Acta neurochirurgica. Supplement
-
Acta Neurochir. Suppl. · Jan 2008
Effect of amantadine sulphate on intracerebral hemorrhage-induced brain injury in rats.
Recent studies have shown that amantadine, an uncompetitive N-methyl-d-aspartate receptor antagonist and dopamine agonist, is effective for the treatment of various cerebral disorders and causes relatively mild side effects. In this study, we investigated whether administration of amantadine will provide a neuroprotective effect in the intracerebral hemorrhage (ICH) rat model. A total of 15 male Sprague Dawley rats (300-380 g) were divided into sham, ICH-untreated, and ICH-treated with amantadine sulphate groups. ⋯ Our data demonstrates that ICH caused significant neurological deficit associated with marked brain edema. Amantadine did not reduce brain injury after ICH; neurological function and brain edema in the treated group were not different from those of the untreated group. We conclude that amantadine sulphate does not offer neuroprotection in acute stage of experimental ICH-induced brain injury.
-
Acta Neurochir. Suppl. · Jan 2008
Effects of superoxide dismutase and catalase derivates on intracerebral hemorrhage-induced brain injury in rats.
The use of exogenous superoxide dismutase (SOD) and catalase (CAT) has been previously evaluated against various reactive oxygen species-mediated brain injuries, especially those associated with ischemia/ reperfusion. In this study, we investigated effects of these enzymatic antioxidants on intracerebral hemorrhage (ICH)-induced brain injury. A total of 65 male Sprague-Dawley rats (300-380 g) were divided into a sham group, an untreated ICH group, 3 groups of ICH rats treated with lecithinized SOD (PC-SOD) at doses of 0.1, 0.3, and 1 mg/kg, and a group treated with polyethylene glycol conjugated CAT (PEG-CAT) at a dose of 10,000 U/kg. ⋯ Our results demonstrated that ICH caused significant neurological deficit associated with remarkable brain edema. Treatment with PC-SOD, PEG-CAT, or PC-SOD in combination with PEG-CAT did not reduce brain edema or neurological deficit after ICH. We conclude that intravenously administered PC-SOD and/or PEG-CAT do not reduce brain injury in the collagenase-induced ICH rat model.
-
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.
-
Acta Neurochir. Suppl. · Jan 2008
ReviewVasospasm after aneurysmal subarachnoid hemorrhage: need for further study.
Cerebral vasospasm is the classic cause of delayed neurological deterioration leading to cerebral ischemia and infarction, and thus, poor outcome and occasionally death, after aneurysmal subarachnoid hemorrhage (SAH). Advances in diagnosis and treatment, principally nimodipine, intensive care management, hemodynamic manipulations, and endovascular neuroradiology procedures, have improved the prospects for these patients, but outcomes remain disappointing. A phase 2b clinical trial (CONSCIOUS-1) demonstrated marked prevention of vasospasm with the endothelin antagonist, clazosentan, yet patient outcome was not improved. ⋯ Clazosentan reduced angiographic vasospasm in a dose-dependent manner in patients with aneurysmal SAH following coiling or clipping of the aneurysm. Reducing the incidence of vasospasm should have an important effect on clinical outcome. A phase 3 clinical trial (CONSCIOUS-2) will focus on quantifying this outcome in patients undergoing aneurysm clipping receiving placebo or 5 mg/h of clazosentan.
-
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.