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1 proteinuria, coagulopathy and peripheral and cerebral oedema.
2 e patients had intracranial hypertension and cerebral oedema.
3 ts with large hemispheric stroke at risk for cerebral oedema.
4 rmalities such as haematomas, contusions and cerebral oedema.
5 are commonly used perioperatively to control cerebral oedema and are frequently continued throughout
6 metabolism presenting with life-threatening cerebral oedema and dysmyelination in affected individua
10 ry mediators have a role in the formation of cerebral oedema and there is evidence that cGMP is an im
12 omising modality of treatment for refractory cerebral oedema, but the only form of treatment known to
14 racranial hypertension, but in most patients cerebral oedema contributes to death or places them at t
15 ion of hypernatraemia over 4-24 h results in cerebral oedema, due primarily to failure of brain amino
16 five [2%] in the placebo group), symptomatic cerebral oedema (five [2%] vs four [2%]), and major haem
17 e mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mech
18 or modified Fisher scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia
20 mination of NPSLE brains reveals presence of cerebral oedema, loss of neurons and myelinated axons, m
22 n ONSD correlated with occurrence of diffuse cerebral oedema, presence of subdural and extradural hem
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