Inhibition of P2X4 and P2X7 receptors improves histological and behavioral outcomes after experimental traumatic brain injury in rats.

Release of large amounts of adenosine triphosphate (ATP), a gliotransmitter, into the extracellular space by traumatic brain injury (TBI) is considered to activate the microglia followed by release of inflammatory cytokines resulting in excessive inflammatory response that induces secondary brain injury. The present study investigated whether antagonists of ATP receptors (P2X4 and/or P2X7) on microglia are beneficial for reducing the post-injury inflammatory response that leads to secondary injury, a prognostic aggravation factor of TBI. Adult male Sprague-Dawley rats were subjected to cortical contusion injury (CCI) and randomly assigned to injury and drug treatment conditions, as follows: i) No surgical intervention (naïve group); ii) dimethyl sulfoxide treatment after CCI (CCI-control group); iii) 5-BDBD (antagonist of P2X4 receptor) treatment after CCI (CCI-5-BDBD group); iv) CCI-AZ11645373 (antagonist of P2X7 receptor) treatment after CCI (CCI-AZ11645373 group); v) or 5-BDBD and AZ11645373 treatment after CCI (CCI-5-BDBD + AZ11645373 group).

Glibenclamide reduces secondary brain injury in a SAH rat model by reducing brain swelling and modulating inflammatory response.

Background: Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is a new therapeutic target. Sulfonylurea receptor 1 (SUR1) is expressed in nerve cells, glial cells, and vascular endothelial cells in EBI. SUR1 promotes intracellular inflow of Na and Ca ions, resulting in cell swelling and depolarization, and finally cell death.

Anti-inflammatory effect of P2Y1 receptor blocker MRS2179 in a rat model of traumatic brain injury.

The aim of the current study was to determine the effects of cerebral contusion injury with purinergic adenosine triphosphate Y1 (P2Y1) receptor blockers on postinjury inflammatory responses. Adenosine triphosphate (ATP) is released into the extracellular space in several in vivo models, including traumatic brain injury. Released ATP triggers neuroinflammation via activation of microglial cells.

Massive efflux of adenosine triphosphate into the extracellular space immediately after experimental traumatic brain injury.

The aim of the current study was to determine effects of mild traumatic brain injury (TBI), with or without blockade of purinergic ATP Y1 (P2Y1) receptors or store-operated calcium channels, on extracellular levels of ATP, glutamate, glucose and lactate. Concentrations of ATP, glutamate, glucose and lactate were measured in cerebral microdialysis samples obtained from the ipsilateral cortex and underlying hippocampus of rats with mild unilateral controlled cortical impact (CCI) or sham injury. Immediately after CCI, a large release of ATP was observed in the cortex (3.

High-dose-infliximab-associated Cerebral Venous Sinus Thrombosis: A Case Report and Review of the Literature.

A 28-year-old woman experienced severe headache and right homonymous hemianopia after receiving high-dose infliximab for Crohn's disease. Computed tomography showed hemorrhagic infarction in the left temporal and parietal lobes. An angiogram revealed left transverse to sigmoid sinus occlusion and a stagnated Labbe vein.

Unusual presentation of a skull base mass lesion in sarcoidosis mimicking malignant neoplasm: a case report.

Background: Sarcoidosis is a multi-organ disease of unknown etiology characterised by the presence of epithelioid granulomas, without caseous necrosis. Systemic sarcoidosis is rare among children, while neurosarcoidosis in children is even rarer whether it is systemic or not.

Case Presentation: We described the case of a 12-year-old boy who presented with monocular vision loss accompanied by unusual MRI features of an extensive meningeal infiltrating mass lesion.

Solitary primary intracranial leptomeningeal glioblastoma invading the normal cortex: Case report.

Solitary primary intracranial leptomeningeal glioma (PLG) is a rare entity of glioma. PLG arises from the heterotopic glial tissue in the subarachnoid space and usually grows there without parenchymal invasion. The present study reported a case of solitary PLG, pathologically diagnosed as glioblastoma, that invaded the temporal cortex and finally disseminated to the spinal cord.

Pyruvate treatment attenuates cerebral metabolic depression and neuronal loss after experimental traumatic brain injury.

Experimental traumatic brain injury (TBI) is known to produce an acute increase in cerebral glucose utilization, followed rapidly by a generalized cerebral metabolic depression. The current studies determined effects of single or multiple treatments with sodium pyruvate (SP; 1000mg/kg, i.p.

Glucose administration after traumatic brain injury improves cerebral metabolism and reduces secondary neuronal injury.

Clinical studies have indicated an association between acute hyperglycemia and poor outcomes in patients with traumatic brain injury (TBI), although optimal blood glucose levels needed to maximize outcomes for these patients' remain under investigation. Previous results from experimental animal models suggest that post-TBI hyperglycemia may be harmful, neutral, or beneficial. The current studies determined the effects of single or multiple episodes of acute hyperglycemia on cerebral glucose metabolism and neuronal injury in a rodent model of unilateral controlled cortical impact (CCI) injury.

Is the circulating plasma volume sufficiently maintained? Fluid management of an aneurysmal subarachnoid hemorrhage in the acute phase.

Cerebral vasospasm is a well-known cause of mortality and morbidity following aneurysmal subarachnoid hemorrhage (SAH). Prevention of symptomatic cerebral vasospasm is the basic management after SAH. Numerous pharmaceutical therapies and endovascular treatments are available against cerebral vasospasm, but none of them have so far proven to improve the outcome.

Delayed sodium pyruvate treatment improves working memory following experimental traumatic brain injury.

Prior work indicates that cerebral glycolysis is impaired following traumatic brain injury (TBI) and that pyruvate treatment acutely after TBI can improve cerebral metabolism and is neuroprotective. Since extracellular levels of glucose decrease during periods of increased cognitive demand and exogenous glucose improves cognitive performance, we hypothesized that pyruvate treatment prior to testing could ameliorate cognitive deficits in rats with TBI. Based on pre-surgical spatial alternation performance in a 4-arm plus-maze, adult male rats were randomized to receive either sham injury or unilateral (left) cortical contusion injury (CCI).

Beneficial effects of sodium or ethyl pyruvate after traumatic brain injury in the rat.

Sodium pyruvate (SP) treatment initiated within 5 min post-injury is neuroprotective in a rat model of unilateral cortical contusion injury (CCI). The current studies examined: (1) effects of delayed SP treatments (1000 mg/kg, i.p.

Metabolic and histologic effects of sodium pyruvate treatment in the rat after cortical contusion injury.

This study determined the effects of intraperitoneal sodium pyruvate (SP) treatment on the levels of circulating fuels and on cerebral microdialysis levels of glucose (MD(glc)), lactate (MD(lac)), and pyruvate (MD(pyr)), and the effects of SP treatment on neuropathology after left cortical contusion injury (CCI) in rats. SP injection (1000 mg/kg) 5 min after sham injury (Sham-SP) or CCI (CCI-SP) significantly increased arterial pyruvate (p < 0.005) and lactate (p < 0.

Duration of ATP reduction affects extent of CA1 cell death in rat models of fluid percussion injury combined with secondary ischemia.

Secondary ischemia (SI) following traumatic brain injury (TBI) increases damage to the brain in both animals and humans. The current study determined if SI after TBI alters the extent or duration of reduced energy production within the first 24 h post-injury and hippocampal cell loss at one week post-injury. Adult male rats were subjected to sham injury, lateral (LFPI) or central fluid percussion injury (CFPI) only, or to combined LFPI or CFPI with SI.

Prediction of symptomatic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage: relationship to cerebral salt wasting syndrome.

Objectives: Symptomatic cerebral vasospasm is a major complication in patients with subarachnoid hemorrhage (SAH). Symptomatic cerebral vasospasm has been reported to be related to the patient's blood volume which is influenced by cerebral salt wasting syndrome (CSWS). We undertook a prospective study to assess whether the onset of symptomatic cerebral vasospasm was predictable or not, by observing the phenomena of CSWS (natriuresis and osmotic diuresis).

A randomized controlled trial of hydrocortisone against hyponatremia in patients with aneurysmal subarachnoid hemorrhage.

Background And Purpose: Hyponatremia is common after aneurysmal subarachnoid hemorrhage (SAH). It is caused by natriuresis, which induces osmotic diuresis and decreases blood volume, contributing to symptomatic cerebral vasospasm (SCV). Hypervolemic therapy to prevent SCV will not be efficient under this condition.

Traumatic cervical internal carotid artery occlusion in an infant. Case report.

A 10-month-old boy presented with traumatic internal carotid artery (ICA) occlusion caused by blunt injury after falling from a baby carrier attached to a standing bicycle. Physical examination found bruises on the scalp in the right temporal region and the right shoulder, but no wound in the neck. Chest radiography showed a right clavicular fracture.

Sagittal magnetic resonance imaging of intramural hematoma from non-traumatic dissection of the anterior cerebral artery. Case report.

A 46-year-old woman presented with non-traumatic anterior cerebral artery dissection manifesting as sudden onset of headache and motor weakness of the right lower limb. Angiography revealed luminal narrowing of the left anterior cerebral artery from the A(3) portion to the distal portion. Sagittal T(1)-weighted magnetic resonance imaging showed hyperintensity due to an intramural hematoma around the flow void signal of the affected anterior cerebral artery.

Prophylactic management of excessive natriuresis with hydrocortisone for efficient hypervolemic therapy after subarachnoid hemorrhage.

Background And Purpose: Hyponatremia caused by excessive natriuresis is common in patients with aneurysmal subarachnoid hemorrhage (SAH). Natriuresis decreases the total blood volume through osmotic diuresis and increases the risk of symptomatic cerebral vasospasm. In such patients, hypervolemic therapy is difficult to achieve without causing hyponatremia because sodium replacement provokes further natriuresis and osmotic diuresis.