Articles: brain-injuries.
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Previous studies have shown that traumatic brain injury (TBI) significantly reduces cerebral blood flow determined in vivo and reduces vascular reactivity in the pial circulation measured with cranial window preparations. We have now tested the hypothesis that TBI induces these changes by impairing intrinsic contractile activity of cerebral arteries. Anesthetized rats underwent moderate (2.2 atm) and severe (3.0 atm) midline fluid percussion TBI or sham injury following which posterior cerebral or middle cerebral arteries were isolated and isometric force generation was measured. ⋯ Acetylcholine induced an endothelium-dependent relaxation of posterior and middle cerebral arteries; the magnitude of the response was unaffected by moderate TBI. To determine whether prolonged in situ exposure of vessels to the traumatized cerebral milieu could reveal an alteration in intrinsic contractility, posterior cerebral arteries were isolated 30 min after TBI; again, no differences in the tension or relaxation responses were observed. It is concluded that midline fluid percussion TBI did not affect contraction or relaxation of proximal middle or posterior cerebral arteries in rats.
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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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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.