Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Seifman, Marc A.; Adamides, Alexios A.; Nguyen, Phuong Nga; Vallance, Shirley; Cooper, Jamie; Kossmann, Thomas; Rosenfeld, Jeffrey V.; Morganti-Kossmann, Maria Cristina

doi:10.1038/sj.jcbfm.9600603

Cited by 79 publications

(74 citation statements)

References 43 publications

(48 reference statements)

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“…This is the case despite the finding that the lipid peroxidation markers F2-isoprostane and malondialdehyde are increased in brain tissue, serum, and CSF after experimental and clinical TBI. [142][143][144] More importantly, this increase in lipid peroxidation is associated with worse clinical outcomes in patients with severe TBI. 145,146 Also unique is the fact that phospholipids in different regions of the brain differ in their fatty acid compositions and side chains, 132-134 but association among types of phospholipids, regions of brain injury, and rates of coagulopathy has not been examined.…”

Section: Phosphatidylserine and Brain Phospholipidsmentioning

confidence: 99%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

123

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Traumatic injury is a common cause of coagulopathy, primarily due to blood loss and hemodilution secondary to fluid resuscitation. Traumatic injury-associated coagulopathy often follows a course of transition from hyper- to hypocoagulable state exemplified in disseminated intravascular coagulation. The incidence of coagulopathy is significantly higher in patients with traumatic brain injury (TBI), especially those with penetrating trauma compared to injury to the trunk and limbs. This occurs despite the fact that patients with isolated TBI bleed less and receive restricted volume load of fluids. TBI-associated coagulopathy is extensively documented to associate with poor clinical outcomes, but its pathophysiology remains poorly understood. Studies in the past have shown that brain tissue is highly enriched in key procoagulant molecules. This review focuses on the biochemical and cellular characteristics of these molecules and pathways that could make brain uniquely procoagulant and prone to coagulopathy. Understanding this unique procoagulant environment will help to identify new therapeutic targets that could reverse a state of coagulopathy with minimal impacts on hemostasis, a critical requirement for neurosurgical treatments of TBI.

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Section: Phosphatidylserine and Brain Phospholipidsmentioning

confidence: 99%

Traumatic Brain Injury-Associated Coagulopathy

Zhang

Jiang

Liu

et al. 2012

Journal of Neurotrauma

123

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“…81 Multiple studies have shown that brain injuries increase the levels of F2-isoprostane both in the CSF and the serum of TBI patients. [82][83][84] For example, Varma et al 85 demonstrated that in children who had severe TBI, the level of F2-isoprostane was elevated by 6-fold compared with that observed in uninjured controls. This marker was found to correlate well with the appearance of NSE, further supporting its use as an indicator of brain damage.…”

Section: F2-isoprostanementioning

confidence: 99%

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

et al. 2010

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“…To our knowledge, no study has examined whether IsoFs are altered in the CSF of patients after aSAH. Increased CSF F 2 -IsoPs have been reported in TBI patients (2,(7)(8)(9). To date, no study has examined IsoFs and F 4 -NeuroPs in patients with TBI.…”

Section: Innovationmentioning

confidence: 99%

Are Isofurans and Neuroprostanes Increased After Subarachnoid Hemorrhage and Traumatic Brain Injury?

Corcoran

Mas

Barden

et al. 2011

Antioxidants & Redox Signaling

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Current diagnostic tools to assess neurological injury after aneurysmal subarachnoid hemorrhage (aSAH) and traumatic brain injury (TBI) have poor discriminatory abilities. Free radicals are associated with the pathophysiology of secondary damage after brain trauma. We examined cerebrospinal fluid (CSF) lipid markers of oxidative stress, isofurans (IsoFs), F 4 -neuroprostanes (F 4 -NeuroPs), and F 2 -isoprostanes (F 2 -IsoPs), in two casecontrolled studies in patients with aSAH or severe TBI. Patients with aSAH (n = 18) or TBI (n = 18) were age and gender matched with separate control groups. CSF samples were collected from patients within 24 h of the injury. CSF IsoFs and F 4 -NeuroPs were increased in aSAH patients compared with their controls. In TBI patients, IsoFs and F 4 -NeuroPs were increased compared with their controls. F 2 -IsoPs were increased in aSAH patients, but not in TBI patients, compared with their respective controls. CSF IsoFs and F 4 -NeuroPs are consistently increased after a catastrophic central nervous system injury. These results suggest their measurement may enhance the management of unconscious patients in neurological care. Antioxid. Redox Signal. 15, 2663-2667. Brain Injury and Oxidative StressA neurysmal subarachnoid hemorrhage (aSAH) and traumatic brain injury (TBI) are associated with devastating central nervous system (CNS) injury. aSAH is associated with a high mortality rate and substantial lifelong morbidity in survivors. TBI is a major health and socioeconomic problem more prevalent in young male adults. The most common secondary injury resulting from aSAH and TBI is attributable to vasospasm-induced microvascular injury and cerebral ischemia. Diagnostic tools use surrogate measures such as intracranial pressure changes and interval changes in neuroimaging, which have poor discriminatory abilities.After acute brain injury, there is a disruption of calcium homeostasis, excitotoxicity from release of neurotransmitters such as glutamate, overproduction of reactive oxygen species (ROS), and opening of the mitochondrial permeability transition pore, all key factors in promoting mitochondrial InnovationAneurysmal subarachnoid hemorrhage (aSAH) and traumatic brain injury (TBI) associate with catastrophic central nervous system (CNS) injury. Diagnostic tools to assess neurological injury after aSAH and TBI currently have poor discriminatory capacity. Free radicals are likely to be involved in mediating secondary damage after brain trauma. In two case-controlled studies of patients with aSAH or severe TBI, we examined lipid markers of oxidative stress, isofurans (IsoFs), F 4 -neuroprostanes (F 4 -NeuroPs), and F 2 -isoprostanes (F 2 -IsoPs), in cerebrospinal fluid (CSF) samples. In aSAH and TBI patients, IsoFs and F 4 -NeuroPs were increased compared with their respective controls. F 2 -IsoPs were increased in aSAH patients, but not in TBI patients. Increased IsoFs and F 4 -NeuroPs in the CSF of these patients is a new and important finding that may have important clinical imp...

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Endogenous Melatonin Increases in Cerebrospinal Fluid of Patients after Severe Traumatic Brain Injury and Correlates with Oxidative Stress and Metabolic Disarray

Cited by 79 publications

References 43 publications

Traumatic Brain Injury-Associated Coagulopathy

Traumatic Brain Injury-Associated Coagulopathy

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

Are Isofurans and Neuroprostanes Increased After Subarachnoid Hemorrhage and Traumatic Brain Injury?

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