3. NEED for ECOG
• Scalp EEG is limited - activity from deep or mesial brain areas are not recorded
• Discharges recorded in the scalp are attenuated and distorted by different layers (scalp, bone, meninges)
The skull attenuates the signal considerably (approx. factor 5)
Example:
Generator in the hippocampus, potential of 500 μV, 0.5 cm from the generator
4 cm from the generator (8 times further), on the temporal neocortex, the potential is 64 times smaller(8 μV)
On the scalp, the potential is reduced by a factor of 5 (1.6 μV)
• 6cm2 of brain cortex is needed to discharge synchronously to generate detectable potential in scalp EEG.
Activity generated by a smaller cortical surface, substandard amplitudes, or midline structures are not
reflected on scalp EEG
• Difficult to localize and determine the extend of the cortical area from scalp EEG
• The skull attenuates frequencies above 10 000 Hz
4. Intraoperative ECOG
• Initially pioneered in human patients by Hans Berger 1929
• First used by Penfield and Jasper in 1950 to map epileptic activity
• Electrodes can be placed almost anywhere with a relatively low risk
• ECOG is of very high quality, without the main artifacts visible on the scalp (movement, eye movements,
EMG)
• Electrodes can be very close to neuronal generators
• Electrodes can be used for stimulation, to trigger seizures or for functional mapping
7. Indications for combination of ECoG and functional mapping
I General indication:
Whenever the irritative zones/epileptic foci are or could be in close proximity to eloquent cortex
II Goals Guiding the surgical approach
1. Extent of resection 2. Subpial transections
III Specific situations
1. Left temporal foci 2. Frontal or parietal foci
3. Multifocal epilepsy 4. Neurodevelopmental lesions
8. Electrodes
• Recording electrodes usually made of Platinum-iridium or stainless steel or less commonly carbon or silver
• Platinum slightly more stable when current is passed and used with MRI/MEG
• Stainless steel may possibly diffuse metal ions across the electrode-pial interface (significant over longer
periods of stimulation)
Montage
• Bipolar
• Referential - identify complex electrical spike field
- avoid bipolar cancellation of potentials
Voltage
• 5-6 times higher than scalp EEG
• around 300-500 microV
• sensitivity often set at 30-70 microV/mm
ECOG duration
• Minutes (intraoperative) to days (extraoperative 7-14 days)
9. Recording Technique
Sampling:
• Usually at 500 Hz but with increased recognized relevance of HFO, sampling rate of 1000-2000 Hz is used (prevent
aliasing)
Amplification:
• ECOG signal need amplification and amplifier must have – a) amplitude linearity, b) adequate bandwidth, c) phase
linearity, d) low noise
Filtering:
• Depending of waveform that need to be seen (low freq vs HFO)
Electrical safety:
(1) using power receptacles and adaptors with a ground prong
(2) connecting all the patient associated equipment to 1 cluster of power receptacles, ideally with separation between
lines and with removal of other sources of power from the patient environment
(3) avoiding contact between the patient and low-resistant pathways such as metal beds, plumbing, metal architectural
elements, or liquids
10. Influence of antiepileptic drug reduction or withdrawal
• Absent or subtherapeutic drug level leads to increase seizure frequency
• Secondary generalization is more often seen after drug reduction/withdrawal
• Interestingly – localization, morphology at seizure onset, time to spread to contralateral and coherence of EEG
discharges do not change
• During seizure cluster, some areas of brain can start to seize that usually do not spontaneously
Influence of Anesthetic agents
• Enhance epileptiform activity – methohexital, fentanyl, remifentanil, propofol, thiopental
• Decreases or increases epileptiform activity – isoflurane, sevoflurane
• Dexmedetomidine (Precedex) – alpha 2 receptor agonist – produce natural sleep pattern, reduce need for propofol
Factors modifying ECOG/epileptiform activity
11. Electrical stimulation of the cortex
• Electrical stimulation of cortex can elicit after discharges, subclinical seizures, habitual or nonhabitual auras, and
habitual and nonhabitual clinical seizures
• Electrically induced auras and seizures frequently correlate with seizure onset zone (unilateral focus) (concordance
75-100% , Schulz et al., 1997; Bernier et al., 1990)
• >1 Seizure onset focus - have decrease concordance
• After-discharge threshold not a reliable predictors of spontaneous SOZ
• After discharge, after discharge evolving to clinical seizure, or after discharge > 10 seconds – does not
topographically correlate to SOZ (Blume et al., 2004)
• Localization value of auras and clinical seizures is superior to after discharges
12. Volume (invasiveness) of depth electrodes
• Depth contact 50 mm length:
If 0.8 mm diameter, volume 25 mm3
If 1.2 mm diameter, volume 56 mm3
• If we place 20 electrodes = 500 to 1000 mm3 or 0.5 to 1 cm3
• Brain volume 1300 cm3
• Sampling area = 0.5 /1300 = 0.04%
• Sampling area = 1/1300 = 0.08%
One electrode explores ~5mm brain volume beyond its border
• 1 multi-contact electrode «captures» a cylinder of ~ 1 cm in diameter and 6 cm in length= 5 cm3
• 10 electrodes (100 contacts) = 50 cm3
• One hemisphere ~ 650 cm3
• 10 electrodes = 8% of one hemisphere
13. Subdural grids
• 1 grid contact captures a disk of ~ 2 cm in diameter (3 cm2)
• One 8 x 8 grid explores 64 x 3 ~ 200 cm2
• One hemisphere~ 5,000 cm2
• One 8 x 8 grid covers about 4% of the cortical surface of one hemisphere
14. Different generator size, same spike amplitude
• The amplitude of the scalp EEG is largely function of the size (surface) of the generator. EEG
electrodes are at approximately the same electrical distance to the generator
• The amplitude of the ECOG is largely a function of the distance between the electrode and the
generator
15. 1. Repetitive electrographic seizures
• Recruiting/derecruiting frequency around 12 to 16 Hz.
2. Repetitive bursting patterns
• High frequency (10 to 20 Hz) lasting for 5 to 10 seconds
3. Continuous or quasi-continuous rhythmic spiking
• Prolonged trains of rhythmic 2-8 Hz spikes
ECoG Patterns Associated with Cortical Dysplasia
Palmini A, Gambardella A, Andermann F, et al. Intrinsic epileptogenicity of human dysplastic cortex as suggested by corticography and surgical results. Ann Neurol 1995;37:476-87
20. (1) Sporadic spikes: spikes occurring at irregular
time intervals at several sites
(2) Continuous spiking: spikes occurring
rhythmically at regular time intervals for at least
10 seconds, the interval between two subsequent
spikes being 1 second at the most (frequency ≥ 1
Hz)
(3) Bursts of spikes: sudden occurrence of spikes
for at least 1 second with a frequency of 10 Hz or
greater
(4) Recruiting discharges: rhythmic spike activity
characterized by increased amplitude and
decreased frequency
Electrocorticographic Patterns in Epilepsy Surgery
and Long-Term Outcome
San-Juan, et al. 2017
22. • Intraoperative ECOG in children in intractable neocortical epilepsy reliable if spike frequency > 10 spike/min1
• Spike frequency <1/min is largely unreliable for localization of seizure focus1
• In temporal lobe epilepsy, pre-resection ECOG showing >18spike/min associated with good outcome2 and
<1spike/4 min associated with poor outcome
1Asano E, Benedek K, Shah A, et al. Is intraoperative electrocorticography reliable in children with intractable neocortical epilepsy. Epilepsia 2004;45(9):1091-9
2McBride MC, Binnie CD, Janota I, Polkey CE. Predictive value of intraoperative electrocorticograms in resective epilepsy surgery. Ann Neurol 1991;30:526-32
Reliability of Intraoperative ECOG
24. Post Surgical Interictal Spikes and Seizure Outcome
• Arise from unresected epileptogenic tissue with potential to cause seizures
• Secondary to cortical isolation, to surgical trauma or activation secondary to partial excision
• Surgical isolation of normal cortex can cause burst suppression, spike-burst suppression
• Surgical injury to cortex can cause postoperative spikes
• Activation of partial excision – minor secondary focus that was suppressed by its proximity to a dominant
focus
25. Post Surgical Interictal Spikes and Seizure Outcome
• Arise from unresected epileptogenic tissue with potential to cause seizures
• Secondary to cortical isolation, to surgical trauma or activation secondary to partial excision
• Surgical isolation of normal cortex can cause burst suppression, spike-burst suppression
• Surgical injury to cortex can cause postoperative spikes
• Activation of partial excision – minor secondary focus that was suppressed by its proximity to a dominant
focus
No general agreement in the value of postoperative ECoG to predict seizure outcome (Nair and Najm, 2008)
In 80 patients with refractory temporal epilepsy, the presence of spikes in postresection ECoG was more
frequent in patients with postoperative seizures (72%) than in seizure-free patients (47%) (Fiol et al., 1991)
In 87 patients with temporal lobe epilepsy, postresection spikes and the change from preresection to
postresection spikes did not correlate with seizure outcome (Kanazawa et al., 1996)
26. Post Surgical Interictal Spikes and Seizure Outcome
• In 47 patients with medial temporal lobe epilepsy, there was no correlation between the presence or absence of
postresection spikes and seizure outcome (Tran et al., 1995)
• In 36 patients with brain tumor and seizures who underwent resection limited to the tumor margins, a correlation
between preresection or postresection spikes, and seizure outcome could not be found (Tran et al., 1997)
• In 94 patients with refractory temporal epilepsy, the presence of spikes in the postsurgical ECoG did not predict
seizure outcome (Benifla et al., 2006)
• In small study of 15 patients with refractory temporal lobe epilepsy, there was nonsignificant better seizure outcome
in patients with spikes than in patients without spikes in the postresection ECoG: seizure freedom was achieved by 8
of 10 (80%) patients with residual spikes and by 3 of 5 (60%) patients with no postsurgical spikes (Chen et al., 2006)
• In 140 patients with refractory mesial temporal lobe epilepsy - patients with hippocampal (but not cortical or
parahippocampal) spikes in postresection ECoG had a significantly worse seizure outcome (McKhann et al., 2000)
Engel class I seizure outcome was achieved in 29% patients with hippocampal spikes
73% patients who had no spikes in the hippocampus
76% patients with no spikes at all
• Postresection ECoG may be of prognostic significance, especially when spikes are residual, not newly appearing spikes
(Binnie et al., 2001)
27. Functional Mapping and Cortical Stimulation
• Luigi Rolando first used galvanic current to stimulate cerebral cortex of living animals in 1809
• Fritz and Hitzig in 1870 first used cortical stimulation in dogs to delineate motor cortex
• Performed to optimize the extend of resection and minimize or avoid deficit
• Bipolar stimulation if used for FM with cathode/anode at the target tissue
• Potential brain injury can happen with cortical stimulation and is depended on charge density
• Charge density is the function of charge and cross-sectional area of the electrode surface in contact with the
brain
• Brain injury is usually seen with continuous stimulation. Never been reported with intermittent stimulation
(which is commonly used in humans for FM)
28. • To avoid tissue damage, critical measurement is charge density measured in μCoulombs/cm2/phase
• Safe maximum is considered to be 50 to 60 μC/cm2/phase
• Charge (Coulombs) = current density (I) x pulse duration (D)
• 1 μC = 1 mA x 1 ms = 2 mA x 0.5 ms
• Charge Density CD = C/ACE (ACE = area of stimulating electrode)
• Subdural grid leads will deliver charge densities of 54 to 57 microcoulombs/cm2 per phase for peak
currents of 13.6 to 15 mA
Charge Density
29. Stimulation intensity (mA) plotted against charge density ([mu]C/cm2) of commonly used SEEG, grid/strip, and
intraoperative probe electrodes (top). Charge density is segregated into "safe," "risky," and "dangerous" categories
based on criteria used by the FDA for the approval of the predicate stimulator device (bottom). These safety
criteria do not take into account other important factors in safety, including interelectrode distance, and presence
(electrocorticographic) or absence (stereo-electroencephalographic) of current shunting through cerebrospinal
fluid, for example.
Animal studies with continuous
stimulation of upto 50 hours
30. Geometry (to scale) of exposed "effective" surfaces available for stimulation of commonly used surface
(grid/strip), depth (stereo-electroencephalographic) and probe (intraoperative handheld) electrodes
31. Oscillatory classes in the cortex
Ripple: 80-150 Hz
Fast Ripple: 150 – 500 Hz
Ultra Fast Ripple: 500 – 2000 Hz
32. Ripple classification helps to localize the seizure‐onset zone in neocortical epilepsy
Epilepsia, Volume: 54, Issue: 2, Pages: 370-376, First published: 25 October 2012, DOI: (10.1111/j.1528-1167.2012.03721.x)
Pathological ?Physiological
(w/o spike)
33. The 14&6/sec positive spikes normal EEG variant is correlated exclusively with hippocampal activity
(Kokkinos. 2019)
The variant is time-locked to high-amplitude spike bursts overlaid on low-amplitude slow waves
38. Seizures from end chain electrodes not reliable for seizure localization
Ictal onset and spread can look similar
39. 2 x 6 strip lateral L temp, 1 anterior
1 x6 strip inferior L temp, 1 mesial
1 x 4 strip L temporal pole, 1 wrapped at pole
40. 2 x 6 strip lateral L temp, 1 anterior
1 x6 strip inferior L temp, 1 mesial
1 x 4 strip L temporal pole, 1 wrapped at pole
Attenuated anterior L temporal with burst suppression (C1-3, C7-9)
Pulse artifact C13-14, C17-18
Attenuated anterior lateral L temporal at pole, asynchronous spike waves
Depth electrode for temporal lobe surgery came to light in 1963
: (1) amplitude linearity: the relationship between input and output signals must be linear, (2) adequate bandwidth: the amplifier should amplify signals centered in the range of frequencies that are relevant to what is wanted to measure, (3) phase linearity: the shifts in time should be equal for all the frequencies, and (4) low noise: signals generated within the instrumentation should be minimized and should not interfere with the recorded signal
Schulz R, Luders HO, Tuxhorn I, et al. Localization of epileptic auras induced on stimulation by subdural electrodes. Epilepsia 1997;38:1321–1329.
Bernier GP, Richer F, Giard N, et al. Electrical stimulation of the human brain in epilepsy. Epilepsia 1990;31:513–520.
Blume WT, Jones DC, Pathak P. Properties of after-discharges from cortical electrical stimulation in focal epilepsies. Clin Neurophysiol 2004;115:982–989.
1Berger MS, Ghatan S, Haglund MM, Dobbins J, Ojemann GA. Low-grade gliomas associated with intractable epilepsy: seizure outcome utilizing electrocorticography during tumor resection. J Neurosurg 1993;79(1):62-9
1Berger MS, Ghatan S, Haglund MM, Dobbins J, Ojemann GA. Low-grade gliomas associated with intractable epilepsy: seizure outcome utilizing electrocorticography during tumor resection. J Neurosurg 1993;79(1):62-9
Nair DR, Najm I. Intraoperative cortical mapping and intraoperative electrocorticography. In: Lüders H, ed. Textbook of epilepsy surgery. London: Informa Healthcare, 2008:1073–1080.
Fiol ME, Gates JR, Torres F, Maxwell RE. The prognostic value of residual spikes in the postexcision electrocorticogram after temporal lobectomy. Neurology 1991;41:512–516.
Kanazawa O, Blume WT, Girvin JP. Significance of spikes at temporal lobe electrocorticography. Epilepsia 1996;37:50–55.
Tran TA, Spencer SS, Marks D, et al. Significance of spikes recorded on electrocorticography in nonlesional medial temporal lobe epilepsy. Ann Neurol 1995;38:763–770.
Tran TA, Spencer SS, Javidan M, et al. Significance of spikes recorded on intraoperative electrocorticography in patients with brain tumor and epilepsy. Epilepsia 1997;38:1132–1139.
Chen X, Sure U, Haag A, et al. Predictive value of electrocorticography in epilepsy patients with unilateral hippocampal sclerosis undergoing selective amygdalohippocampectomy. Neurosurg Rev 2006;29:108–113.
Nair DR, Najm I. Intraoperative cortical mapping and intraoperative electrocorticography. In: Lüders H, ed. Textbook of epilepsy surgery. London: Informa Healthcare, 2008:1073–1080.
Fiol ME, Gates JR, Torres F, Maxwell RE. The prognostic value of residual spikes in the postexcision electrocorticogram after temporal lobectomy. Neurology 1991;41:512–516.
Kanazawa O, Blume WT, Girvin JP. Significance of spikes at temporal lobe electrocorticography. Epilepsia 1996;37:50–55.
Tran TA, Spencer SS, Marks D, et al. Significance of spikes recorded on electrocorticography in nonlesional medial temporal lobe epilepsy. Ann Neurol 1995;38:763–770.
Tran TA, Spencer SS, Javidan M, et al. Significance of spikes recorded on intraoperative electrocorticography in patients with brain tumor and epilepsy. Epilepsia 1997;38:1132–1139.
Chen X, Sure U, Haag A, et al. Predictive value of electrocorticography in epilepsy patients with unilateral hippocampal sclerosis undergoing selective amygdalohippocampectomy. Neurosurg Rev 2006;29:108–113.
Nair DR, Najm I. Intraoperative cortical mapping and intraoperative electrocorticography. In: Lüders H, ed. Textbook of epilepsy surgery. London: Informa Healthcare, 2008:1073–1080.
Fiol ME, Gates JR, Torres F, Maxwell RE. The prognostic value of residual spikes in the postexcision electrocorticogram after temporal lobectomy. Neurology 1991;41:512–516.
Kanazawa O, Blume WT, Girvin JP. Significance of spikes at temporal lobe electrocorticography. Epilepsia 1996;37:50–55.
Tran TA, Spencer SS, Marks D, et al. Significance of spikes recorded on electrocorticography in nonlesional medial temporal lobe epilepsy. Ann Neurol 1995;38:763–770.
Tran TA, Spencer SS, Javidan M, et al. Significance of spikes recorded on intraoperative electrocorticography in patients with brain tumor and epilepsy. Epilepsia 1997;38:1132–1139.
Chen X, Sure U, Haag A, et al. Predictive value of electrocorticography in epilepsy patients with unilateral hippocampal sclerosis undergoing selective amygdalohippocampectomy. Neurosurg Rev 2006;29:108–113.
McKhann GM II, Schoenfeld-McNeill J, Born DE, et al. Intraoperative hippocampal electrocorticography to predict the extent of hippocampal resection in temporal lobe epilepsy surgery. J Neurosurg 2000;93:44–52.
Binnie CD, Polkey CE, Alarcón G. Electrocorticography. In: Lüders H, Comair Y, eds. Epilepsy surgery. Philadelphia: Lippincott Williams & Wilkins, 2001: 637–641.
Significance: Neocortical fast ripples and type I ripples are specific markers of the SOZ, whereas type II ripples are not. Type I ripples are found more readily than fast ripples in human neocortical epilepsy. Type II‐O ripples may represent spontaneous physiologic ripples in the human neocortex.
Illustration of type I and II ripples and their time frequency analysis. Top panel shows three types of HFO events. Note different amplitude calibrations. Type I ripple is superimposed on a spike or a fast activity. The fast activity here is sharply contoured beta waves found interictally and which evolved into an ictal pattern in a patient with parietal lobe epilepsy. Type II ripple occurs independently of epileptiform discharges. The middle panel shows the signals after high‐pass filtering. Events are manually marked and its parameters automatically calculated by Multiview software, as exemplified in the type II ripple. Bottom panels show the time frequency analysis for all three ripples, demonstrating isolated peaks at 100–150 Hz range.
Purpose: Fast ripples are reported to be highly localizing to the epileptogenic or seizure‐onset zone (SOZ) but may not be readily found in neocortical epilepsy, whereas ripples are insufficiently localizing. Herein we classified interictal neocortical ripples by associated characteristics to identify a subtype that may help to localize the SOZ in neocortical epilepsy. We hypothesize that ripples associated with an interictal epileptiform discharge (IED) are more pathologic, since the IED is not a normal physiologic event.
Methods: We studied 35 patients with epilepsy with neocortical epilepsy who underwent invasive electroencephalography (EEG) evaluation by stereotactic EEG (SEEG) or subdural grid electrodes. Interictal fast ripples and ripples were visually marked during slow‐wave sleep lasting 10–30 min. Neocortical ripples were classified as type I when superimposed on epileptiform discharges such as paroxysmal fast, spike, or sharp wave, and as type II when independent of epileptiform discharges.
Key Findings: In 21 patients with a defined SOZ, neocortical fast ripples were detected in the SOZ of only four patients. Type I ripples were detected in 14 cases almost exclusively in the SOZ or primary propagation area (PP) and marked the SOZ with higher specificity than interictal spikes. In contrast, type II ripples were not correlated with the SOZ. In 14 patients with two or more presumed SOZs or nonlocalizable onset pattern, type I but not type II ripples also occurred in the SOZs. We found the areas with only type II ripples outside of the SOZ (type II‐O ripples) in SEEG that localized to the primary motor cortex and primary visual cortex.
The intracranial correlate of the 14&6/sec positive spikes normal scalp
EEG variant
Vasileios Kokkinos a,c,⇑, Naoir Zaher b,c, Arun Antony b,c, Anto Bagic´ b,c, R. Mark Richardson a,c,d,
Alexandra Urban b,c
Emily Parkhurst – hippocampal seizures
Emily Parkhurst – hippocampal seizures
Standish, Tyler: showing end of chain seizure onset with different channel showing onset if one channel is missing
Standish, Tyler: showing end of chain seizure onset with different channel showing onset if one channel is missing