Search results for "Traumatic Brain Injury"
showing 10 items of 121 documents
<title>Noninvasive detection of intracerebral hemorrhage using near-infrared spectroscopy (NIRS)</title>
1998
Intracerebral Hemorrhage (IH) is an important cause of secondary brain injury in neurosurgical patients. Early identification and treatment improve neurologic outcome. We have tested Near Infrared Spectroscopy (NIRS) as an alternative noninvasive diagnostic tool compared to CT-Scans to detect IH. We prospectively studied 212 patients with neurologic symptoms associated with intracranial pathology before performing a CT-scan. NIRS signals indicated pathologies in 181 cases (sensitivity 0.96; specificity 0.29). In a subgroup of subdural hematomas NIRS detected 45 of 46 hematomas (sensitivity 0.96; specificity 0.79). Identification of intracerebral hemorrhage using NIRS has the potential to al…
Prevention and treatment of intracranial hypertension
2007
Intracranial pressure (ICP) is the pressure exerted by cranial contents on the dural envelope. It comprises the partial pressures of brain, blood and cerebrospinal fluid (CSF). Normal intracranial pressure is somewhere below 10 mmHg; it may increase as a result of traumatic brain injury, stroke, neoplasm, Reye's syndrome, hepatic coma, or other pathologies. When ICP increases above 20 mmHg it may damage neurons and jeopardize cerebral perfusion. If such a condition persists, treatment is indicated. Control of ICP requires measurement, which can only be performed invasively. Standard techniques include direct ventricular manometry or measurement in the parenchyma with electronic or fiberopti…
Administration of all‐ trans retinoic acid after experimental traumatic brain injury is brain protective
2020
BACKGROUND AND PURPOSE: All‐trans retinoic acid (ATRA) is a vitamin A metabolite, important in the developing and mature brain. Pre‐injury ATRA administration ameliorates ischaemic brain insults in rodents. This study examined the effects of post‐traumatic ATRA treatment in experimental traumatic brain injury (TBI). EXPERIMENTAL APPROACH: Male adult mice were subjected to the controlled cortical impact model of TBI or sham procedure and killed at 7 or 30 days post‐injury (dpi). ATRA (10 mg kg−1, i.p.) was given immediately after the injury and 1, 2 and 3 dpi. Neurological function and sensorimotor coordination were evaluated. Brains were processed for (immuno‐) histological, mRNA and protei…
Plasminogen activator inhibitor‐1 augments damage by impairing fibrinolysis after traumatic brain injury
2019
Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation b…
Single intracerebroventricular progranulin injection adversely affects the blood–brain barrier in experimental traumatic brain injury
2021
Progranulin (PGRN) is a neurotrophic and anti-inflammatory factor with protective effects in animal models of ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury (TBI). Administration of recombinant (r) PGRN prevents exaggerated brain pathology after TBI in Grn-deficient mice, suggesting that local injection of recombinant progranulin (rPGRN) provides therapeutic benefit in the acute phase of TBI. To test this hypothesis, we subjected adult male C57Bl/6N mice to the controlled cortical impact model of TBI, administered a single dose of rPGRN intracerebroventricularly (ICV) shortly before the injury, and examined behavioral and biological effects up to 5 days post injury (dp…
RS1 (Rsc1A1) deficiency limits cerebral SGLT1 expression and delays brain damage after experimental traumatic brain injury
2018
Acute cerebral lesions are associated with dysregulation of brain glucose homeostasis. Previous studies showed that knockdown of Na+ -D-glucose cotransporter SGLT1 impaired outcome after middle cerebral artery occlusion and that widely expressed intracellular RS1 (RSC1A1) is involved in transcriptional and post-translational down-regulation of SGLT1. In the present study, we investigated whether SGLT1 is up-regulated during traumatic brain injury (TBI) and whether removal of RS1 in mice (RS1-KO) influences SGLT1 expression and outcome. Unexpectedly, brain SGLT1 mRNA in RS1-KO was similar to wild-type whereas it was increased in small intestine and decreased in kidney. One day after TBI, SGL…
Occurrence of Spontaneous Cortical Spreading Depression Is Increased by Blood Constituents and Impairs Neurological Recovery after Subdural Hematoma …
2019
Acute subdural hemorrhage (ASDH) is common and associated with severe morbidity and mortality. To date, the role of spontaneous cortical spreading depression (sCSD) in exaggerating secondary injury after ASDH, is poorly understood. The present study contains two experimental groups: First, we investigated and characterized the occurrence of sCSD after subdural blood infusion (300 μL) via tissue impedance (IMP) measurement in a rat model. Second, we compared the occurrence and influence of sCSD on lesion growth and neurological deficit in the presence and absence of whole blood constituents. In the first experimental group, three IMP traits could be distinguished after ASDH: no sCSD, recurre…
Deficiency of Plasminogen Activator Inhibitor Type 2 Limits Brain Edema Formation after Traumatic Brain Injury
2019
Plasminogen activator inhibitor-2 (PAI-2/SerpinB2) inhibits extracellular urokinase plasminogen activator (uPA). Under physiological conditions, PAI-2 is expressed at low levels but is rapidly induced by inflammatory triggers. It is a negative regulator of fibrinolysis and serves to stabilize clots. In the present study, PAI-2 expression is upregulated 25-fold in pericontusional brain tissue at 6 h after traumatic brain injury (TBI), with a maximum increase of 87-fold at 12 h. To investigate a potentially detrimental influence of PAI-2 on secondary post-traumatic processes, male PAI-2-deficient (PAI-2-KO) and wild-type mice (WT) were subjected to TBI by controlled cortical impact injury. Br…
Skull Fractures Induce Neuroinflammation and Worsen Outcomes after Closed Head Injury in Mice
2020
The weight-drop model is used widely to replicate closed-head injuries in mice; however, the histopathological and functional outcomes may vary significantly between laboratories. Because skull fractures are reported to occur in this model, we aimed to evaluate whether these breaks may influence the variability of the weight-drop (WD) model. Male Swiss Webster mice underwent WD injury with either a 2 or 5 mm cone tip, and behavior was assessed at 2 h and 24 h thereafter using the neurological severity score. The expression of interleukin (IL)-6, IL-1β, tumor necrosis factor-α, matrix metalloproteinase-9, and tissue inhibitor of metalloproteinase-1 genes was m…
Delayed inhibition of angiotensin II receptor type 1 reduces secondary brain damage and improves functional recovery after experimental brain trauma*
2011
OBJECTIVE:: To investigate the regulation of the cerebral renin-angiotensin system and the effect of angiotensin II receptor type 1 inhibition on secondary brain damage, cerebral inflammation, and neurologic outcome after head trauma. DESIGN:: The expression of renin-angiotensin system components was determined at 15 mins, 3 hrs, 6 hrs, 12 hrs, and 24 hrs after controlled cortical impact in mice. Angiotensin II receptor type 1 was inhibited using candesartan (0.1, 0.5, 1 mg/kg) after trauma to determine its effect on secondary brain damage, brain edema formation, and inflammation. The window of opportunity was tested by delaying angiotensin II receptor type 1 inhibition for 30 mins, 1 hr, 2…