Insights into inflammation and epilepsy from the basic and clinical sciences

Silveira, Gustavo Scheffer da; Oliveira, Antônio Carlos Pinheiro de; Teixeira, Antônio Lúcio

doi:10.1016/j.jocn.2011.10.011

Cited by 29 publications

(15 citation statements)

References 83 publications

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“…Besides causing inflammation, cytokines/chemokines also act as neuromodulators, causing neuronal excitability . IL‐6, IL‐8, and TNF‐α, have been shown to increase adhesion molecule expression and activate inflammatory cascade, leading to neurotoxicity, neuronal excitability, blood‐brain barrier disruption, and hippocampal injury in the long term . Previous studies have reported that seizures can perpetuate inflammation, thus activating a vicious cycle that in turn fosters aberrant hyperexcitability contributing to seizure recurrence and severity …”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory cytokines are soluble biological peptide molecules that help in the proliferation, differentiation, and migration of inflammatory cells to the site of inflammation and are commonly used as biomarkers of inflammation. There is rapidly growing evidence regarding the role of inflammation in acute epilepsy and chronic epilepsy groups using cytokine/chemokine analysis in human and experimental studies …”

Section: Introductionmentioning

confidence: 99%

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Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection‐related epilepsy syndrome and febrile status epilepticus

et al. 2019

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Objective To investigate intrathecal inflammation using cerebrospinal fluid (CSF) cytokines and chemokines in a subgroup of pediatric epilepsy patients with frequent daily seizures. Methods We measured 32 cytokines/chemokines using multiplex immunoassay in CSF collected from pediatric patients with febrile infection‐related epilepsy syndrome (FIRES)/FIRES‐related disorders (FRD; n = 6), febrile status epilepticus (FSE; n = 8), afebrile status epilepticus (ASE; n = 8), and chronic epilepsy with frequent daily seizures (n = 21) and compared the results with noninflammatory neurological disorders (NIND; n = 20) and encephalitis (n = 43). We also performed longitudinal CSF cytokine/chemokine studies in three cases with FIRES/FRD. Results The median age of onset of seizures was 2.4 years (range = 0.08‐12.5). Median CSF timing from the onset of seizures was longer in chronic epilepsy (540 days), whereas FIRES, FSE, and ASE had CSF tested within 1‐2 days of onset of seizures (P < .001). The elevation of cytokines/chemokines was higher in FIRES followed by FSE, when compared to chronic epilepsy and NIND controls. Th1‐associated cytokines/chemokines (TNF‐α, CXCL9, CXCL10, CXCL11), IL‐6, CCL2, CCL19, and CXCL1 (P < .05) were elevated in FIRES, in contrast to the elevation of a broader network of cytokines/chemokines in encephalitis. The cytokines/chemokines (CXCL9, CXCL10, CXCL11, and CCL19) were elevated in FSE when compared to ASE despite the similar median seizure duration and timing of CSF testing in relation to seizures. Chronic epilepsy generally lacked significant elevation of cytokines/chemokines despite frequent daily seizures. The median concentrations of the cytokines/chemokines rapidly declined on serial testing during the course of illness in all three FIRES/FRD cases. Significance We identify significant differences in CSF cytokine/chemokine profile between FIRES/FRD and encephalitis. The prominent elevation of CSF cytokines and chemokines in FIRES/FRD and to a lesser extent FSE highlights that the cytokine/chemokine elevation is significantly associated with the etiology of the underlying process rather than purely reactive. However, it is unclear whether the immune activation contributes to the disease process.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection‐related epilepsy syndrome and febrile status epilepticus

et al. 2019

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“…A proinflammatory response can contribute to the progression of overall network excitability and seizure‐induced cell death, and affect survival of seizure‐induced new adult born neurons and their expression of synaptic proteins . Moreover, suppressing neuroinflammation to limit the epileptogenesis after a precipitating injury has been described widely …”

mentioning

confidence: 99%

“…6 Moreover, suppressing neuroinflammation to limit the epileptogenesis after a precipitating injury has been described widely. [7][8][9][10] Brain inflammation is known to involve a broad spectrum of molecules and processes, and this heterogeneity may limit the therapeutic benefits of a complete inhibition. A typical immune response after an injury leads to a classical M1 immune activation, which contributes to neuropathology by being highly proinflammatory and cytotoxic, but also enables the clearance of damaged tissue.…”

mentioning

confidence: 99%

Intracerebral delivery of the M2 polarizing cytokine interleukin 13 using mesenchymal stem cell implants in a model of temporal lobe epilepsy in mice

et al. 2017

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“…Moreover, it is documented that prostaglandins are found in the brain [23] and their levels are raised through their release from glial cells after seizure induction in animal models [24].…”

Section: Wwwtjprcorg Editor@tjprcorgmentioning

confidence: 99%

Evaluation the Effect of Diclofenac Sodium on Inh-Induced Seizures

al.¹

2017

IJMPS

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Epilepsy is a common and a complex neurological disorder that is characterized by a persisting tendency to generate seizures which affect quality of life. However neuro inflammation may be included as a major contributor to seizure that may be treated via non-steroidal anti-inflammatory drugs. The results: the effect of pre-administration of diclofenac sodium intraperitoneally at a dose of 10 mg/kg on the onset of action was highly significant in comparison with first group p-value < 0.001 and was significant and strongly significant in comparison with both diazepam and the combination groups (p-value = 0.003 and 0.001 respectively). The time recorded as a seizure duration which belong to the effect of diclofenac sodium was 57.4 ± 8.142 seconds with highly significant effect against all remaining groups. However, it was revealed that no death was happening in diclofenac sodium group, but it reaches to 100% in diazepam group while in group of combined treatment it was 60% through 24 hours that followed the study period. AimsConclusion: Diclofenac sodium (non-selective NSAIDs) may display protection against seizures, but this protection is revealed to be a lesser extent when it combined with diazepam.

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Insights into inflammation and epilepsy from the basic and clinical sciences

Cited by 29 publications

References 83 publications

Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection‐related epilepsy syndrome and febrile status epilepticus

Etiology is the key determinant of neuroinflammation in epilepsy: Elevation of cerebrospinal fluid cytokines and chemokines in febrile infection‐related epilepsy syndrome and febrile status epilepticus

Intracerebral delivery of the M2 polarizing cytokine interleukin 13 using mesenchymal stem cell implants in a model of temporal lobe epilepsy in mice

Evaluation the Effect of Diclofenac Sodium on Inh-Induced Seizures

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