Chapter 7
Activation Procedures
A met hod used to bring out abnormalities in the EEG,
such as hyperventilation, photic stimulation and sleep.
These procedures are known to activate or stimulate
abnormalities in some patients. For example,
Hyperventilation and photic stimulation are most
useful for activating epileptiform abnormalities,
whereas drowsiness and sleep are useful for activating
all forms of EEG abnormalities as well as normal
epileptiform patterns (so-called pseudoepileptiform
patterns).
Hyperventilation
Hyperventilation is perhaps the most widely used
activation procedure in EEG laboratories. The procedure,
which is simple and relatively safe, consists of three to
five minutes of deep breathing. It is, however, difficult to
perform in patients who are uncooperative, mentally
retarded, or below the age of 4 or 5 years, and it is
preferable to avoid in patients with recent myocardial
infarction, chronic obstructive pulmonary disease, and
other conditions causing difficulty in breathing. Although
hyperventilation has become a common procedure during
routine EEG recording, it is of special importance in the
case of patients suspected of having seizure disorders,
particularly absence seizures.
Procedure
The standard procedure is to have the patient take deep
breaths at the rate of about 20 per minute for three to
five minutes. The first is to explain the procedure in
detail to the patient. Tell the patient to relax, keep the
eyes closed and mouth open, and to breath deeply in
and out at a regular pace until told to stop. A minimum
1 minute baseline recording is made before starting
hyperventilation. The effect of hyperventilation on the
EEG begins earlier in children than adults and is
apparent in 50% of cases within the first minute and
90% within the first 2 minutes.
As recommended by the American Clinical
Neurophysiology Society, hyperventilation should not
be performed in certain clinical settings, including
acute stroke, recent intracranial hemorrhage, large-
vessel severe stenosis and associated TIA , documented
moyamoya disease, severe cardiopulmonary disease,
and sickle cell disease or trait.
Normal and abnormal responses
The normal response to hyperventilation consists of
the occurrence of symmetrical slow activity on both
sides. The absence of any change in the EEG is also
normal. Although this slow activity may be diffuse
theta activity, a more characteristic finding is the
occurrence of intermittent or continuous 3 to 4 Hz high
amplitude activity that is frontally or occipitally
dominant. If the activity is continuous, it may build up
gradually to amplitudes in excess of 250µV. The slow
activity may persist for up to a minute after
hyperventilation ceases, and the EEG may not return to
its prehyperventilation state for two to three minutes.
The amplitude and frequency of the slow activity are of
no clinical importance unless there is consistent
asymmetry between the two hemispheres. The side that
shows a slower frequency and/or a lower amplitude is
usually considered to be the abnormal side.
On the other hand, the hyperventilation response
often includes frontal intermittent rhythmic delta
activity (FIRDA) or, particularly in children, occipital
intermittent rhythmic delta activity (OIRDA).
Although spontaneously occurring FIRDA or OIRDA
76 Review Of Clinical Electroencephalography
indicates the presence of a diffuse cerebral
dysfunction,their isolated appearance in
hyperventilation is considered normal.
The most striking EEG abnormality seen during
hyperventilation is 3 Hz spike and wave discharges often
brought on in patients with absence seizures. These
discharges usually are frontally dominant and may occur
in brief epochs, or they may persist for several seconds
during which time an episode of unresponsiveness may
be documented. Sometimes, other types of epileptiform
abnormalities, such as generalized spike discharges or
even focal spikes, may be brought on by
hyperventilation.
How does hyperventilation bring about such
dramatic changes in the EEG? The major biochemical
finding during hyperventilation is a drop in carbon
dioxide content of the blood(hypocarbia). It is well
known that the most important vasodilatory stimulus
Posterior delta activity produced by hyperventilation in a 6-year-old boy. Older adolescents and adults
typically show anterior-dominant slowing in response to hyperventilation.
for the blood vessels of the brain is carbon dioxide.
The higher the carbon dioxide content, the greater the
vasodilatation. So when there is hypocarbia, the
reverse occurs, namely, vasoconstriction. This
presumably alters the metabolic rate of the neurons and
leads to the slow activity.
The effect of hyperventilation on the EEG is
much more marked in children than in adults, with
children,s EEGs sometimes showing an enormous
buildup of slow activity. Blood sugar level also appears
to influence the response to hyperventilation. The
lower the blood sugar, the more marked the
hyperventilation-induced slow activity. When an adult
EEG shows marked and prolonged slowing as a result
of hyperventilation, one should consider the possibility
of hypoglycemia and should repeat the procedure 15 to
30 minutes after giving a drink containing gloucose.
Activation Procedures 77
78 Review Of Clinical Electroencephalography

response:(1)visual evoked response (2) photic driving,

Photic stimulation (3) the photomyogenic (formerly referred to as
photomyoclonic) response, and (4) the
Visual stimuli are perhaps one of the most effective
photoepileptiform response (PER) (also referred to as
means of stimulating the brain. The ready availability
the photoparoxysmal response [PPR]).
of user friendly stroboscopes has resulted in the routine
use of intermittent photic stimulation(IPS) as an
activation procedure during EEG. The method is most Visual evoked response
valuable in documenting photosensitivity, which has a
The visual evoked response is the same potential which
high clinical correlation with primary generalized
is recorded during evoked potentials. The difference in
epilepsy.
appearance is because of the method of data display
and the absence of averaging. The VER is seen with
Technique low flash frequencies, usually most prominent at and
below 5/sec.
The device used is called a stroboscope or photic
stimulator. It is capable of delivering single or
Photic evoked potential: Flash at 5/sec produces an
continuous bright flashes of light at frequencies
evoked potential in the fourth channel, due to activity
ranging from 1 to 50 flashes per second.
in the occcipital lead. The upgoing potential in this
The test begins by explaining the procedure to the
bipolar montage indicates positivity at the O1
patient. Tell the patient he or she will be seeing very
electrode. The positivity is delayed from the stimulus
bright flashes of light(bright even with the eyes closed)
by about 100 msec, indicating that this is an evoked
and to keep the eyes closed or open as instructed
potential rather than a photic response.
during the course of the test. The flash lamp is
The absence of a VER is not abnormal unless
positioned approximately 30cm in front of the eyes.
unilateral. Such asymmetry suggests abnormality in
Start with one or two flashes per second and increase
projections from one lateral geniculate to the cortex, or
the rate gradually up to 30 flashes per second. Each
the calcarine cortex, itself.
flash rate is presented for a duration of about 10
seconds, and the eyes are kept closed in the first 5
Photic Driving Response
seconds and open in the next 5 seconds. If a
The driving response appears as the flash frequency
photoparoxysmal response (explained later) is elicited,
accelerates beyond 7/sec, and the next evoked potential
the IPS should be stopped to avoid precipitating a
starts before the last evoked potential has ended. It is
seizure. If the response occurs only during a brief part
created by the visual evoked responses merging into
of the stimulation, the technician needs to confirm that
each other.
it is indeed a photoparoxysmal response by cautiously
repeating the stimulation at the same flash rate.
The photic driving response consists of rhythmic,
occipital-dominant waveforms that either show a one-
Responses to photic stimulation to-one relationship with each flash or appear as a
harmonic (an integer multiple) or subharmonic (an
It was found that diffuse light stimulation produces
integer dividend) of the flash frequency.
four main categories of electrographic
 Activation Procedures 79

Photic driving response: Photic driving response is time-locked to the stimulus and appears at faster frequencies
than the photic evoked response

Just as POSTS or lambda waves may be strikingly
asymmetrical in normal individuals, an asymmetrical
driving response is considered normal unless
accompanied by other EEG abnormalities . In normal
individuals, asymmetrical POSTS or lambda waves are
usually associated with a similar asymmetry of the
driving response Cortical epileptogenic lesions or skull
defects can enhance the amplitude of the photic driving
response ipsilaterally, whereas destructive lesions can
attenuate it ipsilaterally.

Photic driving
80 Review Of Clinical Electroencephalography

Photomyogenic Response or Photomyoclonic

Response
The photomyoclonic response is not cerebral in origin,
but rather is electrical activity in the frontal scalp
muscles which is induced by the flash stimulus in
susceptible individuals. Repeated contraction of these
muscles produces EMG activity which is time-locked
to the stimulus, and recorded from the frontal
leads. There is a delay of 50-60 msec between the flash
and the EMG activity.
The main problem with the photomyoclonic response
is in differentiation of this from photoepileptiform
response. Some general guidelines are discussed in the
next table.

Differentiation of photomyogenic from photoepileptiform responses

Feature Photomyogenic Photoepileptiform

Spatial distribution Anterior Posterior or generalized
Termination End of the stimulus May stop before the end of the stimulus
or outlast the stimulus.
Rise time of the spike Fast (EMG) spikes Slower, spike-and-wave complexes most
common.
Frequency Sale frequency as the flash Frequency is independent of the flash
frequency, usually slower.

Photomyogenic (photomyoclonic) response to 14-Hz

photic stimulation. Prominent frontalis and temporalis
myogenic potentials time locked to the flash stimulus
end with a whole-body jerk.

Photoepileptiform or Photoparoxysmal
Responses
The photoepileptiform response is characterized by
spike-wave complexes during photic stimulation. The
discharge is usually activated only by a few specific
flash frequencies. This response is a marker for seizure
tendency, and most often noted with generalized
epilepsies. Less commonly, photosensitivity is noted
Photoparoxysmal response to 15-Hz
photic stimulation with initial fast activity
evolving into a typical generalized 3-Hz
spike-and-wave pattern. Eye fluttering
typical of a myoclonic absence seizure
was observed.
Activation Procedures 81
with partial epilepsy (occipital lobe epilepsy, and even
less commonly temporal lobe epilepsy). While some
patients will have already noticed that there is photic
trigger of their seizures, this is not always the case.
Some patients with photosensitivity have never had a
spontaneous seizure. The correlation of a
photoparoxysmal discharge with seizures is greatest if
the discharge continues after the end of the flash train.
Photoparoxysmal response to 8-Hz photic stimulation
in a 6-year-old girl. Note the irregular spike-and-wave
complexes and greater amplitudes in more anterior
derivations
82 Review Of Clinical Electroencephalography
Photoparoxysmal response
SLEEP ACTIVATION
Activation during Sleep
Sleep is a highly effective method for eliciting both
generalized and focal interictal epileptiform discharges
(IEDs). In as many as onethird of patients with
complex partial epilepsy, IEDs may not be present
during wakefulness but appear only during sleep .
Epileptiform discharges are also often more easily
detected during sleep. Recordings during wakefulness
are often obscured by muscle and movement artifacts,
especially in children and adults who are unable to
cooperate or relax during the recording. Nearly all
patients with IEDs during daytime nap recording have
their first discharge within 15-30 minutes of sleep
onset . Thus outpatient EEGs in patients with suspected
seizures should always include sleep, but the actual
sleep recording generally does not have to exceed 30
minutes in duration. When a sleep EEG recording is
clinically indicated and the patient is unable to fall
asleep, a short-acting sedative can be used to help
induce sleep. Short-acting barbiturates and chloral
hydrate are two agents that have been used for this
purpose. Chloral hydrate is generally preferred
because, unlike barbiturates, it does not induce beta-
frequency activity in the background EEG. Every
patient considered for sedation should be medically
assessed for the risk of sedation. Patients should also
be counseled about restricting their activities until the
effect of sedation has worn off.
Epilepsy syndromes that commonly show activation
with sleep are listed below:
1. Benign occipital epilepsy in infancy
2. Generalized tonic seizures in chronic childhood
epileptic encephalopathies (e.g., Lennox-Gastaut
syndrome)
3. benign rolandic epilepsy
4. Benign juvenile myoclonic epilepsy (i.e., on
awakening)
5. Frontal lobe epilepsy
Activation by Sleep Deprivation
Sleep deprivation increases the possibility of seeing
epileptiform activity in some patients, and also
increases the chance of obtaining sleep. Sleep
deprivation increases the yield of epileptiform
discharges beyond that expected from sleep alone, and
therefore is considered a separate physiologic
activation method. It is often used for patients in whom
routine EEG has not been able to identify interictal
epileptiform activity. Sleep deprivation may be a
particularly potent activation method in patients with
juvenile myoclonic epilepsy. In these patients, the
highest yield is in recording most of the EEG after
arousal from a brief nap following sleep deprivation.