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.     

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.     

Spatiotemporal neuronal correlates of seizure generation in focal epilepsy

Purpose: Focal seizures are thought to reflect simultaneous activation of a large population of neurons within a discrete region of pathologic brain. Resective surgery targeting this focus is an effective treatment in carefully selected patients, but not all. Although in vivo recordings of single‐neuron (i.e., “unit”) activity in patients with epilepsy have a long history, no studies have examined long‐term firing rates leading into seizures and the spatial relationship of unit activity with respect to the seizure‐onset zone. Methods: Microelectrode arrays recorded action potentials from neurons in mesial temporal structures (often including contralateral mesial temporal structures) in seven patients with mesial temporal lobe epilepsy. Key Findings: Only 7.6% of microelectrode recordings showed increased firing rates before seizure onset and only 32.4% of microelectrodes showed any seizure‐related activity changes. Surprisingly, firing rates on the majority of microelectrodes (67.6%) did not change throughout the seizure, including some microelectrodes located within the seizure‐onset zone. Furthermore, changes in firing rate before and at seizure onset were observed on microelectrodes located outside the seizure‐onset zone and even in contralateral mesial temporal lobe. These early changes varied from seizure to seizure, demonstrating the heterogeneity of ensemble activity underlying the generation of focal seizures. Increased neuronal synchrony was primarily observed only following seizure onset. Significance: These results suggest that cellular correlates of seizure initiation and sustained ictal discharge in mesial temporal lobe epilepsy involve a small subset of the neurons within and outside the seizure‐onset zone. These results further suggest that the “epileptic ensemble or network” responsible for seizure generation are more complex and heterogeneous than previously thought and that future studies may find mechanistic insights and therapeutic treatments outside the clinical seizure‐onset zone.     

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.     

Lateralizing and localizing values of ictal onset recorded on the scalp: evidence from simultaneous recordings with intracranial foramen ovale electrodes

PURPOSE: The value of scalp recordings to localize and lateralize seizure onset in temporal lobe epilepsy has been assessed by comparing simultaneous scalp and intracranial foramen ovale (FO) recordings during presurgical assessment. The sensitivity of scalp recordings for detecting mesial temporal ictal onset has been compared with a "gold standard" provided by simultaneous deep intracranial FO recordings from the mesial aspect of the temporal lobe. As FO electrodes are introduced via anatomic holes, they provide a unique opportunity to record simultaneously from scalp and mesial temporal structures without disrupting the conducting properties of the brain coverings by burr holes and wounds, which can otherwise make simultaneous scalp and intracranial recordings unrepresentative of the habitual EEG. METHODS: Simultaneous FO and scalp recordings from 314 seizures have been studied in 110 patients under telemetric presurgical assessment for temporal lobe epilepsy. Seizure onset was identified on scalp records while blind to recordings from FO electrodes and vice versa. RESULTS: Bilateral onset (symmetric or asymmetric) was more commonly found in scalp than in FO recordings. The contrary was true for unilateral seizure onset. In seizures with bilateral asymmetric onset on the scalp, the topography of largest-amplitude scalp changes at onset does not have localizing or lateralizing value. However, 75-76% of seizures showing unilateral scalp onset with largest amplitude at T1/T2 or T3/T4 had mesial temporal onset. This proportion dropped to 42% among all seizures with a unilateral scalp onset at other locations. Of those seizures with unilateral onset on the scalp at T1/T2, 65.2% showed an ipsilateral mesial temporal onset, and 10.9% had scalp onset incorrectly lateralized with respect to the mesial temporal onset seen on FO recordings. In seizures with a unilateral onset on the scalp at electrodes other than T1/T2, the proportions of seizures with correctly and incorrectly lateralized mesial temporal onset were 37.5 and 4.2%, respectively. Thus the ratio between incorrectly and correctly lateralized mesial temporal onsets is largely similar for seizures with unilateral scalp onset at T1/T2 (16.7%) and for seizures with unilateral scalp onset at electrodes other than T1/T2 (11.2%). The onset of scalp changes before the onset of clinical manifestations is not associated with a lower proportion of seizures with bilateral onset on the scalp, or with a higher percentage of mesial temporal seizures or of mesial temporal seizures starting ipsilateral to the side of scalp onset. In contrast, the majority (78.4%) of mesial temporal seizures showed clinical manifestations starting after ictal onset on FO recordings. CONCLUSIONS: A bilateral scalp onset (symmetric or asymmetric) is compatible with a mesial temporal onset, and should not deter further surgical assessment. Although a unilateral scalp onset at T1/T2 or T3/T4 is associated with a higher probability of mesial temporal onset, a unilateral onset at other scalp electrodes does not exclude mesial temporal onset. A unilateral scalp onset at electrodes other than T1/T2 is less likely to be associated with mesial temporal onset, but its lateralizing value is similar to that of unilateral scalp onset at T1/T2. The presence of clinical manifestations preceding scalp onset does not reduce the localizing or lateralizing values of scalp recordings.     

Morphological Patterns of Seizures Recorded Intracranially

We analyzed the frequency and morphological characteristics of the initial EEG manifestations of spontaneous seizures recorded from depth and subdural electrodes in 26 patients for whom pathological analysis of the area of seizure onset was available after resective surgery. Pathological features considered to be positive findings included well-defined structural lesions (hamartoma, neoplasm) or strictly defined mesial temporal sclerosis. Seizure onset was characterized by the frequency of the rhythmic discharge greater than 2 Hz in the first second and by the presence or absence of periodic low-frequency spikes (less than 2 Hz) preceding this stable change in background frequency. These features were correlated with the presence or absence of pathologic abnormalities in temporal and extratemporal locations. Although all patterns and frequencies of seizure onset were recorded in both medial temporal and extratemporal locations, medial temporal seizure onset was significantly more likely to have high frequency (greater than 13 Hz, p less than 0.00001) and tended to show periodic spikes prior to the seizure when it was associated with medial temporal sclerosis compared to when it was not. Extratemporal seizure onset associated with abnormal pathological substrate was significantly more likely to have a lower frequency (less than 13 Hz, p less than 0.05) and no periodic spikes before seizure onset (p less than 0.00001) than extratemporal seizure onset recorded from areas without pathological findings. Variability of seizure onset frequency was a characteristic of temporal, but not extratemporal, seizures (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

24-hour rhythmicity of seizures in refractory focal epilepsy

The occurrence of seizures in specific types of epilepsies can follow a 24-hour nonuniform or nonrandom pattern. We described the 24-hour pattern of clinical seizures in patients with focal refractory epilepsy who underwent video-electroencephalography monitoring. Only patients who were candidates for epilepsy surgery with an unequivocal seizure focus were included in the study. A total of 544 seizures from 123 consecutive patients were analyzed. Specific time of seizures were distributed along 3- or 4-hour time blocks or bins throughout the 24-hour period. The mean age of the subjects was 37.7 years, with standard deviation of 11.5 years, median of 37. The majority were females (70/56%). The majority of patients had a seizure focus located in the mesial temporal lobe (102/83%) and in the neocortical temporal lobe (13/11%). The remaining patients had a seizure focus located in the extratemporal lobe (8/6%). The most common etiology was mesial temporal sclerosis (86/69.9%). Nonuniform seizure distribution was observed in seizures arising from the temporal lobe (mesial temporal lobe and neocortical temporal lobe), with two peaks found in both 3- and 4-hour bins: 10:00–13:00/16:00–19:00 and 08:00–12:00/16:00–20:00 respectively (p = 0.004). No specific 24-hour pattern was identified in seizures from extratemporal location. The 24-hour rhythmicity of seizure distribution is recognized in certain types of epilepsy, but studies on the topic are scarce. Their replication and validation is therefore needed. Our study confirms the bimodal pattern of temporal lobe epilepsy independently of the nature of the lesion. However, peak times differ between different studies, suggesting that the ambient, rhythmic exogenous factors or environmental/social zeitgebers, may modulate the 24-hour rhythmicity of seizures. Characterization of these 24-hour patterns of seizure occurrence can influence diagnosis and treatment in selected types of epilepsy, such as the case of temporal lobe epilepsy, the most common drug-resistant epilepsy.     

Hypomotor seizures in infants and children

PURPOSE: Hypomotor seizures (characterized by diminished behavioral activity with indeterminate level of consciousness) have been identified as an important seizure type in infants. Our goal was to investigate further the clinical and EEG features of hypomotor seizures. METHODS: We retrospectively reviewed 110 hypomotor seizures from 34 patients recorded with video-EEG. RESULTS: Twenty-seven (79%) patients were younger than 48 months, and seven (21%) were aged 4 to 15 years. Seventy-one (64%) seizures had regional or lateralized EEG onset, arising predominantly from temporal or parietal lobe regions. The other 39 (35%) seizures had generalized onset, usually with abrupt onset of diffuse rhythmic high-amplitude theta activity or diffuse electrodecrement and only rarely (two patients) with slow spike-wave complexes or 3-Hz spike-wave complexes. Hypomotor seizures with generalized EEG onset were significantly shorter than those with regional or lateralized onset (p = 0.01, GEE model). Unsustained head or eye movements and subtle mouth automatisms were commonly seen in hypomotor seizures with either focal or generalized onset. Seventeen percent of hypomotor seizures with focal onset evolved to include version of head and eyes or jerking of one arm, whereas 2% of generalized hypomotor seizures evolved to a cluster of spasms. CONCLUSIONS: Hypomotor seizures may be either focal or generalized. Regional EEG onsets were most often temporal or parietal, suggesting that focal hypomotor seizures may be a bland form of "complex partial" seizures with no or minimal automatisms, seen predominantly in infants. Generalized hypomotor seizures were rarely associated with an ictal pattern of generalized spike-wave complexes, suggesting a different mechanism from absence seizures seen later in life.     

Sleep-Wake Patterns of Seizures in Children With Lesional Epilepsy

This study examined diurnal patterns of seizures and their occurrence during wakefulness and sleep in children with lesional focal epilepsy. We reviewed 332 consecutive children with lesional focal epilepsy and video-electroencephalogram monitoring during a 3-year period. Data were analyzed in relationship to clock time, wakefulness/sleep, and seizure localization. The distribution of lesions in 66 children (259 seizures) included mesial temporal, 29%; neocortical temporal, 18%; frontal, 29%; parietal, 13.5%; and occipital, 12%. Seizures in patients with frontal lesions occurred mostly during sleep (72%). Seizures in mesial temporal (64%), neocortical temporal (71%), and occipital (66%) lesional epilepsy occurred mostly during wakefulness. Temporal lobe seizures occurred more frequently during wakefulness (66%), compared with extratemporal seizures (32%) (odds ratio, 2.67; 95% confidence interval, 1.61-4.42). Temporal lobe seizures peaked between 9:00 am and noon and 3:00-6:00 pm, whereas extratemporal seizures peaked between 6:00-9:00 am. Sleep, not clock time, provides a more robust stimulus for seizure onset, especially for frontal lobe seizures. Temporal lobe seizures are more frequent during wakefulness than are extratemporal seizures. Circadian patterns of seizures may provide additional diagnostic and treatment options, such as differential medication dosing and sleep-schedule adjustments.     

Neocortical temporal lobe epilepsy: intracranial EEG features and surgical outcome.

Patients with neocortical temporal lobe epilepsy (NTLE) may have less favorable outcome with anterior temporal lobectomy than those with mesial temporal foci. The authors analyzed ictal intracranial electroencephalograms (EEGs) in patients with NTLE to identify features that predict surgical outcome. The following intracranial ictal EEG features in 31 consecutive medically intractable NTLE patients were studied: Frequency (i.e., low-voltage fast [>20 Hz], recruiting ictal-onset spikes, ictal-onset rhythms less than 5 Hz, ictal-onset rhythms with repetitive sharp waves between 5 and 20 Hz); extent of ictal onset (focal, sublobar, and lobar); localization within the temporal lobe (anterior, posterior, or regional); and the time to seizure spread outside the temporal lobe (rapid, intermediate, and slow). The average follow-up period was 36.7 months (range, 18 to 60 months). Findings between two outcome groups were compared: class I group (seizure-free) and class II to IV group (persistent seizures). Twenty-one (66.7%) of 31 patients with NTLE were seizure-free. Intracranial EEG features which were significantly associated with seizure-free outcome were focal or sublobar onset, anterior temporal onset, and slow propagation time (P < 0.05). There was a trend for patients with ictal onset morphologies of slow ictal-onset rhythm and repetitive sharp waves to be seizure-free (P = 0.07). Intracranial EEG is helpful in predicting surgical outcome in NTLE patients.     

Speech During Partial Seizures: Intracranial EEG Correlates

Vocalization during a seizure may help predict the location of seizure onset or identify structures ultimately involved in the seizure. Spontaneous vocalization during seizures was studied retrospectively in 22 patients with refractory complex partial seizures evaluated with bilateral intracranial electrodes. Of 22 patients, 12 vocalized during seizures. Seizures were as likely to originate from language-dominant (6/12) as from language-nondominant mesial temporal cortex (6/12). Fluent speech frequently occurred as seizure activity was recorded from language-dominant temporal lobe neocortex (6/12 seizures). Of the patients with well-localized seizure onsets who did not speak (6/10), seizures arose from both language-dominant and -nondominant mesial temporal cortex. We conclude that the presence or absence of vocalizations during a seizure does not reliably indicate the anatomic regions in which the seizure begins or spreads.     

Intractable epilepsy secondary to cyclosporine toxicity in children undergoing allogeneic hematopoietic bone marrow transplantation

The long-term evolution to intractable epilepsy in children treated with cyclosporine administered for graft-versus-host-disease after hematopoietic stem cell transplantation was evaluated. In a group of 185 children treated with cyclosporine after bone marrow transplantation, 15 (8%) presented with acute seizures that were generalized in 7 and focal in 7 and had absence status in 1. Electroencephalography (EEG) and neuroimaging showed predominant abnormalities in the occipital regions. One patient died shortly after the seizure; in seven cases, seizures remitted, whereas relapses were observed in seven others. After the first year, seizures persisted chronically in four cases and evolved to intractable epilepsy. Focal temporal epilepsy was diagnosed in three cases, whereas in the fourth case, a multifocal epilepsy was observed. Magnetic resonance imaging (MRI) detected mesial temporal sclerosis in all of these cases. The risk factors associated with evolution to epilepsy included lower age at transplantation (3-5 years), more than one relapsing seizure in the first year after transplantation, and longer treatment with cyclosporine. Not only can cyclosporine cause acute central nervous system toxicity, it can also determine intractable epilepsy associated with mesial temporal sclerosis.     

Electrophysiologic Analysis of a Chronic Seizure Model After Unilateral Hippocampal KA Injection

PURPOSE: Unilateral intrahippocampal injections of kainic acid (KA) in rats produce spontaneous recurrent limbic seizures and morphologic changes in hippocampus that resemble hippocampal sclerosis in patients with medically refractory mesial temporal lobe epilepsy (MTLE), that form of temporal lobe epilepsy (TLE) associated with hippocampal sclerosis. Interictal in vivo electrophysiologic studies have revealed high-frequency (250-500 Hz) oscillations, termed fast ripples (FRs). These oscillations may uniquely occur in or adjacent to the site of hippocampal KA injection, in areas that generate spontaneous seizures. Similar field potentials also have been demonstrated in the epileptogenic region of patients with TLE. We have now characterized ictal electrographic patterns in this rat model for comparison with those in human TLE and begun to evaluate the role of FRs in the transition to ictus in the KA-treated rat. METHODS: Rats received unilateral intrahippocampal injections of KA and, after the development of spontaneous seizures, were implanted with multiple fixed and moveable microelectrodes for single unit, field potential, and EEG recording. They were then monitored by using video-EEG telemetry for several weeks to capture and evaluate electrographic and behavioral seizure types. Results were correlated with Timm's stain demonstration of mossy fiber sprouting. RESULTS: Low-voltage fast (LVF) and hypersynchronous electrographic ictal-onset patterns were seen in the KA-treated rat that resembled similar ictal-onset patterns in patients with TLE. Hypersynchronous, but not LVF, ictal discharges were associated with recurrent FRs. As in the human, hypersynchronous ictal onsets originated predominantly in hippocampus, whereas LVF ictal onsets more often involved extrahippocampal structures. LVF ictal onsets occurred during wakefulness or paradoxical sleep and were usually associated with motor behavior, whereas hypersynchronous ictal onsets occurred during slow-wave sleep or periods of immobility and were not associated with motor behavior unless there was transition to another ictal electrographic pattern. Mossy fiber sprouting did not correlate with the frequency of ictal EEG discharges exhibited by each rat but was greater in those rats that demonstrated frequent behavioral seizures. CONCLUSIONS: The electrographic features of spontaneous seizures in the KA-treated rat resemble those of patients with medically refractory TLE with respect to EEG pattern and localization. Our data suggest that hypersynchronous ictal onsets represent epileptogenic disturbances in hippocampal circuits, whereas LVF ictal onsets may involve extrahippocampal areas having more direct connections to the motor system. Hypersynchronous seizures may involve the same neuronal mechanisms that generate interictal FRs.     

Electroencephalography,clinical seizures,and neuronal involvement in experimental encephalitis

EEG and clinical seizures in an animal model of herpes simplex encephalitis are presented. After implantation of AM radio transmitters, designed for EEG telemetry, baseline recordings from the rabbits showed preinoculation rhythms in the alpha and beta ranges. The animals were then given a focal encephalitis by inoculation of the olfactory bulb with herpes simplex virus, type 1. Three clinical seizure types were demonstrated and consisted of syndromes analogous to human partial simple, partial complex, and generalized (tonic) seizures. EEG tracings showed that partial complex seizure patterns, manifested clinically as stereotypic circling episodes, were associated with 15-Hz beta rhythms that progressed to a 1.5-Hz delta rhythm with spikes after several circuits, and finally to even slower, polymorphic, 1-Hz delta activity that coincided with the end of the seizure. Episodes of rhythmic facial movements and bruxism were associated with different 2-Hz, high-amplitude EEG tracings. Tonic episodes (with some clonic activity occurring afterward) were characterized by 25-Hz rhythms alternating with activity in the 5–10-Hz range. Interictal tracings in animals noted to have clinical seizures showed nearly continuous rhythmic theta activity (3–8 Hz) not associated with any obvious clinical manifestations. All animals had a viral encephalitis by histologic and immunohistochemical criteria.     

Medial Temporal Objective Lobe Epilepsy: Videotape Analysis of Clinical Seizure Characteristics

Summary: Purpose: The syndrome of temporal lobe epilepsy has been described in great detail. Here we focus specifically on the clinical manifestations of seizures originating in the hippocampus and surrounding mesial temporal structures.
Methods: Seizure origin was confirmed in 67 cases by depth EEG recording and surgical cure after mesial temporal resection.
Results: Among nonlateralized manifestations, we commonly found oral automatisms, pupillary dilatation, impaired consciousness, and generalized rigidity. Appendicular automatisms were often ipsilateral to the seizure focus, whereas dystonia and postictal hemiparesis were usually contralateral. Head deviation, when it occurred early in the seizure, was an ipsilateral finding, but was contralateral to the seizure focus when it occurred late. Clear Ictal speech and quick recovery were found when seizures originated in the non-language-dominant hemisphere, but postictal aphasia and prolonged recovery time were characteristic of seizure origin in the language-dominant hemisphere.
Conclusions: These signs help to define the mesial temporal lobe epilepsy (MTLE) syndrome and often provide information as to the side of seizure origin.     

Relations Between EEG Seizure Morphology, Interhemispheric Spread, and Mesial Temporal Atrophy in Bitemporal Epilepsy

Summary: Purpose: A strong relation exists between lateralization of seizure onset in temporal-lobe epilepsy and atrophic mesial structures measured by volumetric magnetic resonance imaging (MRI). We examined whether this relation extended to subregions of the mesial temporal lobe and whether the trend for seizures to spread contralaterally could be related to the localization of atrophy. Methods: We analyzed 362 seizures (with and without clinical signs) from 23 patients having bitemporal epilepsy in whom intracerebral electrodes were implanted for presurgical evaluation. Patients had measurements of hippocampal and amygdala volumes, including comparison with normal controls. We assessed on EEG the laterialization and localization of seizure onset and the trend to spread to the contralateral side (proportion of seizures that spread for each patient). We included all seizures, independent of the presence of clinical manifestations. These features were related to presence and localization of atrophy. Results: Among the 19 patients with mesial atrophy, agreement between side of prevalent seizure onset and predominant atrophy was found in 10 (53%). From 99 seizures starting in a temporal lobe with atrophy limited to the hippocampus, 67% started simultaneously in amygdala and hippocampus, 20% in hippocampus, and 13% in amygdala. From 137 seizures starting in a temporal lobe with amygdala and hippocampal atrophy, 47% started in amygdala and hippocampus, 48% in hippocampus, and 5% in amygdala. The trend to spread was 45% to the most atrophic side and 62% to the normal or less atrophic side. Conclusions: When examining amygdala and hippocampus in this group of patients with bitemporal epilepsy, regions of seizure onset did not correspond to regions of predominant atrophy. The likelihood that seizures spread contralaterally was not influenced by atrophy in the region targeted by the spread. Precise relation between mesial temporal atrophy and seizures remain to be elucidated.     

Focal Status Epilepticus: Clinical Features and Significance of Different EEG Patterns

PURPOSE: Focal status epilepticus is typically diagnosed by the observation of continuous jerking motor activity, but many other manifestations have been described. EEG evidence of focal status may take several forms, and their interpretation is controversial. We detailed the clinical spectrum of focal status in patients diagnosed by both clinical deficit and EEG criteria and contrasted clinical manifestations in patients with different EEG patterns. METHODS: Patients were diagnosed with a neurologic deficit and discrete recurrent focal electrographic seizures or rapid, continuous focal epileptiform discharges on EEG. Clinical findings were determined by chart review. RESULTS: Of 41 patients with focal status, acute vascular disease was the cause in 21; 10 of 41 had exacerbations of prior epilepsy. A variety of clinical seizure types occurred, both before and after the EEG diagnosis, but the diagnosis was not expected in 28 patients before the EEG. Three had no obvious clinical seizures. Focal motor seizures and an abnormal mental status were the most common manifestations at the time of the EEG. With antiepileptic drugs, almost all had control of clinical seizures, and most improved in mental status. Patients with rapid continuous focal epileptiform discharges were nearly identical in presentation, likelihood of diagnosis, subsequent seizures, response to medication, and outcome to those with discrete seizures on EEG. CONCLUSIONS: Focal status epilepticus may be seen with a wide variety of clinical seizure types or without obvious clinical seizures. The diagnosis is often delayed or missed and should be considered after strokes or clinical seizures when patients do not stabilize or improve as expected. The diagnosis should be made equally whether patients have discrete electrographic seizures or continuous rapid focal epileptiform discharges on the EEG, and the same response to medications and outcome should be anticipated for the two groups.     

Ictal spikes: a marker of specific hippocampal cell loss.

Spontaneous seizures recorded from mesial temporal depth electrodes in the human are commonly manifested by one of two onset patterns: a high frequency discharge or a periodic spike discharge morphologically similar but clearly distinguished from ongoing interictal activity. We categorized medial temporal lobe seizure onset for the presence of periodic ictal spikes at a frequency of less than 2 Hz lasting for more than 5 sec to investigate the relationship of this ictal pattern to anatomical changes in the resected temporal lobe tissue. Fifty-one patients had hippocampal depth electrode recordings of spontaneous seizures, subsequent hippocampal resection, and quantitative cell counts of hippocampal subfields. Thirty-two of these patients had ictal spikes lasting at least 5 sec in more than 50% of their seizures. The presence of ictal spikes was significantly correlated with decreased cells in CA1 only (P = 0.015). The correlation of a common ictal pattern with focal cell loss in the hippocampus suggests that electrophysiological manifestations of seizures provide a clue to the underlying pathological substrate. Ictal spikes may be a cause or result of the cell loss. These observations should be correlated with independent investigations in humans and animal models that reflect the CA1 cell loss associated with temporal lobe epilepsy.     

Ictal EEG wave forms from epidural electrodes predictive of seizure control after temporal lobectomy.

Ictal wave form characteristics--frequency, spatial distribution, and duration--were analyzed for 140 complex partial seizures recorded from epidural strip electrodes implanted in 28 patients. None had abnormalities on imaging studies. All had bilateral electrode placements, unilateral seizure onsets, temporal lobectomies, and were followed for a mean of 33 months postoperatively. Sixteen patients (57%) became free of complex partial seizures: 12 had reductions in seizure frequency of at least 50% but were not seizure-free. The only predictor of the seizure-free state was the presence of low voltage fast activity (LVF), in the alpha or beta ranges, localized to one gyrus. This phenomenon occurred in 14/16 seizure-free patients, 2/12 of others (P < 0.001). As seizures progressed, LVF typically increased in amplitude, propagated, and slowed into the theta range. Wave forms were classified into 8 categories based upon their frequency and morphology. Stepwise discriminant analysis of these wave forms, with consideration of whether they were localized or regional, revealed that both frequency and localization were critical for the post-surgical prognosis. The mere presence of a localized seizure onset was unreliable unless the wave form was taken into account. Well-localized rhythmic activity over 8 Hz at seizure onset from epidural subtemporal electrodes predicts surgical success. Slower rhythms imply greater separation in space and time from seizure onset.     

Ictal spikes: a marker of specific hippocampal cell loss

Spontaneous seizures recorded from mesial temporal depth electrodes in the human are commonly manifested by one of two onset patterns: a high frequency discharge or a periodic spike discharge morphologically similar but clearly distinguished from ongoing interictal activity. We categorized medial temporal lobe seizure onset for the presence of periodic ictal spikes at a frequency of less than 2 Hz lasting for more than 5 sec to investigate the relationship of this ictal pattern to anatomical changes in the resected temporal lobe tissue. Fifty-one patients had hippocampal depth electrode recordings of spontaneous seizures, subsequent hippocampal resection, and quantitative cell counts of hippocampal subfields. Thirty-two of these patients had ictal spikes lasting at least 5 sec in more than 50% of their seizures. The presence of ictal spikes was significantly correlated with decreased cells in CA1 only (P=0.015). The correlation of a common ictal pattern with focal cell loss in the hippocampus suggests that electrophysiological manifestations of seizures provide a clue to the underlying pathological substrate. Ictal spikes may be a cause or result of the cell loss. These observations should be correlated with independent investigations in humans and animal models that reflect the CA1 cell loss associated with temporal lobe epilepsy.