Relation of cerebral energy metabolism and extracellular nitrite and nitrate concentrations in patients after aneurysmal subarachnoid hemorrhage.

In a prospective clinical investigation on neurochemical intensive care monitoring, the authors' aim was to elucidate the temporal profile of nitric oxide metabolite concentrations-that is, nitrite and nitrate (NO(x))--and compounds related to energy-metabolism in the cerebral interstitium of patients after aneurysmal subarachnoid hemorrhage (SAH). During aneurysm surgery, microdialysis probes were implanted in cerebral white matter of the vascular territory most likely affected by vasospasm. Temporal profiles of NO(x) were analyzed in a subset of 10 patients (7 female, 3 male, mean age = 47 +/- 14 years).

Early expression of glutamate transporter proteins in ramified microglia after controlled cortical impact injury in the rat.

Traumatic brain injury is followed by increased extracellular glutamate concentration. Uptake of glutamate is mainly mediated by the glial glutamate transporters GLAST and GLT-1. Extent and distribution of GLAST and GLT-1 were studied in a rat model of controlled cortical impact injury (CCII).

Visualization of rat pial microcirculation using the novel orthogonal polarized spectral (OPS) imaging after brain injury.

Recently, the novel optical system, orthogonal polarized spectral (OPS) imaging was developed to visualize microcirculation. Investigation of changes in microcirculation is essential for physiological, pathophysiological, and pharmacological studies. In the present study applicability of OPS imaging was assessed to study pial microcirculation in normal and traumatized rat brain.

Isoflurane doubles plasma glutamate and increases posttraumatic brain edema.

Increased plasma and cerebral glutamate levels may contribute to posttraumatic edema formation. Since volatile anesthetics elevate plasma amino acid concentrations, the influence of isoflurane on arterial plasma glutamate levels and brain edema formation was investigated in brain-injured rats. Rats were anesthetized with chloral hydrate (380 mg/kg i.

Bradykinin 2 receptor antagonist LF 16-0687Ms reduces posttraumatic brain edema.

Activation of the kallikrein-kinin system contributes to traumatic brain edema formation. Inhibition of bradykinin 2 (B2) receptors has been shown to successfully reduce brain edema formation. The purpose of this study was to investigate the protective effect of the novel nonpeptide B2 receptor antagonist LF 16-0687Ms in brain-injured rats.

Intensive care management of head-injured patients in Europe: a survey from the European brain injury consortium.

Objectives: (a) to describe current practice in the monitoring and treatment of moderate and severe head injuries in Europe; (b) to report on intracranial pressure and cerebral perfusion pressure monitoring, occurrence of measured and reported intracranial hypertension, and complications related to this monitoring; (c) to investigate the relationship between the severity of injury, the frequency of monitoring and management, and outcome.

Methods: A three-page questionnaire comprising 60 items of information has been compiled by 67 centres in 12 European countries. Information was collected prospectively regarding all severe and moderate head injuries in adults (> 16 years) admitted to neurosurgery within 24 h of injury.

Secondary insults in severe head injury--do multiply injured patients do worse?

Objectives: To study the occurrence of secondary insults and the influence of extracranial injuries on cerebral oxygenation and outcome in patients with closed severe head injury (Glasgow Coma Scale score < or =8).

Design: Two-year prospective, clinical study.

Setting: Two intensive care units in a level III trauma center.

Effects of tacrolimus on hemispheric water content and cerebrospinal fluid levels of glutamate, hypoxanthine, interleukin-6, and tumor necrosis factor-alpha following controlled cortical impact injury in rats.

Object: Disturbance of calcium homeostasis contributes to evolving tissue damage and energetic impairment following traumatic brain injury (TBI). Calcium-mediated activation of calcineurin results in production of tissue-damaging nitric oxide and free oxygen radicals. Inhibition of calcineurin induced by the immunosuppressant tacrolimus (FK506) has been shown to reduce structural and functional damage after ischemia.

Role of bedside microdialysis in the diagnosis of cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

Object: Ischemia due to vasospasm is a feared complication in patients following aneurysmal subarachnoid hemorrhage (SAH). Cerebral online microdialysis monitoring may detect the metabolic changes in the extracellular fluid associated with ischemia. The aims of the present study were to correlate clinical course, microdialysis-recorded data, transcranial Doppler (TCD) ultrasonography findings, and angiographic findings in patients with SAH.

Current recommendations for neurotrauma.

Diagnostic and monitoring procedures for patients with head injury are aimed at early detection of mass lesions and secondary insults. Our therapeutic approach is based on our understanding of pathophysiologic mechanisms that cause secondary brain damage, and includes evacuation of mass lesions and prevention of secondary insults. Basic research has greatly increased our knowledge of these pathophysiologic mechanisms and has prompted the development of many neuroprotective agents, targeted to selected mechanisms.

Secondary abscess formation in pituitary adenoma after tooth extraction. Case report.

The presence of an abscess in a pituitary tumor is a very rare finding. The authors report the case of a 69-year-old man with a pituitary adenoma confirmed by neuroimaging results, in whom a high fever, meningismus, and left-sided ophthalmoplegia developed 4 days after tooth extraction. The results of serial cranial magnetic resonance imaging were highly indicative of an abscess formation within the pituitary adenoma.

Neuroprotective effect of melatonin on cortical impact injury in the rat.

The pineal hormone melatonin is a highly efficient physiological scavenger of free radicals involved in secondary brain damage. A variety of experimental studies have demonstrated a neuroprotective effect for melatonin, based on its antioxidant activity. The purpose of the present study was to investigate the time-dependency and a possible protective effect of exogenous melatonin in the cortical impact model in rats.

Riluzole reduces brain swelling and contusion volume in rats following controlled cortical impact injury.

Modulation of the glutamatergic and excitotoxic pathway may attenuate secondary damage following traumatic brain injury by reducing presynaptic glutamate release and blocking sodium channels in their inactivated state. The aim of the present study was to investigate the neuroprotective potential of riluzole in traumatic brain-injured rats. A left temporoparietal contusion was induced in 70 male Sprague-Dawley rats (controlled cortical impact injury).

Hemicraniectomy in elderly patients with space occupying media infarction: improved survival but poor functional outcome.

Objective: To assess the survival rate and functional outcome in elderly patients with space occupying supratentorial infarction who underwent hemicraniectomy compared with those who received medical treatment alone.

Methods: All patients older than 55 years with space occupying middle cerebral artery (MCA) infarction treated in our clinic between January 1998 and July 1999 were included in this retrospective analysis. Patients were eligible for decompressive surgery if they were younger than 75 and had no severe comorbidity.

Effects of dopamine on posttraumatic cerebral blood flow, brain edema, and cerebrospinal fluid glutamate and hypoxanthine concentrations.

Objectives: Dopamine is often used in the treatment of traumatic brain injury to maintain cerebral perfusion pressure. However, it remains unclear whether dopamine contributes to secondary brain injury caused by vasoconstriction and resulting diminished cerebral perfusion. The present study investigated the effects of dopamine in different concentrations on posttraumatic cortical cerebral blood flow (CBF), brain edema formation, and cerebrospinal fluid concentrations of glutamate and hypoxanthine.

Increased cerebrospinal fluid glutamate and taurine concentrations are associated with traumatic brain edema formation in rats.

Glutamate-mediated excitotoxicity results in cell swelling and contributes to brain edema formation. Since increased extracellular taurine reflects glutamate-induced cell swelling in vitro, elevated CSF taurine could therefore unmask glutamate-mediated cytotoxic edema formation under in vivo conditions. For this, the temporal profile of brain edema and changes in cisternal CSF glutamate and taurine levels were determined in 28 rats following focal traumatic brain injury.

Temporal profile of cerebrospinal fluid glutamate, interleukin-6, and tumor necrosis factor-alpha in relation to brain edema and contusion following controlled cortical impact injury in rats.

Traumatic brain injury is associated with release of the excitotoxin glutamate and production of pro-inflammatory cytokines IL-6 and tumor necrosis factor-alpha (TNF-alpha). Following controlled cortical impact injury, cerebrospinal fluid (CSF) glutamate, IL-6, and TNF-alpha concentrations were measured to investigate their relationship to evolving tissue damage. Compared to non-traumatized rats CSF glutamate, IL-6 and TNF-alpha levels were significantly increased by 8 h after trauma (P<0.

Significant reduction in brain swelling by administration of nonpeptide kinin B2 receptor antagonist LF 16-0687Ms after controlled cortical impact injury in rats.

Object: Identification of new therapeutic agents aimed at attenuating posttraumatic brain edema formation remains an unresolved challenge. Among others, activation of bradykinin B2 receptors is known to mediate the formation of brain edema. The purpose of this study was to investigate the protective effect of the novel nonpeptide B2 receptor antagonist, LF 16-0687Ms, in brain-injured rats.

The value of the "worst" computed tomographic scan in clinical studies of moderate and severe head injury. European Brain Injury Consortium.

Objective: Computed tomographic (CT) scanning can reveal the pattern and severity of structural brain damage after head injury. With the proliferation of CT scanners in general hospitals, and with improvements in patient transport, the interval from injury to the first CT scan is decreasing. The potential result is an "admission" scan missing an evolving and potentially operable lesion.

Challenges in translating the efficacy of neuroprotective agents in experimental models into knowledge of clinical benefits in head injured patients.

Many agents have been shown to reduce brain damage in experimental models of brain injury; this is proving difficult to translate into improved outcome of patients for reasons that are reviewed in this article. It is possible that, even if fundamental mechanisms are similar, injury processes modelled experimentally may be proportionately less important in human cases, and there also may have been insufficient attention to ensuring that dosage regimens for patients are therapeutically appropriate both in terms of concentration and time window. The distribution of outcomes after head injury means that, in unselected populations, a proportional improvement to the extent usually sought may be difficult to achieve.

Lubeluzole following traumatic brain injury in the rat.

Lubeluzole, a novel nitric oxide synthase (NOS) pathway modulator, was shown to be neuroprotective in cerebral ischemia as studied in animal models and clinical trials. The present study investigated the effect of lubeluzole on contusion volume and brain edema following traumatic brain injury. Sprague-Dawley rats (n = 36) were subjected to cortical impact injury.