Initial EEG Research Articles

Ictal wideband ECoG: Direct comparison between ictal slow shifts and high frequency oscillations

Objective With advanced electroencephalography (EEG) technology, ‘wideband EEG’ ranging from slow shift to high frequency oscillation (HFO) is clinically available to study human epileptogenesis. The purpose of our study is to clarify the relationship between slow shift, HFO and conventional electrocorticographic (ECoG) change. Methods A patient with right temporal lobe epilepsy who underwent presurgical evaluation with subdural electrodes was studied. Slow shift and HFO were evaluated in 16 habitual seizures with wideband EEG technique (bandpass filter of 0.016–600 Hz). Results Upon seizure occurrence in wideband ECoG, negative slow shifts coexisted with HFO (100–300 Hz) in the ictal onset zone in all investigated seizures. The former always preceded HFO and conventional initial EEG changes by mean value of 1.6 and 20.4 s, respectively. The slow shifts and HFOs were observed only in the restricted ictal onset zone. Conclusions In this particular patient, wideband EEG could delineate both ictal slow shift and HFO to define ictal onset zone, and the earliest occurrence of slow shifts may suggest an early role of glia in slow EEG shift generation than neurons. Significance The time difference of the onset between ictal HFO and slow shift may help to understand epileptogenesis.

Clinical Progress of Epilepsy in Children with Tuberous Sclerosis: Prognostic Factors for Seizure Outcome

The incidence and outcome of epilepsy in tuberous sclerosis (TS) patients have not yet been thoroughly investigated. The aim of this study was to evaluate the clinical features and prognosis of epileptic seizures associated with TS. The medical records of 29 patients who satisfied the diagnostic criteria for TS and were followed up for at least 2 years at the Department of Pediatrics, Chonnam National University Hospital (CNUH), between January 2000 and December 2010 were reviewed. Onset age of seizure, initial electroencephalography (EEG) findings, and efficacy of treatment were evaluated. Brain imaging studies were reanalyzed to determine the number of cortical tubers and subependymal nodules present. A total of 26 (89.6%) cases presented with seizures. In the seizure-controlled group (n=9, 34.6%), the mean number of cortical tubers was 4.5 (range, 0-16) and the mean number of subependymal nodules was 6.2 (range, 0-14). Initial EEG identified epileptiform discharges in 4 (44.5%) of these cases. In the seizure-sustained group (n=17, 58.6%), 10 patients had initial seizures before 1 year of age. In this group, the mean number of cortical tubers was 6.0 (range, 0-20) and the mean number of subependymal nodules was 6.0 (range, 1-11). A total of 15 (88.2%) had epileptiform discharges on their initial EEGs. In three patients who did not show any seizures during the observation period, the mean number of cortical tubers was 1.3 (range, 0-2), and the mean number of subependymal nodules was 4.6 (range, 0-13). Medical intractability of epilepsy in conjunction with TS did not correlate with age at onset of seizure, the number of cortical tubers, or subependymal nodules, but was associated with initial EEG findings.

Transient global amnesia with post-hyperventilation temporal sharp waves—A case report

We report a 55-year-old woman, who presented with transient amnesia for 7h following underwater swimming. There was no evidence of neurological disturbance except global amnesia. Sharp waves in both temporal regions were registered during the initial EEG recording, which was accentuated by hyperventilation. Right hippocampal high signal intensity was observed in DWI performed 56 h after symptom onset. The sharp waves were all disappeared on follow-up EEG recordings.

Presence of epileptiform discharges on initial EEGs are associated with failure of retention on first antiepileptic drug in newly diagnosed cryptogenic partial epilepsy: A 2-year observational study

Approximately two-thirds of the patients with newly diagnosed partial epilepsy remained on their first antiepileptic drug (AED) for 2 years in clinical practice. We aimed to analyze retention on the first AED for 2 years in newly diagnosed cryptogenic partial epilepsy patients in clinical practice and whether the presence of epileptiform discharges on the initial EEG was a predictor of the failure of retention on the first AED. For the purpose of this study, we retrospectively reviewed epilepsy database. On the Epilepsy Database, we found 495 newly diagnosed epilepsy patients who had been followed up for at least 2 years. Of these 495 newly diagnosed epilepsy patients, 172 patients had cryptogenic partial epilepsy. The outcome of this study was the retention rate for the first AED for 2 years. In addition, we analyzed the retention on first AED according to the presence or absence of epileptiform discharges on the initial EEG using Kaplan-Meier survival analysis. Overall, retention rate on the first AED for 2 years was 51%. The main lesion of retention failure was a lack of tolerance. The presence of epileptiform discharges on the initial EEGs was significantly related to the failure of retention on the first AED (p=0.003). In newly diagnosed cryptogenic partial epilepsy, overall retention on the first AED was not significantly different from that in newly diagnosed partial epilepsy. In clinical practice, epileptiform discharges on the initial EEG could predict the failure of retention on the first AED for 2 years.

Diagnostic Pitfalls in a Patient With Posttraumatic Exaggerated Startle Response and Mutistic Stupor

Back to table of contents Previous article Next article LETTERFull AccessDiagnostic Pitfalls in a Patient With Posttraumatic Exaggerated Startle Response and Mutistic StuporAgorastos Agorastos M.D.Christoph Muhtz M.D.Michael Kellner M.D., Ph.D.,Agorastos Agorastos M.D.Search for more papers by this authorChristoph Muhtz M.D.Search for more papers by this authorMichael Kellner M.D., Ph.D.Search for more papers by this author,Published Online:1 Jul 2010https://doi.org/10.1176/jnp.2010.22.3.352.e18AboutSectionsView articleView PDFView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail View articleTo the Editor: The differentiation of organic and psychogenic stupor is of major relevance in clinical practice. Mutistic stupor is a clinical manifestation of many psychiatric disorders in which the basal ganglia, frontal lobes, and limbic system are involved. 1 We report an unusual case of sporadic Creutzfeldt-Jakob disease with mutistic stupor, initially suspected as a posttraumatic dissociative reaction. Case ReportMrs. D, a 62-year-old Caucasian woman, presented to our hospital in December 2008 with mutistic stupor. Her daughter reported an acute onset of symptoms directly after a bombing attack very close to their house in Georgia. Since that point Mrs. D was reputedly numbed, showing avoidance behavior, hyperarousal, exaggerated startle, anxiety, disorientation, dissociation with memory loss, insomnia, and progressive mutism. One month earlier she was attacked by heavily armed criminals in her own apartment. Mrs. D had already been treated with sulpiride and risperidone without showing improvement but experienced extrapyramidal side effects (early dyskinesia, parkinsonism, and orofacial dystonic reactions). A subsequent vast exacerbation of the symptoms, with persisting mutism and akinesia, finally led to the admission in our clinic. Our patient showed a broad spectrum of posttraumatic-typical symptoms following exposure to traumatic events. The history of traumatization, the initial nonpathological neurological status, preadmission outpatient MRI, blood testing and lumbar puncture, as well as the nonspecific alterations of the initial EEG, underlined the hypothesis of a posttraumatic reaction. Only a subsequent conduction of all diagnostic measures and the later-on emerged myoclonias provided enough findings in order to revise this hypothesis: The control MRI displayed bilateral hyperintensities in the basal ganglia, the control EEG showed bi- and triphasic synchronized sharp wave complexes, and the liquor serology elevated 14-3-3 proteins, as typically reported in sporadic Creutzfeldt-Jakob disease patients. 2 , 3Discussion Sporadic Creutzfeldt-Jakob disease is a rare neurodegenerative disease with rapidly progressive course and extensively observed psychiatric symptoms, which appear mostly within 100 days of onset, often including exaggerated startle. 2 , 4 Approximately 10% of these patients are first admitted to psychiatric clinics with erroneous clinical diagnoses. 5 This case demonstrates that symptoms caused by the sporadic onset of Creutzfeldt-Jakob disease may mimic posttraumatic symptoms. Exaggerated startle response and stupor after severe traumatic experiences may sometimes have non-trauma-related etiopathogenesis and require a careful differential diagnostic procedure. Department for Psychiatry and Psychotherapy, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany

Ictal EEG patterns in epilepsy with centro-temporal spikes

Purpose: To describe the EEG pattern of seizures in patients with benign childhood epilepsy with centro-temporal spikes (BCECTS). Methods: The clinical and EEG data of 701 BCECTS patients with at least a 3 years follow-up were reviewed from 10 epilepsy centers. Results: Thirty-four seizures were recorded in 30 patients. Four different ictal EEG patterns (A–D) were identified. The most frequent (pattern A) was characterized by low voltage activity of fast rhythmic spikes, increasing in amplitude and decreasing in frequency, and occurred in 14 children. Pattern B (six patients) was constituted by a discharge of spikes intermixed with sharp waves increasing in frequency and amplitude. Pattern C (seven children) consisted of monomorphic theta which progressively formed a discharge increasing in amplitude and decreasing in frequency. Pattern D (5 children) was characterized by a initial focal depression of the electrical activity, followed by one of the three above described patterns. In 21 out of 28 children, the initial ictal pattern, altered from one pattern to another one. No clinical or EEG feature was predictive of a specific ictal pattern. Discussion: We failed to identify a unique ictal EEG pattern in our patients with BCECTS. The occurrence of per-ictal features, e.g., initial EEG depression or post-ictal slowing, is common and should not be interpreted with prejudice. Alteration of ictal EEG pattern from one to another is not in conflict with the diagnosis of BCECTS.

Herpes Encephalitis Presenting With an Opercular Syndrome and Epilepsia Partialis Continua

The opercular syndrome is a rare form of pseudobulbar palsy that is characterized by automatic-voluntary dissociative weakness of the face in addition to weak masticatory and pharyngeal muscles. It is typically seen in the setting of an acute stroke or in association with various congenital malformations of the cortex. It has also been described rarely in association with herpes encephalitis but with an abnormal cerebrospinal fluid (CSF) cell count. We report on a 65-year-old-man with an opercular syndrome associated with epilepsia partialis continua (EPC) secondary to acute herpes simplex virus encephalitis despite an initial near normal CSF analysis. Initial EEG was unremarkable while CSF analysis revealed changes suggestive of a traumatic tap. An opercular syndrome was diagnosed based on the classic presentation of dysarthria, facial diplegia, and hypersalivation, with corresponding MRI brain changes in the operculum. During admission, EPC developed, with continuous right facial twitching and an electroencephalographic correlate in the left centrotemporal region. The EPC initially responded to intravenous lorazepam. Phenytoin was then added for seizure prophylaxis. Herpes virus DNA was later on detected in the CSF. The patient improved with antiviral treatment except for very mild residual dysarthria. Neurologists should be aware of the possible predilection of the herpes simplex virus for the opercular area and the need to empirically treat for herpes encephalitis even in the setting of near normal initial CSF studies in patients with a suggestive clinical presentation.

Repeated exposure to low-level extremely low frequency-modulated microwaves affects cortex-hypothalamus interplay in freely moving rats: EEG study

Purpose: To compare the effects of repeated exposure to extremely low frequency-modulated microwaves (ELF-MW) on cortical and hypothalamic electroencephalograms (EEG).Materials and methods: In 10 freely moving rats with carbon electrodes implanted into the cortex and dorsomedial hypothalamus, averaged frequency spectra (0.5–30 Hz) of the EEG were studied for five consecutive days either under sham exposures (five rats) or under mixed sham/MW-exposures (five rats). The rats were exposed to ELF-MW (915 MHz, 20-ms pulse duration, ∼0.3 mW/cm2, 4 Hz) intermittently (1-min ‘On’, 1-min ‘Off’) for 10 min (specific absorption rate, SAR, ∼0.7 mW/g on average) several times per day, with 10-min pre- and post-exposure periods.Results: In baseline EEG, the activities of 3.2–6.0 Hz and 17.8–30.5 Hz dominated in the cortex and of 6.0–17.8 Hz in the hypothalamus. This cortical-hypothalamic imbalance was relatively stable at sham-exposures and insensitive to ELF-MW in all frequency ranges but one. ELF-MW increased the beta2 (17.8–30.5 Hz) level in the hypothalamus to a greater extent than in the cortex, causing significant diminishing of the initial EEG bias between them. Moreover, a cumulative phenomenon under repeated exposures to ELF-MW was revealed.Conclusions: These results are in line with evidence that repeated low-level exposure to ELF-MW affects brain functioning and provide an additional approach when analysing underlying mechanisms.

Teaching the Teachers: Data to Benefit School Systems and Doctors about Children with Newly Diagnosed Epilepsy

Neuropsychological Status at Seizure Onset in Children: Risk Factors for Early Cognitive Deficits. Fastenau PS, Johnson CS, Perkins SM, Byars AW, deGrauw TJ, Austin JK, Dunn DW. Neurology 2009;73(7):526–534. OBJECTIVE: This large, prospective, community-based study characterized neuropsychological functioning and academic achievement at the time of the first recognized seizure and identified risk factors for cognitive deficits. METHODS: We compared 282 children (ages 6–14 years, IQ ≥ 70) with a first recognized seizure to 147 healthy siblings on a battery of well-standardized and widely used neuropsychological and academic achievement tests and examined relationships with demographic and clinical variables. RESULTS: In this intellectually normal cohort, 27% with just one seizure and up to 40% of those with risk factors exhibited neuropsychological deficits at or near onset. Risk factors associated with neuropsychological deficits included multiple seizures (i.e., second unprovoked seizure; odds ratio [OR] = 1.96), use of antiepileptic drugs (OR = 2.27), symptomatic/cryptogenic etiology (OR = 2.15), and epileptiform activity on the initial EEG (OR = 1.90); a child with all 4 risks is 3.00 times more likely than healthy siblings to experience neuropsychological deficits by the first clinic visit. Absence epilepsy carried increased odds for neuropsychological impairment (OR = 2.00). CONCLUSIONS: A subgroup of intellectually normal children with seizures showed neuropsychological deficits at onset. Academic achievement was unaffected, suggesting that there is a window early in the disorder for intervention to ameliorate the impact on school performance. Therefore, the risk factors identified here (especially if multiple risks are present) warrant swift referral for neuropsychological evaluation early in the course of the condition.

Magnetoencephalographic Findings in Two Cases of Juvenile Myoclonus Epilepsy

The aim of this study is to investigate the electromagnetic sources of epileptic activity in two patients with juvenile myoclonus epilepsy (JME). The first patient was a 22-year old female with JME diagnosis by the age of 17 years old. Her initial EEG recording showed characteristic paroxysmal generalized activity with polyspike-wave complexes. She was on remission for 9 months. The second patient was a 29-year old male with JME diagnosis by the age 18 of years old. He showed an EEG recording with generalized spike-wave complexes of 3.5-4 Hz and presented a great improvement after therapeutic treatment. The MRI examinations for both patients did not disclose any focal lesions or areas of abnormal signal intensity or enhancement by contrast media. Magnetoencephalography (MEG) was recorded with a 122-channel whole-head system, 5 years after the disease onset for the first patient and 11 years for the second patient. For the first patient dipolar sources of MEG paroxysmal activity were localised at the vermis with extension up to the occipital region, whereas, for the second patient dipolar sources of MEG paroxysmal activity were localised at the cerebellar area (vermis and hemisphere). Implication of the cerebellum in JME, as suggested by MEG data in this study, is in accordance with previous reports employing functional MRI or cerebral blood flow evaluation in JME.

Acute atomoxetine effects on the EEG of children with Attention-Deficit/Hyperactivity Disorder

Although stimulant medications are the most commonly-used treatments for Attention-Deficit/Hyperactivity Disorder (AD/HD), as many as 20% of treated children do not respond clinically to stimulants. This study investigated the effects of an acute dose of atomoxetine, a selective noradrenaline reuptake inhibitor (SNRI), on the electroencephalogram (EEG) and performance of children with AD/HD. An initial pre-medication EEG was recorded during an eyes-closed resting condition. Within two weeks, a second EEG was recorded 1 h after ingestion of 20 mg of atomoxetine. Data were Fourier transformed to provide absolute and relative power estimates for the delta, theta, alpha, beta and gamma bands. Compared to controls, the unmedicated AD/HD children had significantly elevated global absolute and relative delta, with reduced global relative alpha, and absolute and relative gamma, and many topographic differences. Atomoxetine produced significant global increases in absolute and relative beta, with several topographic changes in other bands, and a significant reduction in omission errors on a Continuous Performance Task. These results indicate that SNRIs can produce substantial normalisation of the AD/HD EEG profile, together with behavioural performance improvements. Although EEG changes induced by acute administration of psychostimulants (methylphenidate/dexamphetamine) and atomoxetine are not identical, both classes of AD/HD drugs produce similar EEG band changes. Further analysis of EEG responses to SNRIs and psychostimulants could reveal common neurophysiological processes closely linked to clinical improvement of AD/HD symptoms in response to pharmacotherapy, providing translational markers for clinical efficacy studies and potential translational biomarkers for AD/HD drug discovery.

Neuropsychological status at seizure onset in children

This large, prospective, community-based study characterized neuropsychological functioning and academic achievement at the time of the first recognized seizure and identified risk factors for cognitive deficits. We compared 282 children (ages 6-14 years, IQ > or =70) with a first recognized seizure to 147 healthy siblings on a battery of well-standardized and widely used neuropsychological and academic achievement tests and examined relationships with demographic and clinical variables. In this intellectually normal cohort, 27% with just one seizure and up to 40% of those with risk factors exhibited neuropsychological deficits at or near onset. Risk factors associated with neuropsychological deficits included multiple seizures (i.e., second unprovoked seizure; odds ratio [OR] = 1.96), use of antiepileptic drugs (OR = 2.27), symptomatic/cryptogenic etiology (OR = 2.15), and epileptiform activity on the initial EEG (OR = 1.90); a child with all 4 risks is 3.00 times more likely than healthy siblings to experience neuropsychological deficits by the first clinic visit. Absence epilepsy carried increased odds for neuropsychological impairment (OR = 2.00). A subgroup of intellectually normal children with seizures showed neuropsychological deficits at onset. Academic achievement was unaffected, suggesting that there is a window early in the disorder for intervention to ameliorate the impact on school performance. Therefore, the risk factors identified here (especially if multiple risks are present) warrant swift referral for neuropsychological evaluation early in the course of the condition.

14 & 6Hz positive spikes coinciding with PLEDs

We describe the coincidence of 14 & 6Hz positive spikes with PLEDs in a patient with clonic status epilepticus of the left upper extremity and the persistence of 14 & 6Hz positive spikes after cessation of status. Digital video-EEG recordings were performed using 32-channel EEG equipment (XLTEK, Canada) with all electrodes of the international 10-20 system and additional anterior temporal electrodes in a patient during clonic status epilepticus and 2 months later after cessation of status. The initial EEG during clonic status epilepticus showed right hemispheric PLEDs and right lateral temporal 14 & 6Hz positive spikes in between the PLEDs. Follow up EEG recording 2 months later after cessation of status revealed an absence of PLEDs, a continuous slowing over the right hemisphere and the occipital background of 7Hz. Right lateral temporal 14 & 6Hz positive spikes were recorded in the same frequency and the same localization as in the previous status EEG. This case demonstrates that a hemisphere which is in a status epilepticus as clinically reflected by clonic status of the left hand and PLEDs in the EEG is still capable to produce a benign variant pattern like 14 & 6Hz positive spikes. The generator of 14 & 6Hz positive spikes may still persist despite the presence of severe structural and epileptogenic lesions in the same hemisphere.

Status epilepticus in children with Alpers’ disease caused by POLG1 mutations: EEG and MRI features

Refractory convulsive status epilepticus in infancy and childhood is a rare emergency situation. Metabolic disorders frequently underlie this condition, in particular Alpers' disease caused by POLG1 mutations. Status epilepticus may be the first symptom. A pathognomonic electroencephalography (EEG) signature may facilitate diagnosis of Alpers' disease and allow timely avoidance of valproic acid, which is contraindicated in this disorder because it may trigger fatal liver failure. We present five patients with Alpers' disease caused by mutations in POLG1. Age of onset ranged from 7 months to 10 years. Three of the five children died after 3 to 12 months after onset of status epilepticus. Two of these had liver failure associated with use of valproic acid; liver transplantation in one child did not prevent a fatal neurologic outcome. Convulsive status epilepticus was the first obvious sign of Alpers' disease in all children. All had focal clonic and complex-focal seizures; four of them developed epilepsia partialis continua. In four children, initial EEG showed unilateral occipital rhythmic high-amplitude delta with superimposed (poly)spikes (RHADS). Magnetic resonance imaging (MRI) revealed cortical and thalamic involvement in all, although there were only discrete abnormalities in one child. Metabolic investigations remained normal in three children. Alpers' disease is an important differential diagnosis in childhood refractory convulsive status epilepticus. Its EEG hallmark of RHADS is important for timely diagnosis, management, and counseling.

A 4-month-old Boy with Cardiopulmonary Arrest

<P>This previously healthy 4-month-old boy was transferred from an outside hospital at the parents’ request for a second opinion regarding his neurologic status following cardiopulmonary arrest. Four days previously, he uneventfully received his 4-month immunizations. His father fed him formula and left to take a shower. The baby was placed in the swing while the father was in the shower. Upon returning approximately 15 minutes later, he found the boy slumped over with vomit on his face. He could not palpate a pulse. He picked the baby up and noted that he was limp and not breathing. Because he felt it was fastest for him to get to the hospital by himself, the child drove to the nearest hospital, which is a 5-minute drive. At presentation there, he was noted to be asystolic for at least 20 to 30 minutes before the reestablishment of a pulse. His initial arterial blood gas pH was 6.7. He had upper extremity tonic and clonic movements following resuscitation. He was given ceftriaxone, vancomycin, acyclovir, fosphenytoin, phenobarbital, and transferred to the intensive care unit at the outside hospital. Initial EEG and follow-up EEG 24 hours later each showed diffuse slowing. He stayed there for 8 days prior to transfer.</P>

Levetiracetam as monotherapy for seizures in a neonate with acute lymphoblastic leukemia

Congenital acute lymphoblastic leukemia (ALL) is a relatively rare disorder that is characterized by frequent central nervous system involvement that may increase the risk for seizures. Appropriate choice of anticonvulsant therapy with respect to ongoing oncologic treatment is not established in this age group. We report the case of a neonate with ALL who was successfully treated for seizures with levetiracetam monotherapy. This full-term boy did well until 3 days of age when he had an episode of left extremity jerking (07/06/07). Computed tomography of the head demonstrated extensive multifocal intraparenchymal hemorrhages. Initial EEG demonstrated multifocal epileptiform activity. Patient was loaded with Phenobarbital at 20 mg/kg. Complete blood count revealed leukocytosis (78 × 103/mm 3). Peripheral blood smear contained blastocytes and DNA analysis confirmed B-cell ALL. A second focal seizure was reported on the same day and he was re-loaded with Phenobarbital. Maintenance dosing of Phenobarbital was initiated and no further seizures were noted. A repeat EEG on 7/10/07 remained abnormal with excessive multifocal sharp waves. Continuation of anticonvulsant therapy was recommended. Given concern for interaction between Phenobarbital and planned chemotherapy regimen, oncology requested a non-enzyme inducing anticonvulsant. Phenobarbital was subsequently weaned and Levetiracetam monotherapy initiated at 40 mg/kg/day (07/10/2007). Currently, the patient is seizure free at 8 months of age on Levetiracetam monotherapy. The use of Levetiracetam as monotherapy in neonates has not been formally evaluated and experience is limited. We report the successful use of levetiracetam monotherapy after Phenobarbital load in a neonate with leukemia and localization-related epilepsy.

Sequential EEG findings and symptoms in partial seizures of temporal lobe origin.

45 cases of partial seizures of temporal lobe origin undergoing sequential EEG investigation first with routine and then methohexitone activated EEG, 31 supplemented by sphenoidal electrodes, are reported. Methohexitone activated foci from temporal lobes which had previously not displayed temporal spike or sharp wave discharges in 15 (33.3%) cases. In 11 (24.4%) this was the first evidence of the focus in 15 (33.3%) cases. In 11 (24.8%) this was the first evidence of the focus in either temporal lobe and in 4 (8.9%) the focus was contralateral to one already seen in routine EEG. In 3 (6.7%) cases the sphenoidal electrodes were essential for demonstrating the focus. Methohexitone evoked temporal spikes or sharp waves irrespective of the nature of the initial routine EEG which was either normal, had non "epileptic" temporal abnormalities or abnormalities outside the temporal region. 2 X 2 chi 2 tests, comparing the frequency with which a particular symptom was accompanied by an EEG in a sequence with temporal discharges, showed that only in the case of evolution to generalised tonic/clonic seizures (secondary generalization) was the association statistically significant: chi 2 4.28, P less than 0.025. Similar testing of length of history and frequency of attacks against the frequency with which temporal discharges occurred failed to establish a statistically significant association.

Interhemispheric propagation time and temporal lobe epileptogenicity

Long-term subdural electroencephalographic (EEG) recording was performed in a series of patients with medically intractable complex partial seizures to test the hypothesis that ictal interhemispheric propagation time (IHPT) is correlated with temporal lobe epileptogenicity. In 41 patients, the duration from initial subdural EEG seizure onset to the first appearance of subdural EEG epileptic activity in the contralateral hemisphere (IHPT) was measured in seconds and analyzed for a quantitative relationship to temporal lobe seizure interval (frequency −1), in hours. A statistically significant, nonlinear correlation between IHPT and seizure interval was found (Arctan y = −0.009 x 2 + 0.598 x + 75.187, y = IHPT, in seconds, x = seizure interval, in hours, r = 0.326, d.f. = 39, t = 2.15, p < 0.05). The results suggest that, for seizure intervals less than 33 h, increasing IHPT is associated with increasing seizure interval (i.e. decreasing epileptogenicity). Conversely, for seizure intervals greater than 33 h, decreasing IHPT is associated with increasing seizure interval. Because the relationship between IHPT and seizure interval is a trigonometric (i.e. arctangent) function of a second degree polynomial, small changes in IHPT are associated with substantial changes in seizure interval. These findings suggest that temporal lobe epileptogenicity is a complex, nonlinear function of the electrocorticographic EEG time factor (i.e. IHPT) involved in the transmission of ictal epileptic activity from the seizure focus to the contralateral hemisphere. The results suggest that, on an electrophysiologic basis, patients with temporal lobe epilepsy represent two distinct populations based on seizure interval. The results should improve the understanding of the electrocorticographic pathophysiology of temporal lobe epilepsy. The development of cortical neuromodulation strategies designed to suppress temporal lobe seizures should consider this complex relationship between temporal lobe interhemispheric propagation time and epileptogenicity.

Schlaf, Epilepsie und EEG

The very close and strong relationship between the circadian rhythm and epilepsy has been studied for more than a century. Thus, numerous details of their mutual interactions have been elucidated, and meanwhile a considerable body of knowledge has emerged. In many epilepsy disorders, seizures are activated by sleep or arousal. The extent of this activation depends on the epilepsy syndrome, with idiopathic generalised epilepsies showing the greatest activation. On the other hand, sleep deprivation also enhances the likelihood of seizure occurrence, again more in certain epilepsy disorders than in others. With regard to to the EEG, interictal epileptiform abnormalities are seen more commonly during sleep, namely in the non-rapid eye movement sleep. Besides this increase in frequency, the morphology and distribution of epileptiform potentials, especially generalised ones, may be altered. Sleep deprivation also leads to more frequently occurring epileptiform activity, both in the awake and the sleep stages. Thus, it is reasonable to perform an EEG after sleep deprivation if the initial EEG recordings already included sleep and failed to show epileptiform potentials. This review covers the influence of sleep and sleep deprivation on epileptic seizures and epileptiform activity.

Seizure Aggravation—Evidence that Oxcarbazepine Requires Monitoring

Aggravation of Seizures and/or EEG Features in Children Treated with Oxcarbazepine Monotherapy. Vendrame M, Khurana DS, Cruz M, Melvin J, Valencia I, Legido A, Kothare SV. Epilepsia 2007;48(11):2116–2120. Epub 2007 Jul 21. PURPOSE: Exacerbation of epilepsy may occur following initiation of therapy with antiepileptic drugs (AEDs). The aim of this study is to analyze the clinical and EEG characteristics of a group of pediatric patients with worsening of seizures and/or EEG deterioration while on oxcarbazepine (OXC). METHODS: A retrospective analysis of a clinical database was performed to identify patients with epilepsy treated with OXC over the past 3 years. History, neurological examination, and EEG findings were reviewed to identify any who had developed exacerbation of seizures or new abnormalities on EEG. RESULTS: Of 290 patients on OXC, we identified 12 patients with new onset seizures, all with initial normal neurological exam and normal EEG, who developed either worsening of preexisting seizures, new seizure types, and/or EEG deterioration following introduction of OXC monotherapy. EEG changes were primarily characterized by new onset of generalized epileptiform activity not reported on the initial baseline EEG. Following substitution of OXC with a broad spectrum AED, significant improvement of seizure control and improvement in the EEG was observed. CONCLUSIONS: These findings suggest that OXC can aggravate seizures and/or worsen EEG features in children. Following initiation of therapy with OXC, monitoring of patients with follow-up EEGs may be important, especially in patients who do not show adequate response to therapy.