Diagnosing Complicated Epilepsy: Mapping of the Epileptic...
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Diagnosing Complicated Epilepsy:
Mapping of the Epileptic Circuitry
Michael R. Sperling, M.D.Thomas Jefferson University
Philadelphia, PA
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OverviewDefinition of epileptic circuitryMethods of mapping epileptic circuits
EEG: focus of this talkOnly tool to provide high degree of temporal resolution – millisecond level
Other: behavioral, SPECT, fMRI, DTI, fcMRI, MEGResults of mapping studies
Seizure initiation sitesPropagation routes
Mapping cortical functionConclusion
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Epileptic CircuitryInterictal: spikes and dysfunctional areas (examination, neuropsychological deficits, EEG, PET, CBF)
Areas that participate in seizure initiation or spread Ictal onset zone – where seizures begin
Aura and early ictal behaviors provide important clues regarding location of onset zoneEEG shows electrical evidence of seizure initiation
Areas of seizure propagation or spreadProgressive involvement of non-primary areas in ictal discharge
Orderly or “explosive” spread or involvementDetermine behaviors seen during and after a seizureBilateral spread vs. unilateral spread; subcortical spread
Termination patternsSynchronous vs asynchronous – influence late behavior
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Ictal Onset ZoneArea where seizures beginNon-invasively defined by concordance of test data
History, MRI, EEG, PET, MEG suggest abnormality in same area/lobe
Invasively defined by EEGIntracranial electrodes placed directly over or within suspect cortexEstablish area where seizures start
End result: excision of cortex implicated in initiating seizures
Must determine that excision is reasonably safe and will not produce major deficit
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Intracranial EEGDifferent electrode types are used
Depth electrodesSubdural or epidural electrodes
Neurosurgical procedure required for insertion Prior to electrode placement, a hypothesis is needed regarding location of seizure onset
Good luck – essential Associated risk is small
Permanent neurological deficit: 1%Need depends upon epilepsy syndrome/seizure type
Lacking a structural lesion, often needed
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Depth Electrode
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Depth Electrodes
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Subdural Electrodes
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Thomas Jefferson UniversityPatient: Andrew HersheyMRN: 3515185Date: 11/15/07
40 39 38 37
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FPG
LPB
LF
LOF
LAT
LSTA
LSTB
LPA
LAT 129
LOF 121
LF 111
LSTA 119
LSTB 131
LPA 116
LPB 135
LPC 64
LSG 648
LPP/LAP/LMP
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Ictal onset
Interictal spikes
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Interictal EEG
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Ictal EEG PatternsOnset Patterns
FocalRegionalLobarMultilobar
Spread patternsVariable, depend upon site of originWith hippocampal and orbitofrontal seizures, often slow, orderly propagation to other areasWith neocortical seizures, often rapid spread throughout brain
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Focal Anterior Hippocampal OnsetRhythmic spikes start Rhythmic spikes continue
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Focal Anterior Hippocampal OnsetTransition to faster activity Fast activity evolves
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Focal Anterior Hippocampal Onset
spread
Spread to subdural contacts with flattening of amplitude
Symptoms begin
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Regional Seizure Onset inLeft Hippocampus (not focal)
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Lobar Seizure Onset in Right Temporal Neocortex and Hippocampus
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Spread to Left Hippocampus
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Multilobar Seizure Onset
Temporal
Frontal,Interhemispheric
Frontal,Dorsolateral
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Seizure PropagationMultiple methods to study propagation
EEG offers best and most precise temporal resolution though sometime difficult to define (MEG has practical limitations)PET, SPECT, optical imaging, behavior all have poor temporal resolution
Location of seizure onset associated with predictable spread patterns
Medial frontal to contralateral homotopic firstOrbitofrontal to contralateral OF or ipsilateral mesial temporal firstDorsolateral frontal to ipsilateral temporal firstMesial temporal to ipsilateral temporal > contra temporal > ipsifrontal firstTemporal neocortical has variable spreadParietal to ipsilateral frontal > ipsilateral temporal firstOccipital to ipsilateral temporal first
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Onset Location Determines Propagation Times
Zone Mean IPT (sec) Mean CPT (sec)
Med Front 3.5 0.6Lat Front 9.0 14.2Orb Front 47.3 41.5
Med Temp 12.4 35.5Lat Temp 15.5 17.6
Par ietal 6.7 23.3Occipital 18.1 35.5
IPT = Ipsilateral propagation time
CPT = Contralateral propagation time
Jenssen and Sperling, submitted
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Propagation and Prognosis
For hippocampal seizures, time to contralateral spread correlates with surgical outcome
< 5 second to contralateral spread = poor outcome > 50 seconds to contralateral spread = best outcome
Shorter contralateral propagation time correlates with lower neuronal hippocampal cell count in CA 4 (has contralateral commissural connections) Rapid propagation associated with worse surgical outcome in neocortical seizures as wellConclusion: knowledge of typical routes of spread and timing help verify presumed source of seizures and offer prognostic information
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Video
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Ictal SPECT Reveals Early Propagation of Seizures
Huberfield et al 2006 Isotope uptake over 1 minute
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Limitations: Intracranial EEG Need electrodes in the right place – electrode might be in area of spread rather than onset zone Seizure onset can be difficult to discernCould have multiple onset zones Could have variable propagation routes from one seizure to the next, making interpretation difficult Despite multiple onset zones, successful surgery could still be performed if a structural lesion is presentDespite well-localized single onset zone, surgery might still be unsuccessful – only 20-60% seizure-freeMight not record any seizures – bad luckMight cause brain injury with electrode placement, causing deficits or false seizure onset
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Cortical Mapping: Rationale
Practical: reduce risk of causing neurosurgical deficits
Epilepsy surgeryTumor surgery
Academic: enhance understanding of brain function, organizationThis talk will address electrical stimulation and evoked potential mappingMEG, fMRI and other techniques can be used
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Electrical StimulationCurrent is applied directly to pial surfaceTwo types of response
Positive: e.g., jerking of limb, auditory or visual hallucinationNegative: speech arrest
Constant current stimulation fixed charge densityBiphasic square wave pulse to avoid ion deposition0.1-0.3 millisecond pulse duration
5-60 Hz, 1-15 milliamperes, train duration of 2-15 seconds Maintain charge density below 55 uC/sq cm
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Electrical Stimulation: Clinical Effects
Motor cortex: jerking or tonic contractionPremotor cortex: tonic contraction or negative motor, may be bilateral in SMA Somatosensory cortex: tinglingVisual cortex: unformed or formed illusions
Temporal lobe: variable findings, including memories, complex visual or auditory illusions, psychic feelings, naming defectBroca’s area: speech arrestOther speech areas: isolated deficits
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Localization of Language
Morris et al 1984Ojemann et al 1989
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Stimulation Frequency in Cortical Brain Mapping
Zangaladze et al. Epilepsia, 2008
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Localization of Neurologic Function: Caution
Patients may not have “read the book” - specific neurological functions may be atypically localized or widely distributedOne cannot be certain that a function is not located in a particular area unless its location is demonstrated elsewhere Postop deficits may occur despite lack of stimulation effect (how well do we test?)No postop deficit may occur though stimulation shows an area is not safe (redundant function)
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Evoked Potential MappingSomatosensoryevoked potentials locate the post-central gyrusUsual peripheral nerve stimulation technique is used, recording from cortex instead of scalpCan use fast nerve stimulation rate to speed data acquisition, few stimuli per trial
Thomas Jefferson UniversityPatient:MRN:Date:
Thomas Jefferson UniversityPatient:Winegrad,RMRN:Date:8/2/078 7 6 5 4 3 2 1
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LFPALFPB
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DEPTHS
STRIPS
LFA – 481
LFB-487
LFPA-493
LFPB-483
LFPC-810
LIH-822
Intracranial monitoringLEFT SIDE
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Median SSEP: N20 at 21.1 msec
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Posterior Tibial SSEP: P38 at 35.7 msec
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ConclusionUse of intracranial EEG enables some patients to have epilepsy surgery who would otherwise not be candidates
Offers unparalleled temporal resolutionOffers spatial precisionSuffers from significant limitations – not a “gold standard”
Intracranial EEG electrodes can be used to map cortical function
Reduces risk of neurological deficitEpilepsy surgery involves balancing risks and benefits
Risks of surgery generally outweigh the risks of uncontrolled seizures
Key skill is knowing which patients are good candidates and which are poor candidates
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First Site of Seizure PropagationMedial frontal
70% to contralateral mesial frontal zone, 30% to ipsilateral frontal lobe
Lateral frontal70% to ipsilateral temporal lobe, 30% to frontal lobe
OrbitofrontalAll to contralateral oritofrontal area and ipsilateral temporal lobe
Mesial temporal50% to ipsilateral lateral temporal zone 35% to contralateral mesialtemporal 15% to ipsilateral frontal lobe
Lateral temporal62% to ipsilateral mesialtemporal zone 28% to contralateral lateral temporal 10% to frontal lobes
Parietal60% to ipsilateral frontal lobe 33% to ipsilateral temporal lobe 7% to occipital lobe
Occipitalall to ipsilateral temporal lobe
Jenssen and Sperling, submitted
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Subclinical Seizures:Seizures with Insufficient Spread
to Produce SymptomsOccurred in 64% of patients (n = 111) Infrequently spread to other areas within the same lobe, and rarely spread outside their lobe of origin83% of SCS did not spread beyond the area of origin12% of SCS spread within the lobe and only 5% spread beyond the lobe, predominantly in the ipsilateral hemisphere
Zangaladze et al. Epilepsia 2008
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Subclinical Seizures and Outcome
Percent seizure-freeWith SCS: 68%Without SCS: 66%
Percent seizure-free*Complete co-localization 77.5%Incomplete co-localization 37.5%
ConclusionSCS should count as seizures for prognostic purposes Varying sites of onset is less desirable
* p = .003 Zangaladze et al. Epilepsia 2008