, it was the EEG
that revealed the anatomic and physiologic underpinnings of the behavioral change.
 Case 5: Frontal Lobe Status Epilepticus Versus End-of-Life Personality Changes
Miss X was a 58-year-old woman who had been fighting breast cancer for 7 years. She had had a
mastectomy, chemotherapy, and radiation over the multiple recurrences of the disease, but its latest
manifestation—meningeal metastases—was the most dire. The latest cancer recurrence had made
planning for the end of her life a prominent concern. She was undergoing palliative whole-brain
irradiation and discussing hospice placement with her inpatient oncology team when her mental status
dramatically changed. Where she had formerly been practical, no-nonsense, and intimately involved in
organizing her care, she became—overnight—uninterested in the details of her hospice care plan. As if a
switch had been turned on, she suddenly waxed grandiose, vague, expansively spiritual in terms that fit
no known religious practice. She intoned in poetic and dramatic terms about the universe and her place
in it but seemed unable to discuss these ideas with an examiner who found it difficult even to make eye
contact with her as she gazed off into the middle distance. A neurologist and psychiatrist were consulted.
The neurologist found nothing untoward in her presentation and adamantly refused to authorize the
EEG that the psychiatrist wanted, until the patient had a partial complex seizure witnessed by a member
of the neurology team. The patient was found to be in frontal-lobe status epilepticus, a finding that
explained her abrupt mental status change.
SUMMARY
The psychiatrist considering recommending an EEG should look for acute changes in the history or
examination suggestive of an organic cause. If he or she judges that the EEG will help to clarify or
confirm the diagnostic impression already formulated, it is worth considering whether adding
provocative maneuvers could increase the yield. The authors cannot overemphasize the importance of
using the EEG in correlation to further inform old-fashioned clinical detective work already in process,
particularly when the EEG could rule out a potential organic contributor to a psychiatric phenotype. For
routine screening without an elevated index of suspicion or for thoughtless “fishing expeditions,” EEG
results will surely disappoint.
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