Indicators of inflammation after recent tonic–clonic epileptic seizures correlate with plasma interleukin-6 levels

Abstract

Cerebrospinal fluid (CSF) and peripheral blood pleocytosis have been observed after epileptic seizures without any evidence of infections, but no systematic studies on the acute phase reaction in such patients have been performed. We have previously reported increased levels of interleukin-6 (IL-6) in patients with recent tonic--clonic seizures. Because IL-6 is a major inducer of the systemic acute phase reaction, we decided to study various indicators of inflammation in the blood as well as their correlation with plasma and CSF IL-6 levels. CSF and blood samples were studied from 37 patients with previously undiagnosed and untreated tonic-clonic seizures without any clinical evidence of systemic or central nervous system infections as well as from 40 controls. The mean peripheral blood and CSF-leukocyte counts were significantly higher in patients compared with controls ( 7.9 x 10(9)vs. 6.1 x 10(9), P= 0.002 and 1.9 x 10(6)vs. 1.1 x 10(6), P= 0.032, respectively). There was some indication of increased concentration of C-reactive protein (CRP) and no difference in haptoglobin levels. There was a significant correlation between plasma but not CSF IL-6 concentration and those of both B-leukocyte count ( r= 0.051, P= 0.009) and CRP ( r= 0.42, P= 0.009). Epileptic seizures provoke a production of cytokines such as IL-6 that may in turn cause an activation of the acute phase reaction. Thus, CSF pleocytosis and increase in some indicators of inflammation should not automatically be attributed to systemic or CNS infections in patients with acute seizures.

Interleukin-6 Upregulates Neuronal Adenosine A1 Receptors: Implications for Neuromodulation and Neuroprotection

“…Rapid induction of IL-6 expression in the brain is known to occur in most (if not all) neuropathological conditions, including seizures in humans (Lehtimäki et al, 2003(Lehtimäki et al, , 2004Peltola et al, 1998Peltola et al, , 2002Jankowsky and Patterson, 1999) where IL-6 levels in the cerebrospinal fluid up to 100 pg/ml have been found (Peltola et al, 2000). Astrocytes are a major source of IL-6 in the brain (van Wagoner and Benveniste, 1999).…”

“…It is known that the expression of A 1 receptors in WT mice is increased after neuropathological events, such as seizures Vanore et al, 2001;Angelatou et al, 1991Angelatou et al, , 1993. On the other hand, several reports have shown that those noxious conditions trigger the release of IL-6 (Lehtimäki et al, 2003;Peltola et al, 1998Peltola et al, , 2002. Accordingly, we used WT animals and IL-6-deficient mice to evaluate the relationship between the expression of IL-6 and the upregulation of adenosine A 1 receptors in response to PTZ-induced seizures.…”

Early Atherosclerotic Changes in the Patients with Idiopathic Epilepsy: Egyptian Preliminary Study

“…There was a significant positive correlation between the common carotid artery intima media thickness and duration of illness which could be attributed to the role of epilepsy itself through the oxidative stress and the effect of epileptic seizures on the production of interleukin-6 (IL-6) promoting atherosclerosis [17,32].…”

Myoclonus and Metabolic Alkalosis from Licorice in Antacid

“…On the other hand, it is known that activation of inflammation may occur after epileptic seizures without any evidence of systemic or central nervous system infection (14). According to Peltola et al, production of interleukin-6 (IL-6) in the central nervous system can stimulate increased production of IL-6 in peripheral blood, which subsequently activates the acute phase reaction (14). The acute phase reaction in this case may be explained by this mechanism.…”

“…It is reported that convulsions produce changes in muscle tissue membranes that persist for three to eight days and result in CPK leakage into plasma and extracellular fluid (13). On the other hand, it is known that activation of inflammation may occur after epileptic seizures without any evidence of systemic or central nervous system infection (14). According to Peltola et al, production of interleukin-6 (IL-6) in the central nervous system can stimulate increased production of IL-6 in peripheral blood, which subsequently activates the acute phase reaction (14).…”