Journal of neurotrauma
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Journal of neurotrauma · Sep 2007
Chronic cognitive deficits and long-term histopathological alterations following contusive brain injury in the immature rat.
Although diffuse axonal injury is the primary pathology in pediatric brain trauma, the additional presence of focal contusions may contribute to the poor prognosis in brain-injured children younger than 4 years of age. Because existing models of pediatric brain trauma focus on diffuse brain injury, a model of contusive brain trauma was developed using postnatal day (PND) 11 and 17 rats, ages that are neurologically equivalent to a human infant and toddler, respectively. Closed head injury was modeled by subjecting the intact skull over the left parietal cortex of the immature rat to an impact with a metal-tipped indenter. ⋯ In contrast, in PND17 rats, the contused cortex observed at 3 days post-injury matured into a pronounced cavity lined with a glia limitans at 14 days; reactive astrocytes were present in both the hippocampus and thalamus up to 28 days post-injury. No evidence of traumatic axonal injury was observed in any region of the brain-injured PND17 rat. These data suggest that contusive brain trauma in the immature rat is associated with chronic cognitive deficits, but underscore the effect of the age-at-injury on behavioral and histopathologic outcomes.
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Journal of neurotrauma · Sep 2007
Diffusion tensor imaging detects clinically important axonal damage after mild traumatic brain injury: a pilot study.
The goal of the current investigation was to detect clinically important axonal damage in cerebral white matter after mild traumatic brain injury (TBI) using diffusion tensor imaging (DTI). To this end, we evaluated a prospective, pilot study of six subjects with isolated mild TBI and six matched orthopedic controls. All subjects underwent DTI scanning, post-concussive symptom (PCS) assessment, and neurobehavioral testing within 72 h of injury. ⋯ Collectively, DTI detected significantly lower trace and elevated FA values in mild TBI subjects compared to controls. These abnormalities correlated to poor clinical outcome. We believe these findings represent axonal swelling, an early step in the process of axonal injury.
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Journal of neurotrauma · Sep 2007
Traumatic brain injuries in a well-defined population: epidemiological aspects and severity.
The aim was to describe epidemiological and medical aspects of 449 cases of traumatic brain injury (TBI) from a well-defined geographical area with a population of 137,000 inhabitants. An episode of disturbed consciousness was a prerequisite for inclusion in the study. The incidence of TBI was 354/100,000 inhabitants. ⋯ CT was performed on 163 cases (36%) revealing 34 cases with intracranial hemorrhage (ICH) which is 21% of the examined or 8% of all the injured. The rate of ICH increased with increasing age (from 3% among children to 17% among the elderly persons) and also increased with decreasing GCS from 6% in the group of mild TBI to 60% among those with severe TBI. Attention should be directed to acute management of mild TBI in order to detect potentially dangerous ICH as well as to preventive actions against falls and vehicle related accidents.
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Journal of neurotrauma · Sep 2007
Low concentration of isoflurane promotes the development of neurogenic pulmonary edema in spinal cord injured rats.
Anesthetics can either promote or inhibit the development of neurogenic pulmonary edema (NPE) after central nervous system (CNS) injury. The influence of isoflurane was examined in male Wistar rats using 1.5%, 2%, 2.5%, 3%, 4%, or 5% isoflurane in air. Epidural balloon compression of the thoracic spinal cord was performed. ⋯ Animals from the 3% group recovered behaviorally more rapidly than did the animals from the 1.5% group; morphometry and MRI of the lesions showed no differences. Thus, low levels of isoflurane anesthesia promote NPE in rats with a compressed spinal cord and significantly complicates their recovery. The optimal concentration of anesthesia for performing a spinal cord compression lesion is 2.5-3% isoflurane in air.
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Journal of neurotrauma · Sep 2007
Anti-apoptotic effect of insulin in the control of cell death and neurologic deficit after acute spinal cord injury in rats.
Recent studies confirmed that the new cell survival signal pathway of Insulin-PI3K-Akt exerted cyto-protective actions involving anti-apoptosis. This study was undertaken to investigate the potential neuroprotective effects of insulin in the pathogenesis of spinal cord injury (SCI) and evaluate its therapeutic effects in adult rats. SCI was produced by extradural compression using modified Allen's stall with damage energy of 40 g-cm force. ⋯ Neuronal apoptosis was detected by TUNEL, and spinal cord blood flow (SCBF) was measured by laser-Doppler flowmetry (LDF). Ultimately, the data established the effectiveness of insulin treatment in improving neurologic recovery, increasing the expression of anti-apoptotic bcl-2 proteins, inhibiting caspase-3 expression decreasing neuronal apoptosis, reducing the expression of proinflammatory cytokines iNOS and COX-2, and ameliorating microcirculation of injured spinal cord after moderate contusive SCI in rats. In sum, this study reported the beneficial effects of insulin in the treatment of SCI, with the suggestion that insulin should be considered as a potential therapeutic agent.