Acta neurochirurgica. Supplement
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Acute brain edema formation contributes to brain injury after intracerebral hemorrhage (ICH). It has been reported that hyperbaric oxygen (HBO) is neuroprotective in cerebral ischemia, subarachnoid hemorrhage, and brain trauma. In this study, we investigated the effects of HBO on brain edema following ICH in rats. ⋯ In summary, HBO reduced early perihematomal brain edema and HSP-32 levels in brain. HBO-related brain protection does not occur through reduction in thrombin toxicity because HBO failed to attenuate thrombin-induced brain edema. Our results also indicate that HBO treatment after hematoma lysis for ICH may be harmful, since HBO amplifies iron-induced brain edema.
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Acta Neurochir. Suppl. · Jan 2008
Multicenter Study Controlled Clinical TrialPosttraumatic rehabilitation and one year outcome following acute traumatic brain injury (TBI): data from the well defined population based German Prospective Study 2000-2002.
Follow-up examination to review the one-year outcome of patients after craniocerebral trauma with respect to health related quality of life (QoL) and social reintegration. The data are derived from the prospective controlled, well defined population based, multiple centre study that was performed in Germany for the first time in the years 2000-2001 with emphasis on quality management (structural, process, outcome) and regarding the patient's age, physical troubles, and impaired mental-cognitive, neurobehavioral functioning. TBI severity assessment is according to the Glasgow Coma Scale (GCS) score. ⋯ One hundred and sixty patients (= 3.8%) could manage their daily life only partly; 75 TBI (= 87.2%) following mild, 5.8% moderate, and 7% severe TBI. One hundred and sixteen patients could not at all manage their activities in training, at school, or in their jobs (N = 33 MTBI respectively 54%), 6 (= 10%) moderate, and 22 (= 36%) severe TBI. 2.8% of individuals failed when compared with their pre-traumatic situation. TBI severity, patient's age, concomitant organ lesions, and complications influence health related QoL and early social reintegration.
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Acta Neurochir. Suppl. · Jan 2008
Clinical TrialIntracranial pressure and cerebral oxygenation changes after decompressive craniectomy in children with severe traumatic brain injury.
There has been a resurgence of interest in decompressive craniectomy for traumatic brain injury (TBI), but the impact of craniectomy on intracranial pressure (ICP) and cerebral oxygenation has not been well described for diffuse injury in children. ⋯ In selected pediatric patients with TBI, craniectomy for diffuse brain swelling can significantly improve ICP and cerebral oxygenation control. The use of the procedure in appropriate settings does not appear to increase the proportion of disabled survivors.
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Acta Neurochir. Suppl. · Jan 2008
Noninvasive estimation of intracranial compliance in idiopathic NPH using MRI.
The pathophysiology of idiopathic normal pressure hydrocephalus (I-NPH) is still unclear and the diagnosis is sometimes difficult. The aim of this study was to assess the biophysics of I-NPH by measuring intracranial compliance using cine MRI. ⋯ It is possible to estimate intracranial compliance as CI non-invasively using cine MRI. CI could become a useful method for the diagnosis of I-NPH.
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Acta Neurochir. Suppl. · Jan 2008
ReviewDysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH.
Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation, and chemoregulation. Subarachnoid haemorrhage (SAH) interrupts this regulation of cerebral blood flow. ⋯ CSF ADMA levels are closely associated with the degree and time-course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, the exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme (IPRMT3) or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of preclinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.