Cerebral edema is a significant cause of morbidity and mortality after ischemic and hemorrhagic stroke. The underlying molecular pathophysiology remains incompletely understood, limiting treatment efficacy. After stroke occurs, hypoxia, inflammation, and oxidative stresses initiate the expression and functional alteration of the ion/water channels of cells comprising the neurovascular unit, leading to three dynamic forms of edema: cytotoxic, ionic, and vasogenic.
Many studies have proposed that dysfunction of the neurovascular unit increases the brain’s extravascular volume, which contributes to the re-equilibration of solutes and water across the cerebrospinal fluid (CSF)-blood and the blood-brain barriers (BBB). Recent descriptions of the glymphatic system have led to the formulation of a novel hypothesis. In this hypothesis, glymphatic system is responsible for the perivascular, interstitial, and intracellular fluid exchange. After injury, the immediate influx of CSF from the perivascular space into the parenchyma lead to the first stage of edema formation. In addition, the impairment of the glymphatic system hinders the efflux of the interstitial space fluid, further exacerbating the accumulation of fluid within the parenchyma.
In this Research Topic, we welcome original research and review articles in all topics associated with cerebral edema in stroke, from underlying molecular and cellular pathophysiology to clinical transformation. In addition, we are also interested in research aiming to predict the occurrence of cerebral edema, so as to prevent the formation of edema rather than dealing with the treatment afterwards.
Specific themes relevant to this Research Topic are listed below:
1. Mechanisms of cerebral edema formation and glymphatic system, including the underlying molecular and cellular pathophysiology.
2. Roles of BBB and glymphatic system dysfunction in cerebral edema.
3. Novel techniques or technologies to measure the cerebral edema and glymphatic system.
4. Drug developments targeting cerebral edema.
Cerebral edema is a significant cause of morbidity and mortality after ischemic and hemorrhagic stroke. The underlying molecular pathophysiology remains incompletely understood, limiting treatment efficacy. After stroke occurs, hypoxia, inflammation, and oxidative stresses initiate the expression and functional alteration of the ion/water channels of cells comprising the neurovascular unit, leading to three dynamic forms of edema: cytotoxic, ionic, and vasogenic.
Many studies have proposed that dysfunction of the neurovascular unit increases the brain’s extravascular volume, which contributes to the re-equilibration of solutes and water across the cerebrospinal fluid (CSF)-blood and the blood-brain barriers (BBB). Recent descriptions of the glymphatic system have led to the formulation of a novel hypothesis. In this hypothesis, glymphatic system is responsible for the perivascular, interstitial, and intracellular fluid exchange. After injury, the immediate influx of CSF from the perivascular space into the parenchyma lead to the first stage of edema formation. In addition, the impairment of the glymphatic system hinders the efflux of the interstitial space fluid, further exacerbating the accumulation of fluid within the parenchyma.
In this Research Topic, we welcome original research and review articles in all topics associated with cerebral edema in stroke, from underlying molecular and cellular pathophysiology to clinical transformation. In addition, we are also interested in research aiming to predict the occurrence of cerebral edema, so as to prevent the formation of edema rather than dealing with the treatment afterwards.
Specific themes relevant to this Research Topic are listed below:
1. Mechanisms of cerebral edema formation and glymphatic system, including the underlying molecular and cellular pathophysiology.
2. Roles of BBB and glymphatic system dysfunction in cerebral edema.
3. Novel techniques or technologies to measure the cerebral edema and glymphatic system.
4. Drug developments targeting cerebral edema.