Xenon improves neurologic outcome and reduces secondary injury following trauma in an in vivo model of traumatic brain injury.

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Abstract

To determine the neuroprotective efficacy of the inert gas xenon following traumatic brain injury and to determine whether application of xenon has a clinically relevant therapeutic time window.

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A model of parasagittal controlled cortical impact in the mouse: cognitive and histopathologic effects.

George D W Smith, D Meaney, Meryl K Perlman … (1995)

Controlled cortical impact (CCI), using a pneumatically driven impactor to produce traumatic brain injury, has been characterized previously in both the ferret and in the rat. In the present study, we applied this technique to establish and characterize the CCI model of brain injury in another species, the mouse, evaluating cognitive and histopathologic outcome. In anesthetized (sodium pentobarbital, 65 mg/kg) male C57BL mice, we performed sham treatment (no injury, n = 12) or CCI injury (n = 12) at a velocity of 5.7-6.2 m/sec and depth of 1 mm, using a 3-mm diameter rounded-tip impounder, positioned over the left parietotemporal cortex (parasagittal). At this level of injury, we observed highly significant deficits in memory retention of a Morris water maze task 2 days following injury (p < 0.001). Postmortem histopathologic analysis performed at 48 h following injury revealed substantial cortical tissue loss in the region of impact and selective hippocampal neuronal cell loss in the CA2, CA3, and CA3c regions, using Nissl staining. Analysis of degenerating neurons using modified Gallyas silver staining techniques demonstrated consistent ipsilateral injury of neurons in the cortex adjacent to the impact site and in the dentate gyrus of the ipsilateral hippocampus. Bilateral degeneration was observed at the gray matter-white matter interface along the corpus callosum. Glial fibrillary acidic protein (GFAP) immunohistochemistry revealed extensive reactive gliosis appearing diffusely through the bilateral cortices, hippocampi, and thalami at 48 h postinjury. Breakdown of the blood-brain barrier was demonstrated with antimouse IgG immunohistochemistry, revealing extravasation of endogenous IgG throughout the ipsilateral cortex, hippocampus, and thalamus. These results suggest that this new model of parasagittal CCI in the mouse mimics a number of well-established sequelae observed in previously characterized brain injury models using other rodent species. This mouse model may be a particularly useful experimental tool for comparing behavioral and histopathologic characteristics of traumatic brain injury in wild-type and genetically altered mice.

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Monitoring intracranial pressure in traumatic brain injury.

Martin Smith (2007)

Increased intracranial pressure (ICP) is an important cause of secondary brain injury, and ICP monitoring has become an established component of brain monitoring after traumatic brain injury. ICP cannot be reliably estimated from any specific clinical feature or computed tomography finding and must actually be measured. Different methods of monitoring ICP have been described but intraventricular catheters and microtransducer systems are most widely used in clinical practice. ICP is a complex variable that links ICP and cerebral perfusion pressure and provides additional information from identification and analysis of pathologic ICP wave forms. ICP monitoring can also be augmented by measurement of indices describing cerebrovascular pressure reactivity and pressure-volume compensatory reserve. There is considerable variability in the use of ICP monitoring and treatment modalities among head injury centers. However, there is a large body of clinical evidence supporting the use of ICP monitoring to detect intracranial mass lesions early, guide therapeutic interventions, and assess prognosis, and it is recommended by consensus guidelines for head injury management. There remains a need for a prospective, randomized, controlled trial to identify the value of ICP monitoring and management after head injury.