Effect of pretreatment with a tyrosine kinase inhibitor (PP1) on brain oedema and neurological function in an automated cortical cryoinjury model in mice

Turel, Mazda K; Moorthy, Ranjith K; Sam, Gift Ajay; Samuel, Prasanna; Murthy, M. Shankara; Babu, K.Srinivas; Rajshekhar, Vedantam

doi:10.1016/j.jocn.2012.06.009

Cited by 3 publications

(1 citation statement)

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“…17 Standard medical management of cerebral edema involves using a systemic approach, from general measures, that is, optimal head and neck positioning for facilitating intracranial venous outflow, proper airway, avoidance of dehydration, and systemic hypotension, and maintenance of normothermia, to specific therapeutic interventions like controlled hyperventilation, administration of diuretics, osmotherapy, and pharmacological cerebral metabolic suppression. 17,20,21 Some of the drugs clinically used and others under experimental studies are listed in ►Table 1.…”

Section: Treatment Of Brain Edemamentioning

confidence: 99%

Brain Edema: Newer Concept of Treatment

Mohanty

Swain

Biswal

2019

Annals of the National Academy of Medical Sciences (India)

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Brain edema is excess accumulation of water in intracellular or extracellular spaces of the brain. It may be due to traumatic brain injury, neoplasm, infection, or following surgery. Advent of electron microscope and molecular pathophysiology of fluid transport through blood–brain barrier has elucidated the mechanism of edema formation, that is, ion channels and transport of fluid into extracellular space. Currently approved treatments, such as decompressive craniectomy and osmotherapy, controlled hyperventilation, and administration of diuretics, were developed prior to any knowledge of modern cerebral edema pathophysiology. These therapies attempt to manage downstream end-stage events without directly attenuating the underlying molecular mechanisms of cerebral edema. Next few years will yield new knowledge of how particular proteins drive edema influx, paving the way for rationally designed therapeutics that directly target key steps in cerebral edema formation, thereby achieving what currently approved therapies do not. Pharmacological agents which can block edema formation are being tried experimentally and clinically. Development in imaging, that is, computed tomography and diffusion tensor magnetic resonance imaging, has helped in antemortem assessment of evolution and resolution of brain edema as a dynamic pathophysiology. Animal studies shows release of vasoactive substances, that is, histamine, serotonin, adrenaline, nitric oxide, substance P, prostaglandins, tumor necrosis factor-α, and cytokines, in the injured brain results in activation of inflammatory cascade, which is the important cause of brain edema.

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