Do Interictal Discharges Promote or Control Seizures? Experimental Evidence from an In Vitro Model of Epileptiform Discharge

Summary: Interictal and ictal discharges are recorded from limbic structures in temporal lobe epilepsy patients. In clinical practice, interictal spikes are used to localize the epileptogenic area, but they also are assumed to promote ictal events. Here I review data obtained from combined slices of mouse hippocampus–entorhinal cortex that indicate an inverse relation between interictal and ictal events. In this preparation, application of 4-aminopyridine or Mg²⁺-free medium induce (a) interictal discharges that originated from CA3 and propagate (via the Schaffer collaterals) to CA1 and entorhinal cortex, to return to the hippocampus through the dentate area; and (b) ictal discharges that initiate in the entorhinal cortex and propagate to the hippocampus via the dentate gyrus. Interictal activity occurs throughout the experiment (up to 6 h), whereas ictal discharges disappear after 1–2 h. Schaffer collateral cut abolishes interictal discharges in CA1, entorhinal cortex, and dentate and reestablishes entorhinal ictal discharges. Moreover, ictal discharge generation in the entorhinal cortex after Schaffer collateral cut is prevented by mimicking CA3 activity with rhythmic electrical stimulation of CA1 outputs. Thus hippocampal interictal activity controls the ability of the entorhinal cortex to generate seizures. It also may be proposed that Schaffer collateral cut may model the epileptic condition in which CA3 damage results in loss of hippocampal control over the entorhinal cortex. In conclusion, these experiments demonstrate that interictal activity controls rather than promotes ictal events, and functional integrity of CA3 constitutes a critical control mechanism in temporal lobe epilepsy.     

New Topographic Mapping of Temporal Lobe Seizures

A unique topographic map has been developed based on EEG data of ictal events originating from the basal/mesiotemporal lobe regions. This technique involves a new mapping method of temporal lobe seizures as opposed to the interictal activity maps of most commercially available software. The map integrates data from sphenoidal electrodes as well as the standard 10–20 surface electrodes recorded with bipolar montages. A basal view is ideal for visualization of onset of temporal lobe ictal discharges recorded with chronic sphenoidal electrodes. We used the last 150 ictal events from 40 patients with basal/mediotemporal lobe epilepsy to develop this technique. Results indicate that a topographic view incorporating sphenoidal and scalp electrodes may provide a useful adjunct for interpretation of EEG recordings and a basis for comparison between and among patient groups for both ictal and interictal epileptic discharges.     

Celiac Disease, Bilateral Occipital Calcifications and Intractable Epilepsy: Mechanisms of Seizure Origin

Summary: Purpose: To elucidate the mechanisms of seizure origin in patients with celiac disease and bilateral occipital calcifications (CEBOC). Individuals with CEBOC frequently present with occipital lobe seizures, but additional lesions and additional attack patterns may occur.
Methods: We studied two men and one woman who had CEBOC. Villous atrophy was revealed in the two patients who underwent duodenal biopsy. All had a comprehensive presurgical evaluation, including prolonged video-EEG recordings. Two had magnetic resonance imaging (MRI) with volumetric study of mesial temporal structures (MRIV). One patient had undergone stereotactic intracranial depth electrode studies (SEEG).
Results: All patients presented with intractable complex partial seizures. Two had partial simple seizures with visual aura. Neurologic examination was normal; one was of normal intelligence, and two were mildly retarded. Neuroimaging studies showed that each had bilateral occipital calcifications as well as epileptiform abnormalities over temporal lobes. In one, MRI showed an additional right frontal lesion, but SEEG demonstrated right occipital lobe seizure origin with anterior spread; this male patient later underwent a right occipital lobe resection. Another with a history of prolonged febrile convulsions had bilateral hippocampal and amygdalar atrophy demonstrated by MRIV.
Conclusions: In one patient, SEEG confirmed that seizures originated in the occipital lobe. The presence of dual pathology was demonstrated in another, raising the possibility of both occipital and temporal seizure onset. The presence of extraoccipital lesions or of mesial temporal atrophy requires SEEG for clarification of seizure onset. In the absence of confounding factors and when laterality can be demonstrated, surgical treatment may be considered.     

Palliative temporal resection for the treatment of intractable bioccipital epilepsy.

RATIONALE: Temporal resection is usually ineffective in patients with occipital seizures. However, when seizures are unilateral occipital resections are now, occasionally, considered. When bilateral seizures and visual field defects exist, occipital resection can not be carried out. When predominantly lateralized, temporal seizure onset can be shown in such patients, palliative temporal resection may be justified. METHODS: We report two patients with medically refractory, bilateral occipital lobe seizures. Clinical and electrophysiological patterns suggested consistent spread of the ictal discharge to temporal lobe structures. Long-term EEG video monitoring was followed by stereoelectroencephalography (SEEG) to assess involvement of temporal and occipital regions symmetrically. RESULTS: Both patients had non-lateralized, elementary visual aura followed by loss of contact, automatisms, frequent falls and occasionally secondary generalization. Brain MR imaging revealed bilateral parieto-occipital ischemic lesions without concomitant temporal volumetric abnormalities. They had bilateral or unilateral visual field defects. Scalp EEGs showed bilateral temporal or temporo-parieto-occipital interictal and ictal epileptic abnormalities. Intracranial SEEG recordings confirmed the presence of multifocal, temporo-occipital epileptic abnormalities. In both however, disabling seizures originated in, or rapidly spread to the right hippocampus. Since occipital resections were inadvisable, both patients underwent selective, right amygdalohippocampectomy. Seizures continued in both (two-year follow-up), but were much less severe, not associated with falling or secondary generalization, not followed by fatigue or headache and with faster recovery. CONCLUSION: When occipital resection is inadvisable because of bilateral or diffuse visual problems, palliative temporal resection may be considered in patients with lesional, bilateral occipital lobe epilepsy, and rapid seizure spread to mesial temporal structures. (Published with videosequences).     

Clinical manifestations of insular lobe seizures: a stereo-electroencephalographic study

PURPOSE: In this study, we report the clinical features of insular lobe seizures based on data from video and stereo-electroencephalographic (SEEG) ictal recordings and direct electric insular stimulation of the insular cortex performed in patients referred for presurgical evaluation of temporal lobe epilepsy (TLE). METHODS: Since our first recordings of insular seizures, the insular cortex has been included as one of the targets of stereo-electroencephalographic (SEEG) electrode implantation in 50 consecutive patients with TLE whose seizures were suspected to originate from, or rapidly to propagate to, the perisylvian cortex. In six, a stereotyped sequence of ictal symptoms associated with intrainsular discharges could be identified. RESULTS: This ictal sequence occurred in full consciousness, beginning with a sensation of laryngeal constriction and paresthesiae, often unpleasant, affecting large cutaneous territories, most often at the onset of a complex partial seizure (five of the six patients). It was eventually followed by dysarthric speech and focal motor convulsive symptoms. The insular origin of these symptoms was supported by the data from functional cortical mapping of the insula by using direct cortical stimulations. CONCLUSIONS: This sequence of ictal symptoms looks reliable enough to characterize insular lobe epileptic seizures (ILESs). Observation of this clinical sequence at the onset of seizures on video-EEG recordings in TLE patients strongly suggests that the seizure-onset zone is located not in the temporal but in the insular lobe; recording directly from the insular cortex should occur before making any decision regarding epilepsy surgery.     

Ictal spitting in non‐dominant temporal lobe epilepsy: an anatomo‐electrophysiological correlation

We report a patient presenting drug‐resistant, non‐dominant temporal lobe epilepsy with ictal spitting and prosopometamorphopsia, both extremely rare semiologies. Second‐phase pre‐surgical monitoring was performed using SEEG due to lesion‐negative imaging and the rare semiology. The seizure onset zone was delimited to the right anterior hippocampus and the temporobasal cortex, with the propagation zone within the entorhinal cortex. Interestingly, direct electrical stimulation to the entorhinal cortex, which was reproduced in a number of trials, evoked spitting without leading to seizures or post‐discharges. After the resection of the epileptogenic zone, the patient remained seizure‐free without AEDs for a follow‐up period of five years (Engel Class 1a). The neuropathology revealed a focal cortical dysplasia type FCD‐Ia. Spectral analysis of intracranial ictal EEG (iEEG) data suggested a possible role of the basal temporal and entorhinal cortex as a necessary node in ictal spitting. [Published with video sequences on www.epilepticdisorders.com ].     

Epileptiform ictal discharges are prevented by periodic interictal spiking in the olfactory cortex

Interictal potentials are commonly observed between seizures in human epilepsies and in animal models of epilepsy. It is uncertain whether interictal spiking in partial epilepsies is causally related with the onset of an ictal discharge. To analyze the reciprocal correlation between interictal and ictal epileptiform events, we performed extracellular recordings in the limbic system of the in vitro isolated guinea pig brain preparation. Arterial perfusion of bicuculline (50 microM) in vitro consistently induced a focal ictal discharge in the hippocampal-entorhinal region that in one third of the experiments was associated with periodic interictal spikes in the piriform cortex. In the absence of active interictal spiking, the piriform cortex was secondarily invaded by the ictal discharge initiated in the hippocampal-entorhinal region, whereas no secondary ictal entrainment was observed in the presence of periodic piriform cortex spikes at circa 0.1 to 0.2 Hz. Similarly, ictal events never occurred when arterial perfusion of bicuculline was preceded by a local injection of the same drug in the piriform cortex, a procedure that induces a sustained interictal spiking. A reduced responsiveness to incoming paroxysmal discharges generated in the hippocampus was observed during the interval between two interictal spikes in the piriform cortex.     

Focal cooling suppresses spontaneous epileptiform activity without changing the cortical motor threshold

PURPOSE: Focal cerebral cooling has been shown to reduce epileptiform activity in animals. There are, however, few reports of this phenomenon in humans. METHODS: Electrocorticography was performed before resection of a right frontal tumor in a patient with partial seizures. Cold saline was applied to the interictal spike focus, and its effect on the epileptiform discharges was observed. RESULTS: Application of cold saline to the spike focus resulted in a transient, complete cessation of spiking. This effect was reproduced with a second application of cold saline. The motor threshold for electrical stimulation remained unchanged during the application of saline. CONCLUSIONS: In this patient with tumor-related epilepsy, focal cooling of the cortex reproducibly abolished interictal epileptiform discharges without changing the motor threshold to electrical stimulation.     

Interictal Spikes Increase Cerebral Glucose Metabolism and Blood Flow: A PET Study

Summary: Purpose: In patients with reflex epilepsy, it is sometimes possible to evoke interictal spikes predictably, thus providing an uncommon but important experimental paradigm for examining the physiological changes produced by epileptiform discharges.
Methods: To examine the changes in regional cerebral blood flow (rCBF) and glucose consumption (rCMRglc) produced by interictal spikes, we performed positron emission tomography (PET) scans with the blood-flow tracer [¹⁵O]H₂O and with [¹⁸F]fluorodeoxyglucose in a patient with fixation-off epilepsy. The scans were performed in states of high and low spike frequency produced by eye closure and opening, respectively.
Results: The rCBF study revealed a focal increase in blood flow associated with the state of increased interictal spiking. The focus was in the posterior portion of the left superior parietal lobule (Talairach coordinates: x: -36, y: -71, z: 39; t = 4.5; p <0.05) and corresponded to the site of maximal ictal EEG abnormality recorded with implanted electrodes. In a volume of interest of 10-mm diameter centered on the t statistic peak in the rCBF study, the mean rCMRglc was 39.1 μmol/100 g/min with eyes open and 44.1 μmol/100 g/min (13% increase) with eyes closed. An identical activation paradigm was used in six normal subjects studied with functional magnetic resonance imaging. In the normal subjects, no significant activation was observed in the parieto-occipital region, indicating that the changes observed in the patient were due to interictal spiking rather than to task performance alone.
Conclusions: Interictal spiking produces focal increases in cerebral blood flow and glucose metabolism.     

Dipole Modeling in Epilepsy Surgery Candidates

Summary: Purpose : The validity and clinical significance of dipole modeling in epilepsy surgery candidates is not fully established.
Patients and Methods : Interictal and ictal dipole modeling was performed in 43 patients with refractory complex partial seizures (CPS) and intracranial structural abnormalities demonstrated with optimum magnetic resonance imaging (MRI: space–occupying, n = 15; atrophic, n = 26; dysplastic, n = 2). Video–EEG monitoring showed CPS in all patients. In 12 patients, additional intracranial EEG monitoring demonstrated hippocampal seizure onset in 11 patients and medial occipital ictal onset in 1.
Results : Spatiotemporal dipole mapping of averaged interictal spikes and epochs of early ictal discharges revealed two distinct dipole patterns. Patients with lesions located in the medial (± lateral) temporal lobe (n = 34) and medial occipital lobe (n = 1) uniformly presented a combined interictal dipole that consisted of a radial and a tangential component with a high degree of elevation relative to the axial plane. Eight of 9 patients with extratemporal lesions had a less stable dipole with a predominant radial component. Ictal dipole modeling identified the ictal onset zone correctly as compared with intracranial EEG recordings from bilateral hippocampal depth electrodes. Ictal dipoles showed a striking correspondence with the interictal dipoles in individual patients.
Conclusions : Interictal and ictal dipole mapping provided additional, reliable, and relevant localizing information in surgical candidates for refractory CPS. Ictal dipole analysis may limit the number of patients who require intracranial electrodes.     

Intralesional recordings and epileptogenic zone in focal polymicrogyria

PURPOSE: Polymicrogyria (PMG) is recognized as an epileptogenic lesion but few data concerning organization of the epileptogenic zone (EZ) are available. METHODS: We analyzed the distribution of the EZ according to Stereo-EEG (SEEG) with intralesional recordings in four patients evaluated for intractable partial epilepsy associated with focal unilateral PMG, involving the posterior temporal region in two, the perisylvian area in one and the temporoparietal junction in the other. All had ictal scalp EEG, high-resolution structural and functional MRI, fluorodeoxyglucose positron emission tomography (FDG-PET), and SEEG. For each patient, several depth electrodes were implanted both within the PMG and in extralesional areas. RESULTS: In three patients, the PMG displayed high-frequency spiking activity. However, interictal and ictal recordings demonstrated a large epileptogenic network, which was more widespread than the PMG, including the mesial temporal structures in two. In another patient, interictal spiking and seizure onset site were located within the hippocampus and outside of the PMG, although it was rapidly involved during seizure spread. Overall, EZ was considered to be larger than the PMG in all patients although hypometabolic areas detected by PET were concordant with EZ. Three patients underwent extensive surgery including the PMG and are seizure free with a follow-up >2 years. DISCUSSION: Although intralesional recordings demonstrated intrinsic epileptogenicity in PMG, our data provide evidence that unilateral focal PMG belongs to a large epileptogenic network extending beyond the MRI lesion. SEEG may be helpful for planning surgery with favorable outcome, providing large resections are feasible, even in apparently focal PMG.     

Fear as the main feature of epileptic seizures

OBJECTIVES: There are circumstances in which partial seizures may be misdiagnosed as acute psychiatric disturbances. In particular, when fear is the prominent feature the patient may be considered for years as having panic attacks. Eight patients in whom fear was the main symptom of the seizures are reported on. Patients who had a proved lack of consciousness during the fits and patients in whom fear was just fear of having a seizure were excluded. The ictal involvement of temporal limbic and frontal structures in those patients with fear of particular intensity was studied. METHODS: The localisation of the epileptogenic zone was assessed by prolonged interictal EEG recordings as well as ictal video-EEG recording of at least one seizure in every patient; five had ictal SPECT and four had chronic stereotactic implantation of depth electrodes (SEEG). In six patients, a cortical resection was performed with an Engel's class 1 outcome (minimum 28 months follow up, except for two patients). RESULTS: Localisations of primary epileptogenic zones were right temporal in three patients, left temporal in three, bitemporal in one, and frontal in one. In all cases, diagnosis of epileptic seizures could be clinically evoked because of the stereotypy of fits and of associated symptoms. The association of a fear sensation, autonomic symptoms, and coordinated behaviour suggests disturbance of a particular system. The SEEG data argue for temporolimbic and prefrontal lobe involvement in the expression of ictal fear. CONCLUSIONS: In intense ictal fear, with coordinated behaviour and autonomic features, the discharge may involve or interfere with a physiological complex information processing network. This network involves orbitoprefrontal, anterior cingulate, and temporal limbic cortices.     

Interictal-ictal interactions and limbic seizure generation.

Interictal discharges are used in clinical practice to localize the epileptogenic focus in patients with partial epilepsy. However, the interaction between interictal and ictal discharges remains debatable. For instance, interictal events may lead to seizure onset in some models of epileptiform discharge. By contrast, in other models, disappearance of interictal activity (for example by activation of GABAB receptors) induces or potentiates ictal events. We have recently obtained new evidence for a control exerted by interictal discharges on ictal activity in rodent combined slices of hippocampus-entorhinal cortex. In this preparation continuous application of 4-aminopyridine induces: (i) interictal activity which initiates in CA3 and propagates via CA1 and subiculum to the entorhinal cortex, and return to the hippocampus through the dentate gyrus; and (ii) ictal discharges, which originate in the entorhinal cortex and propagate via the dentate gyrus to the hippocampus. Ictal discharges disappear over time, while synchronous interictal discharges continue to occur. Lesioning the Schaffer collaterals abolishes interictal discharges in CA1, entorhinal cortex and dentate gyrus and discloses entorhinal ictal discharges that propagate, via the dentate gyrus, to the CA3 subfield. Interictal activity of CA3 origin also prevents the occurrence of ictal events recorded in the entorhinal cortex in Mg(2+)-free medium. Moreover, in both models, ictal discharge generation in the entorhinal cortex after Schaffer collateral cut is prevented by mimicking CA3 activity through rhythmic electrical stimulation of CA1 hippocampal outputs. Hence, our data demonstrate that hippocampus interictal discharges control the expression of electrographic seizures in entorhinal cortex. Sectioning the Schaffer collaterals may model the epileptic condition in which cell damage in the CA3 subfield results in loss of CA3 control over the entorhinal cortex. Hence, the functional integrity of hippocampal CA3 neurons may represent a critical control point in temporal lobe epilepsy.     

Ictal Single Photon Emission Computed Tomography in Occipital Lobe Seizures

Summary: Purpose: Ictal single photon emission computed tomography (SPECT) has been evaluated as an adjunctive localizing technique in temporal lobe epilepsies and, to a lesser degree, in some extratemporal epilepsies. The purpose of this study was to determine whether occipital lobe seizures are associated with distinctive ictal cerebral blood perfusion (rCP) patterns.
Methods : SPECT was used with the tracer ^99mTc HMPAO to image ictal rCP in 6 patients in whom clinical, EEG, and imaging data indicated occipital lobe seizures.
Results : Two patterns of rCP were seen. Four patients had hyperperfusion that was restricted to the occipital lobe, and two patients had hyperperfusion of the occipital lobe and the ipsilateral mesial temporal lobe, with hypoperfusion of the lateral temporal lobe. The latter 2 patients had clinical and surface EEG evidence of temporal lobe involvement in the seizure discharge.
Conclusions : Ictal rCP patterns in occipital lobe seizures are distinct from those in temporal lobe seizures and may vary according to whether or not ipsilateral temporal lobe structures are involved in the ictal discharge.     

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.     

Five-Year Outcome After Epilepsy Surgery in Nonmonitored and Monitored Surgical Candidates

Summary: Purpose : We wished to compare outcome 5 years after temporal lobectomy in 28 patients selected for surgery on the basis of interictal EEG patterns with that in 46 patients who underwent EEG-video monitoring studies as part of their preoperative evaluation during the same era.
Methods : The 28 nonmonitored patients had interictal EEG patterns that demonstrated a consistent, unilateral, anterior-midtemporal epileptiform focus, without discordant findings from other studies. Outcomes were assessed for years 4 and 5 after operation.
Results : Twenty-six of 28 (92.9%) nonmonitored patients were seizure-free or had at least 75% reduction in seizures. Twenty-nine of 46 (63.0%) monitored patients were seizure-free or had at least 75% reduction in seizures. Preoperative interictal EEGs of 29 of these patients showed independently localized bitemporal, ex-tratemporal, midposterior temporal, or diffuse epileptiform patterns. The remaining 17 monitored patients had preoperative strictly unilateral anterior-midtemporal interictal discharges, and their outcome was comparable to the nonmonitored group, with 15 (88.8%) seizure-free or with at least 75% reduction in seizures.
Conclusions : A proportion of candidates for epilepsy surgery can be selected without ictal recordings provided that interictal EEGs demonstrate consistent unilateral anterior-midtemporal epileptiform discharges and that other data are not discordant.     

Periventricular nodular heterotopia: classification, epileptic history, and genesis of epileptic discharges

PURPOSE: Periventricular nodular heterotopia (PNH) is among the most common malformations of cortical development, and affected patients are frequently characterized by focal drug-resistant epilepsy. Here we analyzed clinical, MRI, and electrophysiologic findings in 54 PNH patients to reevaluate the classification of PNH, relate the anatomic features to epileptic outcome, and ascertain the contribution of PNH nodules to the onset of epileptic discharges. METHODS: The patients were followed up for a prolonged period at the Epilepsy Center of our Institute. In all cases, we related MRI findings to clinical and epileptic outcome and analyzed interictal and ictal EEG abnormalities. In one patient, EEG and stereo-EEG (SEEG) recordings of seizures were compared. RESULTS: We included cases with periventricular nodules, also extending to white matter and cortex, provided that anatomic continuity was present between nodules and malformed cortex. Based on imaging and clinical data, patients were subdivided into five PNH groups: (a) bilateral and symmetrical; (b) bilateral single-noduled; (c) bilateral and asymmetrical; (d) unilateral; and (e) unilateral with extension to neocortex. The latter three groups were characterized by worse epileptic outcome. No differences in outcome were found between unilateral PNH patients regardless the presence of cortical involvement. Interictal as well as ictal EEG abnormalities were always related to PNH location. CONCLUSIONS: The distinctive clinical features and epileptic outcomes in each group of patients confirm the reliability of the proposed classification. Ictal EEG and SEEG recordings suggest that seizures are generated by abnormal anatomic circuitries including the heterotopic nodules and adjacent cortical areas.     

Correlation Between Interictal Regional Cerebral Blood Flow and Depth-Recorded Interictal Spiking in Temporal Lobe Epilepsy

Summary: Purpose: Single photon emission computed tomography (SPECT) is used as an adjunctive method in preoperative localization of epileptic foci. In temporal lobe epilepsy (TLE), interictal hypoperfusion is observed in 60–70% of cases. Correlation with ictal EEG changes is observed in ～50–60% of cases. Relationships with interictal EEG have been studied less. We compared interictal SPECT data obtained in 20 patients with their interictal intracerebral electrical activity recorded by depth electrodes to evaluate a potential relationship. Methods: We studied 20 sequential patients whose clinical, surface, and depth EEG data indicated seizure originating in the temporal lobe and who had interictal [^99mTc]hexamethyl-propylene amine oxime (HMPAO)-SPECT stereo-EEG (SEEG). Intracerebral electrodes were placed according to the patient's profile. The interictal extent of epileptiform activity allowed delineation of the irritative zone. Interictal spike frequency was also analyzed semiquantitatively. Visual and numerical SPECT analysis was performed blind to SEEG data. Results: Interictal hypoperfusion was observed in 16 patients, involving the epileptogenic temporal lobe in 14. Except for 1 patient who manifested lateral temporal hypoperfusion corresponding to a mass lesion, two distinctive patterns of hypoperfusion were noted: (a) mesial hypoperfusion (5 patients), and (b) global temporal hypoperfusion (8 patients). In 8 patients, hypoperfusion had also extended into the adjacent cortex. Temporal mesial hypoperfusion was associated with spiking limited to the mesial structures, whereas global temporal hypoperfusion or hypoperfusion extending beyond the temporal lobe was associated with a similar topographic pattern of spikes. Conclusions: Comparison between SPECT and SEEG data collected in the interictal phase indicated that the extent of the hypoperfused area correlated topographically with that of the underlying irritative zone.