Focal cortical high-frequency oscillations trigger epileptic spasms: Confirmation by digital video subdural EEG

OBJECTIVE: To localize high-frequency oscillations (HFOs) on the cortex during epileptic spasms using video subdural EEG and Multiple Band Frequency Analysis (MBFA). METHODS: Using video subdural EEG sampled at 1 kHz, we studied a 14-year-old boy with asymmetric epileptic spasms of possible left frontal origin. We identified HFOs, then analyzed and localized their distributions by MBFA. We correlated HFO distribution to clinical spasm intensity. RESULTS: Ictal subdural EEG recorded HFOs at 60-150 Hz lasting 0.3-4 s. MBFA showed extensive but noncontiguous distribution of HFOs predominantly over the left frontal and temporal regions. HFOs began and became quasiperiodic before manifestation of clinical spasms. As clinical spasms intensified, HFOs persisted in regions where they initiated subclinically but were of higher frequency and greater power than HFOs in other regions. We performed cortical resections over the left frontal and temporal regions with predominant HFOs. Six months after surgery, the patient remained seizure free. CONCLUSIONS: HFOs were present over the ictal onset zone during epileptic spasms. Periodic spasms in this patient had the characteristics of partial seizures. SIGNIFICANCE: We show that HFOs occurred over the cerebral cortex during epileptic spasms, and we suggest that these focal cortical HFOs triggered the spasms.     

Epileptic spasms in older pediatric patients: MEG and ictal high-frequency oscillations suggest focal-onset seizures in a subset of epileptic spasms

OBJECTIVES: To elucidate the pathophysiology of intractable epileptic spasms in older children by describing the interictal magnetoencephalography spike sources (MEGSSs), intracranial EEG ictal-onset zones (IOZs) and their ictal high-frequency oscillations (HFOs) and surgical outcomes. METHODS: We studied five patients (4.5-14 years) who underwent surgery following intracranial video-EEG (VEEG) monitoring. We analyzed clinical profiles, MRIs, scalp and intracranial VEEGs, and MEGSSs. We localized ictal HFOs using a sampling rate of 1000 Hz and multiple band frequency analysis (MBFA). RESULTS: Seizure onset ranged from 0.4 to 8 years. Three patients presented with asymmetrical spasms. Interictal scalp VEEG recorded predominantly unilateral epileptiform discharges in four; generalized and multifocal in one. Ictal scalp VEEG showed generalized high-amplitude slow waves with superimposed fast waves in four patients; hemispheric electrodecremental episodes in one. MRI findings were normal in three, hemispheric polymicrogyria and periventricular heterotopia in one each. All patients had unilateral MEGSS clusters. Ictal HFOs, ranging from 150 to 250 Hz, localized over Rolandic and frontal regions in four, with one also having extensive temporo-occipital HFOs. After cortical resection, three patients were seizure free; one had >90% reduction in seizure frequency. One patient experienced residual seizures after resection of the hemispheric ictal HFO region. CONCLUSION: Unilateral clusters of MEGSSs overlapped regional IOZs in older patients with epileptic spasms. High spatio-temporal MBFA before and during spasms revealed the regional ictal HFOs. Seizure-free outcomes following resection of zone with MEGSS clusters and ictal HFOs suggested that a subset of epileptic spasms was focal-onset seizures.     

Spatial localization and time-dependant changes of electrographic high frequency oscillations in human temporal lobe epilepsy

Purpose:   High frequency oscillations (HFOs) >200 Hz are believed to be associated with epileptic processes. The spatial distribution of HFOs and their evolution over time leading up to seizure onset is unknown. Also, recording HFOs through conventional intracranial electrodes is not well established. We therefore wished to determine whether HFOs could be recorded using commercially available depth macroelectrodes. We also examined the spatial distribution and temporal progression of HFOs during the transition to seizure activity.
Methods:   Intracranial electroencephalography (EEG) recordings of 19 seizures were obtained from seven patients with temporal lobe epilepsy using commercial depth or subdural electrodes. EEG recordings were analyzed for frequency content in five spectral bands spanning DC-500 Hz. We examined the spatial distribution of the different spectral bands 5 s before and 5 s after seizure onset. Temporal changes in the spectral bands were studied in the 30-s period leading up to seizure onset.
Results:   Three main observations were made. First, HFOs (100–500 Hz) can be recorded using commercial depth and subdural grid electrodes. Second, HFOs, but not <100 Hz oscillations, were localized to channels of ictal onset (100–200, 400–500 Hz, p < 0.05; 300–400 Hz, p < 0.001). Third, temporal analysis showed increased HFO power for approximately 8 s prior to electrographic onset (p < 0.05).
Conclusions:   These results suggest that HFOs can be recorded by depth macroelectrodes. Also, HFOs are localized to the region of primary ictal onset and can exhibit increased power during the transition to seizure. Thus, HFOs likely represent important precursors to seizure initiation.     

Topographic movie of intracranial ictal high-frequency oscillations with seizure semiology: epileptic network in Jacksonian seizures

Purpose: We developed a technique to produce images of dynamic changes in ictal high‐frequency oscillations (HFOs) >40 Hz recorded on subdural electroencephalography (EEG) that are time‐locked to the ictal EEG and ictal semiology video. We applied this technique to Jacksonian seizures to demonstrate ictal HFO propagation along the homunculus in the primary sensory‐motor cortex to visualize the underlying epileptic network. Methods: We analyzed intracranial ictal EEGs from two patients with intractable Jacksonian seizures who underwent epilepsy surgery. We calculated the degrees of increase in amplitude within 40–80, 80–200, and 200–300 Hz frequency bands compared to the interictal period and converted them into topographic movies projected onto the brain surface picture. We combined these data with the ictal EEGs and video of the patient demonstrating ictal semiology. Key Findings: The ictal HFOs began in the sensory cortex and appeared concomitantly with the sensory aura. They then propagated to the motor cortex at the same time that focal motor symptoms evolved. As the seizure progressed, the ictal HFOs spread or reverberated in the rolandic region. However, even when the seizure became secondarily generalized, the ictal HFOs were confined to the rolandic region. In both cases, there was increased amplitude of higher frequency bands during seizure initiation compared to seizure progression. Significance: This combined movie showed the ictal HFO propagation corresponding to the ictal semiology in Jacksonian seizures and revealed the epileptic network involved in seizure initiation and progression. This method may advance understanding of neural network activities relating to clinical seizure generation and propagation.     

High-frequency oscillations of ictal muscle activity and epileptogenic discharges on intracranial EEG in a temporal lobe epilepsy patient.

OBJECTIVE: During seizures, intracranial EEG electrodes can record ictal muscle movements. Our purpose was to differentiate the high-frequency oscillations (HFOs) of extracranial muscle contractions from those of intracranial epileptogenic discharges. METHODS: Using intracranial video-EEG (IVEEG), we recorded seizures in a 17-year-old boy with left mesial-temporal lobe epilepsy. We used multiple band frequency analysis (MBFA) to differentiate extracranial HFOs of craniofacial muscle activities from intracranial HFOs recorded ictally and interictally. RESULTS: During 11 seizures, IVEEG showed low-amplitude fast waves ( approximately 60Hz) starting at the left mesial-temporal electrodes. Ictal facial grimacing projected low-amplitude ( approximately 20muV) fast waves ( approximately 160Hz) on inferior lateral-temporal electrodes. Interictal chewing projected medium-amplitude ( approximately 100muV) fast waves ( approximately 140Hz) correlating to mouth movements. MBFA topographic power spectrograms revealed a sustained, consistent ictal fast-frequency band from electrodes in the seizure-onset zone and randomly scattered HFOs without a specific frequency band from ictal and interictal extracranial muscle contractions. CONCLUSIONS: MBFA power spectrograms differentiated randomly scattered muscle HFOs without a specific frequency band at electrodes close to temporal muscles from ictal epileptic HFOs with a sustained, fast-frequency band in the seizure-onset zone. SIGNIFICANCE: The pattern and distribution of frequency power spectrograms of extracranial HFOs differ from those of intracranial HFOs.     

Statistical mapping of ictal high-frequency oscillations in epileptic spasms

Purpose: We assessed 636 epileptic spasms seen in 11 children (median 44 spasms per child) and determined the spatial and temporal characteristics of ictal high‐frequency oscillations (HFOs) in relation to the onset of spasms. Methods: Electrocorticography (ECoG) signals were sampled from 104–148 cortical sites per child, and the dynamic changes of ictal HFOs were animated on each individual’s three‐dimensional (3D) magnetic resonance (MR) image surface. Key Findings: Visual assessment of ictal ECoG recordings revealed that each spasm event was characterized by augmentation of HFOs. Time‐frequency analysis demonstrated that ictal augmentation of HFOs at 80–200 Hz was most prominent and generally preceded those at 210–300 Hz and at 70 Hz and slower. Recruitment of HFOs in the rolandic cortex preceded the clinical onset objectively visualized as electromyographic deflection. The presence or absence of ictal motor symptoms was related more to the amplitude of HFOs in the Rolandic cortex than in the seizure‐onset zone. In a substantial proportion of epileptic spasms, seizure termination began at the seizure‐onset zone and propagated to the surrounding areas; we referred to this observation as the “ictal doughnut phenomenon.” Univariate analysis suggested that complete resection of the sites showing the earliest augmentation of ictal HFOs was associated with a good surgical outcome. Significance: Recruitment of HFOs at 80–200 Hz in the rolandic area may play a role in determining seizure semiology in epileptic spasms. Our study using macroelectrodes demonstrated that ictal HFOs at 80–200 Hz preceded those at 210–300 Hz.     

Subdural Recording of Ictal DC Shifts in Neocortical Seizures in Humans

Summary: Purpose: Invasive ictal EEG recording is often necessary to delineate epileptogenic areas in patients with intractable partial epilepsy, but even intracranial ictal recordings often reveal ill-defined onset zones in neocortical epilepsy. We studied the physiologic significance of ictal direct current (DC) potentials recorded intracranially in human epilepsy.
Methods: We made intracranial ictal EEG recordings in three patients with intractable partial seizures arising from frontal, lateral temporal, and parietal neocortical areas by using closely spaced subdural electrodes (platinum in two patients and stainless steel in one patient) with both standard (1.5 Hz) and open (0.016 Hz) low-frequency filter (LFF) settings.
Results: The initial ictal pattern was localized to two to nine subdural electrodes and characterized by very low voltage and high-frequency rhythmic activity ("electrode-cremental pattern"). A slow-rising negative potential (DC potential) was seen in a slightly more restricted area (two to six electrodes) and occurred 1–10 s before the initial ictal EEG discharges in two patients.
Conclusions: These results agree with those of previous studies of ictal DC shifts in animals and suggest that ictal DC shifts may be helpful in delineating the epileptogenic area more precisely in human epilepsy.     

Time from ictal subdural EEG seizure onset to clinical seizure onset: prognostic value for selecting temporal lobectomy candidates

Long-term subdural EEG recording was performed to test the hypothesis that the duration from ictal subdural EEG seizure onset (ECOT) is prognostic for seizure-free outcome following temporal lobectomy. In 48 patients with complex partial seizures, temporal lobectomy was based on invasive localization of the ictal seizure focus. Subdural EEG data were analyzed for association with seizure-free outcome (seizure-free: yes or no) at a minimum of one year following temporal lobectomy. As the duration from ictal subdural EEG seizure onset to clinical seizure onset increased, the odds of being seizure-free postoperatively increased. The best fitting statistical model for predicting seizure-free outcome included seizure onset (unilateral vs. bilateral) and duration from ictal subdural EEG seizure onset to clinical seizure onset. While selection of temporal lobectomy candidates has increasingly emphasized noninvasive recording, some scalp-EEG monitored patients cannot be offered surgery for various reasons, one of which may include ictal EEG seizure onset following clinical seizure onset. When subdural EEG monitoring is performed for selection of temporal lobectomy candidates, analysis of the duration from subdural EEG seizure onset to clinical seizure onset should improve the prognostic value of the subdural EEG data for seizure-free outcome following temporal lobectomy.     

Topographic movie of ictal high-frequency oscillations on the brain surface using subdural EEG in neocortical epilepsy

PURPOSE: To understand the rapid dynamic changes of ictal intracranial high-frequency oscillations (HFOs) in neocortical epilepsy. METHODS: We integrated multiple band frequency analysis and brain-surface topographic maps of HFOs from ictal subdural EEG (SDEEG) recordings. We used SDEEG to record partial seizures consisting of right-arm jerks with secondary generalization in a 17-year-old right-handed girl. We selected 20-s EEG sections that included preclinical seizure recordings. We averaged the HFO power between 60 and 120 Hz for 25 selected electrodes, made topographic maps from these averaged powers, and superimposed the maps on the brain-surface image. We filmed consecutive HFO maps at a 10-ms frame rate. RESULTS: Before clinical seizure onset, high-power HFOs emerged at the superior portion of the left precentral gyrus, then appeared in the middle of the left postcentral gyrus, and subsequently reverberated between both regions as well as the posterior portion of the left postcentral gyrus. Right-arm extension and facial grimacing started as the HFO power decreased. As generalized tonic-clonic seizures evolved, HFO power increased but remained within the central region. CONCLUSIONS: Topographic movies of intracranial HFOs on the brain surface allow visualization of the dynamic ictal changes in neocortical epilepsy.     

Ictal high-frequency oscillations at 80-200 Hz coupled with delta phase in epileptic spasms

Previous studies of epileptic spasms reported that ictal events were associated with high-frequency oscillations (HFOs) or delta waves involving widespread regions. We determined whether ictal HFOs at 80-200 Hz were coupled with a phase of slow-wave, whether ictal slow-waves were diffusely or locally synchronous signals, and whether the mode of coupling between HFOs and slow-wave phases differed between ictal and interictal states. We studied 11 children who underwent extraoperative electrocorticography (ECoG) recording. The phases and amplitudes of slow-waves were measured at the peak of ictal and interictal HFOs in the seizure-onset sites. Ictal HFOs were locked tightly to the phase of slow-wave at ≤1 Hz. Ictal slow-waves propagated from the seizure-onset site to other regions. In contrast, interictal HFOs in the seizure-onset site were loosely locked to the phase of slow-wave at ≤1 Hz but tightly to that of ≥3-Hz. Ictal slow-waves coupled with HFOs can be explained as near-field and locally synchronized potentials generated by the neocortex rather than far-field potentials generated by subcortical structures. Ictal slow-waves in epileptic spasms may be generated by a mechanism different from what generates interictal HFOs-slow-wave complexes.     

Two magneto-encephalographic epileptic foci did not coincide with the electrocorticographic ictal onset zone in a patient with temporal lobe epilepsy.

To evaluate the usefulness and limitations of magneto-encephalography (MEG) for epilepsy surgery, we compared 'interictal' epileptic spike fields on MEG with ictal electrocorticography (ECoG) using invasive chronic subdural electrodes in a patient with intractable medial temporal lobe epilepsy (MTLE) associated with vitamin K deficiency intracerebral hemorrhage. A 19-year-old male with an 8-year history of refractory complex partial seizures, secondarily generalized, and right hemispheric atrophy and porencephaly in the right frontal lobe on MRI, was studied with MEG to define the interictal paroxysmal sources based on the single-dipole model. This was followed by invasive ECoG monitoring to delineate the epileptogenic zone. MEG demonstrated two paroxysmal foci, one each on the right lateral temporal and frontal lobes. Ictal ECoG recordings revealed an ictal onset zone on the right medial temporal lobe, which was different from that defined by MEG. Anterior temporal lobectomy with hippocampectomy was performed and the patient has been seizure free for two years. Our results indicate that interictal MEG does not always define the epileptogenic zone in patients with MTLE.     

Induction of partial epileptic seizures by flumazenil

PURPOSE: This study addressed the efficacy of flumazenil (FMZ) to induce or activate interictal or ictal epileptic discharges in patients with medically intractable partial epilepsies. METHODS: Flumazenil, 1 mg, was injected intravenously in 67 patients undergoing presurgical monitoring for epilepsy surgery, 49 of whom had been treated with benzodiazepines (BZDs) before flumazenil was given. Continuous video electroencephalogram (EEG) monitoring with surface or intracranial electrodes was used to evaluate interictal EEG activity, ictal discharges, and the occurrence and semiology of clinically manifest epileptic seizures. RESULTS: Interictal epileptiform potentials did not change in frequency or distribution after FMZ. In patients not pretreated with BZDs, epileptic seizures could not be provoked. In eight of the 49 patients pretreated with BZDs, epileptic seizures occurred within 30 min of FMZ application. Seizure semiology and regional EEG onset were identical to seizures recorded without FMZ. Patients operated on according to seizure-onset localization with FMZ had a >75% reduction in seizure frequency or became seizure free. CONCLUSIONS: Seizure induction by FMZ seems to be a valid method for evaluating seizure semiology and localization of the seizure-onset zone during presurgical monitoring of patients with medically intractable localization-related epilepsies.     

False lateralization by surface EEG of seizure onset in patients with temporal lobe epilepsy and gross focal cerebral lesions

Medically intractable temporal lobe seizures developed in 3 patients with radiological and clinical evidence of a gross focal cerebral lesion acquired early in life. All had bilateral independent epileptogenic discharges from the lateral and inferomesial regions of both hemispheres. Scalp and sphenoidal electroencephalographic (EEG) recordings suggested that the seizures originated from the side contralateral to the known cerebral lesion. Because the lateralizing evidence presented by the ictal EEG conflicted with the clinical data, depth electrodes were implanted stereotaxically to determine the side of onset of the seizures. These studies showed that the seizures originated from the limbic structures of the damaged hemisphere in all 3 patients. At operation the mesial temporal lobe structures showed gliotic changes in all. The patients have remained seizure-free for 3 to 13 years postoperatively. These findings suggest that depth electrode recordings may be required to clarify the lateralization of seizure onset in such cases. Extracranial EEG findings must be interpreted with caution in epileptic patients who have gross focal lesions.     

Magnetoencephalographic localization in pediatric epilepsy surgery: comparison with invasive intracranial electroencephalography.

The object of this study was to determine the concordance of the anatomical location of interictal magnetoencephalographic (MEG) spike foci with the location of ictal onset zones identified by invasive ictal intracranial electroencephalographic recordings in children undergoing evaluation for epilepsy surgery. MEG was performed in 11 children with intractable, nonlesional, extratemporal, localization-related epilepsy. Subsequently, chronic invasive intracranial electroencephalographic monitoring was performed by using subdural electrodes to localize the ictal onset zone and eloquent cortex. Based on the invasive monitoring data, all children had excision of, or multiple subpial transections through, ictal onset cortex and surrounding irritative zones. In 10 of 11 patients, the anatomical location of the epileptiform discharges as determined by MEG corresponded to the ictal onset zone established by ictal intracranial recordings. In all children, the anatomical location of the somatosensory hand area, determined by functional mapping through the subdural electrode array, was the same as that delineated by MEG. Nine of 11 patients became either seizure-free or had a greater than 90% reduction in seizures after surgery, with a mean follow-up of 24 months. MEG is a powerful and accurate tool in the presurgical evaluation of children with refractory nonlesional extratemporal epilepsy.     

Somatosensory evoked high frequency oscillations recorded from subdural electrodes

OBJECTIVES: To examine high frequency oscillations (HFOs) of somatosensory evoked potentials (SEPs) recorded directly from subdural electrodes to investigate the relationship between the primary somatosensory cortex and HFOs. METHODS: SEPs were recorded directly from subdural electrodes previously implanted in 3 patients for clinical evaluation prior to surgical treatment of intractable epilepsy. RESULTS: The primary sensory cortex (area 3b) was proposed as the source of somatosensory HFOs, because the distribution of HFOs recorded from the subdural electrodes agreed with the distribution of the N20-P20 components of the somatosensory evoked potential. The somatosensory HFOs showed a strictly somatotopic source arrangement. There was a polarity inversion of the prophase component and also the N20-P20 component of HFOs across the central sulcus. However, the phase was synchronized in the latter part of the HFOs. CONCLUSIONS: We propose that the origins of the early and latter parts of HFOs are different, and that there was a clear somatotopy.     

Ictal SPECT in supplementary motor area seizures

OBJECTIVES: We used ictal single photon emission computed tomography (SPECT) to clarify the propagation pathways of epileptic discharges in patients with supplementary motor area (SMA) seizure. METHODS: In four patients (four males, age range, 18-27 years) with SMA seizures, SPECT studies by radioisotope 99mTc-ECD were performed as a preoperative evaluation. Two of the patients remained seizure-free after complete resection of the focal cortical dysplasia on magnetic resonance (MR) images including epileptic foci. In the other two patients, MR images were normal, but subdural electrode monitoring allowed for verifying the ictal onset in the left SMA. After partial resection of the SMA including epileptic foci, these patients experienced a significant (>90%) reduction of seizure frequency. Regional cerebral blood flow (rCBF) measurements obtained under ictal and interictal conditions were compared on a voxel-by-voxel basis by means of the SPM99 paired t-test option (uncorrected p<0.001). RESULTS: Significant increases in rCBF under ictal conditions were identified in the bilateral anterior cingulate cortex (ACC), the globus pallidus ipsilateral to epileptic foci and the contralateral cerebellar hemisphere. The right ACC included a cluster with a submaximum in the right primary sensorimotor area. DISCUSSION: In patients with SMA seizures, the hyperperfusion areas of ictal SPECT did not localize within the SMA but spread to the adjacent cortex such as the ACC and sensorimotor cortex ipsilateral to epileptic foci. Additionally, the epileptic discharges propagated to the remote areas such as the globus pallidus and cerebellum. We caution that ictal SPECT localization in patients with SMA seizures is not always concordant to epileptic focus but reveals already spread seizure activities.     

Time from ictal subdural EEG seizure onset to clinical seizure onset: an electrocorticographic time factor associated with temporal lobe epileptogenicity

Long-term subdural video/electroencephalographic (EEG) monitoring was performed in a series of patients with medically intractable complex partial seizures, in a study of diagnostic accuracy, to test the hypothesis that the time from ictal subdural EEG seizure onset to clinical seizure onset (ECOT) is correlated with temporal lobe epileptogenicity and confirm measures of validity of ECOT for predicting seizure-free outcome following anterior temporal lobectomy and amygdalohippocampectomy (ATL/AH). In 34 patients with refractory temporal lobe epilepsy, subdural EEG monitoring localized the ictal epileptogenic focus to a single temporal lobe. In each patient, ECOT was analysed for correlation with temporal lobe epileptogenicity as measured by seizure interval in hours. Patients in whom ECOT was equal to or less than the mean (i.e. subdural EEG seizure onset preceding clinical seizure onset by at least 11.7 seconds) had a significantly greater likelihood of becoming seizure-free following ATL/AH compared to patients in whom ECOT was greater than the mean (i.e. subdural EEG seizure onset preceding clinical seizure onset by less than 11.7 seconds) (x(2) = 5.78, p<0.05). The validity of ECOT for predicting seizure-free outcome following ATL/AH is confirmed to have sensitivity of 55.0%, specificity of 85.7%, false positive rate of 15.4%, false negative rate of 42.9%, diagnostic value of 84.6% and diagnostic accuracy of 67.6%. In addition, a significant correlation, described by a second order polynomial relationship, was found between the natural exponential function of ECOT and seizure interval [f(x=0.415x(2) -25.554x + 267.036, r= 0.731, df= 32, t =6.05, p<0.001, where f(x)=e(ECOT) and x= seizure interval). This result provides the epileptologist with a quantitative tool capable of predicting seizure interval based on ECOT. The capability of ECOT to predict seizure interval may allow the patient and epileptologist to anticipate future seizure onset based on ECOT, potentially facilitating accurate timing of ictal seizure focus localization techniques and clinical intervention to abort seizure onset using various available central and peripheral nervous system stimulation therapeutic strategies. The results suggest a relationship between ECOT and seizure interval. Fundamental pathophysiologic processes involved in the transition from ictal EEG to clinical seizure onset may be responsible for temporal lobe epileptogenicity.     

The effects of stimulus rates on high frequency oscillations of median nerve somatosensory-evoked potentials--direct recording study from the human cerebral cortex.

OBJECTIVES: To study the effects of different stimulus rates on high-frequency oscillations (HFOs) of somatosensory-evoked potentials (SEPs), we recorded median nerve SEPs directly from the human cerebral cortex. METHODS: SEPs were recorded from subdural electrodes in 5 patients with intractable epilepsy, under the conditions of low (3.3Hz) and high (12.3Hz) stimulus rates. RESULTS: Increased stimulus rates to the median nerve from 3.3 to 12.3Hz showed a pronounced amplitude reduction of HFOs when compared with the primary N20-P20, area 3b, and P25, area 1, responses. CONCLUSIONS: HFOs were more sensitive to a high stimulus rate than the primary cortical responses, suggesting that the post-synaptic intracortical activities may greatly contribute to the HFO generation.     

Intracranial EEG findings in patients with lesional lateral temporal lobe epilepsy

PURPOSE: Intracranial EEG in patients with lesional lateral temporal lobe epilepsy is rarely reported. Therefore, the number of patients with seizures arising independently from ipsilateral mesial structures or contralateral hemisphere has not been clarified. We analyzed the intracranial EEG of cases with localized lesion in the lateral temporal cortex. METHODS: We studied 15 patients who satisfied the following criteria: (1) MRI depicted a lesion less than 4cm in diameter located lateral to the collateral sulcus and at least 3cm posterior to the temporal pole; (2) intracranial EEG with electrodes placed on bilateral temporal lobes captured at least one complex partial seizure; and (3) postoperative follow-up period of 2 years or longer. The mean age of seizure onset was 16.6 years (range, 11-25) and that at surgery was 26.7 years (range, 16-36). RESULTS: A total of 147 complex partial seizures, 51 simple partial seizures, 16 secondarily generalized seizures, and over 80 subclinical seizures were recorded. On the lesional side, many clinical seizures were recorded from the lateral cortex. Independent of the lateral temporal onset seizures, ictal discharges originating from the mesial temporal structures were recorded in 7 of 15 patients (47%). Moreover, onset of ictal discharges from the contralateral temporal lobe was recorded in 7 of 15 patients (47%). Interictal spikes from ipsilateral mesial structures were recorded in all patients. The presence of ipsilateral mesial onset seizures was not associated with hippocampal neuron losses. CONCLUSION: Intracranial EEG analysis revealed that approximately one-half of the patients with structural lesions in the lateral cortex showed independent epileptogenic areas in ipsilateral mesial structures. Although ictal discharges originating from the contralateral temporal lobe were recorded in a half of these patients, this finding does not constitute a contraindication of resective surgery. Interictal spike is not an indicator of whether mesial structures should be resected.     

Spectral Analysis of Sphenoidal Evoked Potentials Predicts Epileptic Focus

Sphenoidal evoked potentials (SpEPs) were recorded in 14 patients with intractable temporal lobe epilepsy. Twelve patients had electrographically proven unilateral seizure onset (five left, seven right). Two patients had partial complex seizures and unilateral mesial temporal lobe lesions shown by magnetic resonance imaging (MRI). Thirteen patients subsequently underwent temporal lobectomy. SpEPs were recorded using the P3 tonal oddball paradigm from sphenoidal electrodes referenced to scalp electrodes (i.e., T3, T4, C3, C4, Cz) and were subjected to spectral analysis for whole band (1-12.6 Hz) power. A significant relationship was found for side of seizure focus and reduced spectral power of the sphenoidal-temporal target SpEPs. In 10 of 14 patients, SpEP spectral power was less from the "epileptogenic" than from the "nonepileptogenic" temporal lobe. Of the remaining 4 patients, 2 had bilaterally equal spectral power, and 2 had lower SpEP power from the nonepileptogenic side. Postoperatively, all 13 patients are seizure-free except for the 2 patients with reduced SpEP power opposite to the ictal onset and 1 patient with fluctuations in SpEP asymmetries. Spectral analysis of SpEPs appears to have utility in the assessment of temporal lobe dysfunction and thus in the preoperative evaluation for epilepsy surgery.