Aquaporins and blood–brain barrier permeability in early edema development after traumatic brain injury

Blixt, Jonas; Svensson, Mikael; Gunnarson, Eli; Wanecek, Michael

doi:10.1016/j.brainres.2015.03.004

Cited by 57 publications

(49 citation statements)

References 60 publications

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“…In the early stage of increased ICP induced by cerebral edema, cerebrospinal fluid (CSF) with the maximal electrical conductivity tissue of the intracranial region played a leading role in regulation [28]. When cerebral edema occurred, the distribution of the cerebrospinal fluid immediately changed [2]. As part of CSF regulation, the ICP had a significant difference later than the MIPS.…”

Section: Resultsmentioning

confidence: 99%

“…Cerebral edema is a common secondary disease following traumatic brain injury (TBI) which can be an important risk factor for mortality and poor outcome [1,2]. Therefore, the real-time continuous monitoring of cerebral edema plays important roles in disease observation, treatment guidance, surgery timing determination and prognosis evaluation for patients after TBI.…”

Section: Introductionmentioning

confidence: 99%

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Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

Sun

et al. 2017

Sensors

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Cerebral edema is a common disease, secondary to craniocerebral injury, and real-time continuous monitoring of cerebral edema is crucial for treating patients after traumatic brain injury. This work established a noninvasive and noncontact system by monitoring the magnetic induction phase shift (MIPS) which is associated with brain tissue conductivity. Sixteen rabbits (experimental group n = 10, control group, n = 6) were used to perform a 24 h MIPS and intracranial pressure (ICP) simultaneously monitored experimental study. For the experimental group, after the establishment of epidural freeze-induced cerebral edema models, the MIPS presented a downward trend within 24 h, with a change magnitude of −13.1121 ± 2.3953°; the ICP presented an upward trend within 24 h, with a change magnitude of 12–41 mmHg. The ICP was negatively correlated with the MIPS. In the control group, the MIPS change amplitude was −0.87795 ± 1.5146 without obvious changes; the ICP fluctuated only slightly at the initial value of 12 mmHg. MIPS had a more sensitive performance than ICP in the early stage of cerebral edema. These results showed that this system is basically capable of monitoring gradual increases in the cerebral edema solution volume. To some extent, the MIPS has the potential to reflect the ICP changes.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

Sun

et al. 2017

Sensors

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“…; Blixt et al . ). Active microglia rapidly induce the expression and release of cytokines and chemokines after injury (Kumar et al .…”

Section: Classic Examples Of Neuroinflammation In the Context Of Centmentioning

confidence: 97%

“…Myriad studies indicate that both focal (penetrating) and diffuse (non-penetrating) TBI induce significant inflammatory processes in the brain mediated, in part, by resident microglia and astrocytes (Tang et al 1997;McCrea et al 2003;Lifshitz et al 2007b;Woodcock and Morganti-Kossmann 2013). Following TBI, microglia respond to damaged cells, other activated glia, and peripherally derived stimuli after the breakdown of the blood-brain barrier (Abdul-Muneer et al 2013;Blixt et al 2015). Active microglia rapidly induce the expression and release of cytokines and chemokines after injury (Kumar et al 2015;Witcher et al 2015).…”

Section: Classic Examples Of Neuroinflammation In the Context Of Centmentioning

confidence: 99%

Neuroinflammation: the devil is in the details

DiSabato

Quan

Godbout

2016

Journal of Neurochemistry

1,169

737

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There is significant interest in understanding inflammatory responses within the brain and spinal cord. Inflammatory responses that are centralized within the brain and spinal cord are generally referred to as “neuroinflammatory”. Aspects of neuroinflammation vary within the context of disease, injury, infection or stress. The context, course, and duration of these inflammatory responses are all critical aspects in the understanding of these processes and their corresponding physiological, biochemical and behavioral consequences. Microglia, innate immune cells of the central nervous system (CNS), play key roles in mediating these neuroinflammatory responses. Because the connotation of neuroinflammation is inherently negative and maladaptive, the majority of research focus is on the pathological aspects of neuroinflammation. There are, however, several degrees of neuroinflammatory responses, some of which are positive. In many circumstances including CNS injury, there is a balance of inflammatory and intrinsic repair processes that influences functional recovery. In addition, there are several other examples where communication between the brain and immune system involves neuroinflammatory processes that are beneficial and adaptive. The purpose of this review is to distinguish different variations of neuroinflammation in a context-specific manner and detail both positive and negative aspects of neuroinflammatory processes.

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“…In the context of injury, microglia respond to damaged cells, other activated glia, and peripherally derived stimuli following breakdown of the blood brain barrier (BBB). For instance, TBI causes down-regulation of gap-junction proteins as early as 6 hours after injury [34] that persists for up to 4 days [35], allowing blood components to enter the brain. This is relevant because fibrinogen [36], a component of the clotting cascade, and ferritin [37], an iron storage molecule, cause microglial activation and chemotaxis.…”

Section: Acute Activation Of Microglia After Tbimentioning

confidence: 99%

Priming the Inflammatory Pump of the CNS after Traumatic Brain Injury

Witcher

Eiferman

Godbout

2015

Trends in Neurosciences

191

157

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Traumatic brain injury (TBI) can lead to secondary neuropsychiatric problems that develop and persist years after injury. Mounting evidence indicates that neuroinflammatory processes progress after the initial head injury and worsen with time. Microglia contribute to this inflammation by maintaining a primed profile long after the acute effects of the injury have dissipated. This may set the stage for glial dysfunction and hyperactivity to challenges including subsequent head injury, stress, or induction of a peripheral immune response. The purpose of this review is to discuss the evidence that microglia become primed following TBI and how this corresponds with vulnerability to a “second hit” and subsequent neuropsychiatric and neurodegenerative complications.

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Aquaporins and blood–brain barrier permeability in early edema development after traumatic brain injury

Cited by 57 publications

References 60 publications

Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

Neuroinflammation: the devil is in the details

Priming the Inflammatory Pump of the CNS after Traumatic Brain Injury

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