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Brain edema is believed to be linked to high mortality incidence after severe burns. The present study investigated the molecular pathology of brain damage and responses involving brain edema in forensic autopsy cases of fire fatality (n = 55) compared with sudden cardiac death (n = 11), mechanical
Malignant cerebral edema (MCE) is a life-threatening complication of acute cerebral stroke. To date, the focus has been on symptomatic treatment, rather than on prevention. Therefore, to identify high-risk patients and explore potential therapeutic approaches, we investigated the possible predictors
Patients with middle cerebral artery (MCA) infarction accompanied by MCA occlusion with or without internal carotid artery (ICA) occlusion have a poor prognosis, as a result of brain cell damage caused by both the infarction and by space-occupying and life-threatening edema formation. Multiple
BACKGROUND
Intracranial hemorrhage (ICH) is not an uncommon complication of end-stage renal disease (ESRD), and may be complicated by cerebral edema. Hemodialysis (HD) may induce rapid osmolar and fluid shifts, increasing brain water content with the potential to worsen cerebral edema. The dangers
Background and Purpose: Diabetes mellitus increases stroke incidence and mortality and hampers functional recovery after stroke. Fingolimod has been shown to improve neurofunctional recovery and reduce brain infarction after ischemic injury in mice without comorbidities. In this work, we
Our previous study demonstrated that p53 plays an orchestrating role in the vasospasm and apoptotic cell death after subarachnoid hemorrhage (SAH). We now hypothesize that p53 also plays an important role in brain edema by up-regulating the expression of MMP-9 via the NF-kappaB molecular signaling
Blood-brain barrier permeability is not routinely evaluated in the clinical setting. Global cerebral edema occurs after SAH and is associated with BBB disruption. Detection of global cerebral edema using current imaging techniques is challenging. Our purpose was to apply blood-brain barrier
Glycerol, an effective cerebral dehydrating agent, also has gluconeogenic properties, and can thereby elevate serum glucose to dangerously high levels in predisposed patients treated for cerebral edema. The nonketotic hyperosmolar hyperglycemic state usually occurs in cases of maturity onset
A novel method of long-term telemetric monitoring of mean arterial pressure (MAP) and intracranial pressure (ICP) for the determination of current cerebral perfusion pressure (CPP) and the time course of ICP in freely moving rats under physiological conditions and with increased ICP One of the major mechanisms responsible for tissue injury in hypoxic ischemic brain damage is the formation of free radicals. We studied the efficacy of methylprednisolone, which is claimed to cause rapid congealing of membranes, and to protect the cells against the free radicals present in the
Within the scope of a cerebral magnetic resonance imaging to diagnose a dysphagia in a patient on long-term artificial respiration, the morphological criteria for a HACE (high-altitude cerebral edema) have been met. We found microangiopathic white matter lesions in the area of the corpus callosum
Pichler Hefti, Jacqueline, Philipp Hoigné-Perret, and Raimund Kottke. Extensive microhemorrhages of the cerebellar peduncles after high-altitude cerebral edema. High Alt Med Biol. 18:182-184, 2017.-Neuromagnetic resonance imaging (MRI) of subjects who suffered from high-altitude cerebral edema
Stellate ganglion neural blockade reverses within seconds anoxemia and edema by release of catecholamine vasoconstriction of the small arteries. The factor XII enzyme cascade is controlled by increased oxygenated arterial blood flow and a normal pH. My patient's rapid recovery reflects the
Acute mountain sickness (AMS) is usually a benign and self-limited illness that befalls previously healthy individuals who ascend rapidly to high altitude without sufficient acclimatization. In its more severe forms, AMS can progress to a life-threatening condition in which pulmonary or cerebral
Early hematoma enlargement and delayed clot lysis contribute to brain injury after intracerebral hemorrhage (ICH). We investigated hematoma growth, clot lysis, and brain edema formation in patients with spontaneous ICH. A total of 17 spontaneous ICH patients who received regular medication were