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seizures/infiammazione
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 3170 risultati
Astrocytic TLR4 at the crossroads of inflammation and seizure susceptibility.
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Astrocytes have been implicated in epilepsy development, but their contribution is under debate. In this issue, Shen et al. (2016. J. Cell Biol. https://doi.org/10.1083/jcb.201605046) demonstrate that early postnatal inflammatory stimuli activate toll-like receptor 4 signaling in astrocytes and
Intranasal Delivery of miR-155-5p Antagomir Alleviates Acute Seizures Likely by Inhibiting Hippocampal Inflammation
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Introduction: To confront the resistance to existing antiepileptic drugs, studies have gradually begun to investigate alternative pathologies distinct from the traditional treatments that overwhelmingly target ion channels. Microglia
IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure.
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Interleukin-33 (IL-33) is a novel identified chromatin-associated cytokine of IL-1 family cytokines. It signals through a heterodimer comprised of ST2L and IL-1RAcp, and plays a crucial role in many diseases. However, very little is known about the role and underlying intricate mechanisms of IL-33
Novel Inflammatory Neuropathology in Immature Brain: (1) Fetal Tuberous Sclerosis, (2) Febrile Seizures, (3) α-B-crystallin, and (4) Role of Astrocytes.
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Though the term "inflammation" is traditionally defined as proliferation or infiltration of lymphatic cells of the lymphatic immune system and macrophages or as immunoreactive proteins including cytokines, interleukins and major histocompatibility complexes, recently recognized reactions to tissue
Experimentally induced various inflammatory models and seizure: understanding the role of cytokine in rat.
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BACKGROUND
The mechanism of epileptogenesis is not well established. There is higher incidence of seizures among patients with chronic inflammatory disease. Cytokines are rapidly induced in the brain after a variety of stimuli including inflammation. Aim of this study was to produce various
Resection of the epileptogenic lesion abolishes seizures and reduces inflammatory cytokines of patients with temporal lobe epilepsy.
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Persistent neuroinflammation is implicated in the pathogenesis of seizures and neuronal degeneration of temporal lobe epilepsy (TLE). Circulating level of inflammatory cytokines was determined during inter-ictal period of 25 non-operated and 10 patients (OP) submitted to anterior temporal lobectomy.
Absence of seizures in Rasmussen encephalitis with active inflammation.
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Severe focal motor epilepsy is considered a clinical hallmark of Rasmussen encephalitis (RE). The authors report a 6-year-old girl with progressive right sided hemiparesis, loss of language skills, left sided hemispheric atrophy, and brain pathologic features characteristic for RE. The patient did
Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids with seizures and central pyrexia, in a patient requiring tracheal intubation and mechanical ventilation: A case report.
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Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) has been described in multiple case reports since it was first described in the literature in 2010. The patient described is a 54-year-old man with no significant medical history who presented
DPP4 regulates the inflammatory response in a rat model of febrile seizures.
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Febrile seizures (FS) are the most common seizure disorders in children aged 6 months to 5 years. Children suffering from complex FS have a high risk of developing subsequent temporal lobe epilepsy (TLE). Neuroinflammation is involved in the pathogenesis of FS although the mechanism remains unknown.
Inflammatory pathways of seizure disorders.
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Epilepsy refers to a cluster of neurological diseases characterized by seizures. Although many forms of epilepsy have a well-defined immune etiology, in other forms of epilepsy an altered immune response is only suspected. In general, the hypothesis that inflammation contributes to seizures is
Efficacy of anti-inflammatory therapy in a model of acute seizures and in a population of pediatric drug resistant epileptics.
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Targeting pro-inflammatory events to reduce seizures is gaining momentum. Experimentally, antagonism of inflammatory processes and of blood-brain barrier (BBB) damage has been demonstrated to be beneficial in reducing status epilepticus (SE). Clinically, a role of inflammation in the pathophysiology
Isocortical hyperemia and allocortical inflammation and atrophy following generalized convulsive seizures of thalamic origin in the rat.
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1. Generalized convulsive seizures can be elicited by a single unilateral microinjection of the cholinergic muscarinic agonist, carbachol, into the specific sites of the thalamus including ventral posterolateral and the reticular thalamic nuclei. The implication of the thalamic specific and
Inflammation is a key risk factor for persistent seizures in neurocysticercosis.
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UNASSIGNED
We conducted a retrospective, case-control study of neurocysticercosis patients to ascertain early markers that identify subjects likely to develop treatment-resistant seizures.
UNASSIGNED
Clinical histories and imaging studies from 38 neurocysticercosis patients who had been followed for
Protective effects of maternal administration of curcumin and hesperidin in the rat offspring following repeated febrile seizure: Role of inflammation and TLR4
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Neuroinflammation has a key role in seizure generation and perpetuation in the neonatal period, and toll-like receptor 4 (TLR4) pathway has a prominent role in neuroinflammatory diseases. Administration of antioxidants and targeting TLR4 in the embryonic period may protect rat offspring against the
Volumetric response of the adult brain to seizures depends on the developmental stage when systemic inflammation was induced.
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Inflammation has detrimental influences on the developing brain including triggering the epileptogenesis. On the other hand, seizure episodes may induce inflammatory processes and further increase of brain excitability. The present study focuses on the problem whether transitory systemic
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