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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 due to the induced cerebral edema were studied.
This article was published in the following journal.
Name: Neuro endocrinology letters
Overexposure to 1,2-dichloroethane (1,2-DCE) can induce brain edema, but the underlying mechanisms remain largely unknown. Aquaporin 4 (AQP4) is the most prevalent water channel in the brain, and the ...
Since no definitive treatment has been suggested for diffuse traumatic brain injury (TBI), and also as the effect of exercise has been proven to be beneficial in neurodegenerative diseases, the effect...
Acetaminophen (APAP) administration at therapeutic doses is safe, however overdosing produces hepatocellular injury via a multifactorial mechanism(s) that involves generation of reactive oxygen specie...
BACKGROUND The aim of this study was to construct a radiation-induced brain injury (RBI) model and assess the effects of human recombinant endostatin in the treatment of RBI. MATERIAL AND METHODS In t...
Cerebral edema is a major cause of morbidity in severe traumatic brain injury (TBI) patients. Intraparenchymal thermal conductivity-based probes that measure local cerebral blood flow (CBF) can measur...
Usage of osmotic agents is a standard practice in neuroanesthesia since cerebral edema is a very common situation for patients with pathology in the brain. Cerebral edema is defined as the...
A large number of preclinical studies have confirmed that progesterone and its metabolites have strong neuroprotective effects. As a neuroprotective agent, progesterone has been effective ...
It had been shown that high percentage of severe preeclampsia patients got a high cerebral perfusion pressure (CPP) due to abnormal autoregulation of cerebral blood vessels with associated...
Acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE) are complications of rapid ascent to high altitude. Several features suggest th...
Intracerebral hemorrhage (ICH) is one of the most devastating nontraumatic cerebral vascular diseases. Its exacerbation is often related to a mass effect because of hematoma formation and ...
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
Bleeding within the brain as a result of penetrating and nonpenetrating CRANIOCEREBRAL TRAUMA. Traumatically induced hemorrhages may occur in any area of the brain, including the CEREBRUM; BRAIN STEM (see BRAIN STEM HEMORRHAGE, TRAUMATIC); and CEREBELLUM.
A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.
Conditions characterized by persistent brain damage or dysfunction as sequelae of cranial trauma. This disorder may result from DIFFUSE AXONAL INJURY; INTRACRANIAL HEMORRHAGES; BRAIN EDEMA; and other conditions. Clinical features may include DEMENTIA; focal neurologic deficits; PERSISTENT VEGETATIVE STATE; AKINETIC MUTISM; or COMA.