Clinical and EEG Features of Complex Partial Seizures of Temporal Lobe Origin

Summary: The electrographic and clinical behavioural manifestations of 96 temporal lobe seizures are reviewed from recordings in 19 patients who were submitted to stereotaxic depth electrode implantation in temporal and frontal lobes. Focal onset in hippocampus was recorded in 40% of the seizures. Sixty percent of temporal lobe seizures exhibited a regional seizure onset but in two-thirds of these ictal changes were restricted to amygdaloid and hippocampal structures. Thus, in approximately 80% of seizures, the onset of ictal EEG changes resided in the mesial temporal structures. The main behavioral manifestations observed during seizure discharge restricted to one temporal lobe included warning (67%), motionless stare (24%), automatism (22%), and head-body turning (24%). The predominant ictal behavioural manifestations observed during seizure spread to contralateral temporal and extratemporal structures included warning (3%), motionless stare (36%), automatism (77%), and head-body turning (81%). The direction of head turning did not provide reliable lateralization as to the side of seizure onset.     

Comparison of bitemporal and unitemporal epilepsy defined by depth electroencephalography

Of 166 consecutive patients studied with depth electroencephalography (EEG), 87 had seizures arising from one temporal lobe and 23 had seizures arising independently from each temporal lobe. We retrospectively reviewed and compared those patients with unitemporal and those with bitemporal seizures. There was no statistically significant differences between the two groups in terms of age at onset of seizures, duration of epilepsy, localization of scalp EEG abnormalities, surgical results, or pathological findings. The bitemporal group, however, had significantly fewer patients with a history of febrile seizures (p less than 0.025). Two patients with bitemporal seizures were later found to have extratemporal lesions, and one an extrahippocampal temporal lesion, on magnetic resonance scans; one patient's extratemporal lesion was resected and all habitual seizures stopped. These findings suggest that a single pathophysiological process accounts for unitemporal and some bitemporal epilepsy, but that independent onset of seizures from each temporal lobe detected by depth EEG may also indicate extratemporal foci.     

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.     

Occipitotemporal Epilepsies: Evaluation of Selected Patients Requiring Depth Electrodes Studies and Rationale for Surgical Approaches

Summary: In 8 patients in whom it was uncertain whether they had occipital or temporal lobe (TL) epilepsy, clinical, scalp EEG, and radiologic features were correlated with the sites of seizure onset as determined by depth EEG. The 8 patients were selected from >40 with occipital epilepsy because they had (a) an aura considered to be of occipital lobe (OL) origin, (b) an occipital interictal epileptic focus, (c) an OL lesion, or (d) a combination of all of these. Scalp EEG and clinical patterns suggested temporal involvement in all, however. Extracranial EEG recordings were often misleading, showing multilobar interictal epileptic abnormalities, and seizure onset was of poor localizing value and did not clarify the problem sufficiently. Intracranial EEG recordings showed that seizure onset could be ordered along an Occipitotemporal gradient. Consistent OL seizure onset was observed in patients who had only elementary visual auras. Those who had inconsistent aura or no aura, suggesting OL origin, had onset of most attacks in the TL. All patients had a seizure spread pattern suggesting early TL involvement. To prevent visual field defect, surgical approaches included temporal resection when temporal seizure origin or spread was demonstrated; although occasionally this produced excellent results, it was of limited benefit in most patients, even when some seizures were proven to originate in TL structures. In patients with malignant epilepsy and in those with an occipital lesion, occipital resection should be considered.     

Intracranial, Intraaxial, Space-Occupying Lesions in Patients with Intractable Partial Seizures: An Anatomoclinical, Neuropsychological, and Surgical Correlation

Fifty of approximately 250 patients evaluated for intractable partial seizures were shown to have a space-occupying lesion detected with radiographs and/or neuroimaging. Twenty-eight males and 22 females had a mean age at seizure onset of 13 years and a mean duration of seizures of 11 years. All patients had closed-circuit television with EEG monitoring and complete neurologic and neuropsychological assessment. Findings were correlated with lesion location and surgical data. Twenty-seven lesions (54%) were located in the temporal lobe. Thirty-five lesions (70%) were neoplastic. All patients with temporal lobe lesions had complex partial seizures, as did 74% of patients with extratemporal lesions. A good correlation between clinical seizure characteristics and lesion localization was found with the temporal, occipital, and frontal lesions but not with the parietal lesions. Sixty-six percent of patients had focal interictal EEG findings. Lateralization corresponded to the side of the lesion in 64% and was localized to the region of the lesion in 30%. Lateralized ictal EEGs occurred in 58% of patients, corresponding with the side of the lesion in all but one patient. Abnormal findings on neuropsychological testing were congruent with lesion lateralization in 56% of patients and were localized to the region in 26%. Thirty-nine of 47 patients who underwent a subtotal lobectomy to include the lesion are seizure-free after greater than or equal to 1 year of follow-up, and five others are markedly improved.     

Falsely localizing ictal onsets with depth EEG telemetry during anticonvulsant withdrawal

A patient with partial complex seizures evaluated for surgery with chronic depth electrode recordings demonstrated falsely localizing ictal onsets during anticonvulsant drug withdrawal. When phenytoin was being reduced, more seizures appeared to originate from the left temporal lobe than from the right. Right anterior temporal lobectomy, performed on the basis of other findings, revealed a small unsuspected tumor in the resected specimen, and the patient has remained seizure free for 3 years. The seizures that originated from the left temporal lobe were different from the patient's habitual attacks and appeared to be the result of anticonvulsant withdrawal and, perhaps, electrode irritation. Four other patients who received anterior temporal lobectomies at UCLA between 1977 and 1980 had at least one stereotaxic EEG (SEEG)-recorded contralateral seizure onset, and all have benefited from surgery. Although multifocal SEEG-recorded ictal onsets should be considered a poor prognostic sign, distant sites that give rise to atypical seizures during drug withdrawal may not generate spontaneous seizures postoperatively. Consequently, this finding should not be used as a sole criterion against the recommendation of surgical therapy.     

Intracranial EEG Substrates of Scalp Ictal Patterns from Temporal Lobe Foci

Summary: Purpose: To determine the intracranial EEG features responsible for producing the various ictal scalp rhythms, which we previously identified in a new EEG classification for temporal lobe seizures. Methods: In 24 patients, we analyzed simultaneous intracranial and surface ictal EEG recordings (64 total channels) obtained from a combination of intracerebral depth, subd-ural strip, and scalp electrodes. Results: Four of four patients with Type 1 scalp seizure patterns had mesial temporal seizure onsets. However, discharges confined to the hippocampus produced no scalp EEG rhythms. The regular 5- to 9-Hz subtemporal and temporal EEG pattern of Type 1a seizures required the synchronous recruitment of adjacent inferolateral temporal neocortex. Seizure discharges confined to the mesiobasal temporal cortex produced a vertex dominant rhythm (Type 1c) due to the net vertical orientation of dipolar sources located there. Ten of 13 patients with Type 2 seizures had inferolateral or lateral, temporal neocortical seizure onsets. Initial cerebral ictal activity was typically a focal or regional, low voltage, fast rhythm (20–40 Hz) that was often associated with widespread background flattening. Only an attenuation of normal rhythms was reflected in scalp electrodes. Irregular 2- to 4-Hz cortical ictal rhythms that commonly followed resulted in a comparably slow and irregular scalp EEG pattern (Type 2a). Type 2C seizures showed regional, periodic, 1– to 4-Hz sharp waves following intracranial seizure onset. Seven patients had Type 3 scalp seizures, which were characterized by diffuse slowing or attenuation of background scalp EEG activity. This resulted when seizure activity was confined to the hippocampus, when there was rapid seizure propagation to the contralateral temporal lobe, or when cortical ictal activity failed to achieve widespread synchrony. Conclusions: Type 1, 2, and 3 scalp EEG patterns of temporal lobe seizures are not a reflection of cortical activity at seizure onset. Differences in the subsequent development, propagation, and synchrony of cortical ictal discharges produce the characteristic scalp EEG rhythms.     

Depth electrode investigations in patients with bitemporal epileptiform abnormalities

Fifty-seven patients showing bitemporal independent epileptiform abnormalities on extracranial electroencephalograms (EEGs) in whom the epileptogenic zone could not be localized or lateralized by extracranial EEG and other noninvasive tests were investigated with stereotactic depth electrode recordings. In a majority of 44 patients (77%), seizures originated exclusively or with a strong predominance in one temporal lobe only. Of the remaining 13 patients (23%), 8 had seizures originating independently in either temporal lobe without significant lateralized predominance, and 5 had multiple seizure patterns, which were often diffuse. The patterns of seizure onset as recorded by depth electrodes tended to vary even in the same patient. Electrical stimulation studies and the determination of afterdischarge thresholds were of limited utility for lateralization of seizure onset.     

Interictal indices of temporal seizure origin

Two studies assessed the value of temporal lobe interictal electroencephalographic (EEG) spikes and delta in indicating side of temporal epileptogenesis. The first study determined laterality of spikes/delta in awake recordings of 56 patients whose seizures all began unilaterally as proven by (1) EEG-recorded seizures and (2) >90% improvement after lobectomy. Spikes of 52 (93%) and delta of 46 (82%) patients predominated or appeared exclusively ipsilateral to seizure origin. Neither predominated contralaterally in any patient. The second study investigated laterality of temporal seizures in a separate group of 156 patients with various side vs side spike or delta ratios on 1 to ≥4 awake recordings. Ninety-nine of 104 patients (95%) with temporal spikes on four or more awake recordings had most or all seizures ipsilateral to most spikes, including 79 of 80 (99%) of those with ≥3 side vs side spike ratios. Among the 120 patients with high (≥3) side vs side spike ratios, most or all seizures of 118 (98%) originated ipsilateral to most spikes. Predominant seizure origin also correlated with lateralized arrhythmic delta—from 90% ipsilateral seizures of those with one EEG with delta to 100% with ≥4 such EEGs. Data from these two studies using opposite directions of analysis (seizures ← spikes/delta and spikes/delta → seizures) demonstrate high correlations between laterality of interictal and ictal entities, particularly if temporal spikes clearly predominate on one side and if unilateral temporal delta activity persists over several recordings. Such correlations suggest that the awake interictal scalp EEG cannot be ignored when assessing laterality of temporal epileptogenesis.     

Periodic lateralized epileptiform discharges in neurosyphilis

We report two patients of neurosyphilis with periodic lateralized epileptiform discharges (PLEDs) in the EEG. Patient 1, a 32-yr-old man manifested with rapidly progressive cognitive decline and abnormal behavior and recurrent generalized tonic-clonic seizures. EEG revealed periodic epileptiform discharges arising from the anterior temporal and frontal region, predominantly from the right. Diffusion weighted MRI of brain did not show any focal restricted diffusion. Patient 2, a 33-yr-old woman presented with 2-year history of behavioral abnormalities, generalized tonic-clonic seizures and unconcerned urinary incontinence. EEG revealed PLEDS arising from the left anterior temporal region. Her CT scan showed gross cerebral atrophy. Both the patients improved partially with treatment and PLEDs resolved completely. PLEDs may be recorded in EEG of patients with neurosyphilis without imageological evidence of focal cerebral lesion.     

Autosomal dominant lateral temporal lobe epilepsy associated with a novel reelin mutation

Aims. Reelin mutations are responsible for a minority of families with autosomal dominant lateral temporal lobe epilepsy. Here, we report a novel nuclear family with distinct clinical and neuroradiological findings. Methods. We studied the proband and her mother by means of EEG, video‐EEG, 3T MRI, FDG‐PET and genetic testing. Results. Both patients had a focal drug‐resistant epilepsy with onset at the age of 16 and focal seizures with typical auditory features combined with fear, followed by loss of contact or evolving to bilateral tonic‐clonic seizures. The proband's ictal EEG showed clear left temporal seizure onset, and cerebral MRI revealed subtle left temporal changes (mild hypotrophy, slight blurring of the white and grey matter and hyperintensity) with corresponding left temporal mesial focal hypometabolism on FDG‐PET. Genetic testing identified a missense variant, c.6631C>T (p.Arg2211Cys), in reelin repeat #5 in both patients, which markedly affected the secretion of the protein. Conclusion. The data from this family support previous findings indicating that reelin mutations are a cause of autosomal dominant lateral temporal lobe epilepsy which has a clinical spectrum that may also encompass drug‐resistant epilepsy associated with mild MRI temporal changes.     

Temporal lobectomy in patients with bitemporal epilepsy defined by depth electroencephalography

Patient selection for temporal lobectomy was reviewed for 23 patients with seizures that arose independently from each temporal lobe as detected by depth electroencephalography (EEG). Although neuropsychological testing, interictal EEG findings, imaging studies, and subclinical seizures were also considered, all patients offered temporal lobectomy had (1) at least 50% of the clinical seizures originating from the lobe to be resected, (2) adequate contralateral memory on testing with amobarbital, and (3) no clear evidence of an extratemporal focus. Eleven patients underwent temporal lobectomy. Pathological findings were considered positive in all nine specimens reviewed. Nine patients had no seizures, one had greater than 75% reduction in seizure frequency, and 1 had 50 to 75% reduction. Pathological features and clinical outcome were similar in the 6 patients with fewer than 80% and the 5 patients with at least 80% of seizures originating from the resected lobe. Thus, having fewer than 80% of seizures originate from one temporal lobe should not be an absolute contraindication for temporal lobectomy.     

Source localization in refractory partial epilepsy.

In this paper, 51 patients with refractory complex partial seizures (CPS) and intracranial structural abnormalities demonstrated with optimum MR (space-occupying: n = 16; atrophic: n = 32; dysplastic: n = 3) were studied. Video-EEG monitoring showed CPS in all patients. In 13 patients, additional intracranial EEG monitoring demonstrated hippocampal seizure onset in 12 and medial occipital ictal onset in 1 patient. Interictal and ictal dipole modeling using a spherical head model and realistic electrode coordinates were performed. Spatiotemporal dipole mapping of interictal epileptic discharges revealed two distinct dipole patterns. Patients with lesions located in the medial temporal lobe (n = 41) and medial occipital lobe (n = 2) uniformly presented a dipole with an elevation of more than 15 degrees relative to the axial plane. Eight out of ten patients with extratemporal lesions and 1 patient with a pure neocortical temporal lesion had a less stable dipole with an elevation less than 15 degrees relative to the axial plane. Dipole modeling of epochs of early ictal discharges revealed a striking correspondence with the interictal findings in individual patients. Ictal dipole modeling identified the ictal onset zone correctly when compared with intracranial EEG recordings from bilateral hippocampal depth electrodes in patients with medial temporal seizure onset. Mapping of dipoles on MR images of individual patients facilitated clinical interpretation of the EEG data. Interictal and ictal dipole mapping provided additional and clinically relevant information and may obviate the need for intracranial EEG studies in some surgical candidates for refractory CPS.     

Prognostic implication of contralateral secondary electrographic seizures in temporal lobe epilepsy

PURPOSE: Interhemispheric propagation of seizures in temporal lobe epilepsy is frequently noted during intracranial EEG monitoring. We hypothesized that a distinct secondary electrographic seizure (DSES) in the temporal lobe contralateral to primary seizure onset may be an unfavorable prognostic indicator. METHODS: We reviewed intracranial depth electrode EEG recordings, 1-year outcome, and medical records of 51 patients (M 29, F 22: age 15-64 years) who underwent anterior temporal lobectomy during 1988-96. We defined DSES as a seizure that spread to the contralateral temporal lobe and produced distinct contralateral EEG features. The distinct feature was focal involvement of one or two electrode contacts at onset, which starts and evolves independently from the ipsilateral temporal lobe. We considered DSES as the predominant seizure pattern when it occurred in more than one half of the patients' recorded seizures. RESULTS: Only nine of 19 (47%) patients with predominant DSES had a 1-year seizure-free outcome, whereas 27 of 32 (84%) patients without predominant DSES had a 1-year seizure-free outcome (p < 0.01). Bitemporal independent seizures were more common in patients with predominant DSES (9/19 versus 0/32; p < 0.001). CONCLUSION: Our results suggest that distinct contralateral secondary electrographic seizure is a predictor of unfavorable outcome and is also more likely to be associated with bitemporal seizures.     

Analysis of dynamics and propagation of parietal cingulate seizures with secondary mesial temporal involvement

Cingulate-onset seizures, particularly those originating from parietal cingulate regions, are inadequately described and confounded by patterns of propagation. We analyzed scalp and depth electrode recordings in a patient whose seizures originated from a lesion in the right posterior cingulate region and produced secondary seizure activity in ipsilateral mesial temporal structures. Analyses included the matching pursuit (MP) method of time-frequency decomposition and the Gabor atom density (GAD) measure of signal complexity. Although scalp recordings suggested a right temporal onset, seizures recorded with depth electrodes clearly began in the parietal cingulate region before producing a secondary discharge in ipsilateral mesial structures. GAD revealed a significant increase in complexity during ictal cingulate activity and a consistent pattern of subsequent complexity changes in the hippocampus 30 seconds later. MP and GAD measures were valuable supplements to confirm the stereotyped pattern of both time-frequency changes and complexity. This provides additional evidence for pathways between the parietal cingulate region and mesial temporal structures and raises questions as to whether parietal cingulate seizures can produce clinical symptoms independent of regional or remote propagation.     

The localizing value of ictal EEG in focal epilepsy.

OBJECTIVE: To investigate the lateralization and localization of ictal EEG in focal epilepsy. METHODS: A total of 486 ictal EEG of 72 patients with focal epilepsy arising from the mesial temporal, neocortical temporal, mesial frontal, dorsolateral frontal, parietal, and occipital regions were analyzed. RESULTS: Surface ictal EEG was adequately localized in 72% of cases, more often in temporal than extratemporal epilepsy. Localized ictal onsets were seen in 57% of seizures and were most common in mesial temporal lobe epilepsy (MTLE), lateral frontal lobe epilepsy (LFLE), and parietal lobe epilepsy, whereas lateralized onsets predominated in neocortical temporal lobe epilepsy and generalized onsets in mesial frontal lobe epilepsy (MFLE) and occipital lobe epilepsy. Approximately two-thirds of seizures were localized, 22% generalized, 4% lateralized, and 6% mislocalized/lateralized. False localization/lateralization occurred in 28% of occipital and 16% of parietal seizures. Rhythmic temporal theta at ictal onset was seen exclusively in temporal lobe seizures, whereas localized repetitive epileptiform activity was highly predictive of LFLE. Seizures arising from the lateral convexity and mesial regions were differentiated by a high incidence of repetitive epileptiform activity at ictal onset in the former and rhythmic theta activity in the latter. CONCLUSIONS: With the exception of mesial frontal lobe epilepsy, ictal recordings are very useful in the localization/lateralization of focal seizures. Some patterns are highly accurate in localizing the epileptogenic lobe. One limitation of ictal EEG is the potential for false localization/lateralization in occipital and parietal lobe epilepsies.     

Reliability and accuracy of localization by scalp ictal EEG

One hundred forty-four scalp ictal EEGs from 54 patients were analyzed independently by three electroencephalographers for side and lobe of seizure onset. Observers did not know the patients' identities. Accuracy was determined by depth EEG. We found 58 to 60% agreement between observers for lobe, and 64 to 74% for side, of seizure onset; 21 to 38% agreement with depth EEG for lobe, and 46 to 49% agreement for side, of seizure onset; best accuracy for lateralization of seizure onset in temporal lobe seizures, but erroneous in 3 to 17%. More formal criteria are needed before scalp ictal records can be used reliably or accurately for localization.     

Unilateral hippocampal sclerosis with contralateral temporal scalp ictal onset

PURPOSE: To investigate the clinical characteristics and surgical outcomes in patients with unilateral hippocampal sclerosis whose scalp ictal EEG recordings localize to the opposite temporal lobe. METHODS: We retrospectively reviewed the data of all adult patients who had undergone depth electrode implantation for suspected temporal lobe epilepsy (TLE) at UCLA (1993-2000) or the Montreal Neurological Institute (1991-1998) to identify patients who had (a) unilateral hippocampal atrophy, and (b) surface ictal recordings in which the majority of seizures appeared to initiate in the opposite temporal lobe, with few or none that were concordant with the hippocampal atrophy. RESULTS: Of 109 patients with suspected TLE who underwent depth electrode study at the two centers, five patients met the aforementioned criteria. Four of these five had very severe hippocampal atrophy, whereas the fifth had mild atrophy but extensive signal change on magnetic resonance imaging (MRI). Depth electrode recordings in four of the five patients yielded clear ictal onset in the mesial temporal lobe ipsilateral to the imaging abnormality (contralateral to apparent scalp ictal onset). One patient had an unusual bitemporal onset pattern, which was nonetheless suggestive of onset in the sclerotic hippocampus. No patient had intracranial ictal onset contralateral to the imaging abnormality. All patients underwent resection of the structurally abnormal temporal lobe. After follow-up of > or = 2 years, four (80%) of five patients were seizure free, while the fifth showed lesser improvement (class III). CONCLUSIONS: Some patients with severe hippocampal sclerosis (sometimes called a "burned-out hippocampus") have atypical spread of ictal discharges, resulting in apparent gross discordance between imaging and scalp ictal recordings. These patients nonetheless have excellent surgical outcomes on the whole. Whether such patients may forego intracranial recordings requires further study.     

Considerations of secondary temporalization

In generalized forms of epileptic seizure disorder, secondary focal involvement of the temporal lobe may gradually develop. Such signs of "secondary temporalization" may manifest themselves in the seizures type (occurrence of complex partial seizures) and in the EEG. Fourteen observations of secondary temporalization are reported: 3 of them in cases of primary generalized epilepsy and 11 in patients with Lennox-Gastaut syndrome. In 9 patients, additional depth implants were carried out in order to detect a primary focal epileptogenic lesion. Secondary temporalization is likely to be caused by independent paroxysmal activity evolving in the limbic structures (amygdala, hippocampus) due to their role of "low threshold areas." Postconvulsive hypoxic damage of the hippocampus is possible but a much less likely cause of secondary temporal lobe manifestations.     

Neuronal Complexity Loss in Interictal EEG Recorded with Foramen Ovale Electrodes Predicts Side of Primary Epileptogenic Area in Temporal Lobe Epilepsy: A Replication Study

Summary: Purpose: To investigate whether a correct lateralization of the primary epileptogenic area by means of neuronal complexity loss analysis can be obtained from interictal EEG recordings using semi-invasive foramen ovale electrodes. In a previous study with recordings from intrahippocampal depth and subdural strip electrodes it was shown that the dynamics of the primary epileptogenic area can be characterized by an increased loss of neuronal complexity in patients with unilateral temporal lobe epilepsy (TLE).
Methods: Neuronal complexity loss analysis was applied. This analysis method is derived from the theory of nonlinear dynamics and provides a topological diagnosis even in cases where no actual seizure activity can be recorded. We examined interictal EEG recorded intracranially from multipolar foramen ovale electrodes in 19 patients with unilateral TLE undergoing presurgical evaluation.
Results: The primary epileptogenic area was correctly lateralized in 16 of the 19 investigated patients. The misclassification of the side of seizure onset in three patients might be attributed to the larger distance between the foramen ovale electrodes and the mesial temporal structures as compared to intrahippocampal depth electrodes.
Conclusions: Our results confirm the previous findings and provide further evidence for the usefulness of nonlinear time-series analysis for the characterization of the spatiotemporal dynamics of the primary epileptogenic area in mesial temporal lobe epilepsy.