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1 or the management of glioblastoma-associated cerebral oedema.
2 rmalities such as haematomas, contusions and cerebral oedema.
3 proteinuria, coagulopathy and peripheral and cerebral oedema.
4 e patients had intracranial hypertension and cerebral oedema.
5 ts with large hemispheric stroke at risk for cerebral oedema.
6  breakdown of the blood-brain barrier and to cerebral oedema after reperfusion therapy.
7 are commonly used perioperatively to control cerebral oedema and are frequently continued throughout
8  metabolism presenting with life-threatening cerebral oedema and dysmyelination in affected individua
9                                              Cerebral oedema and increased intracranial pressure can
10            We report here the development of cerebral oedema and increased intracranial pressure in 1
11 rlie the aetiology of neuroleptic associated cerebral oedema and neuroleptic malignant syndrome.
12 ry mediators have a role in the formation of cerebral oedema and there is evidence that cGMP is an im
13  transient response to treatment and died of cerebral oedema before a transplant could be done.
14 omising modality of treatment for refractory cerebral oedema, but the only form of treatment known to
15                                  We detected cerebral oedema by computed axial tomography of the head
16      Clinical baseline covariates, including cerebral oedema, cerebral infarction, respiratory failur
17 racranial hypertension, but in most patients cerebral oedema contributes to death or places them at t
18                                              Cerebral oedema develops after anoxic brain injury.
19 ion of hypernatraemia over 4-24 h results in cerebral oedema, due primarily to failure of brain amino
20 five [2%] in the placebo group), symptomatic cerebral oedema (five [2%] vs four [2%]), and major haem
21 st computational model for the simulation of cerebral oedema following acute ischaemic stroke for the
22 lopment of alternative strategies to prevent cerebral oedema formation after cardiac arrest.
23 acute mountain sickness (AMS), high-altitude cerebral oedema (HACE) and high-altitude pulmonary oedem
24 e mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mech
25 eroid that is frequently prescribed to treat cerebral oedema in patients with glioblastoma-generated
26 or modified Fisher scale, rebleeding, global cerebral oedema, intracranial pressure crisis, pneumonia
27                                              Cerebral oedema is a cause of morbidity and mortality in
28                                              Cerebral oedema is a near-universal occurrence in patien
29                                              Cerebral oedema is associated with morbidity and mortali
30 gly, early brain injury presenting as global cerebral oedema is recognised as a potential treatment t
31 mination of NPSLE brains reveals presence of cerebral oedema, loss of neurons and myelinated axons, m
32 nd had documented intracranial hypertension, cerebral oedema, or both.
33 n ONSD correlated with occurrence of diffuse cerebral oedema, presence of subdural and extradural hem
34                   Hepatic encephalopathy and cerebral oedema remain important and life-threatening co
35           Sepsis with multiorgan failure and cerebral oedema remain the leading causes of death in pa
36 an lead to grave consequences in the form of cerebral oedema, severe neurological impairment and even
37 y phenytoin died as a result of catastrophic cerebral oedema unrelated to either treatment.
38 osis involves pathophysiologically low-grade cerebral oedema with oxidative/nitrosative stress, infla