Prognostic value of brain injury biomarkers in acute encephalitis/encephalopathy

Tsukahara, Hirokazu; Fujii, Yosuke; Matsubara, Kousaku; Yamada, Masaya; Nagaoka, Yoshiharu; Saito, Yukie; Yashiro, Masato; Tsuge, Mitsuru; Goto, Shinichiro; Kitamura, Tatsuya; Hata, Atsuko; Ichiyama, Takashi; Morishima, Tsuneo

doi:10.1111/ped.12094

Cited by 20 publications

(15 citation statements)

References 13 publications

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“…According to the syndromic classification, group 1 had statistically significant unfavorable outcomes (87.5%, p = 0.0010) (Table 3), which coincided with previous reports [2, 6, 13, 14]. On the other hand, patients in group 2 had a remarkably lower risk of clinical deterioration (unfavorable outcome ratio: 14.3%).…”

Section: Discussionsupporting

confidence: 89%

Prognostic Factors for Pediatric Acute Encephalopathy Associated with Severe Brain Edema

Tamura

Inagaki

2021

Pediatr Neurosurg

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Background and Objective: Acute encephalopathy is a life-threatening brain dysfunction in children, often associated with a preceding infection and diffuse noninflammatory brain edema. At present, the role of decompressive craniectomy (DC) over the swollen area of the brain is unclear. The risk factors for predicting clinical deterioration also need clarification. Methods: A retrospective study of pediatric patients admitted between 2015 and 2019 with acute cerebral encephalopathy was carried out. Patients were classified according to: (1) the preceding pathogens, (2) the syndromic classification, and (3) the extent of brain edema. The syndromic classification is a relatively new classification of acute encephalopathy proposed in 2016 and divides patients into 3 groups: those with systemic inflammatory reactions or “cytokine storms” (group 1), those with status epilepticus but no cytokine storm (group 2), and others (group 3). Glasgow Outcome Scale (GOS) scores of 1–3 were defined as unfavorable, while a GOS score of 4 or 5 was defined as a favorable outcome in this study. DC was performed for select patients with life-threatening signs of brainstem compression. Results: Nineteen patients (mean age: 23.3 months) were included in the study, 8 (42.1%) of whom had an unfavorable outcome. There was no significant correlation between the types of pathogens and outcome. Unfavorable outcomes were observed in significantly more patients in group 1 (87.5%) than group 2 (14.3%) and group 3 (0%). There was a significant association between diffuse brain edema and unfavorable outcomes (72.7%). Neurosurgical DC was performed in 2 patients to alleviate life-threatening brainstem compression: one with a cytokine storm and diffuse bilateral brain edema, and the other with prolonged status epilepticus causing diffuse right-sided brain edema. The GOS score was 3 and 4, respectively. Conclusion: The risk factors for clinical deterioration in pediatric acute encephalopathy were evaluated based on a variety of classifications, including the new syndromic classification. Laboratory features of cytokine storms and radiological evidence of diffuse brain edema were associated with unfavorable outcomes. The role of surgical decompression is still controversial and should be assessed on a case-by-case basis.

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Section: Discussionsupporting

confidence: 89%

Prognostic Factors for Pediatric Acute Encephalopathy Associated with Severe Brain Edema

Tamura

Inagaki

2021

Pediatr Neurosurg

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“…Notably, the onset of neurological manifestations was also paralleled by an increase in serum levels of S100B protein (reflecting an increased BBB permeability)[10]. Elevated serum S100B levels have been previously reported in other acute encephalitis and immune effector cell neurotoxicity syndrome (ICANS)[15][16][17].CRS is a potentially fatal complication of different infectious (e.g., influenza, SARS, Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis) and noninfectious (e.g., multiple organ dysfunction syndrome, multiple sclerosis) diseases. Moreover, it can have a iatrogenic origin during the course of T and B lymphocyte engaging therapies like chimeric antigen receptor (CAR)-T-cell immunotherapy, rituximab, and immune check-point inhibitors [18,13].…”

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confidence: 77%

Cytokine Release Syndrome-Associated Encephalopathy in Patients with COVID-19

Perrin¹,

Collongues²,

Baloglu³

et al. 2020

Preprint

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Severe disease and uremia are risk factors for neurological complications of coronavirus disease-2019 (COVID-19). An in-depth analysis of a case series was conducted to describe the neurological manifestations of patients with COVID-19 and gain pathophysiological insights that may guide clinical decision-making – especially with respect to the cytokine release syndrome (CRS). Extensive clinical, laboratory, and imaging phenotyping was performed in five patients. Neurological presentation included confusion, tremor, cerebellar ataxia, behavioral alterations, aphasia, pyramidal syndrome, coma, cranial nerve palsy, dysautonomia, and central hypothyroidism. Neurological disturbances were remarkably accompanied by laboratory evidence of CRS. SARS-CoV-2 was undetectable in the cerebrospinal fluid. Hyperalbuminorachy and increased levels of the astroglial protein S100B were suggestive of blood-brain barrier (BBB) dysfunction. Brain MRI findings comprised evidence of acute leukoencephalitis (n = 3, of whom one with a hemorrhagic form), cytotoxic edema mimicking ischemic stroke (n = 1), or normal results (n = 2). Treatment with corticosteroids and/or intravenous immunoglobulins was attempted – resulting in rapid recovery from neurological disturbances in two cases. Patients with COVID-19 can develop neurological manifestations that share clinical, laboratory, and imaging similarities with those of chimeric antigen receptor-T cell-related encephalopathy. The pathophysiological underpinnings appear to involve CRS, endothelial activation, BBB dysfunction, and immune-mediated mechanisms.

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“…64 There has also been interest in the development of blood and CSF-based biomarkers of prognosis, including elevated levels of neural proteins or inflammatory cytokines which may correlate with poor outcome. [65][66][67] Overall, however, there exists a relative paucity of clinically useful biomarkers for prognosis following encephalitis and thus there is considerable interest in developing neuroimaging biomarkers. Below we will describe outcomes and neuroimaging correlates for selected infectious and autoimmune causes of encephalitis.…”

Section: Neuroimaging Biomarkers and Outcomesmentioning

confidence: 99%

Imaging in Encephalitis

Venkatesan

Jagdish

2019

Semin Neurol

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Despite recent advances in diagnostic and therapeutic modalities for infectious and autoimmune encephalitis, the management of patients with suspected or confirmed encephalitis poses a great challenge to physicians. Neuroimaging, including magnetic resonance imaging (MRI) and positron emission tomography (PET) scanning, can play a crucial role in substantiating the diagnosis of encephalitis and eliminating clinical mimics of encephalitis from consideration. Moreover, characteristic neuroimaging patterns can aid in defining specific infectious and autoimmune etiologies. Volumetric and functional MRI, in particular, are being increasingly used to characterize outcomes following encephalitis and can shed light on brain reorganization and function after the acute phase of disease has resolved. Here, we discuss the uses of structural, functional, and PET neuroimaging in the clinical assessment of the acute and recovery phases of encephalitis.

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Prognostic value of brain injury biomarkers in acute encephalitis/encephalopathy

Abstract: Our findings suggest that combined measurement and scoring assessment of the markers, especially S-100B and tau, show promise as predictors of clinical outcomes in children with AEE.

Cited by 20 publications

References 13 publications

Prognostic Factors for Pediatric Acute Encephalopathy Associated with Severe Brain Edema

Prognostic Factors for Pediatric Acute Encephalopathy Associated with Severe Brain Edema

Cytokine Release Syndrome-Associated Encephalopathy in Patients with COVID-19

Imaging in Encephalitis

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