bluuebunny/crossref_metadata_2025_split huggingface dataset:
Headache Associated With the Chiari Type I Malformation.
Authors: Stovner Lars Jacob 
Published: June 2005

SYNOPSISThe main purpose of the present study was to define and understand more clearly the headache, and in particular the long‐lasting attacks or continuous pain associated with the Chiari type I malformation. Of 34 patients with the malformation, the 20 patients who had or had had headache problems were interviewed according to a standardized questionnaire. Many patients had several headache types. Ten patients had shortlasting “cough headache” attacks lasting less than 5 minutes, 14 patients had relatively long‐lasting attacks lasting from 3 hours to several days, and 8 patients had continuous headache. Unlike the short‐lasting cough headache attacks, long‐lasting attacks were usually not precipitated by Valsalva‐like maneuvers. With discriminant analysis, this headache could rather well be differentiated from that of migraine and cervicogenic headache patients. In many respects, however, this headache resembled cervicogenic headache with occipital and neck pain, pain In the arm, restriction of neck movement, and dizziness often accompanying the headache. Dizziness was the meat distinguishing feature in the Chiari patients. These features, together with a beneficial effect of surgical treatment in some patients, suggest a causal relationship between the malformation and headache. From the histories of a few Illustrative cases, It is suggested that the malformation may cause long‐lasting headache attacks or continuous head pain by compression of the brainstem, central cord degeneration or intracranial hypertension.
Headache in College Students: A Comparison of Four Populations
Authors: Forgays Donald G. , Rzewnicki Randy , Ober Allison J. , Forgays Deborah K. 
Published: June 2005

SYNOPSISRecent studies have reported a much lower rate of headache prevalence for Australian college students as compared with those for two campuses in the United States. We present such data here for a third U.S. campus and make several comparisons of these data for the four campuses. While the gender difference of higher female over male headache frequency was found for all four campuses, the same measure for combined genders is reliably higher for all three U.S. groups over their Australian counterpart and there are significant differences among the U.S. groups as well. Possible reasons for these campus differences in headache prevalence are outlined and discussed and further research is indicated.
Episodic Paroxysmal Hemicrania: 3 New Cases and a Review of the Literature
Authors: Newman Lawrence C. , Lipton Richard B. , Solomon Seymour 
Published: June 2005

SYNOPSISEpisodic paroxysmal hemicrania (EPH) is a rare, benign disorder characterized by discrete bouts of hemicranial headaches separated by periods of pain‐free remissions. EPH is frequently mistaken for episodic cluster headache because they have similar temporal profiles and clinical features. EPH is differentiated from cluster headaches by an increased frequency and a shorter duration of individual attacks. Establishing the diagnosis of EPH is important because of its unique response to treatment with indomethacin and not standard anti‐cluster headache medications.
Cluster Headache In Identical Twins
Authors: Sjaastad O. , Shen J‐M. , Stovner L.J. , EIsås T. 
Published: June 2005

SYNOPSISTwin brothers with cluster headache are described. Monozygosity was demonstrated by conventional genetic markers and DNA‐typing. Both had “mini‐bouts” in the early stages. In the one, attacks were always excruciatingly severe; in the other, they started out as “mild”, eventually becoming more severe. Both brothers also suffered from paroxysmal tachycardia. The connection between attacks of tachycardia and cluster headache remains enigmatic.The observation of cluster headache in monozygotic twins underscores the importance of genetic factors in the etiology. The ratio between cluster headache prevalence in close family members vs. prevalence in the general population may be higher in cluster headache than in migraine.
Changes of Cortical Interhemispheric Responses after Status Epilepticus in Immature Rats
Authors: Mareš Pavel , Tsenov Grygoriy , Aleksakhina Katarina , Druga Rastislav , Kubová Hana 
Published: June 2005

Summary: Purpose:To study cortical excitability after status epilepticus induced in two age groups of immature rats.Methods:Lithium‐pilocarpine status epilepticus was elicited in 12‐ (SE12) or 25‐day‐old (SE25) rats. Control siblings received saline instead of pilocarpine. Interhemispheric responses were elicited by stimulation of sensorimotor region of cerebral cortex 3, 6, 9, 13, or 26 days after status. Single biphasic pulses with intensities from 0.2 to 4 mA were used for stimulation; eight responses were always averaged. Amplitude of the first positive and negative waves (i.e., monosynaptic transcallosal responses) was measured and used for construction of input–output (I/O) curves. FluoroJade B was used to visualize degenerating neurons 24 h after status in both age groups.Results:No significant changes were found at short intervals, but only a tendency to lower amplitudes 3 days after status in SE12 group. Marked changes appeared 26 days after status. The younger group exhibited lower amplitudes than did control rats, whereas SE25 animals generated responses with higher amplitude than did controls (i.e., the I/O curve was steeper. FluoroJade B‐positive neurons were scarce in SE12 rats, whereas a substantial number of positive neurons was found in SE25 animals. The positive neurons exhibited characteristics of interneurons, and their distribution in cortical layers differed in the two groups.Conclusions:Status epilepticus resulted in neuronal death in both SE12 and SE25 animals. Changes in transcallosal evoked potentials were opposite in the two age groups. Augmented amplitude of responses in SE25 rats may indicate an increased cortical excitability.
Inflammatory Response and Glia Activation in Developing Rat Hippocampus after Status Epilepticus
Authors: Ravizza Teresa , Rizzi Massimo , Perego Carlo , Richichi Cristina , Velískǒvá Jana , Moshé Solomon L. , De Simoni M. Grazia , Vezzani Annamaria 
Published: June 2005

Summary:  Purpose: We investigated the activation of microglia and astrocytes, induction of cytokines, and hippocampal neuronal damage, 4 and 24 h after kainic acid–induced status epilepticus (SE) in postnatal day (PN) 9, 15, and 21 rats. Methods: Limbic seizures were induced by systemic injection of kainic acid. Glia activation and neuronal cell loss were studied by using immunocytochemistry and Western blot. Cytokine expression was analyzed by reverse transcriptase–polymerase chain reaction (RT‐PCR) followed by Southern blot quantification. Results: After SE onset, hippocampal glia activation, cytokine expression, and neuronal damage are all age‐dependent phenomena. In the hippocampus, neuronal injury occurs only when cytokines are induced in glia, and cytokine synthesis precedes the appearance of degenerating neurons. Neuronal injury is more pronounced when interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) are produced in addition to IL‐1β. Conclusions: This study shows that cytokine induction in rat brain after sustained seizures is age dependent, and it is associated with the appearance of cell injury.
Reduced Serotonin and 3‐Hydroxyanthranilic Acid Levels in Serum of Cystatin B‐Deficient Mice, a Model System for Progressive Myoclonus Epilepsy
Authors: Arbatova Jelena , D'Amato Elena , Vaarmann Annika , Zharkovsky Alex , Reeben Mati 
Published: June 2005

Summary:  Purpose: To evaluate the levels of tryptophan and its metabolites along serotonin (5‐HT) and kynurenine (KYN) pathways in serum of progressive myoclonus epilepsy (EPM1) patients and cystatin B (CSTB)‐deficient mice, a model system for EPM1. Methods: Tryptophan and its metabolites along serotonin (5‐HT) and KYN pathways were determined in serum of EPM1 patients and CSTB‐deficient mice by reverse‐phase high‐pressure liquid chromatography (HPLC) with electrochemical detection. Results: Reduced levels of 5‐HT and KYN intermediate metabolite 3‐hydroxyanthranilic acid were found in serum of CSTB‐deficient mice. A similar trend was found in EPM1 patients. Although tryptophan concentration was reduced in serum of EPM1 patients, no such decrease was observed in CSTB‐deficient mice. Conclusions: The present study demonstrates that tryptophan metabolism along 5‐HT and KYN pathways are disrupted in EPM1. Further studies are needed to elucidate the role of KYN pathway in pathogenesis of EPM1.
Alterations in Seizure Susceptibility and in Seizure‐induced Plasticity after Pharmacologic and Genetic Manipulation of the Fibroblast Growth Factor‐2 System
Authors: Zucchini Silvia , Barbieri Mario , Simonato Michele 
Published: June 2005

Summary:  Purpose: The adult brain undergoes activity‐dependent plastic modifications during pathologic processes that are reminiscent of those observed during development. For example, seizures induce neuronal loss, neurogenesis, axonal and dendritic sprouting, gliosis, and circuit remodeling. Neurotrophic factors and fibroblast growth factor‐2 (FGF‐2), in particular, are well‐known mediators in each of these cellular events. The aim of this minireview is to summarize and discuss the data supporting the idea that FGF‐2 may be involved in seizure generation and in their sequelae. Methods: We used epilepsy models of kainate and kindling, with FGF‐2 knockout mice and FGF‐2 overexpressing mice. Results: Seizures increase FGF‐2 mRNA and protein levels in specific brain areas and upregulate the expression of its receptor FGFR‐1. Short‐term intrahippocampal injection of FGF‐2 cause seizures, whereas long‐term i.c.v. infusion of low‐dose FGF‐2 does not affect kainate seizures but promotes behavioral recovery and reduces hippocampal damage. Kainate seizure severity is not altered in FGF‐2 knockout mice, but is increased in FGF‐2 overexpressing mice. Conclusions: FGF‐2 is implicated in seizure susceptibility and in seizure‐induced plasticity.
The Role of Extracellular Potassium in the Epileptogenic Transformation of Recurrent GABAergic Inhibition
Authors: Bihi Rachid Id , Jefferys John G. R. , Vreugdenhil Martin 
Published: June 2005

Summary:  Purpose: Epileptiform burst‐firing can occur in hippocampal area CA1 where recurrent excitation is relatively weak and recurrent inhibition strong. Recent observations suggest that recurrent inhibition can transform into recurrent excitation because of collapse of the chloride gradient. Here we assess the role of potassium in this epileptogenic transformation. Methods: Extracellular field potential recordings, combined with either intracellular recordings from pyramidal neurons or extracellular potassium concentration recordings, were made in vitro from isolated CA1 minislices cut from the rat hippocampus and in vivo from area CA1 in urethane‐anesthetized rats. Burst responses were evoked by 5‐Hz alveus stimulation. Results: The 5‐Hz alveus stimulation in vitro caused a transient period of burst responses that was associated with a transient increase in synaptic input in stratum oriens and a transient shift of the reversal potential of the synaptic potential. These changes were related to the transient increase in extracellular potassium concentration in stratum oriens. Observations in vivo confirmed the relation between bursting and extracellular potassium concentration in stratum oriens. Conclusions: Use‐dependent increase of extracellular potassium concentration in stratum oriens facilitates the collapse of the chloride gradient in the basal dendrites and transforms γ‐aminobutyric acid (GABA)ergic inhibition into GABAergic excitation, giving rise to burst firing. Improvement of intracellular chloride homeostasis or extracellular potassium homeostasis could reduce epileptogenicity.
Detection of Increased Local Excitatory Circuits in the Hippocampus during Epileptogenesis Using Focal Flash Photolysis of Caged Glutamate
Authors: Shao Li‐Rong , Dudek F. Edward 
Published: June 2005

Summary:  Purpose: Local synaptic circuits, particularly recurrent excitation, are hypothesized to contribute to the generation and synchronization of epileptiform activity. The present study tested whether local excitatory circuits in the hippocampus are increased in an animal model of temporal lobe epilepsy, and thus may contribute to epileptic seizures. Methods: Rats were given hourly injections of kainic acid to induce status epilepticus, which led to chronic epilepsy with spontaneous recurrent seizures. Whole‐cell recording was performed in hippocampal slices, and focal flash photolysis of caged glutamate was used to detect local excitatory circuits. Results: In the dentate gyrus of rats with kainate‐induced epilepsy and mossy fiber sprouting, focal stimulations with caged glutamate at many different sites in the granule cell layer consistently evoked repetitive excitatory postsynaptic currents (EPSCs) in normal medium and prolonged bursts of action potentials in bicuculline; these responses were not observed in similarly treated slices from control rats. In CA1, focal flash photolysis of caged glutamate in stratum pyramidale revealed significantly more excitatory connections between CA1 pyramidal cells in rats with kainate‐induced epilepsy than saline‐treated control animals. Conclusion: Focal flash photolysis of caged glutamate revealed that new local excitatory circuits are formed in both the dentate gyrus and CA1 area of rats with kainate‐induced epilepsy, which supports the hypothesis that the progressive formation of new local excitatory circuits occurs in many locations during epileptogenesis.
Autoantibodies and Cell‐mediated Autoimmunity to NMDA‐type GluRɛ2 in Patients with Rasmussen's Encephalitis and Chronic Progressive Epilepsia Partialis Continua
Authors: Takahashi Yukitoshi , Mori Hisashi , Mishina Masayoshi , Watanabe Masahiko , Kondo Naomi , Shimomura Jiro , Kubota Yuko , Matsuda Kazumi , Fukushima Katsuyuki , Shiroma Naohide , Akasaka Noriyuki , Nishida Hiroshi , Imamura Atsushi , Watanabe Hiroo , Sugiyama Nobuyoshi , Ikezawa Makoto , Fujiwara Tateki 
Published: June 2005

Summary:  Purpose: To evaluate antibody‐mediated and cytotoxic T cell–mediated pathogenicity that has been implicated as the autoimmune pathophysiological mechanism in Rasmussen's encephalitis. Methods: We examined autoantibodies against the N‐methyl‐d‐aspartate glutamate receptor (NMDA‐type GluR) ɛ2 subunit and its epitopes in serum and CSF samples from 20 patients [five histologically proven (definitive) Rasmussen's encephalitis with epilepsia partialis continua (EPC), four definitive Rasmussen's encephalitis without EPC, and 11 clinical Rasmussen's encephalitis with EPC]. We examined 3H‐thymidine uptake into lymphocytes after stimulation by GluRs. Results: All nine definitive patients (five patients with EPC and four without EPC), and 10 of 11 clinical Rasmussen's encephalitis patients had the autoantibodies. In four patients, the autoantibodies were absent in early stage when epileptic seizures had already become frequent, and appeared subsequently. In two patients, the autoantibodies persisted in the serum after frontal lobe resection or functional hemispherectomy, although epileptic seizures were completely controlled. Autoantibodies to the C2 epitope predominated, while autoantibodies to the extracellular N epitope were rare. The mean 3H‐thymidine uptake ratios (stimulation by GluRɛ2‐containing homogenates/stimulation by PHA) were significantly higher in definitive and clinical Rasmussen encephalitis patients than in controls. The mean 3H‐thymidine uptake ratios (relative to PHA) were significantly higher for GluRɛ2‐containing homogenate than for control homogenate or GluRδ2‐containing homogenate. Conclusions: Autoantibodies against GluRɛ2 may be one of the diagnostic markers for Rasmussen's encephalitis with and without EPC. Patients have activated T cells stimulated by GluRɛ2 in peripheral blood circulation. We speculate that cellular autoimmunity and the subsequent humoral autoimmunity against GluRɛ2 may contribute to the pathophysiological processes in Rasmussen's encephalitis.
Long‐term Effect of Convulsive Behavior on the Density of Adenosine A1 and A2A Receptors in the Rat Cerebral Cortex
Authors: Rebola Nelson , Porciúncula Lisiane O. , Lopes Luísa V. , Oliveira Catarina R. , Soares‐da‐Silva Patrício , Cunha Rodrigo A. 
Published: June 2005

Summary:  Purpose: Adenosine is a neuromodulator that has been proposed to act as an anticonvulsant mainly via inhibitory A1 receptors, but recent data show that genetic deletion of facilitatory A2A receptors might also attenuate convulsions. Since both A1 and A2A receptors are prone to down‐ and upregulation in different stressful situations, we investigated if convulsive behavior leads to a long‐term change in A1 and A2A receptor density in the rat cerebral cortex. Methods: Stage 4‐5 convulsions (Racine's scale) were induced in adult Wistar rats either through amygdala stimulation (kindling) or by intraperitoneal injection of kainate (10 mg/ml). Rats were killed after 4 weeks to evaluate adenosine A1 and A2A receptor density in the cerebral cortex using both Western blot and membrane binding assays. Results: The binding density of the A1 antagonist, 3H‐DPCPX, decreased by 40. ± 4.4% and by 20.7 ± 0.5% after kindling or kainate injection. Likewise, A1 receptor immunoreactivity in cortical membranes from kindled or kainate‐injected rats decreased by 19.1 ± 3.3% and 12.7 ± 5.7%, respectively. In contrast, the binding density of the A2A receptor antagonist 3H‐SCH 58261 increased by 293 ± 34% and by 159 ± 32% in cortical membranes from kindled or kainate‐injected rats, and A2A receptor immunoreactivity also increased by 151 ± 12% and 79.6 ± 7.0%. Conclusions: This indicates that after convulsive behavior there is a long‐term decrease of A1 receptors accompanied by an increased density of A2A receptors, suggesting that A2A antagonists rather than A1 agonists may be more promising anticonvulsive drugs.
Modulation of Seizures and Synaptic Plasticity by Adenosinergic Receptors in an Experimental Model of Temporal Lobe Epilepsy Induced by Pilocarpine in Rats
Authors: Vianna Eduardo Paulo Morowsky , Ferreira Alice Teixeira , Doná Flávia , Cavalheiro Esper Abrão , Da Silva Fernandes Maria José 
Published: June 2005

Summary:  Purpose: Adenosine is a major negative neuromodulator of synaptic activity in the central nervous system and can exert anticonvulsant and neuroprotective effects in many experimental models of epilepsy. Extracellular adenosine can be formed by a membrane‐anchored enzyme ecto‐5′‐nucleotidase. The purposes of this study were to characterize the role of adenosine receptors in modulating status epilepticus (SE) induced by pilocarpine and evaluate its neuroprotective action. Ecto‐5′‐nucleotidase activity was studied during the different phases of pilocarpine‐induced epilepsy in rats. Methods: Adult rats were pretreated with different adenosinergic agents to evaluate the latency and incidence of SE induced by pilocarpine in rats. The neuroprotective effect also was evaluated. Results: A proconvulsant effect was observed with DPCPX and DMPX that reduced the latency of SE in almost all rats. Pretreatment with the MRS 1220 did not alter the incidence of SE but reduced the latency to develop SE. An anticonvulsant and neuroprotective effect was detected with R‐PIA. Rats pretreated with R‐PIA had a decreased number of apoptotic cells in the hippocampus, whereas pretreatment with DPCPX did not modify the hippocampal damage. An intensification of neuronal death was observed in the dentate gyrus and CA3 when rats were pretreated with DMPX. MRS‐1220 did not modify the number of apoptotic cells in the hippocampus. An increase in the ecto‐5´‐nucleotidase staining was detected in the hippocampus during silent and chronic phases. Conclusions: The present data show that adenosine released during pilocarpine‐induced SE via A1‐receptor stimulation can exhibit neuroprotective and anticonvulsant roles. Similar effects could also be inferred with A2a and A3 adenosinergic agents, but further experiments are necessary to confirm their roles. Ecto‐5´‐nucleotidase activity during silent and chronic phases might have a role in blocking spontaneous seizures by production of inhibitory neuromodulator adenosine, besides taking part in the mechanism that controls sprouting.
The RADAR repository: a resource for studies of infectious agents and their transmissibility by transfusion
Authors: Kleinman S.H. , Glynn S.A. , Higgins M.J. , Triulzi D.J. , Smith J.W. , Nass C.C. , Garratty George , Murphy E.L. , LeParc G.F. , Schreiber G.B. , King M.R. , Chamberland M.E. , Nemo G.J. 
Published: June 2005

BACKGROUND: An ongoing issue in transfusion medicine is whether newly identified or emerging pathogens can be transmitted by transfusion. One method to study this question is through the use of a contemporary linked donor‐recipient repository.STUDY DESIGN AND METHODS: The Retrovirus Epidemiology Donor Study Allogeneic Donor and Recipient (RADAR) repository was established between 2000 and 2003 by seven blood centers and eight collaborating hospitals. Specimens from consented donors were collected, components from their donations were routed to participating hospitals, and recipients of these units gave enrollment and follow‐up specimens for long‐term storage. The repository was designed to show that zero transmissions to enrolled recipients would indicate with 95 percent confidence that the transfusion transmission rate of an agent with prevalence of 0.05 to 1 percent was lower than 25 percent.RESULTS: The repository contains pre‐ and posttransfusion specimens from 3,575 cardiac, vascular, and orthopedic surgery patients, linked to 13,201 donation specimens. The mean number of RADAR donation exposures per recipient is 3.85. The distribution of components transfused is 77 percent red cells, 13 percent whole blood–derived platelet concentrates, and 10 percent fresh frozen plasma. A supplementary unlinked donation repository containing 99,906 specimens from 84,339 donors was also established and can be used to evaluate the prevalence of an agent and validate assay(s) performance before accessing the donor‐recipient–linked repository. Recipient testing conducted during the establishment of RADAR revealed no transmissions of human immunodeficiency virus, hepatitis C virus, or human T‐lymphotropic virus.CONCLUSIONS: RADAR is a contemporary donor‐recipient repository that can be accessed to study the transfusion transmissibility of emerging agents.
Hemostatic effects of fibrinogen γ‐chain dodecapeptide‐conjugated polymerized albumin particles in vitro and in vivo
Authors: Okamura Yosuke , Takeoka Shinji , Teramura Yuji , Maruyama Hitomi , Tsuchida Eishun , Handa Makoto , Ikeda Yasuo 
Published: June 2005

BACKGROUND: Prototypes of platelet (PLT) substitutes have been studied and the focus was on a dodecapeptide, HHLGGAKQAGDV (H12), which is a fibrinogen γ‐chain carboxy‐terminal sequence (γ 400‐411) and exists only in the fibrinogen domain.STUDY DESIGN AND METHODS: H12 was conjugated to the surface of polymerized albumin particles (polyAlb) as biocompatible and biodegradable particles with a mean diameter of 260 ± 60 nm, and the hemostatic ability of H12‐conjugated polyAlb (H12‐polyAlb) under flow conditions and thrombocytopenic rats have been studied.RESULTS: H12‐polyAlb enhanced the in vitro thrombus formation of activated PLTs on a collagen‐immobilized plate when exposed to the flowing thrombocytopenic imitation blood. Furthermore, the analysis of the tail bleeding time of rats that were made thrombocytopenic by busulfan injection showed that H12‐polyAlb had a hemostatic effect. Based on the bleeding time and the amount injected, the hemostatic capacity of 20 H12‐polyAlb was estimated to correspond to that of one PLT.CONCLUSION: These results were important first steps toward the development of PLT substitutes and indicated that H12‐polyAlb may be a suitable candidate for an alternative to human PLT concentrates transfused into thrombocytopenic patients in the future.