bluuebunny/crossref_metadata_2025_split huggingface dataset:
Platelet 3H Ketanserin Binding in Tension‐type Headache
Authors: Shukla R. , Husain M. , Tandon R. , Khanna V.K. , Nag D. , Dikshit M. , Srimal R.C. , Seth P.K. 
Published: March 2003

Objective.—The present study was undertaken to investigate the alterations in platelet 5‐HT2 receptor binding in patients with tension‐type headache.Background.—Serotonin (5‐HT) has an important but complex role in pain modulation. The involvement of serotonin in tension‐type headache has been investigated by studying serotonin in peripheral blood, but results have been inconclusive. There are, however, only a few investigations in which the status of platelet serotonin transporters has been studied by 3H imipramine and 3H paroxetine. The present study was undertaken to investigate alterations in platelet 5‐HT2A receptors using 3H ketanserin as a ligand.Methods.—Platelet 3H ketanserin binding was studied in 14 patients with tension‐type headache and in 15 healthy controls. The binding characteristics, equilibrium dissociation constant and maximal number of binding sites were determined by Scatchard analysis.Results.—There was no change in the equilibrium dissociation constant in the patients with headache as compared to the control group, but subgroup analysis revealed that patients with tension‐type headache with a headache index of less than 360 had a significantly lower equilibrium dissociation constant as compared to those with a headache index of more than 360; there was a significant correlation between the equilibrium dissociation constant and the headache index. A significant decrease was observed in the maximal number of binding sites in tension‐type headache. No correlation was observed between the maximal number of binding sites and age, duration of illness, or headache intensity.Conclusions.—The findings of the present study show that there is a decrease in the number of binding sites of 5‐HT2A receptors in some patients with tension‐type headache, suggesting postsynaptic serotonergic dysfunction and the involvement of serotonin in that group.
Tolerability and Safety of Frovatriptan With Short‐ and Long‐term Use for Treatment of Migraine and in Comparison With Sumatriptan
Authors: Géraud Gilles , Spierings Egilius L.H. , Keywood Charlotte 
Published: March 2003

Objective.—To evaluate the tolerability and safety of frovatriptan 2.5 mg in patients with migraine.Background.—Frovatriptan is a new, selective serotonin agonist (triptan) developed for the acute treatment of migraine. Dose range‐finding studies identified 2.5 mg as the dose that conferred the optimal combination of efficacy and tolerability.Methods.—The tolerability and safety of frovatriptan 2.5 mg were assessed during controlled, acute migraine treatment studies, including a study that compared frovatriptan 2.5 mg with sumatriptan 100 mg, as well as a 12‐month open‐label study during which patients could take up to three doses of frovatriptan 2.5 mg within a 24‐hour period. Safety and tolerability were assessed through the collection of adverse events, monitoring of heart rate and blood pressure performance of 12‐lead electrocardiogram, hematology screen, and blood chemistry studies.Results.—In the short‐term studies, 1554 patients took frovatriptan 2.5 mg and 838 took placebo. In the 12‐month study, 496 patients treated 13  878 migraine attacks. Frovatriptan was well tolerated in the short‐ and long‐term studies with 1% of patients in the short‐term studies and 5% of patients in the long‐term study withdrawing due to lack of tolerability. The incidence of adverse events was higher in the frovatriptan‐treated patients than in the patients who took placebo (47% versus 34%) and the spectrum of adverse events was similar. When compared to sumatriptan 100 mg, significantly fewer patients taking frovatriptan experienced adverse events (43% versus 36%; P=.03) and the number of adverse events was lower (0.62 versus 0.91), there were also fewer adverse events suggestive of cardiovascular symptoms in the frovatriptan group. Analysis of the entire clinical database (n=2392) demonstrated that frovatriptan was well tolerated by the patients regardless of their age, gender, race, concomitant medication, or the presence of cardiovascular risk factors. No effects of frovatriptan on heart rate, blood pressure, 12‐lead electrocardiogram, hematology screen, or blood chemistry were observed. No patient suffered any treatment‐related serious adverse event.Conclusions.—Short‐ and long‐term use of frovatriptan 2.5 mg was well tolerated by a wide variety of patients. Frovatriptan treatment produced an adverse events profile similar to that of placebo, and in a direct comparison study was better tolerated than sumatriptan 100 mg.
Heart Rate and Heart Rate Variability Changes in the Intracarotid Sodium Amobarbital Test
Authors: Ahern Geoffrey L. , Sollers John J. , Lane Richard D. , Labiner David M. , Herring Anne M. , Weinand Martin E. , Hutzler Ronald , Thayer Julian F. 
Published: March 2003

Summary:  Purpose: Changes in heart rate and heart rate variability have been found in prior studies performed during the intracarotid sodium amobarbital (ISA) test. However, these results are not entirely consistent with current models of differential cerebral involvement in the modulation of the heart. This study was designed to re‐investigate this topic with a larger N than has heretofore been used.Methods: The electrocardiogram was recorded during left and right ISAs in 73 subjects. Raw heart rate and heart rate variability were calculated.Results: Raw heart rate increased during inactivation of either hemisphere, but more so for the right hemisphere. Heart rate variability changes consistent with decreasing parasympathetic tone also were found to occur during either ISA, but to a significant degree, only during right ISA.Conclusions: The right hemisphere appears to have a greater role in cerebral regulation of cardiac function, perhaps by virtue of the modification of parasympathetic effects.
Epilepsy in Estonia: A Quality‐of‐Life Study
Authors: Herodes Marju , Õun Andre , Haldre Sulev , Kaasik Ain‐Elmar 
Published: March 2003

Summary: Purpose: To study the impact of epilepsy and its treatment on people with epilepsy in Estonia and to analyze how it is affected by the characteristics of epilepsy.Methods: Clinical and demographic data about patients were obtained from medical notes and mailed self‐completed questionnaires (including the RAND 36‐Items Health Survey 1.0 (RAND‐36)).Results: Information was collected from 203 patients aged 20–74 years, who all had active epilepsy. A third of the respondents had been seizure free during the last year. Eighty‐four percent were receiving monotherapy. More than half of respondents felt stigmatized by epilepsy, 24.7% of them highly so. A third were working full‐time, 31.9% were underemployed workers, and 11%, unemployed. Sixty‐two percent of these same unemployed or underemployed workers considered their epilepsy to be a significant reason for this situation. Overall, 44% believed they had been treated unfairly at work or when trying to get a job. Study respondents scored lower in all domains on the RAND‐36 than did persons from the control group. The biggest differences were found in five domains: Social functioning, Role limitations–physical, Role limitations–emotional, General health, and Vitality.Conclusions: The clinical characteristics of this study were similar to those of most other series of prevalence cases of epilepsy. The level of employment among persons with epilepsy was not lower than that in the general population. The percentage of stigmatization was high. There were significant differences in the way respondents scored on the stigma scale and on the RAND‐36 domains when measuring their health status, depending above all on seizure frequency and type.
The Effects of Remifentanil on Epileptiform Discharges during Intraoperative Electrocorticography in Patients Undergoing Epilepsy Surgery
Authors: Wass C. Thomas , Grady Robert E. , Fessler A. James , Cascino Gregory D. , Lozada Leonard , Bechtle Perry S. , Marsh W. Richard , Sharbrough Frank W. , Schroeder Darrell R. 
Published: March 2003

Summary:  Purpose: High‐dose i.v. opioids (e.g., alfentanil, 50 μg/kg bolus) are known to increase the intraoperative reading of epileptiform activity during epilepsy surgery (ES), thereby facilitating localization of the epileptogenic zone (i.e., the site of ictal onset and initial seizure propagation). However, this phenomenon has not been studied with remifentanil (i.e., a novel ultra‐short acting opioid). The purpose of the present study was to evaluate the effect of remifentanil on electrocorticography (ECoG) during ES.Methods: After Institutional Review Board approval, 25 adult patients undergoing elective ECoG‐guided anterior temporal corticectomy were enrolled. At the time of ECoG, anesthesia consisted of inhaled isoflurane 0.1% (end‐tidal) in 50% N2O, and i.v. fentanyl, 2 μg/kg/h and vecuronium. Patients were maintained at normocapnia and normoxia during ECoG. After acquisition of baseline ECoG, bolus remifentanil, 2.5 μg/kg i.v., was administered. The number of epileptiform spikes occurring 5 min before and after this bolus were compared by using a one‐sided sign test; p values 0.05 were considered statistically significant.Results: When compared with baseline ECoG, bolus i.v. remifentanil significantly increased the frequency of single spikes or repetitive spike bursts in the epileptogenic zone while suppressing activity in surrounding normal brain.Conclusions: During ES, remifentanil enhanced epileptiform activity during intraoperative ECoG. Such observations facilitate localization of the epileptogenic zone while minimizing resection of nonepileptogenic eloquent brain tissue. Although not specifically evaluated in this study, we speculate that remifentanil's short elimination half‐life will facilitate neurologic function testing immediately after ES. Should this be the case, we envision remifentanil has the potential to supplant other opioids (e.g., alfentanil) during ECoG‐guided ES.
Felbamate Urolithiasis
Authors: Sparagana S. P. , Strand W. R. , Adams R. C. 
Published: March 2003

Summary:  Purpose: To report a case of felbamate (FBM) urolithiasis.Methods: Urographic imaging [sonography, abdominal computed tomography (CT), intravenous pyelogram, voiding cystourethrogram] and urologic procedures (cystoscopy with lithotripsy, ureteral stent) to define and capture the stones. Stone identification was by infrared spectroscopy and gas chromatography/mass spectrometry.Results: A 15‐year‐old boy had painful hematuria, bilateral ureteral obstruction, and urinary retention. Kidney, bladder, and ureteral stones were found, and ureteral stent placement was required to relieve obstruction. The stone material was identified as FBM by chemical analysis. Stone formation ceased with discontinuation of FBM.Conclusions: FBM urolithiasis can occur, and possible contributory factors include high felbamate dosage, drug polypharmacy, and risk factors for forming stones of other types. FBM urolithiasis may be heralded by crystalluria.
An Animal Model of Nonconvulsive Status Epilepticus: A Contribution to Clinical Controversies
Authors: Kršek Pavel , Mikulecká Anna , Druga Rastislav , Hliňák Zdeněk , Kubová Hana , Mareš Pavel 
Published: March 2003

Summary:  Purpose: To characterize electroencephalographic and behavioral effects as well as electrophysiologic and morphologic consequences of a subconvulsive dose of pilocarpine in lithium chloride–pretreated rats.Methods: Pilocarpine (15 mg/kg) was administered intraperitoneally to adult rats pretreated with lithium chloride (3 mEq/kg, i.p.). Behavior was observed for 2 h and videotaped in three consecutive sessions. At the same time, EEG was recorded from the sensorimotor cortex and the dorsal hippocampus. Threshold intensities of currents necessary to elicit hippocampal afterdischarges were determined 24 h and 1 week after the pilocarpine administration. The brains were histologically examined 1 week after pilocarpine administration using Nissl stain.Results: Pilocarpine induced time‐limited nonconvulsive status epilepticus (NCSE). Epileptic EEG activity concurrent with prominent behavioral features was observed both in the neocortex and, predominantly, in the hippocampus. No changes in afterdischarge thresholds were observed in the dorsal hippocampus 24 h and 1 week after NCSE. One week after NCSE, seizure‐related brain damage was found mainly in the motor neocortical fields.Conclusions: Pilocarpine‐induced NCSE in rats strongly resembles a short‐term human complex partial status epilepticus. Our animal model is suitable for studying the possible adverse effects of prolonged nonconvulsive seizures.
Oxcarbazepine in Focal Epilepsy and Hepatic Porphyria: A Case Report
Authors: Gaida‐Hommernick Bernadette , Rieck Karina , Runge Uwe 
Published: March 2003

Summary:  Purpose: Despite the development of new antiepileptic agents (AEDs), the therapy of epilepsies along with hepatic porphyrias remains difficult. Most AEDs such as carbamazepine (CBZ), phenytoin (PHT), valproate (VPA), and lamotrigine (LTG) may precipitate clinically latent porphyria by inducing hepatic metabolism and increasing hepatic heme synthesis. Actually, only gabapentin (GBP), an AED without any hepatic metabolism, is known as a potential therapy for partial seizures in patients having hepatic forms of porphyria.Methods: We present the case of a 28‐year‐old man with porphyria cutanea tarda (PCT) who has had pharmacoresistant epilepsy with complex partial and secondarily generalized seizures since early childhood. Despite having undergone several AED therapies over the years, no seizure‐free interval had been observed. Only CBZ could cause a seizure reduction, but this treatment had to be discontinued as an elevation of the transaminases as well as pruritus and erythema were noted. The patient was then started on oxcarbazepine (OCBZ), a ketoanalogue of CBZ similar in its pharmacologic mechanism as well as its clinical use, but which, in contrast to CBZ, has only a low hepatic induction of microsomal enzymes. A final maintenance dose four times higher than that of CBZ was prescribed.Results: In the follow‐up, the patient stopped having seizures, and his liver functions became normal.Conclusions: It can be concluded that OCBZ can successfully be administered to patients with hepatic porphyria and focal epilepsy who did not respond to treatment with GBP.
Relation between Responsiveness to Neurotransmitters and Complexity of Epileptiform Activity in Rat Hippocampal CA1 Neurons
Authors: Yang Hong‐Jun , Hu San‐Jue , Han Sheng , Liu Guo‐Peng , Xie Yong , Xu Jian‐Xue 
Published: March 2003

Summary:  Purpose: Our previous works suggested that sensitivity of neurons with chaotic firing patterns to stimuli is significantly greater than that in neurons with periodic firing patterns, which shows that responsiveness of neurons may depend on the complexity of the firing series. This study was performed to determine the relation between responsiveness of the hippocampal CA1 neurons with epileptiform activity (EA) to neurotransmitters and their complexity of firing series.Methods: Firing series of CA1 neurons were recorded extracellularly in rat hippocampal slice. Approximate entropy was used to describe the complexity of the interspike interval (ISI) series. EA was induced by local application of penicillin (1,000 IU/ml). The change of firing rate induced by neurotransmitters (glutamate and γ‐aminobutyric acid) was compared with that of the degree of complexity of ISI series in the process of EA.Results: The excitatory responses to glutamate and the inhibitory responses to γ‐aminobutyric acid in CA1 neurons appeared to be decreased during the process of penicillin‐induced EA. However, during this same process, the approximate entropy of the ISI series also was decreased significantly.Conclusions: The results suggest that the reduced responses to neurotransmitters of the CA1 neurons appear to be closely related to the onset of EA. Furthermore, these neurons show that the changes in responsiveness are closely parallel to the decrease of degree of complexity of firing series during penicillin epileptogenesis.
Altered Flurothyl Seizure Induction Latency, Phenotype, and Subsequent Mortality in a Mouse Model of Juvenile Neuronal Ceroid Lipofuscinosis/Batten Disease
Authors: Kriscenski‐Perry Elizabeth , Applegate Craig D. , Serour Andrew , Mhyre Timothy R. , Leonardo Christopher C. , Pearce David A. 
Published: March 2003

Summary:  Purpose: Juvenile neuronal ceroid lipofuscinosis (JNCL), or Batten disease, is a pediatric neurodegenerative disease characterized by vision loss, seizure activity, cognitive decline, and premature death. Discovery of the Batten disease–related gene, CLN3, led to creation of a Cln3 protein‐deficient mouse model (Cln3−/−), which recapitulates some of the histopathologic characteristics of the human condition. We hypothesized that lack of Cln3 would alter seizure‐related behavioral parameters.Methods: Using flurothyl gas inhalation, we examined seizure‐induction latencies in Cln3−/− mice and wildtype (wt) controls at time points that represent late neonatal, immature, mature, and aged time points. We examined latency to first myoclonic jerk (LMJ), latency to loss of posture (LOP), and subsequent mortality.Results: Our results demonstrate an age‐dependent alteration of seizure‐induction latencies in Cln3−/−. Immature Cln−/− mice aged 35–42 days had an increased latency to both LMJ and LOP compared with age‐matched wt controls. There were no significant latency differences between Cln3−/− and wt at other time points examined. Mortality after generalized seizure was high in both Cln3−/− and wt animals at late neonatal and immature developmental stages. No mortality was seen in wt mice past maturity at 6 weeks. Mature and aged Cln3−/− animals retained a vulnerability to death after seizure activity.Conclusions: These results suggest that a deficiency of Cln3 protein in the Batten model mice may result in age‐dependent alteration of the neuroanatomic and biochemical substrates involved in seizure propagation and recovery. This may be important in understanding seizures, neurodegeneration, and premature death in human Batten disease.
Visual Field Constriction in 91 Finnish Children Treated with Vigabatrin
Authors: Vanhatalo Sampsa , Nousiainen Iiris , Eriksson Kai , Rantala Heikki , Vainionpää Leena , Mustonen Kirsi , Äärimaa Tuula , Alen Reija , Aine Marjo‐Riitta , Byring Roger , Hirvasniemi Aune , Nuutila Auli , Walden Tiina , Ritanen‐Mohammed Ulla‐Maija , Karttunen‐Lewandowski Pirkko , Pohjola Leena‐Maria , Kaksonen Satu , Jurvelin Pekka , Granström Marja‐Liisa 
Published: March 2003

Summary:  Purpose: To study the prevalence and features of visual field constrictions (VFCs) associated with vigabatrin (VGB) in children.Methods: A systematic collection of all children with any history of VGB treatment in fifteen Finnish neuropediatric units was performed, and children were included after being able to cooperate reliably in repeated visual field tests by Goldmann kinetic perimetry. This inclusion criterion yielded 91 children (45 boys; 46 girls) between ages 5.6 and 17.9 years. Visual field extent <70 degrees in the temporal meridian was considered abnormal VFC.Results: There was a notable variation in visual field extents between successive test sessions and between different individuals. VFCs <70 degrees were found in repeated test sessions in 17 (18.7%) of 91 children. There was no difference in the ages at the study, the ages at the beginning of treatment, the total duration of the treatment, general cognitive performance, or neuroradiologic findings between the patients with normal visual fields and those with VFC, but the patients with VFC had received a higher total dose of VGB. In linear regression analysis, there were statistically significant inverse correlations between the temporal extent of the visual fields and the total dose and the duration of VGB treatment. The shortest duration of VGB treatment associated with VFC was 15 months, and the lowest total dose 914 g.Conclusions. Because of a wide variation in normal visual‐field test results in children, the prevalence figures of VFCs are highly dependent on the definition of normality. Although our results confirm the previous findings that VFC may occur in children treated with VGB, our study points out the need to reevaluate critically any suspected VFC to avoid misdiagnosis. Nevertheless, our study suggests that the prevalence of VFC may be lower in children than in adults, and that the cumulative dose of VGB or length of VGB therapy may add to the personal predisposition for developing VFC.
Anticonvulsant Profile and Teratogenicity of N‐methyl‐tetramethylcyclopropyl Carboxamide: A New Antiepileptic Drug
Authors: Isoherranen Nina , White H. Steve , Finnell Richard H. , Yagen Boris , Woodhead José H. , Bennett Gregory D. , Wilcox Karen S. , Barton Matthew E. , Bialer Meir 
Published: March 2003

Summary:  Purpose: The studies presented here represent our efforts to investigate the anticonvulsant activity of N‐methyl‐tetramethylcyclopropyl carboxamide (M‐TMCD) and its metabolite tetramethylcyclopropyl carboxamide (TMCD) in various animal (rodent) models of human epilepsy, and to evaluate their ability to induce neural tube defects (NTDs) and neurotoxicity.Methods: The anticonvulsant activity of M‐TMCD and TMCD was determined after intraperitoneal (i.p.) administration to CF#1 mice, and either oral or i.p. administration to Sprague–Dawley rats. The ability of M‐TMCD and TMCD to block electrical‐, chemical‐, or sensory‐induced seizures was examined in eight animal models of epilepsy. The plasma and brain concentrations of M‐TMCD and TMCD were determined in the CF#1 mice after i.p. administration. The induction of NTDs by M‐TMCD and TMCD was evaluated after a single i.p. administration at day 8.5 of gestation in a highly inbred mouse strain (SWV) that is susceptible to valproic acid–induced neural tube defects.Results: In mice, M‐TMCD afforded protection against maximal electroshock (MES)‐induced, pentylenetetrazol (Metrazol)‐induced, and bicuculline‐induced seizures, as well as against 6‐Hz “psychomotor” seizures and sound‐induced seizures with ED50 values of 99, 39, 81, 51, and 10 mg/kg, respectively. In rats, M‐TMCD effectively prevented MES‐ and Metrazol‐induced seizures and secondarily generalized seizures in hippocampal kindled rats (ED50 values of 82, 45, and 39 mg/kg, respectively). Unlike M‐TMCD, TMCD was active only against Metrazol‐induced seizures in mice and rats (ED50 values of 57 and 52 mg/kg, respectively). Neither M‐TMCD nor TMCD was found to induce NTDs in SWV mice.Conclusions: The results obtained in this study show that M‐TMCD is a broad‐spectrum anticonvulsant drug that does not induce NTDs and support additional studies to evaluate its full therapeutic potential.