Disease relevance of Head Injuries, Closed

• METHODS: In a randomized, controlled trial, we compared the effects of moderate hypothermia and normothermia in 82 patients with severe closed head injuries (a score of 3 to 7 on the Glasgow Coma Scale) [1].
• To investigate the role of endogenous apolipoprotein E following acute brain injury, noninvasive magnetic resonance imaging was performed on anesthetized mice following closed head injury [2].
• Vegetative state after closed-head injury. A Traumatic Coma Data Bank Report [3].
• The effects of Rivastigmine, a novel centrally-acting anticholinesterase agent, were evaluated on cerebral edema, neurological and motor deficits, and impairment of spatial memory induced in mice by closed-head injury (CHI) [4].
• Succinylcholine-induced hyperkalemia in a patient with a closed head injury [5].

Psychiatry related information on Head Injuries, Closed

• PATIENTS/CONTROLS: Eleven patients at least 2 years after severe closed head injury (Glasgow Coma Scale score < 8 at admission and duration of posttraumatic amnesia > 48 hours) were compared with a control group matched for age and educational level [6].
• PURPOSE: To determine whether there is an association between the spatial distribution of lesions detected at magnetic resonance (MR) imaging of the brain in children after closed-head injury and the development of secondary attention-deficit/hyperactivity disorder (ADHD) [7].
• Confounding factors (active or previous substance abuse, developmental disabilities, and history of closed head injury or epilepsy) did not significantly affect ERP latencies [8].
• Lethargy, hyperpyrexia, tremor, and rigidity associated with leukocytosis and elevation of the creatine kinase level occurred in a patient with a closed head injury who was being treated with haloperidol for control of agitation [9].
• The earliest stage of recovery from moderate to severe closed head injury is a period of PTA that typically includes memory loss for events preceding and surrounding the injury and memory loss for events occurring since the injury [10].

High impact information on Head Injuries, Closed

• OBJECTIVE: To evaluate outcome of patients with severe closed head injury treated with pegorgotein, a scavenger of oxygen-derived free radicals [11].
• Dynamic changes in N-methyl-D-aspartate receptors after closed head injury in mice: Implications for treatment of neurological and cognitive deficits [12].
• A placebo-controlled trial shows no effect of vasopressin on recovery from closed head injury [13].
• Increase in peripheral benzodiazepine receptors and loss of glutamate NMDA receptors in a mouse model of closed head injury: a quantitative autoradiographic study [14].
• The aim of the present study was to examine whether HA exerts a beneficial effect on the outcome of closed head injury (CHI) in mice and to explore the possible involvement of HIF-1 and Epo in this process [15].

Chemical compound and disease context of Head Injuries, Closed

• In a model of closed head injury (CHI) in the rat we have shown the activation of phospholipase A2 and the production of eicosanoids after injury: at 15 min, mainly 5-hydroxyeicosatetraenoic acid (5-HETE), and at 24 h, mainly prostaglandin E2 [16].
• Mechanism of brain protection by nitroxide radicals in experimental model of closed-head injury [17].
• Pentobarbital disposition was assessed in 10 adults with severe nonpenetrating head injury after an intravenous loading dose of sodium pentobarbital, 10 mg/kg, infused over 1 hour, followed by a continuous infusion at 0.5 to 3.0 mg/kg/hr provided the cerebral perfusion pressure remained greater than 50 torr [18].
• Depression after minor closed head injury: role of dexamethasone suppression test and antidepressants [19].
• The closed head injury patients were treated with phenelzine after a 3- to 7-day washout period [19].

Biological context of Head Injuries, Closed

• Closed head injury induces up-regulation of ErbB-4 receptor at the site of injury [20].
• Localizing and prognostic value of auditory evoked responses in coma after closed head injury [21].
• Oxidative stress in closed-head injury: brain antioxidant capacity as an indicator of functional outcome [22].
• Heat acclimation increases hypoxia-inducible factor 1alpha and erythropoietin receptor expression: implication for neuroprotection after closed head injury in mice [15].
• We evaluated prospectively gentamicin and tobramycin pharmacokinetics in 37 patients with multiple system trauma and seven patients with isolated closed head trauma [23].

Anatomical context of Head Injuries, Closed

• Homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations were measured in the lumbar cerebrospinal fluid of 98 patients after closed head injury [24].
• Strong expression of GFAP mRNA in rat hippocampus after a closed-head injury [25].
• Robust Fos expression was observed in the ipsilateral pyriform cortex following both types of injury but was observed in the ipsilateral dentate gyrus only following closed head injury [26].
• The activity of the sympathetic nervous system during the course of severe closed head injury has been evaluated in 15 patients by measuring plasma levels of epinephrine and norepinephrine [27].
• A case is presented in which a patient sustained a closed head injury with subsequent acute subdural hematoma and delayed posterior dislocation of the atlas without fracture of the odontoid process and with an intact C-1 arch [28].

Gene context of Head Injuries, Closed

• In the brain of mice subjected to closed head injury, neither Fractalkine protein nor mRNA were found to be augmented; however, Fractalkine receptor (CX3CR1) mRNA steadily increased peaking at 1 week postinjury (P < 0.05, one-way analysis of variance) [29].
• Serum S100B concentrations are increased after closed head injury in children: a preliminary study [30].
• In this study, we investigated the effect of transgenic overexpression of IL-1ra on the cytokine expression and neurological damage in a closed head injury (CHI) model of TBI [31].
• In previous studies, drugs that were inhibitors of both COX-1 and COX-2 failed to decrease brain edema formation or improve Neurological Severity Score (NSS) after closed head trauma (CHT), although some did decrease prostaglandin-E2 (PGE2) formation [32].
• The authors investigated the posttraumatic release of IL-18 in murine brains following experimental closed head injury (CHI) and in CSF of CHI patients [33].

Analytical, diagnostic and therapeutic context of Head Injuries, Closed

• The indications for prophylactic inferior vena cava filter insertion included prolonged immobilization with multiple injuries, closed head injury, pelvic fracture, spine fracture, multiple long bone fracture, and attending discretion [34].
• The Traumatic Brain Injury Unit at Gaylord Hospital routinely admits patients over 50 years of age for rehabilitation after significant closed head injury [35].
• In order to determine the effects of steroid administration on the metabolic response to isolated closed-head injury, a longitudinal study was performed [36].
• The responses of the apoE-deficient and control groups to closed head injury were both biphasic and were composed of initial reductions followed by subsequent increases in the levels of reducing antioxidant equivalents [37].
• Impact of traumatic subarachnoid hemorrhage on outcome in nonpenetrating head injury. Part II: relationship to clinical course and outcome variables during acute hospitalization [38].

References