Brain-derived neurotrophic factor and neuron-specific enolase, but not S100β, levels are associated to the occurrence of delirium in intensive care unit patients

Grandi, Carmen; Tomasi, Cristiane Damiani; Fernandes, Keiti; Stertz, Laura; Kapczinski, Flávio; Quevedo, Joao L De; Dal‐Pizzol, Felipe

doi:10.1016/j.jcrc.2010.10.006

Cited by 70 publications

(61 citation statements)

References 15 publications

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“…7 Therefore, we expected that brain markers of injury would be associated with mortality in critically ill patients, even in patients who did not present clinically evident brain dysfunction. An interesting issue is that we had previously demonstrated that NSE levels at admission are associated with the occurrence of delirium in ICU patients, 8 and delirium is a well-defined predictor of death in ICU populations. Nevertheless, we could not determine a clear association between levels of either S100b or NSE at ICU admission and mortality in our sample of critically ill patients.…”

Section: Biomarkers and Mortalitymentioning

confidence: 99%

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Macedo

Tomasi

Giombelli

et al. 2013

Rev. Bras. Psiquiatr.

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Objective: To evaluate the relationship between brain damage biomarkers and mortality in the intensive care unit (ICU). Methods: The sample comprised 70 patients admitted to an ICU. Blood samples were collected from all patients on ICU admission, and levels of S100b and neuron-specific enolase (NSE) were determined by ELISA. Results: Acute Physiologic and Chronic Health Evaluation (APACHE II) score was associated with mortality, but NSE and S100b were not associated with this outcome. In contrast, S100b levels were significantly higher in delirious and non-delirious patients who required mechanical ventilation during ICU stay. Conclusion: Levels of brain biomarkers at the time of ICU admission did not predict mortality in critically ill patients.

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Section: Biomarkers and Mortalitymentioning

confidence: 99%

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Macedo

Tomasi

Giombelli

et al. 2013

Rev. Bras. Psiquiatr.

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“…Other studies, however, did not find similar associations [15-17]. Increased neuron-specific enolase, an enzyme expressed in neurons in the central nervous system [18], has been reported in delirium patients in three studies [19-21], whereas one study in stroke patients could not replicate these findings [22]. Dissimilar study populations as well as lack of tissue specificity for both S100B and neuron-specific enolase may partly explain the divergent reports.…”

Section: Introductionmentioning

confidence: 99%

Neurofilament Light in Serum and Cerebrospinal Fluid of Hip Fracture Patients with Delirium

Halaas

Blennow

Idland

et al. 2018

Dement Geriatr Cogn Disord

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Background: Delirium is associated with new-onset dementia, suggesting that delirium pathophysiology involves neuronal injury. Neurofilament light (NFL) is a sensitive biomarker for neuroaxonal injury. Methods: NFL was measured in cerebrospinal fluid (CSF) (n = 130), preoperative serum (n = 192), and postoperative serum (n = 280) in hip fracture patients, and in CSF (n = 123) and preoperative serum (n = 134) in cognitively normal older adults undergoing elective surgery. Delirium was diagnosed with the Confusion Assessment Method. Results: Median serum NFL (pg/mL) was elevated in delirium in hip fracture patients (94 vs. 54 pre- and 135 vs. 92 postoperatively, both p < 0.001). Median CSF NFL tended to be higher in hip fracture patients with delirium (1,804 vs. 1,636, p = 0.074). Serum and CSF NFL were positively correlated (ρ = 0.56, p < 0.001). Conclusion: Our findings support an association between neuroaxonal injury and delirium. The correlation between serum and CSF NFL supports the use of NFL as a blood biomarker in future delirium studies.

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“…56 In contrast, S-100b is associated with SE, 45 and NSE is associated with delirium in general ICU patients. 57 Sharshar et al 27 demonstrated that septic shock is associated with neuronal and glial apoptosis in autonomic centers in humans, but brain TNF-a expression did not differ between septic shock and control patients. Whether neuronal and glial apoptosis is sufficient to induce clinically relevant brain dysfunction remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Septic encephalopathy: does inflammation drive the brain crazy?

Dal‐Pizzol

Tomasi

Ritter

2014

Rev. Bras. Psiquiatr.

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Sepsis and the multiorgan dysfunction syndrome are among the most common reasons for admission to an intensive care unit, and are a leading cause of death. During sepsis, the central nervous system (CNS) is one of the first organs affected, and this is clinically manifested as sepsis-associated encephalopathy (SAE). It is postulated that the common final pathway that leads to SAE symptoms is the deregulation of neurotransmitters, mainly acetylcholine. Thus, it is supposed that inflammation can affect neurotransmitters, which is associated with SAE development. In this review, we will cover the current evidence (or lack thereof) for the mechanisms by which systemic inflammation interferes with the metabolism of major CNS neurotransmitters, trying to explain how systemic inflammation drives the brain crazy.

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Brain-derived neurotrophic factor and neuron-specific enolase, but not S100β, levels are associated to the occurrence of delirium in intensive care unit patients

Abstract: Our results suggest that admission serum BDNF and NSE levels are associated with the occurrence of delirium in ICU patients.

Cited by 70 publications

References 15 publications

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Lack of association of S100β and neuron-specific enolase with mortality in critically ill patients

Neurofilament Light in Serum and Cerebrospinal Fluid of Hip Fracture Patients with Delirium

Septic encephalopathy: does inflammation drive the brain crazy?

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