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Understanding

Electroencephalography

Mohamed Hamdy
Post graduate teaching
Electrophysiology

Objectives of this lecture

To know what is the basic mechanism of the normal and abnormal


EEG
To know the significance of the EEG in the light of the clinical context
To know when to ask for EEG and what activation technique do you
recommend
To know the variability of findings in different age groups
To use the EEG finding in making the decision in epilepsy
management

Mohamed Hamdy

The skeleton of the topic

Physiology of the EEG waves


Normal variants
Interictal epileptiform abnnormalities
Ictal abnormalities
Maturational aspects from neonates to adulthood
Sleep changes in EEG
EEG monitoring
Example tests
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Recording EEG

EPSP at apical dentritic trees of pyramid


cells
Dentritic membrane depolarized
Potential difference cause a current
flow through volume conductor from the
nonexited membrane of the soma to the
apical dentritic tree
Extracellular currents = secondary /
volume currents

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Recording EEG

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The EEG machine

8 64 identical channels recording


simultaneously from as many different
pairs of electrodes

Electrodes & electrode board


Amplifiers
Filters
Pen & chartdrive (screen)

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The Source of EEG

EEG = a measure of cerebral electrical activity


The generator sources for EEG waves are within the cerebral cortex
Electrical activity recorded on the scalp is produced by extracellular
current flow associated with summated excitatory and inhibitory
postsynaptic potentials (EPSPs and IPSPs)
Individual action potentials do not contribute directly to EEG activity

Mohamed Hamdy

Synaptic Potentials:
The Basis of EEG Activity

Synaptic potentials are of much lower voltage than action


potentials, but the produced current has a much larger distribution
PSPs have a longer duration and involve a larger amount of
membrane surface area than APs

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EPSPs and IPSPs

EPSP produces a change in membrane permeability within a select


portion of the cell membrane resulting in a net influx of + ions that
depolarizes the cell
IPSP selective activation of either Cl- or K+ channels resulting in a
net outward ionic current with hyperpolarization of the cell

Mohamed Hamdy

EEG: A Reflection of Current

Spontaneous EEG activity occurs when currents flow across charged


neuronal membranes
An EEG waveform reflects a summation of PSPs from thousands or
even millions of cortical neurons
The EEG represents the average behavior of large neuronal
aggregates
The current flow from positive to negative is arranged in a dipole

Mohamed Hamdy

The Dipole

Theoretically, the current flows in a 3-dimensional ellipse with the


greatest current density along a straight line connecting the positive
pole to the negative pole
The complex arrangement of the brain and head, differences in cell
type and function within a region, and physical differences between
brain areas result in an approximate dipole that is not a perfect
model.

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Rhythmical vs. Arrhythmical


EEG Activity

When EEG waves are rhythmical, most of the cells within the
given neuronal pool are behaving similarly
With arrhythmic activity, there is less correlation with individual cell
behavior

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Pyamidal Cells:
Principal Current Generators of EEG

Topographical organization within the cortical mantle corresponds


to a dipoles oriented perpendicular to the cortical surface

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Factors Affecting EEG Waveforms

Voltage of the cortical discharge


Area involved in synchronous activity
Degree of synchrony
Location of the dipole generators in relation to the convolutions of the
cortical mantle.

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Factors that Attenuate Voltage

Primarily overlying spinal fluid and dura


Scalp to a lesser extent
Scalp recorded activity represents spatial averaging of electrical activity
from a limited area of cortex
20-70% of epileptiform activity may not be seen on scalp EEG
Involvement of small areas of tissue is associated with much greater attenuation
of activity
Activity arising from cortex within the walls or depths of sulci may not be recorded

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Origin of EEG Rhythmicity

Rhythmical activity sequences of regularly recurring waveforms of similar


shape and duration
Rhythmical activity may be locally generated or occur via projected synaptic
inputs from deeper structures
The thalamus, via an anatomic cellular organization, thalamocortical
projections and mechansims that are not fully understood, governs different
types of rhythmical activity
Sleep spindles
Alpha rhythm in the occipital cortex
3 per second spike and wave associated with absence seizures

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Types of EEG Recording

Routine

analog, digital

with computerized analysis & brain electrical activity


mapping

Long-term Monitoring

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Routine EEG Techniques


20-min or longer sampling of brain activity
Written out or recorded directly on magnetic tape or digitally by
computer
Disc electrodes are applied according to 10-20 system of
electrode placement
Montages: referential, bipolar, changeable with digital recording

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10-20 System Of Electrode


Placement

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International 10-20 System of Electrode


Placement

Established in 1958
Electrodes are spaced at 10% or 20% of distances between specified
anatomic landmarks
Use 21 electrodes, but others can be added
increase spatial resolution
record from specific areas
monitor other electrical activity (e.g. ECG, eye movements)

Odd number electrodes over left and even number over right
hemisphere
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10-10 System Of Electrode


Placement

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10-10 System Of Electrode


Placement

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Routine EEG Techniques


20-min or longer sampling of brain activity
Written out or recorded directly on magnetic tape or digitally by
computer
Disc electrodes are applied according to 10-20 system
Montages: bipolar, referential, changeable with digital recording

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Mohamed Hamdy

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Activations
Routine

Optional

Eye opening and closure


Hyperventilation
Intermittent photic stimulation

1, 5, 10, 15 & 20 Hz
eyes open
eyes closed
eyes closure

Sleep deprivation
Sedated sleep
Specific methods of seizure
precipitation
video games
visual patterns

AED withdrawal

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Strength and Advantages of EEG


Is a measure of brain function;
supplement neuroimaging studies

Provides some spatial or


localization information

Provides direct rather than indirect


evidence of epileptic abnormality

Low cost

May be the only test that shows


abnormalities in epileptic patients

Low morbidity
Readily repeatable
Portable / ambulatory

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The EEG Frequency Spectrum


Waves

Frequenci
es per
second

Amplitude
in V

Characteristics

Beta-waves 14 - 30

5 - 50,
mostly below
30

Sharp spike-waves over 35 Hz,


Frontocentral, precentral &
posterior
Criteria of light sleep stages

Alphawaves

8 - 13

5 - 120,
mostly below
50

Posterior-dominant, awake, eyes


closed, mental inactivity, physical
relaxation

Thetawaves

4-7

20 - 100

Strictly rhythmic or highly


irregular
Awake & drowsiness or light
sleep stages

Deltawaves

0,5 - 3

5 - 250

Abnormality in waking adults,


Accompaniment of deep sleep

Gammawaves

31 - 60

-10 Mohamed Hamdy


Legality of appearance and site
not well established

The EEG Frequency Spectrum

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Posterior Alpha Rhythm


Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2

Mohamed Hamdy

Uses Of EEG In The Management of Seizure


Disorders
To support a clinical diagnosis of epilepsy
To help to classify seizures
To help localize epileptogenic focus, especially in presurgical
candidates
To quantify seizures
To aid in the decision of whether to stop AED treatment
Not a good guide to the effectiveness of treatment, except in
absence seizures

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Analyzing EEG Activities

Morphology
Distribution
Frequency
Voltage
Duration
State of the patient
Background from which activity is arising from
Similarity or dissimilarity to the other ongoing background rhythms

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Guidelines To EEG Interpretation


Each EEG should be read with maximum possible objectivity
Ideally an EEGer should describe the findings and make an EEG
diagnosis without knowledge of the patient's history
Clinical significance of the findings can then be judged by integrating
the EEG diagnosis with the history

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EEG Interpretation

Normal
Lack

of Abnormality

Abnormal
Non-epileptiform
Epileptiform

Patterns

Patterns

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Epileptiform Patterns on Scalp-recorded


EEG

Interictal Epileptiform Pattern


Electrographic Seizure Pattern

Isomorphic seizure pattern

Metamorphic seizure pattern

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Criteria For Potentially Epileptogenic


Transients

Clearly of cerebral and not artifactual origin


Abnormal for the age and the state of the patient
Have a significant epileptiform character and not
one of the benign epileptiform variants

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Sharp Transients

Physiologic Activities That Can Be Confused With Epileptiform Activities

Vertex transients of light sleep


Hypnagogic hypersynchrony
Positive occipital sharp transients of sleep (POST)
Mu rhythm
Lambda waves
Breach rhythms

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Mohamed Hamdy

Breech Rhythm

Benign Variants Of Unknown Clinical Significance


Benign epileptiform transients of sleep (small sharp spikes)
6- and 14-Hz positive spikes
Wicket spikes
Psychomotor variants (rhythmic mid-temporal theta
discharge of drowsiness)
Subclinical rhythmic EEG discharge of adults
Phantom spike and wave

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Mohamed Hamdy

Small Sharp Spikes

FP1
F7
F7 T3
T3
T5
T5
O1
FP2
F8
F8 T4
T4
T6
T6
O2
FP1
F3
F3
C3
C3
P3
P3
O1
FP2

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Wicket Spikes

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Psychomotor Variant

Vertex Wave and Sleep Spindles


Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4

Fp1-F3
F3-C3
C3-P3

P4-O2

P3-O1
Fp1-F7
F7-T3

Fp2-F4

T3-T5

F4-C4

T5-O1

C4-P4

Fp2-F8

P4-O2

F8-T4
T4-T6
T6-O2

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Examples Of Inter-ictal Epileptiform Patterns


Spikes
Sharp waves
Benign Epileptiform Discharges of Childhood
Spike-and-wave complexes
3Hz Spike-and-wave complexes
Slow spike-and-wave complexes
Hypsarrhythmia
Photo-paroxysmal response

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Focal Epileptiform Discharges


and Abnormalities
Spikes and sharp waves
Phase reversal localizes the focus
Recorded seizures
Focal slowing may indicate an underlying epileptogenic focus,
structural lesion or injury, or postictal effect

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Localization: Phase Reversal


Each channel records the potential
difference between two electrodes
G1 G2
Negative is up
If G1 is more negative than G2, the
deflection will be up
If G2 is more negative, the deflection
will be down

FP1-F7

F7-T3

T3-T5

FP1-F7

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Generalized EEG Abnormalities

Generalized spike and wave


Generalized polyspike-wave or multispike-wave
Generalized slow spike and wave
Generalized 3 Hertz spike-wave
Generalized slowing
Generalized suppression
Generalized burst suppression
Electrocerebral silence

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Generalized Spike-Wave
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2

Mohamed Hamdy

Generalized Polyspike Wave


Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2

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3 Hertz Spike and Wave


Fp1-F3

F3-C3

C3-P3

P3-O1

Fp2-F4

F4-C4

C4-P4

P4-O2
1 sec

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50 V

Generalized Delta Slowing


Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2

Mohamed Hamdy

Interictal Spikes / Sharp Waves


Spikes (<70 msec in duration) or Sharp Waves (70-200 msec in
duration)
Usually surface negative; occasionally bipolar or only surface positive
Monophasic, biphasic or polyphasic
Occur alone or accompanied by an after-coming slow wave (usually
surface negative and higher in amplitude than the spike or sharp wave)
Occurs singly or in burst, lasting at most a few seconds
Focal or generalized
No clinical manifestation

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Epileptiform Discharges: Spikes

Indicate susceptibility to seizures


May be generalized or focal
Focal spikes cortical spikes are associated with synchronous
paroxysmal depolarizing bursts occurring in neurons within the
focus resulting in extracellular current flow that is recorded as
surface spikes

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Inter-ictal Epileptiform Patterns

Idiopathic Epilepsies

Symptomatic Epilepsies

Generalized

3 Hz spike-and-wave
Polyspikes
Atypical spike-and-wave

Generalized

Partial / Focal
Benign focal epilepsy of childhood
with centrotemporal spikes
Benign focal epilepsy of childhood
with occipital spikes

Hypsarrhythmia
Slow spike-and-wave
Paroxysmal fast activity
Multiple independent spike foci

Partial / Focal

Temporal
Frontal
Centro-parietal
Occipital
Midline

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3 Hz Spike & Wave Complexes

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3 Hz Spike & Wave Complexes

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Polyspikes

The Spike and Wave Complex

The cellular depolarizing bursts are followed by long-lasting


afterhyperpolarization in cells within the focus
Additional inhibition occurs in surrounding cortex, thalamus and other
subcortical areas
This results in a surface slow wave that follows the individual spike

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Polyspikes & Wave

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Hypsarrhythmia

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Slow Spike & Wave Complexes

Fp1
F7
F7
T3
T3
T5
T5
O1
Fp2
F8
F8
T4
T4
T6
T6
O2
Fp1
F3
F3
C3
C3
P3
P3
O1
Fp2

Benign Epileptiform
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Discharges of Childhood

Focal Inter-ictal Epileptiform Pattern


Temporal, frontal, occipital, centroparietal, centrotemporal, or midline
Relative frequency (Gibbs and Gibbs, 1952)

1396 patients; Temporal: 73%; Frontal: 0.8%

Likelihood of seizures (Kellaway, 3526 children)


Temporal : 90-95% (91%)
Frontal : 70-80% (75%)
Parieto-occipital : 40-50% (48%)
Central : 30-40% (38%)

Focal spikes in a patient with a history of epileptic seizures indicates that


the patient is likely to have focal or localization-related epilepsy
syndrome

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Neuronal Synchronization

The interictal spike may be initiated by a spontaneous burst in one or


a few cells
Each cell has excitatory connections to a number of other cells
Excitatory connections will allow burst propagation if inhibition is
decreased, absent or simply overcome
Loss of effective dendritic inhibitory synapses may occur over time

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Mohamed Hamdy

Sharp Wave, Regional, Left

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Sharp Wave, Regional, Right

Sharp Wave,
Regional,
Right
Mohamed
Hamdy
Posterior Temporal

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Sharp Wave, Regional, Central

Epileptiform Activity In People


Without Epilepsy
Zivin and Ajmone-Marsan, 1980
142/6497 (2.2%) of non-epileptic patients had IEDs
only 20/142 (14.1%) eventually developed epilepsy
Eeg-Olofsson et al, 1971
2.7% and 8.7% of 743 normal children had IEDs during
wakefulness and sleep, respectively
Cavazutti et al, 1980
131/3726 children (3.5%) had IEDs on awake EEG
only 7/131 (5%) eventually developed seizures
Presence of interictal epileptiform discharges (IEDs) is not
diagnostic of epilepsy

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Normal EEG In People With Epilepsy

I know my patient has epilepsy. How can the EEG be


normal?
If the EEG is normal, am I wrong in thinking that my patient
has epilepsy?

Mohamed Hamdy

Normal EEG In People With Epilepsy

Ajmone-Marsan & Zivin, 1970


only 56% of 1824 EEGs from 308 patients (1-64 years) with known
seizures showed IEDs on first EEG
IEDs recorded in another 26% in subsequent records
Holmes, 1986
25% of 24 paediatric patients with documented seizures on longterm monitoring had no IEDs
first and only EEG abnormalities recorded was complex partital
seizures
Patients with well-documented seizures may have normal EEGs

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Factors Responsible For Detection Of Epileptiform


Discharges

Characteristic of Generator Source

Voltage of cortical discharge which is directly related to size/area


of cortex involved in generation of synchronous activity

Distance between electrodes and the generator source

Orientation of dipole

Sampling Time
Activation
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Factors Which Modify Spike Frequency

Sleep
Photic stimulation
Hyperventilation
Temporal relation to a seizure
Age of patient
Effect of anticonvulsant withdrawal

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Recording of Focal Interictal Spikes


Yield of recording focal interictal spikes increases

during NREM sleep, especially stage 3/4


after sleep deprivation
after seizures
during long-term monitoring
? using supplementary electrodes (e.g. sphenoidal)

Occurrence of focal interictal spikes is not affected


by increasing or decreasing the AED dosages or level
by hyperventilation or photic stimulation
before seizures

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Does the Frequency of IEDs Tell Us


Anything?

Probably not
Increases after a seizure
Does not predict severity of epilepsy
Relationship between spikes and ictal activity is not known

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Routine EEG
Concluding Remarks
EEG is the most valuable tool in the evaluation of patients with a
seizure disorder
Interpretation of clinical significance of EEG abnormality(ies) can
only be made by a physician who

is evaluating the patients history and physical findings

has an understanding of the benefits and limitations of EEG recording

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Epileptiform Patterns on Scalp-recorded


EEG

Interictal Epileptiform Pattern


Electrographic Seizure Pattern

Isomorphic seizure pattern

Metamorphic seizure pattern

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Electrographic Seizure Pattern

Rhythmic repetition of components that may or may not have an


epileptiform morphology
Lasting more than several seconds
When this pattern produce clinical symptoms and/or signs, it is called a
clinical electrographic seizure discharge
When it does not produce clinical symptoms, it is called a subclinical
electrographic seizure discharge

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Generalized Spike-and-Wave

A pathological exaggeration of cortical excitability is the basic disturbance


and appears to initiate the process
Cortical spikes precede epileptiform discharges in depths
Thalamocortical connections are necessary for triggering and phasing the
spike-and-wave bursts
The brainstem reticular formation appears to modulate spike-and-wave
activity by modifying the level of cortical excitability.
Substantia nigra involvement in some way is essential in the production of
generalized convulsions.

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Isomorphic Seizure Pattern

Ends as it begins, without progressing through multiple phases


into a postictal phase
Ictal morphology is usually similar to interictal epileptiform
patterns
Differ only in having greater rhythmicity, duration, spatial extent
and amplitude
Almost exclusively seen in generalized seizures
Prototype: 3/s spike-and-wave complexes

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Metamorphic Seizure Pattern

Ends differently from its beginning, commonly progressing


through 2 or more different ictal phases into a postictal state
Ictal morphology can also be dissimilar to interictal epileptiform
patterns
Ictal morphology may consist of smooth sinusoidal rhythms and
has no spike or sharp wave
Seen both in generalized seizures and focal seizures

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Seizure, Regional, Left Temporal

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Seizure, Generalized

ICTAL EEG
Always abnormal in generalized seizures
Almost invariably abnormal during a partial seizures especially
with loss of consciousness
Might be normal for simple partial seizures

Should be correlated with behavioral changes

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Long-term EEG Monitoring

In- or out-patient setting


Methods
Prolonged Conventional
Ambulatory
With video recording of behavior

analog, digital

Telemetered EEG recording


radio, cable

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Video/EEG Monitoring

To obtain a prolonged interictal EEG sample


To record habitual seizures or spells
To make precise EEG / behavioral correlation
To classify seizures (e.g. absence vs. complex partial)
To localize epileptogenic focus, especially in epilepsy surgery
candidates
To quantify seizures when they occur frequently
Evaluate seizure precipitants

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Questions To Be Answered After


Video/EEG Monitoring

Does the patient have epilepsy?


Where do the seizures come from?
Is the patient a candidate for surgical treatment?

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EEG in Neonates

Premature newborn due to the incomplete development of


neuronal connections, synapse formation, myelination, etc., EEG
activity prior to 30 weeks estimated gestational age (EGA) is
disccontinuous and very abnormal appearing
Focal sharp discharges in frontal and temporal regions are normal to
some extent until about 44 weeks EGA

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Trace Discontinue in 27 week EGA Neonate


Fp1-F7
F7-T5
T5-O1
Fp1-F3
F3-P3
P3-O1
Fp2-F4
F4-P4
P4-O2
Fp2-F8
F8-T6
T6-O2

Mohamed Hamdy

2 month old with Enterococcal meningitis and left posterior


temporal focal electrographic seizure
FP1-F7
F7-T5
T5-O1
FP1-F3
F3-P3
P3-O1
Fp2-F4
F4-P4
P4-O2
Fp2-F8

50 V
1 sec

F8-T6
T6-O2

Mohamed Hamdy

2 month old with Enterococcal meningitis with an


electrographic seizure discharge, maximal right frontal
FP1-F7
F7-T5
T5-O1
FP1-F3
F3-P3
P3-O1
Fp2-F4
F4-P4
P4-O2
Fp2-F8

50 V
1 sec

F8-T6
T6-O2

Mohamed Hamdy

2 month old with Enterococcal meningitis and right posterior


temporal focal electrographic seizure
FP1-F7
F7-T5
T5-O1
FP1-F3
F3-P3
P3-O1
Fp2-F4
F4-P4
P4-O2

50 V
1 sec

Fp2-F8
F8-T6
T6-O2

Mohamed Hamdy

2 month old with Enterococcal meningitis and bilateral


independent focal electrographic seizures
FP1-F7
F7-T5
T5-O1
FP1-F3
F3-P3
P3-O1
Fp2-F4
F4-P4
P4-O2
50 V

Fp2-F8
1 sec

F8-T6
T6-O2
Mohamed Hamdy

Progression of EEG in Childhood

Occipital rhythmical activity = Alpha rhythm


3-5 months
12 months
3 years
9 years

3.5-4.5 Hertz
5-6 Hertz
7.5-9.5 Hertz
>9 Hertz

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EEG During Sleep

Stage I sleep
Dropout of alpha rhythm
Intermixed slowing

Stage II sleep
Increased intermixed theta and delta slowing
Vertex waves, sleep spindles and K-complexes
Positive occipital sharp transients of sleep (POSTs)

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Progression of Sleep

Stage III sleep


Increased delta slowing
Central vertex activity diminishes

Stage IV sleep
Marked delta slowing
Absence of vertex activity

Stage III and IV = Slow wave sleep

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Stage 3-4 Sleep


Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2

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REM Sleep
Low voltage mixed frequency activity with faster components
Absent vertex activity
Decreased EMG activity

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EEG in the Evaluation of


Possible Epilepsy

For patients with epilepsy, a single EEG will reveal epileptiform


activity in:
30-40% with an awake EEG only
60-70% with wakefulness and sleep
Some patients will only have an abnormality detected if an actual
seizure is recorded
A normal EEG does not rule out a diagnosis of epilepsy

Mohamed Hamdy

EEG Monitoring in Critical Care

Many patients with head injury, any form of encephalopathy, or severe


illness are at risk for seizures
Patients who are mechanically ventilated are often sedated and
pharmacologically paralyzed and seizures can only be diagnosed with EEG
The diagnosis of nonconvulsive status epilepticus can only be detected and
monitored with EEG
Monitoring progression of coma and potentially cerebral death

Mohamed Hamdy

11 y/o boy with severe cardiomyopathy on ECMO following


cardiac electromechanical disassociation
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4

50 V
1 sec

F4-C4
C4-P4
P4-O2

Mohamed Hamdy

11 y/o boy with severe cardiomyopathy on ECMO with right temporal


electrographic seizure
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
1 sec

F4-C4
C4-P4
P4-O2

Mohamed Hamdy

50 V

Focal Status Epilepticus


Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4
F4-C4
C4-P4
P4-O2

1 sec

Mohamed Hamdy

50 V

11 y/o boy with severe cardiomyopathy on ECMO with left


hemispheric suppression due to infarction
Fp1-F7
F7-T3
T3-T5
T5-O1
Fp2-F8
F8-T4
T4-T6
T6-O2
Fp1-F3
F3-C3
C3-P3
P3-O1
Fp2-F4

50 V
1 sec

F4-C4
C4-P4
P4-O2

Mohamed Hamdy

EEG Monitoring and


Epilepsy Surgery
20% of patients with epilepsy cannot be controlled with
medications
Focal onset seizures can sometimes be selected and treated with
surgical resection of the epileptogenic focus
Multiple methods are can be employed

Mohamed Hamdy

EEG: Recorded Seizure


*Fp1-F3

*F3-C3

*C3-P3

*P3-O1

Fp2-F4

F4-C4

C4-P4
50 V
1 sec

*P4-O2

Mohamed Hamdy

*Fp1-F3

*F3-C3

*C3-P3

*P3-O1

Fp2-F4

50 V
1 sec

F4-C4

C4-P4

*P4-O2

Mohamed Hamdy

*Fp1-F3

*F3-C3

*C3-P3

*P3-O1

Fp2-F4

50 V
1 sec

F4-C4

C4-P4

*P4-O2

Mohamed Hamdy

Electrocortical Seizure Recording


41-42
42-43
43-44
44-45
45-46
49-50
50-51
51-52
52-53
1 sec

53-54
54-55

Mohamed Hamdy

50 V

41-42
42-43
43-44
44-45
45-46
49-50
50-51
51-52
52-53
1 sec

53-54
54-55

Mohamed Hamdy

50 V

41-42
42-43
43-44
44-45
45-46
49-50
50-51
51-52
52-53
53-54

1 sec

50 V

54-55

Mohamed Hamdy

Examples of Clinical cases


Please give me your interpretation

Mohamed Hamdy

Mohamed Hamdy

Mohamed Hamdy

Female patient 20 ys, with attacks of confusional


state, she is awake with the eye closed

Mohamed Hamdy

Mohamed Hamdy

Mohamed Hamdy

Mohamed Hamdy

Male patient
aged 28 years. He has recurrent
Awake
record
attacks of lapses of consciousness

Mohamed Hamdy

Male patient 57 Years with recurrent GTCS


that developed only in the last year

Mohamed Hamdy

Thank you