Increased level of serum interleukin-1 receptor antagonist subsequent to resolution of clinical symptoms in patients with West syndrome

Yamanaka, Gaku; Kawashima, Hisashi; Oana, Shingo; Ishida, Yu; Miyajima, Tasuku; Kashiwagi, Yasuyo; Hoshika, Akinori

doi:10.1016/j.jns.2010.07.018

Cited by 19 publications

(20 citation statements)

References 23 publications

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“…Some related articles were excluded because of unvalued data (Dias De Sousa et al, 2012), lack of specific values (mean ± SD) ( Masuyama et al, 2002;Virta et al, 2002b;Ichiyama et al, 2004Ichiyama et al, , 2008Ichiyama et al, , 2009Stoeck et al, 2006;Yamanaka et al, 2006Yamanaka et al, , 2010Fukumoto et al, 2007;Sinha et al, 2008 Asano et al, 2010;Blyth et al, 2011;Mathieu et al, 2011;Haberlandt et al, 2013), lack of a control group without any neurological complications interfered with immunological response or using baseline references (Billiau et al, 2007;Alapirtti et al, 2009;Bauer et al, 2009;Li et al, 2013;Uludag et al, 2013), concomitant disorders in epileptic cases [e.g., depression (Lehtimäki et al, 2008) and neurocysticercosis (Evans et al, 1998)], concomitant disorders in the control group (e.g., encephalitis) (Ichiyama et al, 1998;Hu et al, 2014), and replicated data (Peltola et al, 2002). Some abstracts seemed to be related, but full-text was not available to make sure if they met the inclusion criteria or not (Ling et al, 1993;Kawakami et al, 1999b;Haspolat et al, 2002;Ganor et al, 2005;Makis et al, 2005;Lehtimäki et al, 2010;Lukaszewicz et al, 2010;Majoie et al, 2010;Mine et al, 2013).…”

Section: Resultsmentioning

confidence: 99%

Proinflammatory and anti-inflammatory cytokines in febrile seizures and epilepsy: systematic review and meta-analysis

Saghazadeh

Gharedaghi

Meysamie

et al. 2014

Reviews in the Neurosciences

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Section: Resultsmentioning

confidence: 99%

Proinflammatory and anti-inflammatory cytokines in febrile seizures and epilepsy: systematic review and meta-analysis

Saghazadeh

Gharedaghi

Meysamie

et al. 2014

Reviews in the Neurosciences

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“…Increased populations of CD3 + and CD4 + T lymphocytes, CD4 + /8 + T cell ratio, and higher serum concentrations of IL-1β, IL-12, and macrophage inflammatory protein 1β were observed in the pre-ACTH treatment patient group compared with the post-ACTH treatment group [106]. Similarly, the IL receptor antagonist (IL-1ra) seems to be decreased during the active stage of IS [107] and increased after the resolution of symptoms of IS [108]. IL-2, interferon-α, and tumor necrosis factor-α were also reported to be increased in the serum of patients with IS [109].…”

Section: Neuroinflammatory Mechanismsmentioning

confidence: 90%

“…IL-2, interferon-α, and tumor necrosis factor-α were also reported to be increased in the serum of patients with IS [109]. These findings were equally relevant for both patients with IS of structural/metabolic or unknown etiology [108,109]. However, cerebrospinal fluid (CSF) concentrations of the classical proinflammatory IL-6 were significantly lower in patients with IS than in patients with generalized tonic-clonic seizures due to infection or trauma [110].…”

Section: Neuroinflammatory Mechanismsmentioning

confidence: 94%

Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

2014

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The mechanisms of epileptogenesis in pediatric epileptic syndromes are diverse, and may involve disturbances of neurodevelopmental trajectories, synaptic homeostasis, and cortical connectivity, which may occur during brain development, early infancy, or childhood. Although genetic or structural/metabolic factors are frequently associated with agespecific epileptic syndromes, such as infantile spasms and West syndrome, other syndromes may be determined by the effect of immunopathogenic mechanisms or energy-dependent processes in response to environmental challenges, such as infections or fever in normally-developed children during early or late childhood. Immune-mediated mechanisms have been suggested in selected pediatric epileptic syndromes in which acute and rapidly progressive encephalopathies preceded by fever and/or infections, such as febrile infection-related epilepsy syndrome, or in chronic progressive encephalopathies, such as Rasmussen encephalitis. A definite involvement of adaptive and innate immune mechanisms driven by cytotoxic CD8 +

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“…Among the studies that correlated the treatment response to the inflammatory indices before and after treatment, there is evidence that some of these changes are linked to treatment response (e.g., IL-1ra elevation or reduction of blood IL-1β or reduction in CD4+ or CD4+/CD8+ ratios (Ohya, Nagai, Araki, Yanagawa, Tanabe, Iyoda et al 2009, Shiihara, Miyashita, Yoshizumi, Watanabe, Yamada & Kato 2010, Yamanaka, Kawashima, Oana, Ishida, Miyajima, Kashiwagi et al 2010). However, conclusive studies are needed as well as confirmation by animal models.…”

Section: Does Activation Of the Inflammatory Pathways In The Brainmentioning

confidence: 99%

Inflammation in Epileptic Encephalopathies

Shandra

Moshé

Galanopoulou

2017

Stress and Inflammation in Disorders

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West syndrome (WS) is an infantile epileptic encephalopathy (EE) that manifests with infantile spasms, hypsarrhythmia (in ~60% of infants) and poor neurodevelopmental outcomes. The etiologies of WS can be structural-metabolic pathologies (~60%), genetic (12–15%) or of unknown origin. The current treatment options include hormonal treatment [adrenocorticotropic hormone (ACTH) and high dose steroids], the GABA aminotransferase inhibitor vigabatrin, while ketogenic diet can be given as add-on treatment in refractory IS. There is a need to identify new therapeutic targets and more effective treatments for WS. Theories about the role of inflammatory pathways in the pathogenesis and treatment of WS have emerged, being supported by both clinical and preclinical data from animal models of WS. Ongoing advances in genetics have revealed numerous genes involved in the pathogenesis of WS, including genes directly or indirectly involved in inflammation. Inflammatory pathways also interact with other signaling pathways implicated in WS, such as the neuroendocrine pathway. Furthermore, seizures may also activate pro-inflammatory pathways raising the possibility that inflammation can be a consequence of seizures and epileptogenic processes. With this targeted review we plan to discuss the evidence pro and against the following key questions. Does activation of inflammatory pathways in the brain cause epilepsy in WS and does it contribute to the associated comorbidities and progression? Can activation of certain inflammatory pathways be a compensatory or protective event? Are there interactions between inflammation and the neuroendocrine system that contribute to the pathogenesis of West syndrome? Does activation of brain inflammatory signaling pathways contribute to the transition of WS to Lennox-Gastaut syndrome? Are there any lead candidates or unexplored targets for future therapy development for WS targeting inflammation?

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Increased level of serum interleukin-1 receptor antagonist subsequent to resolution of clinical symptoms in patients with West syndrome

Cited by 19 publications

References 23 publications

Proinflammatory and anti-inflammatory cytokines in febrile seizures and epilepsy: systematic review and meta-analysis

Proinflammatory and anti-inflammatory cytokines in febrile seizures and epilepsy: systematic review and meta-analysis

Mechanisms of Epileptogenesis in Pediatric Epileptic Syndromes: Rasmussen Encephalitis, Infantile Spasms, and Febrile Infection-related Epilepsy Syndrome (FIRES)

Inflammation in Epileptic Encephalopathies

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