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- Lambert, G, et al.
(författare)
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Sympathetic nervous activation following subarachnoid hemorrhage: Influence of intravenous clonidine.
- 2002
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Ingår i: Acta anaesthesiologica Scandinavica. - 0001-5172. ; 46:2, s. 160-5
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Tidskriftsartikel (refereegranskat)abstract
- Subarachnoid hemorrhage is often accompanied by systemic complications and cerebral vasospasm. Elevated levels of circulating catecholamines may be involved in the pathophysiology behind these events. The alpha-2-agonist clonidine inhibits sympathetic outflow by a central mechanism. Unrestricted sympathoexcitation may be detrimental and administration of clonidine may be beneficial in these patients.
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- Lindvall, Peter, et al.
(författare)
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Reducing intracranial pressure may increase survival among patients with bacterial meningitis
- 2004
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Ingår i: Clinical Infectious Diseases. - Chicago : Univ. of Chicago Press. - 1058-4838 .- 1537-6591. ; 38:3, s. 384-390
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Tidskriftsartikel (refereegranskat)abstract
- We reported findings concerning continuous intracranial pressure (ICP) and cerebral perfusion pressure (CPP) measurements and mortality in patients with severe bacterial meningitis treated on the basis of an ICP-targeted approach. Eighteen patients with severe bacterial meningitis were admitted for neurointensive care at Umeå University Hospital (Umeå, Sweden). In 15 patients, ICP was measured continuously through an ICP measuring device. During care, all patients but one developed intracranial hypertension with an ICP of ⩾15 mm Hg (14 [93%] of 15 patients). Ten (67%) of 15 patients survived and were discharged, and 5 patients (33%) died. Mean ICP was significantly higher and CPP was markedly decreased in nonsurvivors, compared with survivors. Among the survivors, ICP was gradually reduced. Treatment of patients with severe bacterial meningitis should include neurointensive care and continuous ICP measurement. Increased ICP may be reduced by using the ICP-targeted therapy that closely resembles the “Lund concept.”
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- Naredi, Silvana, 1953
(författare)
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Cerebral circulation and the sympathetic nervous system in patients with traumatic brain injury or subarachnoid hemorrhage
- 2000
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Maintenance of adequate cerebral microcirculation is necessary to avoid cerebral ischemia after severe traumatic brain injury and non-traumatic subarachnoid hemorrhage. After severe traumatic brain injury the blood-brain-barrier is disrupted and transcapillary leakage will contribute to the development of vasogenic brain edema. The edema causes a compromised microcirculation.Systemic complications and cerebral vasospasm observed after non-traumatic subarachnoid hemorrhage may be associated with an activated sympathetic nervous system. Although in-creased concentrations of plasma and urinary norepinephrine are found in patients following subarachnoid hemorrhage, this does not necessarily indicate an activated sympathetic nervous system. To adequately assess an activation of the sympathetic nervous system both release and removal processes of norepinephrine must be considered.A therapy focused on physiological principles for volume regulation and preserved microcir-culation following traumatic brain injury was evaluated in two clinical studies. Prostacyclin may improve cerebral microcirculation after severe traumatic brain injury due to its inhibition of platelet/leukocyte aggregation and adhesion to endothe-lium. Safety profile and outcome after prostacyclin administration was evaluated in the sec-ond study. With an isotope dilution technique the duration and magnitude of the sympathetic nervous activation in patients following subarachnoid hemorrhage was measured and the presumed inhibitory effect of clonidine on sympathetic nervous activation was tested.Favorable outcome after severe traumatic brain injury was 71% in both studies and the mor-tality rate was 13% and 3% respectively. Prostacyclin did not cause any severe side effects. Patients following subarachnoid hemorrhage exhibited an extreme elevation in sympathetic nervous system activity that persisted for at least one week after the insult. Contrary to what would be expected, clonidine did not reduce sympathetic nervous activation in patients fol-lowing subarachnoid hemorrhage.
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- Naredi, Silvana, 1953, et al.
(författare)
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Increased sympathetic nervous activity in patients with nontraumatic subarachnoid hemorrhage.
- 2000
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Ingår i: Stroke; a journal of cerebral circulation. - 0039-2499. ; 31:4, s. 901-6
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Tidskriftsartikel (refereegranskat)abstract
- Activation of the sympathetic nervous system, which leads to elevation of circulating catecholamines, is implicated in the genesis of cerebral vasospasm and cardiac aberrations after subarachnoid hemorrhage. To this juncture, sympathetic nervous testing has relied on indirect methods only.
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