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Understanding Electroencephalography

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

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

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
+ + -

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

The Dipole
Theoretically, the current flows in a 3dimensional 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.

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

Pyamidal Cells: Principal Current Generators of EEG

Topographical organization within the cortical mantle corresponds to a dipoles oriented perpendicular to the cortical surface

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.

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

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

2 O- 6 T

6 T- 4 T

4 T- 8 F

2 O- 4 P

8 F- 2 p F

1 O- 5 T

4 P- 4 C

5 T- 3 T

4 C- 4 F

3 T- 7 F

7 F- 1 p F

4 F- 2 p F
2 O- 4 P

1 O- 3 P

4 P- 4 C

4 C- 4 F

3 P- 3 C
4 F- 2 p F

3 C- 3 F

1 O- 3 P

3 F- 1 p F

3 P- 3 C

3 C- 3 F

3 F- 1 p F

Vertex Wave and Sleep Spindles

2 -4P O

4P-4 C

4 -4F C

4F-2pF

1 -3P O

3P-3 C

3 -3F C

3F-1pF

Posterior Alpha Rhythm

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

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

Left Temporal Spikes

Fp1-F7 F7-T3 T3-T5

Spike and slow wave complex

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

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.

EEG Frequencies
Delta Theta Alpha Beta 0 - 4 Hertz 4 - 7 Hertz 8 - 13 Hetrz > 13 Hertz

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

2 -T O6

6 -F T8

8-p F2 F

2 -P O4

4 -F P4

4-p F2 F

1 -P O3

3 -F P3

3-p F1 F

1 -T O5

5 -F T7

7-p F1 F

Trace Discontinue in 27 week EGA Neonate

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 F8-T6 T6-O2 1 sec 50 V

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 F8-T6 T6-O2 1 sec 50 V

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 Fp2-F8 F8-T6 T6-O2 1 sec 50 V

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 Fp2-F8 F8-T6 T6-O2 1 sec 50 V

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

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)

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

2 -6T O

6T-4T

4T-8 F

8 -2p F F

1 -5T O

5T-3T

3T-7 F

7 -1p F F

2 -4 O P

4 -4 P C

4 -4 C F

4 -2p F F

1 -3 O P

3 -3 P C

3 -3 C F

3 -1p F F

Stage 3-4 Sleep

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

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

Localization: Phase Reversal

7F-1PF 7F-1PF 5T-3T 3T-7F

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

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

2O-6 T

6 T-4 T

4 T-8F

8F- 2pF

1O-5 T

5 T-3 T

3 T-7F

7F- 1pF

2O-4P

4P-4C

4C-4F

4F- 2pF

1O-3P

3P-3C

3C-3F

3F- 1pF

Generalized Spike-Wave

2 -T O6

6 -T T4

4 -F T8

8 -p F2 F

1 -T O5

5 -T T3

3 -F T7

7 -p F1 F

2 -P O4

4 -C P4

4 -F C4

4 -p F2 F

1 -P O3

3 -C P3

3 -F C3

3 -p F1 F

Generalized Polyspike Wave

3 Hertz Spike and Wave

Fp1-F3 F3-C3

C3-P3

P3-O1

Fp2-F4

F4-C4

C4-P4

P4-O2 1 sec 50 V

2O-6T

6 T-4T

4 T-8F

8F-2pF

1O-5T

5 T-3T

3 T-7F

7F- 1pF

2O-4P

4P-4C

4C-4F

4F-2pF

1O-3P

3P-3C

3C-3F

3F- 1pF

Generalized Delta Slowing

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

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

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 F4-C4 C4-P4 P4-O2 1 sec 50 V

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 F4-C4 C4-P4 P4-O2 1 sec 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

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 F4-C4 C4-P4 P4-O2 1 sec 50 V

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

Clinical Case
8.5 year old boy with onset of seizures at age 7 Seizures begin with a tingling sensation in the R hand followed by extension and posturing of the R arm Seizures were never completely controlled with about 1 seizure per week for the first year December, 2001: Seizures began to dramatically increase January-March, 2002: Numerous seizures per day with up to 100 in a single day, and episodes of status epilepticus lasting up to 1 hour

Typical Seizure

EEG: Recorded Seizure

*Fp1-F3 *F3-C3

*C3-P3

*P3-O1

Fp2-F4

F4-C4

C4-P4 50 V 1 sec *P4-O2

*Fp1-F3

*F3-C3

*C3-P3

*P3-O1

Fp2-F4 50 V 1 sec F4-C4

C4-P4

*P4-O2

*Fp1-F3

*F3-C3

*C3-P3

*P3-O1

Fp2-F4 50 V 1 sec F4-C4

C4-P4

*P4-O2

MRI Findings

3D-MRI Image

3D-MRI with Coronal Cut

Craniotomy with Lesion Localization

Grid Placement

Cortical Grid Map

Craniotomy Closure

Electrocortical Seizure Recording

41-42 42-43 43-44 44-45 45-46 49-50 50-51 51-52 52-53 53-54 54-55 1 sec 50 V

41-42 42-43 43-44 44-45 45-46 49-50 50-51 51-52 52-53 53-54 54-55 1 sec 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 50 V

Functional Cortical Mapping

Cortical Stimulation: Arm

Functional Cortical Map

Cortical Resection

Second Surgery: Stereotactic Lesion Localization

Depth EEG Recording

43-33 53-43 63-53

100 uV 1 sec

Outcome

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 F8-T6 T6-O2 1 sec 50 V