Cytokines in cerebrospinal fluid of children with West syndrome

Cytokines in cerebrospinal fluid of children with West syndrome

In this study we aimed to determine the levels of tumor necrosis factor beta (TNF-b), interleukin (IL) 1-beta (IL-1b), IL-5, IL-10, and interferon gamma (IFN-g ) in CSF from children during the onset of West syndrome (WS). We observed elevated levels of IL-1b and IFN-g correlated to clinical, EEG, therapeutic response, and follow-up suggesting the involvement of immune response in WS. These results suggest that inflammatory and immunologic mediators may play a role in the pathophysiologic mechanisms of infantile spasms. Our findings may explain the perfusion and cognitive disfunctions and actions of adrenocorticotropic hormone (ACTH), corticosteroids, and intravenous immunoglobulin (IVIg) observed in WS. In conclusion, WS results from association of neurophysiological mechanisms and structural abnormalities with participation of cytokines mainly in symptomatic group.

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Bibliographic Details
Main Authors: Sousa,MA Dias de, Bonatti,RCF, Rodrigues Jr,V, Azevedo,DS, Santos,MHA, Pereira,ROL, Leboreiro-Fernandez,A
Format: Digital revista
Language:English
Published: Liga Brasileira de Epilepsia (LBE) 2012
Online Access:http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1676-26492012000200010
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Summary:In this study we aimed to determine the levels of tumor necrosis factor beta (TNF-b), interleukin (IL) 1-beta (IL-1b), IL-5, IL-10, and interferon gamma (IFN-g ) in CSF from children during the onset of West syndrome (WS). We observed elevated levels of IL-1b and IFN-g correlated to clinical, EEG, therapeutic response, and follow-up suggesting the involvement of immune response in WS. These results suggest that inflammatory and immunologic mediators may play a role in the pathophysiologic mechanisms of infantile spasms. Our findings may explain the perfusion and cognitive disfunctions and actions of adrenocorticotropic hormone (ACTH), corticosteroids, and intravenous immunoglobulin (IVIg) observed in WS. In conclusion, WS results from association of neurophysiological mechanisms and structural abnormalities with participation of cytokines mainly in symptomatic group.

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