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Acute Brain Injury (acute + brain_injury)
Selected AbstractsAcute brain injury in hypoglycaemia-induced hemiplegiaDIABETIC MEDICINE, Issue 9 2005H . Ozer No abstract is available for this article. [source] Acute brain injury in hypoglycaemia-induced hemiplegiaDIABETIC MEDICINE, Issue 6 2004H. Shirayama Abstract Background The development of hemiplegia as a result of hypoglycaemia was first described in 1928. However, the mechanism remains unclear. Case report We report a case of a 58-year-old male with diabetes, who developed left hemiplegia during a severe hypoglycaemic event. Results Diffusion-weighted magnetic resonance imaging detected an increased signal intensity in the pons, indicating that the patient's hemiplegia resulted from acute brain injury. Conclusions This report provides evidence that acute brain injury may be a cause of the neurological deficit. [source] Epileptic Seizures after Treatment with ThiocolchicosideEPILEPSIA, Issue 8 2001Pier Luigi De Riu Summary: ,Purpose: To report the occurrence of epileptic seizures in humans, closely related to the use of the centrally acting muscle relaxant thiocolchicoside. Methods: Description of three case histories. Results: Two patients, affected with complex-partial seizures, sometimes secondarily generalized, receiving antiepileptic therapy, were seizure free for 7 and 9 years, respectively. They had the reappearance of tonic,clonic seizures few days after the continued use of thiocolchicoside, at a cumulative dose of the drug of 52 mg and 76 mg, respectively. The third patient was brain damaged and without a history of seizures. He had a sudden, convulsive seizure a few minutes after 4 mg intramuscular thiocolchicoside. Conclusions: Our case histories indicate that thiocolchicoside has a powerful epileptogenic activity. This drug should be avoided in patients with epilepsy or acute brain injury and possible disruption of the blood,brain barrier. [source] Mitochondrial dysfunction early after traumatic brain injury in immature ratsJOURNAL OF NEUROCHEMISTRY, Issue 5 2007Courtney L. Robertson Abstract Mitochondria play central roles in acute brain injury; however, little is known about mitochondrial function following traumatic brain injury (TBI) to the immature brain. We hypothesized that TBI would cause mitochondrial dysfunction early (<4 h) after injury. Immature rats underwent controlled cortical impact (CCI) or sham injury to the left cortex, and mitochondria were isolated from both hemispheres at 1 and 4 h after TBI. Rates of phosphorylating (State 3) and resting (State 4) respiration were measured with and without bovine serum albumin. The respiratory control ratio was calculated (State 3/State 4). Rates of mitochondrial H2O2 production, pyruvate dehydrogenase complex enzyme activity, and cytochrome c content were measured. Mitochondrial State 4 rates (ipsilateral/contralateral ratios) were higher after TBI at 1 h, which was reversed with bovine serum albumin. Four hours after TBI, pyruvate dehydrogenase complex activity and cytochrome c content (ipsilateral/contralateral ratios) were lower in TBI mitochondria. These data demonstrate abnormal mitochondrial function early (,4 h) after TBI in the developing brain. Future studies directed at reversing mitochondrial abnormalities could guide neuroprotective interventions after pediatric TBI. [source] Expression of interleukin-1 receptors and their role in interleukin-1 actions in murine microglial cellsJOURNAL OF NEUROCHEMISTRY, Issue 4 2002Emmanuel Pinteaux Abstract Interleukin (IL)-1 is an important mediator of acute brain injury and inflammation, and has been implicated in chronic neurodegeneration. The main source of IL-1 in the CNS is microglial cells, which have also been suggested as targets for its action. However, no data exist demonstrating expression of IL-1 receptors [IL-1 type-I receptor (IL-1RI), IL-1 type-II receptor (IL-1RII) and IL-1 receptor accessory protein (IL-1RAcP)] on microglia. In the present study we investigated whether microglia express IL-1 receptors and whether they present target or modulatory properties for IL-1 actions. RT,PCR analysis demonstrated lower expression of IL-1RI and higher expression of IL-1RII mRNAs in mouse microglial cultures compared with mixed glial or pure astrocyte cultures. Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1,, IL-6 and prostaglandin-E2 (PGE2), and activated nuclear factor ,B (NF-,B) and the mitogen-activated protein kinases (MAPKs) p38, and extracellular signal-regulated protein kinase (ERK1/2), but not c-Jun N-terminal kinase (JNK) in microglial cultures. In comparison, IL-1, induced the release of PGE2, IL-6 and activated NF-,B, p38, JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures. IL-1, also failed to affect LPS-primed microglial cells. Interestingly, a neutralizing antibody to IL-1RII significantly increased the concentration of IL-1, in the medium of LPS-treated microglia and exacerbated the IL-1,-induced IL-6 release in mixed glia, providing the first evidence that microglial IL-1RII regulates IL-1, actions by binding excess levels of this cytokine during brain inflammation. [source] Intracortical electroencephalography in acute brain injury,ANNALS OF NEUROLOGY, Issue 3 2009Allen Waziri MD Objective Continuous electroencephalography (EEG) is used in patients with neurological injury to detect electrographic seizures and clinically important changes in brain function. Scalp EEG has poor spatial resolution, is often contaminated by artifact, and frequently demonstrates activity that is suspicious for but not diagnostic of ictal activity. We hypothesized that bedside placement of an intracortical multicontact electrode would allow for improved monitoring of cortical potentials in critically ill neurological patients. Methods Sixteen individuals with brain injury, requiring invasive neuromonitoring, underwent implantation of an eight-contact minidepth electrode. Results Intracortical EEG (ICE) was successfully performed and compared with scalp EEG in 14 of these 16 individuals. ICE provided considerable improvement in signal-to-noise ratio compared with surface EEG, demonstrating clinically important findings in 12 of 14 patients (86%) including electrographic seizures (n = 10) and acute changes related to secondary neurological injury (n = 2, 1 ischemia, 1 hemorrhage). In patients with electrographic seizures detected by ICE, scalp EEG demonstrated no concurrent ictal activity in six, nonictal-appearing rhythmic delta in two, and intermittently correlated ictal activity in two. In two patients with secondary neurological complications, ICE demonstrated prominent attenuation 2 to 6 hours before changes in other neuromonitoring modalities and more than 8 hours before the onset of clinical deterioration. Interpretation ICE can provide high-fidelity intracranial EEG in an intensive care unit setting, can detect ictal discharges not readily apparent on scalp EEG, and can identify early changes in brain activity caused by secondary neurological complications. We predict that ICE will facilitate the development of EEG-based alarm systems and lead to prevention of secondary neuronal injury. Ann Neurol 2009;66:366,377 [source] | ||||||||||