Articles: brain-injuries.
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Randomized Controlled Trial Comparative Study Clinical Trial
Treatment of traumatic brain injury with moderate hypothermia.
Traumatic brain injury initiates several metabolic processes that can exacerbate the injury. There is evidence that hypothermia may limit some of these deleterious metabolic responses. ⋯ Treatment with moderate hypothermia for 24 hours in patients with severe traumatic brain injury and coma scores of 5 to 7 on admission hastened neurologic recovery and may have improved the outcome.
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Acta neuropathologica · Feb 1997
Chronic histopathological consequences of fluid-percussion brain injury in rats: effects of post-traumatic hypothermia.
Early outcome measures of experimental traumatic brain injury (TBI) are useful for characterizing the traumatic severity as well as for clarifying the pathomechanisms underlying patterns of neuronal vulnerability. However, it is increasingly apparent that acute outcome measures may not always be accurate predictors of chronic outcome, particularly when assessing the efficacy of potential therapeutic regimens. This study examined the chronic histopathological outcome in rats 8 weeks following fluid-percussive TBI coupled with moderate post-traumatic brain hypothermia, a protocol that provides acute neuronal protection. ⋯ Lateral ventricles were substantially enlarged in the TBI-normothermia group, an effect which was significantly attenuated by post-TBI hypothermia. The attenuation of lateral ventricular dilation by post-traumatic hypothermia is indicative of chronic neuroprotection in this TBI model. These data provide new information concerning the chronic histopathological consequence of experimental TBI and the relevance of this trauma model to chronic human head injury.
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Journal of neurotrauma · Feb 1997
Motor and cognitive functional deficits following diffuse traumatic brain injury in the immature rat.
To determine the motor and cognitive deficits following a diffuse severe traumatic brain injury (TBI) in immature Sprague Dawley rats (17 days), four groups of animals were injured at different severity levels using a new closed head weight drop model: (sham, severe injury [SI: 100 g/2 m], SH [SI + hypoxemia (30 min of an FiO2 of 8% posttrauma)], and ultra severe injury [US: 150 g/2 m]). Latency on beam balance, grip test performance, and maintenance of body position on an inclined board were measured daily after injury to assess vestibulomotor function. Cognitive function was assessed on days 11-22 using the Morris water maze (MWM). ⋯ US, however, produced significant cognitive dysfunction (vs. sham, SI, and SH), specifically, greater latencies to find the hidden platform through 22 days. Swim speeds were not significantly different between any of the injury groups and shams. These data indicate that (1) beam balance, inclined plane and MWM techniques are useful for assessing motor and cognitive function after TBI in immature rats; (2) SI produces motor but not cognitive deficits, which was not augmented by transient hypoxia; and (3) US created a marked but reversible motor deficit up to 10 days, and a sustained cognitive dysfunction for up to 22 days after TBI.
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Journal of neurosurgery · Feb 1997
Cerebral hyperglycolysis following severe traumatic brain injury in humans: a positron emission tomography study.
Experimental traumatic brain injury studies have shown that cerebral hyperglycolysis is a pathophysiological response to injury-induced ionic and neurochemical cascades. This finding has important implications regarding cellular viability, vulnerability to secondary insults, and the functional capability of affected regions. Prior to this study, posttraumatic hyperglycolysis had not been detected in humans. ⋯ The results of this study indicate that the metabolic state of the traumatically injured brain should be defined differentially in terms of glucose and oxygen metabolism. The use of FDG-PET demonstrates that hyperglycolysis occurs both regionally and globally following severe head injury in humans. The results of this clinical study directly complement those previously reported in experimental brain-injury studies, indicating the capability of imaging a fundamental component of cellular pathophysiology characteristic of head injury.
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Zhonghua Wai Ke Za Zhi · Feb 1997
[Relation of continuous ICP, CPP monitoring with prognosis for severe brain injury].
We analysed the treatment results of two groups of patients. Group I included 50 patients with severe brain injury with GCS 3-8, on whom continuous intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring was performed and Group II included 50 cases of similar patients, on whom no continuous ICP monitoring was performed. ⋯ Group II patients received the same intervention based on clinical observations, but they had relatively worse results. We are of the opinion that continuous ICP and CPP monitoring for severe brain injury patients helps find proper treatments and reduce mortality.