bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interictal and Ictal EEG Activity in the Basal Ganglia: An SEEG Study in Patients with Temporal Lobe Epilepsy
Authors: Rektor Ivan , Kuba Robert , Brázdil Milan 
Published: March 2003

Summary:  Purpose: The interictal and ictal EEG activity in the basal ganglia in patients with temporal lobe epilepsy were studied during invasive EEG monitoring.Methods: Eight epilepsy surgery candidates, each with a proven mesiotemporal seizure‐onset zone, participated in the study. We used two invasive EEG methods to determine the seizure‐onset zone. In both methods, diagonal electrodes were targeted into the amygdalohippocampal complex via a frontal approach and were passed through the basal ganglia with several leads. We analyzed 16 partial epileptic seizures, four of which became secondarily generalized.Results: No epileptic interictal or ictal discharges were noticed in the basal ganglia. The interictal activity in the basal ganglia was a mixture of low‐voltage beta activity and medium‐voltage alpha–theta activity. When the ictal paroxysmal activity remained localized to the seizure‐onset zone, the activity of the basal ganglia did not change. The spread of epileptic activity to other cortical structures was associated with the basal ganglia EEG slowing to a theta–delta range of 3–7 Hz. This slowing was dependent on the spread of ictal discharge within the ipsilateral temporal lobe (related to the investigated basal ganglia structures); alternatively, the slowing occurred in association with the regional spread of ictal activity from the mesiotemporal region to the temporal neocortex contralaterally to the investigated basal ganglia. Secondary generalization was associated with a further slowing of basal ganglia activity.Conclusions: The basal ganglia do not generate specific epileptic EEG activity. Despite the absence of spikes, the basal ganglia participate in changing or reflect changes in the distribution of the ictal epileptic activity.
Randomized Double‐blind Parallel‐group Study Comparing Cognitive Effects of a Low‐dose Lamotrigine with Valproate and Placebo in Healthy Volunteers
Authors: Aldenkamp A. P. , Arends J. , Bootsma H. P. R. , Diepman L. , Hulsman J. , Lambrechts D. , Leenen L. , Majoie M. , Schellekens A. , De Vocht J. 
Published: March 2003

Summary:  Purpose: This study aimed at investigating the cognitive and mood effects of lamotrigine (LTG) versus valproate (VPA) and placebo (PBO).Methods: By studying the effects in healthy volunteers, it is possible to separate the genuine effects of LTG from the cognitive improvements, caused by better seizure control. The study used a pretest–posttest comparison of 50 mg LTG, 900 mg VPA, or PBO in a double‐blind single‐dummy parallel‐group design with 30 healthy volunteers. Study duration was 12 days (with a last control on day 13). Outcome measures included cognitive tests (FePsy neuropsychological test battery), mood scales (ASL; mood‐rating scale), and a scale for subjective complaints (ABNAS Neurotoxicity scale). Total sleep time was controlled with actigraphic recordings. The results were analyzed by comparing the change over time (pretest with posttest) for the three treatments with Student's t tests.Results: Cognitive tests: significant differences between the treatments were found for measurements of cognitive activation (i.e., three of the four simple reaction‐time measurements showed statistically significant differences in change between PBO and LTG in favor of LTG (p = 0.03; 0.03; 0.04); two of four tests showed statistically significant differences in change between LTG and VPA, both in favor of LTG (p = 0.03; 0.05). Subjective complaints: the ABNAS‐neurotoxicity scale reveals a significant reduction of drug‐related cognitive complaints for the subjects taking LTG, relative to VPA (p = 0.02). Mood rating: significant changes were found on the scale assessing “tiredness,” showing increased tiredness/sedation for VPA relative to PBO (p = 0.02) and on the “timid scale” for LTG reporting “being more at ease” compared with both PBO and VPA (p = 0.02; 0.02). The general direction of change for the mood scales was toward “activation” for LTG (five of six scales improved), whereas for VPA, the reverse effect was found (four of six scales showed a change in the direction of “tiredness/sedation”).Conclusions: Short‐term treatment in normal volunteers with a low dose of LTG resulted in improved cognitive activation on simple reaction‐time measurements, a more positive subjective report about the impact of drug treatment relative to VPA, and mood changes concurring with the activating effect demonstrated by the cognitive tests.
Tactile‐evoked Rolandic Discharges: A Benign Finding?
Authors: Langill Lisa , Wong Peter K. H. 
Published: March 2003

Summary:  Purpose: This retrospective study was undertaken to determine if patients having tactile‐evoked rolandic discharges were a more “benign” patient population than those with spontaneously occurring nontactile rolandic discharges and to determine whether the presence of tactile‐evoked rolandic discharges was a marker for the future development of epilepsy, as previously reported.Methods: During this 8‐year study, 304 patients were seen with rolandic discharges. These patients all had tactile stimulation of their hands and/or feet. They formed two groups: patients with spontaneous rolandic discharges that could not be evoked by tactile stimulation (NT) and patients with spontaneous rolandic discharges that could be enhanced with tactile stimulation (TE). Over a 14‐month period, every patient had tactile stimulation of both hands and both feet, resulting in a third group of patients having rolandic discharges seen only with tapping (TO).Results: Tactile‐enhanced discharges constituted 38.2% of all rolandic discharges. Patients with TE and TO discharges had a higher incidence of normal development and intelligence, normal neurologic examinations, and a lower incidence of seizures and focal or generalized background abnormalities on their EEGs. Only one patient with normal background and no coexisting epileptiform abnormalities had partial motor seizures with corresponding contralateral central discharges. Only two patients who had no seizures at the time of their first EEG subsequently went on to develop seizures. Neither fit the pattern of the seizure disorder described in the literature.Conclusions: It is hypothesized that tactile‐evoked rolandic discharges are a benign, age‐related phenomenon, which do not represent a marker for the future development of epilepsy and are not the interictal electrographic correlate to an already existing seizure disorder.
Cardiac Asystole in Epilepsy: Clinical and Neurophysiologic Features
Authors: Rocamora R. , Kurthen M. , Lickfett L. , Von Oertzen J. , Elger C. E. 
Published: March 2003

Summary:  Purpose: Cardiac asystole provoked by epileptic seizures is a rare but important complication in epilepsy and is supposed to be relevant to the pathogenesis of sudden unexplained death in epilepsy (SUDEP). We sought to determine the frequency of this complication in a population of patients with medically intractable epilepsy and to analyze the correlation between EEG, electrocardiogram (ECG), and clinical features obtained from long‐term video‐EEG monitoring.Methods: Retrospective analysis of the clinical records of hospitalized patients from May 1992 to June 2001 who underwent long‐term video‐/EEG monitoring.Results: Of a total of 1,244 patients, five patients had cardiac asystole in the course of ictal events. In these patients, 11 asystolic events, between 4 and 60 s long in a total of 19 seizures, were registered. All seizures had a focal origin with simple partial seizures (n = 13), complex partial seizures (n = 4), and secondarily generalized seizures (n = 2). One patient showed the longest asystole ever reported (60 s) because of a seizure. Cardiac asystole occurred in two patients with left‐sided temporal lobe epilepsy (TLE) and in three patients with frontal lobe epilepsy (FLE; two left‐sided, one bifrontal). Two patients reported previous cardiac disease, but only one had a pathologic ECG by the time of admission. Two patients had a simultaneous central ictal apnea during the asystole. None of the patients had ongoing deficits due to the asystole.Conclusions: These findings confirm that seizure‐induced asystole is a rare complication. The event appeared only in focal epilepsies (frontal and temporal) with a lateralization to the left side. A newly diagnosed or known cardiac disorder could be a risk factor for ictal asystole. Abnormally long postictal periods with altered consciousness might point to reduced cerebral perfusion during the event because of ictal asystole. Central ictal apnea could be a frequent associated phenomenon.
Ih Blockers Have a Potential of Antiepileptic Effects
Authors: Kitayama Masaomi , Miyata Harue , Yano Michiko , Saito Nobuko , Matsuda Yoshiki , Yamauchi Toshio , Kogure Shinichi 
Published: March 2003

Summary:  Purpose: The h current (Ih) is an inwardly mixed cationic conductance activated by membrane hyperpolarization and distributed predominantly in the apical dendrites of hippocampal pyramidal neurons. To verify a hypothesis that an anomalous hyperpolarization generates an abnormal excitation by way of Ih channels, we examined the effects of Ih blockers (CsCl and ZD7288) on electrically induced paroxysmal discharges (PADs).Methods: Fifty‐three adult male rabbits were used. We measured the PAD threshold elicited by stimulation to the apical dendritic layer of the hippocampal CA1 region before and after injecting 50 μl of each Ih blocker or saline extracellularly into the same region.Results: In Ih blocker injection groups (n = 26), we obtained a significant increase in PAD threshold (1 mM CsCl: 163%, p < 0.01; 10 mM CsCl: 265%, p < 0.01; 100 mM CsCl: 199%, p < 0.01; 100 μM ZD7288: 192%, p < 0.05; 1 mM ZD7288: 246%, p < 0.05). Conversely, we did not obtain the increase in PAD threshold in a saline injection group (n = 10, 107%). The magnitude as well as duration of the effect had a tendency to depend on concentration of Ih blockers, although a saturated or declining tendency was observed with the 100 mM CsCl injection.Conclusions: We concluded that Ih channels might contribute to hippocampal epileptiform discharges in vivo. Our hypothesis for epileptogenesis demonstrated in the present experiment offers an idea to develop a new type of antiepileptic drug based on Ih blockers for the treatment of epileptic disorders refractory to current medications.
EEG in Adult‐onset Idiopathic Generalized Epilepsy
Authors: Yenjun Suthida , Harvey A. Simon , Marini Carla , Newton Mark R. , King Mark A. , Berkovic Samuel F. 
Published: March 2003

Summary:  Purpose: It remains controversial whether adult‐onset idiopathic generalized epilepsy (IGE) is a distinct syndrome or a continuum among IGE syndromes. EEG is the only known biologic marker of IGE and helps differentiate many of its classic subsyndromes. In this study, we looked for the differences in the EEG findings of IGE of classic adolescent onset versus adult onset that may suggest syndromic heterogeneity.Methods: Seventy‐six patients (47 adolescent‐onset IGE, 29 adult‐onset IGE) with a clinical and EEG diagnosis of IGE were included. We defined IGE with age at onset of 11–20 years as adolescent‐onset IGE and age at onset of 20 years or after as adult‐onset IGE. Patients with first‐decade onset of seizures, delayed EEGs, and no EEG available for review were excluded. The first EEG was performed within 24 h of the seizure, and if negative, a sleep‐deprived EEG was done. All EEGs were reviewed in detail with respect to the background activity and the generalized spike–wave (GSW) characteristic.Results: EEGs (87; 56 adolescent‐onset IGE, 31 adult‐onset IGE) were systematically reviewed. Background was normal in all patients. The morphology, amplitude, duration, frequency, occurrence, or activation of the GSW pattern did not differ between these two groups.Conclusions: No differences of EEG features were found between the classic adolescent‐onset and the adult‐onset IGE. This supports the hypothesis that they share common biologic determinants and exist along a life‐long age spectrum of classic IGE.
Interlaboratory Variability in the Quantification of New Generation Antiepileptic Drugs Based on External Quality Assessment Data
Authors: Williams John , Bialer Meir , Johannessen Svein I. , Krämer Günther , Levy René , Mattson Richard H. , Perucca Emilio , Patsalos Philip N. , Wilson John F. 
Published: March 2003

Summary:  Purpose: To assess interlaboratory variability in the determination of serum levels of new antiepileptic drugs (AEDs).Methods: Lyophilised serum samples containing clinically relevant concentrations of felbamate (FBM), gabapentin (GBP), lamotrigine (LTG), the monohydroxy derivative of oxcarbazepine (OCBZ; MHD), tiagabine (TGB), topiramate (TPM), and vigabatrin (VGB) were distributed monthly among 70 laboratories participating in the international Heathcontrol External Quality Assessment Scheme (EQAS). Assay results returned over a 15‐month period were evaluated for precision and accuracy.Results: The most frequently measured compound was LTG (65), followed by MHD (39), GBP (19), TPM (18), VGB (15), FBM (16), and TGB (8). High‐performance liquid chromatography was the most commonly used assay technique for all drugs except for TPM, for which two thirds of laboratories used a commercial immunoassay. For all assay methods combined, precision was <11% for MHD, FBM, TPM, and LTG, close to 15% for GBP and VGB, and as high as 54% for TGB (p < 0.001). Mean accuracy values were <10% for all drugs other than TGB, for which measured values were on average 13.9% higher than spiked values, with a high variability around the mean (45%). No differences in precision and accuracy were found between methods, except for TPM, for which gas chromatography showed poorer accuracy compared with immunoassay and gas chromatography–mass spectrometry.Conclusions: With the notable exception of TGB, interlaboratory variability in the determination of new AEDs was comparable to that reported with older‐generation agents. Poor assay performance is related more to individual operators than to the intrinsic characteristics of the method applied. Participation in an EQAS scheme is recommended to ensure adequate control of assay variability in therapeutic drug monitoring.
Antiepileptic Actions of Neuropeptide Y in the Mouse Hippocampus Require Y5 Receptors
Authors: Baraban Scott C. 
Published: March 2003

Summary:  Purpose: Recent evidence suggests an antiepileptic role for neuropeptide Y (NPY) in the central nervous system. The precise receptor subtypes mediating the inhibitory actions of NPY in the hippocampal formation, however, remain unclear. In vitro studies suggest a role for Y2 receptors in modulating excitatory hippocampal synaptic transmission and epileptiform discharge. In vivo studies implicate Y5 receptors. Here we used pharmacologic tools and Y5‐receptor knockout mice to examine the role of Y5 receptors in mediating the antiexcitatory and antiepileptic actions of NPY in the hippocampal formation.Methods: Hippocampal slices were obtained from age‐matched wild‐type (WT; 129 s3/svimj) and Y5‐receptor knockout (Y5R KO) mice generated on the same background strain. Extracellular or whole‐cell voltage‐clamp recordings were obtained in area CA3 pyramidale. Evoked population spikes or excitatory postsynaptic currents were monitored during bath application of NPY, NPY13‐36, or human pancreatic polypeptide (hPP). In some slices, zero‐magnesium cerebrospinal fluid (CSF) was used to evoke spontaneous epileptiform discharges.Results: NPY and NPY agonists with preference for either Y2 (NPY13‐36) or Y5 (hPP) receptor subtypes caused a significant reduction in population spike and excitatory postsynaptic current (EPSC) amplitudes in slices from WT mice. NPY (and NPY agonists) also suppressed zero‐magnesium epileptiform burst discharge in slices from WT mice. In contrast, bath application of NPY, NPY13‐36, or hPP had no effect in slices from Y5R KO mice.Conclusions: NPY modulates excitatory synaptic transmission and inhibits limbic seizure activity in the mouse hippocampus. The antiepileptic actions of NPY, in the mouse, appear to require activation of hippocampal Y5 receptors.
Progesterone Reduces Pentylenetetrazol‐Induced Ictal Activity of Wild‐Type Mice But Not Those Deficient in Type I 5α‐Reductase
Authors: Frye Cheryl A. , Rhodes Madeline E. , Walf Alicia , Harney Jacob 
Published: March 2003

Summary:  Purpose: To investigate the importance of progesterone (P4) metabolism by the 5α‐reductase type I enzyme in mitigating P4 antiseizure effects.Methods: Ovariectomized, female homozygous and heterozygous 5α‐reductase type I knockout mice (n = 23) and their wild‐type siblings (n = 31) were administered P4 (1.0 mg), and their pentylenetetrazol (PTZ)‐induced ictal behaviors were compared with those of vehicle‐administered mice (n = 49).Results: Mice deficient in the 5α‐reductase type I enzyme administered P4, or vehicle‐administered control mice, had significantly shorter latencies and increased incidence of PTZ‐induced hindlimb extension and death than did wild‐type mice administered P4.Conclusions: These data suggest that P4's metabolism by the 5α‐reductase type I enzyme may mitigate some of P4's antiseizure effects in the PTZ‐induced seizure model.
Electrophysiologic Abnormalities of the Hippocampus in the Pilocarpine/Cycloheximide Model of Chronic Spontaneous Seizures
Authors: Longo Beatriz M. , Sanabria Emilio R. G. , Gabriel Siegrun , Mello Luiz E. A. M. 
Published: March 2003

Summary:  Purpose: Mossy fiber sprouting (MFS) and synaptic reorganization in the dentate gyrus (DG) is considered one of the physiopathologic mechanisms in temporal lobe epilepsy. Supragranular MFS can be blocked by cycloheximide (CHX) without interfering with the genesis of spontaneous recurrent seizures. The aim of this study was to investigate electrophysiologic properties of the hippocampus in the CHX/pilocarpine (CHX/PILO) model as compared with the conventional PILO model.Methods: In vitro electrophysiology was performed 2 months after status epilepticus (SE) induction using extracellular recordings in hippocampal slices from PILO (n = 8) and CHX/PILO animals (n = 10). Field potential responses were evoked in the CA1 and DG regions during perfusion with normal artificial cerebrospinal fluid (aCSF) and aCSF containing 3.5, 5, or 8 mM K+ without or with bicuculline added. Neo‐Timm staining was used for the assessment of supragranular MFS.Results: Evoked potentials in PILO‐ and CHX/PILO‐treated rats displayed small‐amplitude polyspiking activity (epileptiform responses) in CA1 and an apparently normal isolated population spike in DG. More important, PILO and CHX/PILO animals did not differ regarding electrophysiologic abnormalities, even under high K+ or high K+/bicuculline. Analysis of the neo‐Timm staining revealed strong supragranular MFS in PILO‐injected rats and significantly less staining in CHX/PILO rats. Thus, occurrence of abnormal stimulus responses and high K+‐ or high K+/bicuculline‐induced epileptiform activities did not depend on the degree of MFS.Conclusions: We therefore suggest that other mechanisms such as anomalous intrinsic bursting and disinhibition rather than MFS might account for the increased hippocampal hyperexcitability in this model.
Behavior and Physiology of Mice Lacking the GABAA‐Receptor δ Subunit
Authors: Spigelman Igor , Li Zhiwei , Banerjee Pradeep K. , Mihalek Robert M. , Homanics Gregg E. , Olsen Richard W. 
Published: March 2003

Summary:  Purpose: Mice with a targeted disruption of the γ‐aminobutyric acid (A) receptor (GABAAR) δ subunit exhibited spontaneous seizures and a strikingly selective attenuation of responses to neuroactive steroids, but not to other neuromodulators. This study further characterized the behavior and physiology of the δ mutants.Methods: Seizure susceptibility to pentylenetetrazol (PTZ) injection, intracellular recordings, and whole‐cell patch recordings in dentate granule neurons was determined.Results: Susceptibility to PTZ‐induced convulsive seizures was significantly higher in −/− versus +/+ mice. In intracellular recordings, the evoked inhibitory postsynaptic potentials (IPSPs) had much faster decay τ in −/− mutants (25 ± 3.5 ms) compared with +/+ controls (51 ± 5.2 ms). In whole‐cell patch recordings, the decay τ of pharmacologically isolated miniature spontaneous GABAAR‐mediated synaptic currents (mIPSCs) from −/− mice was only slightly, but significantly faster (5.7 ± 0.13 ms; n = 18) than that of +/+ controls (6.8 ± 0.32 ms; n = 20). Furthermore, mIPSC prolongation by bath application of alphaxalone (10 μM), was much smaller in −/− mice (52 ± 12%; n = 3) compared with +/+ littermates (192 ± 14%; n = 3).Conclusions: Faster decay of evoked IPSPs and mIPSCs is consistent with altered GABAAR subunit composition in the δ mutants, but suggests predominant extrasynaptic δ subunit location in the dentate gyrus of normal mice. Faster‐decaying IPSPs likely contribute to the proepileptic phenotype of the δ mutants. Reduced neurosteroid sensitivity might also contribute to seizure susceptibility. It remains to be determined whether δ subunit–containing GABAARs represent the actual target of neurosteroids or whether the behavioral and physiologic sensitivity to neurosteroids is indirectly altered in the δ−/− mice.
Die Bedeutung des Helicobacter – auch jenseits des Magens
Authors: Ferenci P. 
Published: March 2003

Zusammenfassung:Die Entdeckung der Rolle des Helicobacter (H.) pylori als Verursacher des Ulcus pepticum war ein Meilenstein in der Gastroenterologie. Neben der Ulkuskrankheit könnte H. pylori auch bei anderen internen Erkrankungen wie der koronaren Herzkrankheit, der rheumatoiden Arthritis, der hepatischen Enzephalopathie und beim Sjoegren‐Syndrom eine Rolle spielen. Alle diese möglichen Assoziationen sind widersprüchlich und bedürfen weiterer Studien. Andere Helicobacterstämme (H. bilis, H. hepaticus, H. rappani, H. pullorum) werden als Erreger chronischer Leber‐ und Gallenwegserkrankungen sowie von Durchfallserkrankungen diskutiert. Besonders die mögliche Rolle dieser Keime für die Krebsentstehung ist hochinteressant und Gegenstand intensiver Forschungsarbeit.
Die Diagnose der Helicobacter pylori‐Infektion
Authors: Hirschl A. M. 
Published: March 2003

Zusammenfassung:Für die Diagnose der Infektion mit H. pylori stehen, wie für kaum eine andere bakterielle Infektion, eine Vielzahl sowohl invasiver als auch nicht‐invasiver Testverfahren zur Verfügung. Zu den bewährten Tests, die in vielen Studien eine einheitlich hohe Aussagekraft gezeigt haben, zählen der Biopsie‐Ureasetest, Histologie, Kultur und der 13C‐Atemtest. Zu den wichtigsten neuen Testansätzen gehören molekularmikrobiologische Verfahren, die u. a. die Möglichkeit der raschen Bestimmung von Virulenzfaktoren und Resistenzgenen eröffnen, sowie der Antigennachweis im Stuhl. Letztgenanntem Nachweisverfahren dürfte, nach Klärung einiger offener Fragen, in Zukunft große Bedeutung zukommen. Die Verfügbarkeit von Atemtests und Antigennachweis schränkt die Notwendigkeit des Einsatzes serologischer Tests ein, zumal die Mehrzahl der verfügbaren Schnelltests nicht ausreichend verläßlich ist. Gut definierte Indikationen zur Behandlung der Infektion mit H. pylori sind eine wesentliche Voraussetzung für einen vernünftigen Einsatz des diagnostischen Repertoirs.