Brain edema

Increased intracranial pressure and brain edema

Authors: Dietrich W, Erbguth F.

In primary and secondary brain diseases, increasing volumes of the three compartments of brain tissue, cerebrospinal fluid, or blood lead to a critical increase in intracranial pressure (ICP). A rising ICP is associated with typical clinical symptoms; however, during analgosedation it can only be detected by invasive ICP monitoring. Other neuromonitoring procedures are not as effective as ICP monitoring; they reflect the ICP changes and their complications by other metabolic and oxygenation parameters. The most relevant parameter for brain perfusion is cerebral perfusion pressure (CPP), which is calculated as the difference between the middle arterial pressure (MAP) and the ICP. A mixed body of evidence exists for the different ICP-reducing treatment measures, such as hyperventilation, hyperosmolar substances, hypothermia, glucocorticosteroids, CSF drainage, and decompressive surgery.

Substance p antagonists as a novel intervention for brain edema and raised intracranial pressure

Authors: Gabrielian L, Helps SC, Thornton E, Turner RJ, Leonard AV, Vink R.

Increased intracranial pressure (ICP) following acute brain injury requires the accumulation of additional water in the intracranial vault. One source of such water is the vasculature, although the mechanisms associated with control of blood-brain barrier permeability are unclear. We have recently shown that acute brain injury, such as neurotrauma and stroke, results in perivascular accumulation of the neuropeptide, substance P. This accumulation is associated with increased blood-brain barrier permeability and formation of vasogenic edema. Administration of a substance P antagonist targeting the tachykinin NK1 receptor profoundly reduced the increased blood-brain barrier permeability and edema formation, and in small animal models of acute brain injury, improved functional outcome. In a large, ovine model of experimental traumatic brain injury, trauma resulted in a significant increase in ICP. Administration of an NK1 antagonist caused a profound reduction in post--traumatic ICP, with levels returning to normal within 4 h of drug administration. Substance P NK1 antagonists offer a novel therapeutic approach to the treatment of acute brain injury.

Increased intracranial pressure and brain edema

(Article in German)

Authors: Dietrich W, Erbguth F. 

In primary and secondary brain diseases, increasing volumes of the three compartments of brain tissue, cerebrospinal fluid, or blood lead to a critical increase in intracranial pressure (ICP). A rising ICP is associated with typical clinical symptoms; however, during analgosedation it can only be detected by invasive ICP monitoring. Other neuromonitoring procedures are not as effective as ICP monitoring; they reflect the ICP changes and their complications by other metabolic and oxygenation parameters. The most relevant parameter for brain perfusion is cerebral perfusion pressure (CPP), which is calculated as the difference between the middle arterial pressure (MAP) and the ICP. A mixed body of evidence exists for the different ICP-reducing treatment measures, such as hyperventilation, hyperosmolar substances, hypothermia, glucocorticosteroids, CSF drainage, and decompressive surgery.

Brain edema in acute liver failure and chronic liver disease: similarities and differences

Authors: Bosoi CR, Rose CF.

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed.

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