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Neuropharmacology Feb 2019Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable prognosis in traumatic brain injury (TBI). CE is a leading cause of... (Review)
Review
Cerebral edema (CE) and resultant intracranial hypertension are associated with unfavorable prognosis in traumatic brain injury (TBI). CE is a leading cause of in-hospital mortality, occurring in >60% of patients with mass lesions, and ∼15% of those with normal initial computed tomography scans. After treatment of mass lesions in severe TBI, an important focus of acute neurocritical care is evaluating and managing the secondary injury process of CE and resultant intracranial hypertension. This review focuses on a contemporary understanding of various pathophysiologic pathways contributing to CE, with a subsequent description of potential targeted therapies. There is a discussion of identified cellular/cytotoxic contributors to CE, as well as mechanisms that influence blood-brain-barrier (BBB) disruption/vasogenic edema, with the caveat that this distinction may be somewhat artificial since molecular processes contributing to these pathways are interrelated. While an exhaustive discussion of all pathways with putative contributions to CE is beyond the scope of this review, the roles of some key contributors are highlighted, and references are provided for further details. Potential future molecular targets for treating CE are presented based on pathophysiologic mechanisms. We thus aim to provide a translational synopsis of present and future strategies targeting CE after TBI in the context of a paradigm shift towards precision medicine. This article is part of the Special Issue entitled "Novel Treatments for Traumatic Brain Injury".
Topics: Animals; Brain Edema; Brain Injuries, Traumatic; Humans; Neuroprotective Agents
PubMed: 30086289
DOI: 10.1016/j.neuropharm.2018.08.004 -
European Respiratory Review : An... Jan 2017At any point 1-5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain... (Review)
Review
At any point 1-5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.
Topics: Acute Disease; Adult; Aged; Altitude; Altitude Sickness; Animals; Brain Edema; Cerebral Arteries; Cerebrovascular Circulation; Female; Humans; Hypertension, Pulmonary; Hypoxia; Inflammation; Male; Middle Aged; Prognosis; Pulmonary Circulation; Risk Factors; Time Factors; Vasoconstriction
PubMed: 28143879
DOI: 10.1183/16000617.0096-2016 -
Journal of Cerebral Blood Flow and... Mar 2016Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of... (Review)
Review
Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema.
Topics: Animals; Aquaporins; Blood-Brain Barrier; Brain; Brain Edema; Humans; Ion Transport; Ions; Permeability; Water
PubMed: 26661240
DOI: 10.1177/0271678X15617172 -
Neurobiology of Disease Jan 2023Intracerebral hemorrhage (ICH) accounts for about 10% of all strokes in the United States of America causing a high degree of disability and mortality. There is initial... (Review)
Review
Intracerebral hemorrhage (ICH) accounts for about 10% of all strokes in the United States of America causing a high degree of disability and mortality. There is initial (primary) brain injury due to the mechanical disruption caused by the hematoma. There is then secondary injury, triggered by the initial injury but also the release of various clot-derived factors (e.g., thrombin and hemoglobin). ICH alters brain fluid homeostasis. Apart from the initial hematoma mass, ICH causes blood-brain barrier disruption and parenchymal cell swelling, which result in brain edema and intracranial hypertension affecting patient prognosis. Reducing brain edema is a critical part of post-ICH care. However, there are limited effective treatment methods for reducing perihematomal cerebral edema and intracranial pressure in ICH. This review discusses the mechanisms underlying perihematomal brain edema formation, the effects of sex and age, as well as how edema is resolved. It examines progress in pharmacotherapy, particularly focusing on drugs which have been or are currently being investigated in clinical trials.
Topics: Humans; Brain Edema; Cerebral Hemorrhage; Brain; Treatment Outcome; Hematoma
PubMed: 36481437
DOI: 10.1016/j.nbd.2022.105948 -
Frontiers in Immunology 2021Intracerebral hemorrhage (ICH) has one of the worst prognoses among patients with stroke. Surgical measures have been adopted to relieve the mass effect of the hematoma,... (Review)
Review
Intracerebral hemorrhage (ICH) has one of the worst prognoses among patients with stroke. Surgical measures have been adopted to relieve the mass effect of the hematoma, and developing targeted therapy against secondary brain injury (SBI) after ICH is equally essential. Numerous preclinical and clinical studies have demonstrated that perihematomal edema (PHE) is a quantifiable marker of SBI after ICH and is associated with a poor prognosis. Thus, PHE has been considered a promising therapeutic target for ICH. However, the findings derived from existing studies on PHE are disparate and unclear. Therefore, it is necessary to classify, compare, and summarize the existing studies on PHE. In this review, we describe the growth characteristics and relevant underlying mechanism of PHE, analyze the contributions of different risk factors to PHE, present the potential impact of PHE on patient outcomes, and discuss the currently available therapeutic strategies.
Topics: Brain; Brain Edema; Cerebral Hemorrhage; Glyburide; Hematoma; Humans; Hypoglycemic Agents; Magnetic Resonance Imaging; Neurogenic Inflammation; Risk Factors
PubMed: 34737745
DOI: 10.3389/fimmu.2021.740632 -
Ugeskrift For Laeger Mar 2023More and more people travel to high altitudes, some develop mountain sickness, a possible life-threatening condition. The most common and benign case of mountain... (Review)
Review
More and more people travel to high altitudes, some develop mountain sickness, a possible life-threatening condition. The most common and benign case of mountain sickness is acute mountain sicknes, this condition is easily treatable by descending or low dose aceatazolamide. Treatment is important to avoid development to the more severe cases of mountain sickness high-altitude cerebral oedema and high-altitude pulmonary oedema. These conditions require early recognition and treatment. This review gives an overview of available treatment of these conditions and how to avoid them in the first place.
Topics: Humans; Altitude Sickness; Acute Disease; Brain Edema; Travel; Hypertension, Pulmonary; Altitude
PubMed: 36999289
DOI: No ID Found -
International Journal of Molecular... Dec 2016The aquaporin (AQP) family of water channels are a group of small, membrane-spanning proteins that are vital for the rapid transport of water across the plasma membrane.... (Review)
Review
The aquaporin (AQP) family of water channels are a group of small, membrane-spanning proteins that are vital for the rapid transport of water across the plasma membrane. These proteins are widely expressed, from tissues such as the renal epithelium and erythrocytes to the various cells of the central nervous system. This review will elucidate the basic structure and distribution of aquaporins and discuss the role of aquaporins in various neuropathologies. AQP1 and AQP4, the two primary aquaporin molecules of the central nervous system, regulate brain water and CSF movement and contribute to cytotoxic and vasogenic edema, where they control the size of the intracellular and extracellular fluid volumes, respectively. AQP4 expression is vital to the cellular migration and angiogenesis at the heart of tumor growth; AQP4 is central to dysfunctions in glutamate metabolism, synaptogenesis, and memory consolidation; and AQP1 and AQP4 adaptations have been seen in obstructive and non-obstructive hydrocephalus and may be therapeutic targets.
Topics: Animals; Aquaporins; Brain Edema; Cell Movement; Epilepsy; Humans; Hydrocephalus; Water-Electrolyte Balance
PubMed: 28036023
DOI: 10.3390/ijms18010055 -
International Journal of Molecular... Apr 2015Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of... (Review)
Review
Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB) and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them.
Topics: Animals; Brain Edema; Glucocorticoids; Humans; Matrix Metalloproteinase Inhibitors; Neuroprotective Agents; Sodium Potassium Chloride Symporter Inhibitors; Vascular Endothelial Growth Factor A
PubMed: 25941935
DOI: 10.3390/ijms16059949 -
Cerebrovascular Diseases (Basel,... 2016Intracerebral hemorrhage (ICH) is a subtype of stroke with a severe high mortality and disability rate and accounts for about 10-15% of all strokes. The oppression and... (Review)
Review
BACKGROUND
Intracerebral hemorrhage (ICH) is a subtype of stroke with a severe high mortality and disability rate and accounts for about 10-15% of all strokes. The oppression and destruction by hematoma to brain tissue cause the primary brain injury. The inflammation and coagulation response after ICH would accelerate the formation of brain edema around hematoma, resulting in a more severe and durable injury. Currently, treatments for ICH are focusing on the primary injury including reducing intracranial hypertension, blood pressure control, and rehabilitation. There is a short-of-effective medical treatment for secondary inflammation and reducing brain edema in ICH patients. So, it is very important to study on the relationship between brain edema and ICH.
SUMMARY
Many molecular and cellular mechanisms contribute to the formation and progress of brain edema after ICH; inhibition of brain edema provides favorable outcome of ICH.
KEY MESSAGES
This review mainly discusses the pathology and mechanism of brain edema, the effects of brain edema on ICH, and the methods of treating brain edema after ICH.
Topics: Animals; Brain; Brain Edema; Cerebral Hemorrhage; Erythrocytes; Humans; Inflammation Mediators; Risk Factors; Signal Transduction; Thrombin; Treatment Outcome
PubMed: 27110940
DOI: 10.1159/000445170 -
Archives of Women's Mental Health Feb 2017Donkin psychoses are eclamptic psychoses without seizures. As symptomatic psychoses resulting from cerebral endothelial damage, they may explain the lucid intervals that...
Donkin psychoses are eclamptic psychoses without seizures. As symptomatic psychoses resulting from cerebral endothelial damage, they may explain the lucid intervals that sometimes occur between eclampsia and the eruption of psychosis. They have the same features as eclamptic psychoses, with onset during pregnancy or the early puerperium, especially in first-time mothers, a short duration and full recovery in most. The clinical picture is usually delirium, but mania is also seen, and some patients have retrograde amnesia or other cognitive defects. Donkin psychosis should be considered in the differential diagnosis of childbearing psychoses, and collaborative research is needed to clarify their differences.
Topics: Adult; Bipolar Disorder; Brain Edema; Eclampsia; Female; Humans; Pregnancy; Psychotic Disorders
PubMed: 27718021
DOI: 10.1007/s00737-016-0677-6