Articles: brain-injuries.
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The purpose of this study was to determine the effect of augmenting NMDA receptor activation on cognitive deficits produced by traumatic brain injury (TBI). Specifically, D-cycloserine (DCS), a partial agonist of the NMDA-associated glycine site, was tested as a potential cognitive enhancer. Rats were injured using lateral fluid percussion TBI (2.8 +/- .10 atm). ⋯ In contrast, the 10 mg/kg dose of DCS was ineffective in reducing injury-induced memory deficits. DCS (30 mg/kg) also significantly improved the spatial memory of sham-injured animals when compared with sham-injured animals treated with vehicle (P < 0.05). In conclusion, chronic, post-injury enhancement of the NMDA receptor is an effective strategy for ameliorating TBI-associated cognitive deficits.
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Comparative Study
Diaspirin cross-linked hemoglobin resuscitation improves cerebral perfusion after head injury and shock.
Shock associated with traumatic brain injury (TBI) doubles the mortality of TBI alone by inducing a secondary ischemic injury. Rapid correction of cerebral perfusion pressure (CPP) is thought to be essential to improving outcome. Diaspirin cross-linked hemoglobin (DCLHb) has been shown to improve cerebral blood flow, increase mean arterial pressure (MAP), and reduce lesion size in models of occlusive cerebral ischemia but has not been evaluated in a model of TBI combined with hemorrhagic shock. ⋯ These data suggest that DCLHb is beneficial in the early resuscitation of head injury and shock and that further investigation is warranted. Key Words: Diaspirin cross-linked hemoglobin, Head injury, Shock, Cerebral perfusion pressure.
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Head traumas frequently occur in polytrauma patients but are also found as isolated injuries. In our hospital trauma center without a neurosurgical department, in a 21-month period, 489 patients with head/brain trauma were treated. This represents 6.5% of all patients treated in the trauma and reconstructive surgery clinic. ⋯ In patients with intracerebral bleeding, bleeding in the dorsal fossa, injury of brain nerves, carotid artery or sinus cavernosus injuries, frontobasal injuries with liquor fistula or pneumonencephalon, transfer of the patients to specialized neurosurgical centers is indicated. With this selection, we obtained the same results in a trauma center without a neurosurgical department as reported in the literature. This avoids overloading neurosurgical centers with head/brain injury patients.
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Am J Phys Med Rehabil · Nov 1996
Revised trauma score: an additive predictor of disability following traumatic brain injury?
Recent studies have clarified the role of hypoxic-ischemic damage as a secondary factor in traumatic brain injury (TBI). Many trauma centers are now consistently using the Revised Trauma Score (Glasgow Coma Scale, systolic blood pressure, and respiratory rate) to assist with triage of multitrauma patients. This study investigated the predictive power of the Revised Trauma Score (RTS) instead of the Glasgow Coma Scale (GCS) in determination of disability as measured by the Disability Rating Scale (DRS). ⋯ Lowest GCS within the first 24 h postinjury also failed to show a strong relationship with DRS at rehabilitation admission (-0.28) and discharge (-0.24). Multiple regression analysis performed on RTS subsets for systolic blood pressure and respiratory rate did not reveal an added predictive value. Although RTS may be important in emergency triage for its ability to predict mortality, this study indicates its limited usefulness in prediction of disability.
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In the last two decades our understanding of the pathophysiology of severe head injury has significantly increased. It has become evident that secondary neuronal damage may occur and should be prevented. It is ischemia, similar to that seen with stroke and aneurysmal subarachnoid hemorrhage, that causes secondary brain damage. ⋯ Moreover, there are some new pharmacological concepts for changing the threshold for ischemia in brain tissue. At the present time, however, valid data concerning clinical use are still not available. Therefore, mild hyperventilation and sedation during the initial post-traumatic phase and lowering of intracranial pressure by osmotherapeutics remain the most important treatment modalities, as they were 20 years ago.