Focal cortical dysplasia at the primary somatosensory cortex could manifest both intractable partial epilepsy and cortical reflex myoclonus]

We report a 31-year-old patient who suffered from the left foot motor seizure since 6 years of age. In addition to spontaneous seizures, the seizures tended to be triggered by somatosensory stimulus to the left foot. Recently, he developed irregular myoclonic jerks of the left foot. Neurologically, he had mild impairment of fine movements of the left foot, but otherwise no weakness or sensory disturbance was noted. Interictal spikes were frequently recorded at the vertex region, where ictal discharges also started during the video-EEG monitoring. Electrical stimulation of the left tibial nerve evoked giant cortical components of somatosensory evoked potentials and C-reflex. Magnetoencephalographic study of both interictal and jerk-locked averaged spikes located the equivalent current dipole of both activities at the left foot primary somatosensory cortex (SI), where 3 tesla MRI revealed a focal abnormality consistent with focal cortical dysplasia. The present non-invasive investigation suggests that focal cortical dysplasia at SI could manifest intrinsic, autonomous, epileptogenicity as well as extrinsic, stimulus-sensitive, hyperexcitability, which are clinically manifested as spontaneous seizures and cortical reflex myoclonus, respectively.     

Suppression of Interictal Spikes and Seizures by Stimulation of the Vagus Nerve

The effects of electrical stimulation of the vagus nerve, a proposed treatment for patients with intractable epilepsy, on focal interictal spikes produced by penicillin and EEG secondarily generalized seizures induced by pentylenetetrazol were assessed in rats. Interictal spike frequency was reduced by 33% during 20 s of stimulation (p < 0.001) and remained low for ≤3 min. Amplitude of residual spikes was also decreased. Cardiac and respiratory rates were suppressed. Cooling the nerve proximal to the point of stimulation abolished the EEG and respiratory effects. A similar reduction in spike frequency of 39% was obtained by heating the animals' tail (p < 0.01). Vagal stimulation at onset of seizures reduced mean seizure duration from 30.2 ± 15.7 s without stimulation to 5.0 ± 1.8 s (p < 0.01). Only the EEG equivalent of the clonic phase of the seizure was affected. These findings suggest that vagus nerve stimulation can be a potent but nonspecific method to reduce cortical epileptiform activity, probably through an indirect effect mediated by the reticular activating system.     

Reorganization of the primary somatosensory area in epilepsy associated with focal cortical dysplasia

A 5-year-old boy with focal cortical dysplasia was referred to our hospital because of epileptic seizures. He showed mild weakness of the left hand without sensory disturbance. Brain MRI revealed extensive cortical dysplasia with pachygyria and microgyria around the right central sulcus. On EEG examination, interictal spikes were noted over the right fronto/centro/parietal region. A 37-channel magnetometer revealed that the sources of the spikes were in a small, restricted region of the normal frontal lobe adjacent to the dysplastic brain. Somatosensory evoked magnetic fields indicated that the location of the current source of N2O was in the same area. Our patient shows a unique case of plasticity and reorganization of the somatosensory function due to cortical dysplasia.     

The Effect of Vagus Nerve Stimulation on Epileptiform Activity Recorded from Hippocampal Depth Electrodes

PURPOSE: To assess the effect of vagus nerve stimulation (VNS) on interictal epileptiform activity in the human hippocampus. Clinical studies have established the efficacy of vagus nerve stimulation in patients with epilepsy (VNS Study Group, 1995), although the electrophysiologic effects of VNS on the human hippocampus and mesial temporal lobe structures remain unknown. METHODS: We report a case study in which a patient with an implanted VNS underwent intracranial electrode recording before temporal lobectomy for intractable complex partial seizures. Epileptiform spikes and sharp waves were recorded from a depth electrode placed in the patient's left hippocampus. Spike frequencies and sharp-wave frequencies before and during VNS were compared using both a 5- and a 30-Hz stimulus. Different stimulation rates were tested on different days, and all analyses were performed using a Student's t test. RESULTS: We found no significant differences in spike frequency between baseline periods and stimulation at 5 and 30 Hz. In contrast, stimulation at 30 Hz produced a significant decrease in the occurrence of epileptiform sharp waves compared with the baseline, whereas stimulation at 5 Hz was associated with a significant increase in the occurrence of epileptiform sharp waves. CONCLUSIONS: VNS produces a measurable electrophysiologic effect on epileptiform activity in the human hippocampus. Although a clinical response to VNS did not occur in our patient before surgery, 30-Hz VNS suppressed interictal epileptiform sharp waves that were similar in appearance to those seen during the patient's actual seizures. In contrast, 5-Hz stimulation appeared to increase the appearance of interictal sharp waves.     

Experimental therapy of epilepsy with transcranial magnetic stimulation: lack of additional benefit with prolonged treatment

OBJECTIVE: To investigate the effect of three months of low-frequency repetitive transcranial magnetic stimulation (rTMS) treatment in intractable epilepsy. METHODS: Five patients (four males, one female; ages 6 to 50 years), were enrolled in the study; their epilepsy could not be controlled by medical treatment and surgery was not indicated. rTMS was performed twice a week for three months; patients kept records of seizure frequency for an equal period of time before, during, and after rTMS sessions. rTMS was delivered to the vertex with a round coil, at an intensity 5% below motor threshold. During rTMS sessions, 100 stimuli (five series of 20 stimuli, with one-minute intervals between series) were delivered at a frequency of 0.3 Hz. RESULTS: Mean daily number of seizures (MDNS) decreased in three patients and increased in two during rTMS--one of these was treated for only one month; the best result was achieved in a patient with focal cortical dysplasia (reduction of 43.09% in MDNS). In the whole patient group, there was a significant (p<0.01) decrease in MDNS of 22.8%. CONCLUSION: Although prolonged rTMS treatment is safe and moderately decreases MDNS in a group of patients with intractable epilepsy, individual patient responses were mostly subtle and clinical relevance of this method is probably low. Our data suggest, however, that patients with focal cortical lesions may indeed benefit from this novel treatment. Further studies should concentrate on that patient subgroup.     

Antiepileptic effects of low-frequency repetitive transcranial magnetic stimulation by different stimulation durations and locations.

OBJECTIVE: To evaluate the antiepileptic effect of low-frequency rTMS (repetitive transcranial magnetic stimulation) in the patients with intractable epilepsy. METHODS: We enrolled 35 patients with localization-related epilepsy who had experienced at least one complex partial seizure or a secondarily generalized seizure per week on a constant antiepileptic drug regimen over an 8-week period. rTMS was administered using a Rapid(2) magnetic stimulator with an air-cooled coil at 0.5Hz for 5 consecutive days at 100% of rMT (resting motor threshold). Patients were divided into a focal stimulation group with a localized epileptic focus, or a non-focal stimulation group with a non-localized or multifocal epileptic focus. These two groups were then randomly subdivided into four subgroups depending on the total number of stimulations administered, i.e., 3000 pulse and 1500 pulse subgroups. Weekly seizure frequencies were determined for 8 weeks before and after rTMS. To compare the number of interictal spikes before and after rTMS, EEG was recorded twice before (1st day) and after rTMS (5th day). RESULTS: Mean weekly seizure frequency was non-significantly decreased after rTMS (8.4-->6.8/week, -13.9%). Longer stimulation subgroups (3000 pulses, -23.0%) tended to have fewer seizures than shorter stimulation subgroups (1500 pulses, -3.0%), without statistical significance. TMS stimulation site and structural brain lesions did not influence seizure outcome. However, interictal spikes significantly decreased (-54.9%, P=0.012) after rTMS and they totally disappeared in 6 patients (17.1%, 6/35). CONCLUSIONS: Low-frequency rTMS reduced interictal spikes, but its effect on seizure outcome was not significant. Focal stimulation for a longer duration tended to further reduce seizure frequency. SIGNIFICANCE: These findings may help clinicians to further investigate the therapeutic potential of the rTMS for patients with intractable epilepsy.     

Temporal lobe epilepsy due to hippocampal sclerosis in pediatric candidates for epilepsy surgery.

OBJECTIVE: To characterize the clinical, EEG, MRI, and histopathologic features and explore seizure outcome in pediatric candidates for epilepsy surgery who have temporal lobe epilepsy (TLE) caused by hippocampal sclerosis (HS). METHODS: The authors studied 17 children (4 to 12 years of age) and 17 adolescents (13 to 20 years of age) who had anteromesial temporal resection between 1990 and 1998. RESULTS: All patients had seizures characterized by decreased awareness and responsiveness. Automatisms were typically mild to moderate in children and moderate to marked in adolescents. Among adolescents, interictal spikes were almost exclusively unilateral anterior temporal, as opposed to children in whom anterior temporal spikes were associated with mid/posterior temporal, bilateral temporal, extratemporal, or generalized spikes in 60% of cases. MRI showed hippocampal sclerosis on the side of EEG seizure onset in all patients. Fifty-four percent of children and 56% of adolescents had significant asymmetry of total hippocampal volumes, whereas the remaining patients had only focal atrophy of the hippocampal head or body. Subtle MRI abnormalities of ipsilateral temporal neocortex were seen in all children and 60% of adolescents studied with FLAIR images. On histopathology, there was an unexpectedly high frequency of dual pathology with mild to moderate cortical dysplasia as well as HS, seen in 79% of children and adolescents. Seventy-eight percent of patients were free of seizures at follow-up (mean, 2.6 years). A tendency for lower seizure-free outcome was observed in patients with bilateral temporal interictal sharp waves or bilateral HS on MRI. The presence of dual pathology did not portend poor postsurgical outcome. CONCLUSIONS: TLE caused by HS similar to those in adults were seen in children as young as 4 years of age. Focal hippocampal atrophy seen on MRI often was not reflected in total hippocampal volumetry. Children may have an especially high frequency of dual pathology, with mild to moderate cortical dysplasia as well as HS, and MRI usually, but not always, predicts this finding. Postsurgical seizure outcome is similar to that in adult series.     

Factors in the interictal record predicting an ictal episode: a case study.

This report deals with a patient with intractable seizures, who had 64 subdural electrodes implanted onto the left frontal and temporal cerebral cortex in anticipation of probable seizure surgery. One specific region on the left frontal lobe proved to be the focus for both the interictal spikes and also for the ictal activity. Our goal was to determine what electrical characteristics in the interictal record predicted the ictal episodes. The number of interictal spikes and also the amount of fast activity (15-128/sec) progressively increased before each of the 5 ictal episodes; an analysis showed that the number of spikes and their frequency proved the more significant variable. One other characteristic that changed before the ictal episodes was a great decrease in the interval between spikes as an example of a diminishing variability or increasing periodicity. Thus, the important factors in the interictal record that lead to an ictal event are the number of spikes, the amount of fast activity and the decreasing variability between the spikes.     

Pharmacologic evidence for abnormal thalamocortical functioning in GABA receptor beta3 subunit-deficient mice, a model of Angelman syndrome

PURPOSE: gamma-Aminobutyric acid receptor (GABA(A)r) subunit beta3-deficient mice model Angelman syndrome by displaying impaired learning, abnormal EEG with interictal spikes and slowing, myoclonus, and convulsions. The beta3-subunit deficiency causes a failure of intrathalamic reticular nucleus inhibition, leading to abnormally synchronized thalamocortical oscillations. We postulated that this pathophysiology underlies the abnormal cortical EEG and triggers interictal spikes and seizures, but extrathalamic regions also contribute to interictal spikes and seizures, so that the EEG slowing should reveal an absence-like response profile, whereas spikes and seizures have dual responsiveness to absence and partial-seizure drugs. METHODS: Recording electrodes were implanted over the parietal cortices of wild-type, heterozygotes, and homozygous null mice. In each experiment, EEG was recorded for 45 min, either drug or vehicle administered, and EEG recorded for another 3 h. Each EEG was scored for slow-wave activity, interictal spikes, and seizures by a reader blinded to treatments. RESULTS: Interictal spiking and percentage of time in EEG slowing in heterozygotes were increased by the proabsence drug baclofen (GABA(B)-receptor agonist), whereas CGP 35348 (GABA(B)-receptor antagonist) had the opposite effect. The antiabsence drug ethosuximide markedly suppressed EEG slowing and interictal spiking in heterozygote and null mice. Broad-spectrum clonazepam and valproate were more effective on interictal spiking than on EEG slowing, and fosphenytoin suppressed only interictal spiking. CONCLUSIONS: The results suggest that this model of Angelman syndrome, although not expressing typical absence seizures, is characterized by hypersynchronous thalamocortical oscillations that possess absence-like pharmacologic responsiveness and promote EEG slowing, interictal spikes, and convulsive seizures.     

Nocturnal frontal lobe epilepsy presenting with restless leg syndrome-like symptoms

We describe the case of a 22-year-old male affected by NFLE reporting paroxysmal RLS-like symptoms. The patient was referred to our Sleep Center due to nocturnal paresthesias and cramps involving the left leg and leading to sleep fragmentation. At age 4, the patient presented with secondary generalized seizures preceded by left leg discomfort, controlled on CBZ. After successive therapy discontinuation, leg symptoms built up in frequency and duration until a secondary generalized seizure re-occurred. On CBZ prompt resumption no further GM seizures occurred albeit persistence of night-time frequent cramps and paraesthesia. Sleep EEG demonstrated asymmetric interictal sharp theta on the right posterior frontal areas, whereas brain MRI results were consistent with a Taylor type right frontal cortical dysplasia. CBZ augmentation and add on therapy with LEV led to further frequency reduction of sensory symptoms.     

Postoperative EEG and seizure outcome in temporal lobe epilepsy surgery.

OBJECTIVE: To assess the prognostic value of scalp electroencephalogram (EEG) after epilepsy surgery, we investigated whether postoperative EEG abnormalities (interictal epileptiform discharges, IED; interictal slow activity, ISA) were associated with seizure outcome and other patient characteristics after resective surgery in patients with temporal lobe epilepsy (TLE). METHODS: Sixty-two patients with medically refractory TLE who underwent surgery were studied. Patients were categorized according to etiology (mesiotemporal sclerosis vs. tumors/cortical dysplasias); extent of surgical resection (extensive vs. limited); and amount of preoperative IED on wake EEG (oligospikers, <1 IED/h, vs. spikers). Patients were also classified as seizure-free (SF) or having persistent seizures/auras (not-SF) during follow up visits 1 month and 1 year after surgery. Preoperative 60-min interictal EEGs were evaluated for IED and ISA, and compared to postoperative wake EEGs. RESULTS: Seizures/auras persisted in 16/62 (25.8%) patients at 1 month and in 8/62 (12.9%) at 1 year follow up. ISA was not significantly related to outcome. Of 42 patients with EEG negative for IED at 1 month, 4 were not-SF; at 1 year, one of 44 such patients was not-SF. IED was significantly associated with seizure/aura persistence in patients categorized as mesiotemporal sclerosis and with extensive surgery. Oligospikers and spikers on preoperative EEG showed no differences in the postoperative seizure outcome, excellent in both cases; moreover, the presence of postoperative IEDs indicated auras/seizures persistence apart from the preoperative EEG spike frequency. CONCLUSIONS: Our study showed that the presence of IED of postoperatve EEG strongly indicates seizure/aura persistence. Therefore, serial EEGs should be included in postoperative follow up schedules as a crucial tool in evaluating seizure outcome.     

Topiramate: effect on EEG interictal abnormalities and background activity in patients affected by focal epilepsy

PURPOSE: To evaluate the effects of topiramate (TPM) on interictal epileptiform abnormalities (IEA) and background activity by means of a computerized EEG analysis, in adult patients affected by focal epilepsy, with or without secondarily generalization, treated with TPM as adjunctive therapy or monotherapy. METHODS: Twenty-four patients affected by symptomatic or cryptogenic focal epilepsy underwent long-term video-EEG recording before and after TPM addition (mean dose 175+/-25 mg per day). RESULTS: TPM addition induced a significant reduction of both partial and secondarily generalized tonic-clonic (SGTC) seizures; treatment responder patients (seizure reduction > or = 50%) were 19 out of 24 patients (79.1%), of whom 5 were seizure-free. Quantitative analysis of IEA showed a significant decrease in the mean number of spikes/10 min during TPM therapy ( 4.2+/-4.2 versus 2.2+/-4.4; P<0.003 ). The analysis of spatial distribution of interictal spikes showed that such reduction was more evident at the level of the epileptogenic area rather than on the spreading component. Statistical analysis revealed only a significant decrease of mean relative power of alpha band in the EEG spectral content, recorded at rest in a group of 18 out of 24 epileptic patients during TPM therapy. In addition, during TPM treatment we observed a significant reduction in alpha reactivity without any important changes of alpha indexes (peak frequency and median frequency). CONCLUSION: These findings suggest that TPM has a strong inhibitory effect on IEA, probably acting on the generating processes, and, if used at low dosage and gradually titrated, seems to have only mild interferences with EEG background activity.     

Effect of cortical cooling on interictal epileptiform activities

ObjectiveTo determine if applying chilled solution to exposed cerebral cortex can reduce interictal epileptiform activities in patients during surgery.MethodsElectrocorticography was used to record the epileptiform activity of 12 patients (ages 18–53) undergoing cortical mapping and resection surgery. Interictal spikes were counted at baseline and compared with spikes after applying room temperature and chilled Lactated Ringer's or normal saline solution.ResultsCortical irrigation with 150-cm³, chilled (4 °C) normal saline solution reduced the mean number of interictal spikes from 11.46 to 4.87 spikes per minute (p = 0.04). There was no significant reduction in the epileptic spike frequency when room temperature normal saline was used.ConclusionThe application of chilled solution directly to the cortex can reduce interictal epileptiform activities, suggesting that seizure potential can be suppressed to avoid evoked seizures during intraoperative surgery.     

Stimulus induced and seizure related changes in extracellular potassium concentration in cat thalamus (VPL).

Extracellular potassium activity (ak) and field potentials (fp) were measured in the nucleus ventro-postero-lateralis (VPL) thalami in order to assess the extent of thalamic participation in cortical seizure activity. Small increases (up to 0.7 mmole/l) or decreases (up to 0.2 mmole/l) in ak were induced by electrical stimulation of the contralateral forepaw. These changes in ak were spatially more limited than the simultaneously recorded fp. Similar observations were made during weak electrical stimulation of the somatosensory cortex and during interictal spikes in a cortical penicillin focus. Large and widespread increases in ak to levels of 11.6 mmoles/l and slow negative fps of 8 mV accompanied seizure generation either in a cortical penicillin focus or during intense repetitive electrical stimulation of the cortical surface. Subsequent to such increases ak fell to subnormal levels. The amplitudes and durations of such undershoots were correlated with the amplitudes of the preceding increases in ak. Sometimes thalamic seizures ceases before cortical epileptic episodes. This resulted in a decrease of cortical EEG amplitudes. After ablation of the sensorimotor cortex seizures in forepaw-VPL could be induced by stimulation of the somatosensory cortex. These results further support the conclusion that specific thalamic nuclei participate in seizure generation and may serve as a subcortical route of seizure spread.     

Double-blind, randomized controlled pilot study of bilateral cerebellar stimulation for treatment of intractable motor seizures

PURPOSE: The efficacy and safety of cerebellar stimulation (CS) was reevaluated in a double-blind, randomized controlled pilot study on five patients with medically refractory motor seizures, and especially generalized tonic-clonic seizures. METHODS: Bilateral modified four-contact plate electrodes were placed on the cerebellar superomedial surface through two suboccipital burr holes. The implanted programmable, battery-operated stimulator was adjusted to 2.0 microC/cm(2)/phase with the stimulator case as the anode; at this level, no patient experienced the stimulation. Patients served as their own controls, comparing their seizure frequency in preimplant basal phase (BL) of 3 months with the postimplant phases from 10 months to 4 years (average, eight epochs of 3 months each). During the month after implantation, the stimulators were not activated. The patient and the evaluator were blinded as to the next 3-month epoch, as to whether stimulation was used. The patients were randomized into two groups: three with the stimulator ON and two with the stimulator OFF. After a 4-month postimplantation period, all patients had their stimulator ON until the end of the study and beyond. Medication was maintained unchanged throughout the study. EEG paroxysmal discharges also were measured. RESULTS: Generalized tonic-clonic seizures: in the initial 3-month double-blind phase, two patients were monitored with the stimulation OFF; no change was found in the mean seizure rate (patient 1, 100%, and patient 5, 85%; mean, 93%), whereas the three patients with the stimulation initially ON had a reduction of seizures to 33% (patient 2, 21%; patient 3, 46%; patient 4, 32%) with a statistically significant difference between OFF and ON phase of p = 0.023. All five patients then were stimulated and monitored. At the end of the next 6 months of stimulation, the five patients had a mean seizure rate of 41% (14-75%) of the BL. The second patient developed an infection in the implanted system, which had to be removed after 11 months of stimulation; the seizures were being reduced with stimulation to a mean of one per month from a mean of 4.7 per month (BL level) before stimulation. At the end of 24 months, three patients were monitored with stimulation, resulting in a further reduction of seizures to 24% (11-38%). Tonic seizures: four patients had these seizures, which at 24 months were reduced to 43% (10-76%). Follow-up surgery was necessary in four patients because of infection in one patient and lead/electrode displacement needing repositioning in three patients. The statistical analysis showed a significant reduction in tonic-clonic seizures (p < 0.001) and tonic seizures (p < 0.05). CONCLUSIONS: The superomedial cerebellar cortex appears to be a significantly effective and safe target for electrical stimulation for decreasing motor seizures over the long term. The effect shows generalized tonic-clonic seizure reduction after 1-2 months and continues to decrease over the first 6 months and then maintains this effectiveness over the study period of 2 years and beyond.     

Intracranial EEG substrates of scalp EEG interictal spikes

PURPOSE: To determine the area of cortical generators of scalp EEG interictal spikes, such as those in the temporal lobe epilepsy. METHODS: We recorded simultaneously 26 channels of scalp EEG with subtemporal supplementary electrodes and 46 to 98 channels of intracranial EEG in 16 surgery candidates with temporal lobe epilepsy. Cerebral discharges with and without scalp EEG correlates were identified, and the area of cortical sources was estimated from the number of electrode contacts demonstrating concurrent depolarization. RESULTS: We reviewed approximately 600 interictal spikes recorded with intracranial EEG. Only a very few of these cortical spikes were associated with scalp recognizable potentials; 90% of cortical spikes with a source area of >10 cm(2) produced scalp EEG spikes, whereas only 10% of cortical spikes having <10 cm(2) of source area produced scalp potentials. Intracranial spikes with <6 cm(2) of area were never associated with scalp EEG spikes. CONCLUSIONS: Cerebral sources of scalp EEG spikes are larger than commonly thought. Synchronous or at least temporally overlapping activation of 10-20 cm(2) of gyral cortex is common. The attenuating property of the skull may actually serve a useful role in filtering out all but the most significant interictal discharges that can recruit substantial surrounding cortex.     

The Absence of Interictal Spikes with Documented Seizures Suggests Extratemporal Epilepsy

PURPOSE: To determine the demographic and clinical characteristics of patients who have documented epileptic seizures on long-term video-EEG monitoring who do not have interictal spikes. METHODS: The records of 1,223 monitoring studies from 919 patients who underwent noninvasive long-term video-EEG monitoring were reviewed. In 28 patients (3.0% of monitored patients, 4.4% of patients with electrographic evidence of epilepsy), no interictal spikes were found despite the occurrence of at least one recorded electrographic seizure. The demographic, medical, neuropsychological, and EEG data of these patients were compared with those of 28 matched control patients with documented interictal spikes. RESULTS: Extratemporal seizures were significantly more frequent in the patients with at least one recorded epileptic seizure but without interictal spikes compared with patients with epileptic seizures and interictal spikes (p = 0.031). The only other significant difference between the groups (p = 0.016) was a later age at seizure onset (18.3 vs. 10.7 years) for the patients without interictal spikes. Age at evaluation, gender, handedness, clinical seizure type, family history of epilepsy, history of febrile seizures, neuropsychological testing, and neurologic and psychiatric history did not differ between the two groups. CONCLUSIONS: In patients with documented epilepsy without interictal spikes on EEG monitoring, the possibility of an extratemporal focus should be considered.     

Interictal afterdischarge in focal penicillin epilepsy: thalamocortical unit activity

The involvement of thalamic versus cortical structures for the initiation and maintenance of brief interictal afterdischarge was evaluated by recording extracellularly units and field potentials from different subcortical and cortical sites. Afterdischarge oscillations at 16 to 22/s that followed interictal spikes with a delay of 170 to 220 ms usually appeared 10 to 30 min after the topical application of penicillin to the cat's precruciate cortex. Units in the ventrolateral nucleus of the thalamus fired in burst discharges during cortical afterdischarge and less reliably during the cortical interictal spike. In contrast, units recorded at the cortical penicillin focus and homologous contralateral site remained silent during afterdischarge but had a typical burst discharge during the interictal spike. Although these data support a thalamic basis for the rhythm, the lack of an afterdischarge-like oscillation in the thalamic field potential and the independent appearance of afterdischarge and cortical recruiting waves elicited by stimulation of the nucleus reticularis would favor its cortical origin. In accordance with its frequency characteristics and data gained from earlier cooling studies we suggest a cortical mechanism requiring thalamic triggering for the generation of afterdischarge.     

Frontal lobe epilepsy may present as myoclonic seizures

We describe a patient with seizures arising from right anterior–inferior frontal lobe presenting as myoclonic epilepsy. A 19-year-old man had experienced frequent paroxysmal bilateral myoclonic jerks involving his upper arms, shoulders, neck, and upper trunk since the age of 10. His baseline EEG showed intermittent right frontal spikes, and his ictal EEG showed rhythmic sharp theta discharges in the same area. MRI revealed cortical dysplasia in the right inferior frontal gyrus, and ictal–interictal SPECT analysis by SPM showed increased signal abnormality in this region. Diffusion tensor imaging (DTI) showed defects in fasciculi in the same area. These findings suggest that frontal lobe epilepsy should be considered in some patients with myoclonic seizures.     

What is more harmful,seizures or epileptic EEG abnormalities? Is there any clinical data?

Cognitive impairment is a common and often devastating co‐morbidity of childhood epilepsy. While the aetiology of the epilepsy is a critical determinant of cognitive outcome, there is considerable evidence from both rodent and human studies that indicate that seizures and interictal epileptiform abnormalities can contribute to cognitive impairment. A critical feature of childhood epilepsy is that the seizures and epileptiform activity occur in a brain with developing, plastic neuronal circuits. The consequences of seizures and interictal epileptiform activity in the developing brain differ from similar paroxysmal events occurring in the relatively fixed circuitry of the mature brain. In animals, it is possible to study interictal spikes independently from seizures, and it has been demonstrated that interictal spikes are as detrimental as seizures during brain development. In the clinic, distinguishing the differences between interictal spikes and seizures is more difficult, since both typically occur together. However, both seizures and interictal spikes result in transient cognitive impairment. Recurrent seizures, particularly when frequent, can lead to cognitive regression. While the clinical data linking interictal spikes to persistent cognitive impairment is limited, interictal spikes occurring during the formation and stabilization of neuronal circuits likely contribute to aberrant connectivity. There is insufficient clinical literature to indicate whether interictal spikes are more detrimental than seizures during brain development.