Serum and CSF levels of cytokines in acute encephalopathy following prolonged febrile seizures

Ichiyama, Takashi; Suenaga, Naoko; Kajimoto, Madoka; Tohyama, Jun; Isumi, Hiroshi; Kubota, Masaya; Mori, Masayuki; Furukawa, Susumu

doi:10.1016/j.braindev.2007.05.008

Cited by 101 publications

(73 citation statements)

References 27 publications

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“…Finally, CSF IFN-g levels have been reported to be elevated in CNS disorders with direct mechanisms, such as herpes simplex encephalitis, but not in CNS disorders caused by an indirect mechanism, such as influenza encephalopathy [Ichiyama et al, 2002[Ichiyama et al, , 2005[Ichiyama et al, , 2008Shoji et al, 2004]. We found that the concentrations of IFN-g were not elevated in the CSF of HHV-6 encephalopathy patients, consistent with a recent report [Ichiyama et al, 2009].…”

Section: Discussionsupporting

confidence: 92%

Comparison of the levels of human herpesvirus 6 (HHV‐6) DNA and cytokines in the cerebrospinal fluid and serum of children with HHV‐6 encephalopathy

Kawabe¹,

Ito²,

Ohta³

et al. 2010

Journal of Medical Virology

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Primary human herpesvirus-6 (HHV-6) infection is a common cause of acute sporadic encephalopathy in Japanese children. Occasionally, HHV-6 is not detected in the cerebrospinal fluid (CSF) of patients with encephalopathy, for example, in those with focal viral encephalitis, such as herpes simplex viral encephalitis. This indicates that HHV-6 encephalopathy is caused by an indirect mechanism, although this is not fully understood. HHV-6 DNA, cytokines (interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12 p70, tumor necrosis factor-alpha, interferon-gamma), and matrix metalloproteinase-9 were quantitated in both the CSF and serum of 13 patients with HHV-6 encephalopathy during the acute phase of the disease. HHV-6 DNA was detected in the CSF of seven patients with HHV-6 encephalopathy. The viral DNA concentration was significantly higher in serum than in CSF (mean 1.64 x 10(4) vs. 5.70 x 10(1) copies/ml; P = 0.003). The lack or low level of viral DNA in the CSF samples suggests that direct invasion of the central nervous system by HHV-6 is not the main cause of encephalopathy. Additionally, the IL-10 concentration was significantly higher in serum than in CSF (P < 0.001), whereas there was no significant difference in IL-6 levels between the CSF and serum samples. Interestingly, the IL-8 concentration was significantly higher in CSF than in serum (P = 0.038). The distribution of these cytokines differed between CSF and serum. The high CSF concentration of IL-8 could play an important role in the pathogenesis of encephalopathy.

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Section: Discussionsupporting

confidence: 92%

Comparison of the levels of human herpesvirus 6 (HHV‐6) DNA and cytokines in the cerebrospinal fluid and serum of children with HHV‐6 encephalopathy

Kawabe¹,

Ito²,

Ohta³

et al. 2010

Journal of Medical Virology

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“…CSF cytokine analysis in AESD showed elevated interleukin (IL)-6 without elevated IL-10 (an anti-inflammatory cytokine) or soluble tumor necrosis factor (TNF) receptor 1 (sTNFR1, reflecting the true biologic activity of inflammatory cytokine, TNF-␣). 8 This profile is distinct from that of a cytokine storm, seen in inflammation and showing elevated IL-6, IL-10, and sTNFR1.…”

Section: Discussionmentioning

confidence: 99%

Excitotoxicity in Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion

Takanashi¹,

Tada²,

Terada³

et al. 2008

AJNR Am J Neuroradiol

113

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SUMMARY:Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a recently described clinicoradiologic syndrome. MR spectroscopy in 3 patients with AESD revealed decreased N-acetylaspartate (NAA) and elevated glutamine/glutamate complex (Glx) during the week of presentation. Afterward, Glx normalized, whereas NAA remained low in 2 patients with neurologic sequelae but nearly normalized in the third patient without neurologic sequelae. These findings support the hypothesis that excitotoxic neuronal damage plays an important role in the pathogenesis of AESD and suggest that MR spectroscopy might be predictive of outcome.A n acute encephalopathy syndrome characterized by biphasic seizures and late reduced diffusion (AESD) was recently reported in 17 Asian children. The syndrome is characterized by a prolonged (Ͼ30 minutes) febrile seizure as the initial neurologic symptom on day 1, followed by secondary seizures (most often in a cluster of complex partial seizures) at days 4 -6; affected children display variable levels of neurologic sequelae.1,2 MR imaging shows no acute abnormality during the first 2 days; reduced diffusion appears in the frontal or frontoparietal subcortical white matter, with sparing of perirolandic region, during days 3-9, then disappears between days 9 and 25. Ultimately, patients develop cerebral atrophy. Other reports have described patients with closely related entities, such as acute encephalopathy with febrile convulsive status epilepticus (AEFCSE).3 Recently, a mild form of AESD with a brief initial febrile seizure (non-status epilepticus) and the absence of permanent neurologic sequelae has also been reported, 2 suggesting that AESD has a wider spectrum than AEFCSE.The exact pathogenesis of AESD is uncertain; excitotoxic injury with delayed (or apoptotic) neuronal death is hypothesized as a possible mechanism.3 Elevated glutamine (Gln)/ glutamate (Glu) complex (Glx, at 2.1-2.5 and 3.8 ppm on MR spectroscopy) was reported in 1 patient with AESD.1 We performed MR spectroscopy in 3 additional patients with AESD to evaluate metabolites in vivo and to test the hypothesis that excitotoxicity is the mechanism of pathogenesis. Case Reports Patient 1A previously healthy 2-year-old Japanese girl presented with a generalized tonic-clonic seizure, lasting an hour, following a 7-hour prodromal illness consisting of a high fever, cough, and rhinorrhea. Blood and CSF examinations findings were normal. Electroencephalography (EEG) showed diffuse high-voltage slow waves. A rapid antigen-detection assay from a nasopharyngeal swab revealed influenza A. She became comatose after cessation of the initial seizure. On day 5, she manifested a cluster of partial seizures, each lasting a few minutes. MR imaging on day 6 revealed reduced diffusion (Fig 1A, B) and T2 and T1 prolongation diffusely in the subcortical white matter with sparing of the perirolandic region; follow-up MR imaging on day 20 showed mild cortical T2 prolongation with mild cerebral atrophy (Fig 1D). On the basis of t...

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“…CSF IFN-γ levels were elevated in the central nervous system (CNS) disorders due to direct viral invasion, such as viral meningitis and HSE (Matsubara et al, 2000;Ichiyama et al, 2005;Ichiyama et al, 2008a), but not in immune-mediated CNS disorders, such as acute disseminated encephalomyelitis, influenzaassociated encephalopathy, and acute encephalopathy following prolonged febrile seizures, and hemolytic uremic syndrome with encephalopathy (Ichiyama et al, 2002;Ichiyama et al, 2004;Ichiyama et al, 2008b;Shiraishi et al, 2008). IFN-γ, which is produced by NK cells, CD8+ and Th1 type CD4+ T lymphocytes, plays an important role in host defense against viral infection, and inhibits viral replication (Samuel., 1991).…”

Section: Pathogenesismentioning

confidence: 99%

Non-Herpetic Acute Limbic Encephalitis: A New Subgroup of Limbic Encephalitis?

Shoji¹,

Kimura²,

Kumamoto³

et al. 2011

Pathogenesis of Encephalitis

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Serum and CSF levels of cytokines in acute encephalopathy following prolonged febrile seizures

Cited by 101 publications

References 27 publications

Comparison of the levels of human herpesvirus 6 (HHV‐6) DNA and cytokines in the cerebrospinal fluid and serum of children with HHV‐6 encephalopathy

Comparison of the levels of human herpesvirus 6 (HHV‐6) DNA and cytokines in the cerebrospinal fluid and serum of children with HHV‐6 encephalopathy

Excitotoxicity in Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion

Non-Herpetic Acute Limbic Encephalitis: A New Subgroup of Limbic Encephalitis?

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