Articles: brain-injuries.
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Although glucose is the main carbohydrate energy substrate for the normal brain, several studies published over the last 10 years now challenge this assumption. The activated brain increases its metabolism to meet increased energy demands by glycolysis after injury. In vitro studies now show that lactate alone can serve as an energy source to maintain synaptic function. ⋯ After 30 min, the brain was removed, frozen, and cut into 20 microm sections for autoradiography. Uptake of 14C-label was mainly concentrated at the injury site (2.5 times greater) although uninjured brain also took up the 14C-label. This increased concentration of radioactive lactate at the injury site suggests that the injured brain may use the lactate as an energy source.
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Traumatic brain injury (TBI) can produce chronic cognitive learning/memory deficits that are thought to be mediated, in part, by impaired hippocampal function. Experimentally induced TBI is associated with deficits in hippocampal synaptic plasticity (long-term potentiation, or LTP) at acute post-injury intervals but plasticity has not been examined at long-term survival periods. The present study was conducted to assess the temporal profile of LTP after injury and to evaluate the effects of injury severity on plasticity. ⋯ These experiments reveal a previously unknown effect of TBI whereby experimentally induced injury results in a chronic inability of the CA1 hippocampus to maintain synaptic plasticity. They also provide evidence that sham surgical procedures can significantly influence hippocampal physiology at the acute post-TBI intervals. The results have implications for the mechanisms underlying the impaired synaptic plasticity following TBI.
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J Neurosurg Anesthesiol · Apr 2000
The use of hyperventilation in the treatment of plateau waves in two patients with severe traumatic brain injury: contrasting effects on cerebral oxygenation.
We present the case reports of two patients with severe traumatic brain injury who, in the absence of external stimuli, developed episodes of acute elevation of intracranial pressure (plateau waves) associated with jugular bulb oxyhemoglobin (SjO2) desaturation, severe reduction of cerebral tissue PO2 (PbrO2), and deterioration of neurological status. In all of these episodes hyperventilation was successful in extinguishing plateau waves, but in one patient it was associated with an improvement of both the global (increased SjO2) and local (increased PbrO2) cerebral perfusion, while in the other patient it was associated with a reduction of both SjO2 and PbrO2. In both patients the effects of hyperventilation (and other pharmacological treatments) were short-lived; plateau waves reappeared and the patients had to be submitted to decompressive craniotomy (first patient) and cerebrospinal fluid (CSF) drainage (second patient). We conclude that hyperventilation can be useful as a temporary measure to treat plateau waves, but cerebral oxygenation should always be monitored to avoid iatrogenic cerebral ischemia.
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Journal of neurotrauma · Apr 2000
Ethanol reduces metabolic uncoupling following experimental head injury.
Previous investigations have shown that ethanol is neuroprotective following experimental traumatic brain injury (TBI). This study sought to determine if the neuroprotective effects of ethanol in a controlled cortical impact (CCI) injury model are related to its effects on cerebral glucose metabolism and blood flow. Adult rats were given ethanol (1.0 g/kg) or saline by intraperitoneal injection followed 40 min later by injury. ⋯ Simultaneously, the reduction in CBF typically seen within the contusion core and penumbra after CCI is less severe when ethanol is present. The net effect of these changes is a decreased degree of uncoupling between glucose metabolism and CBF that otherwise occurs in the absence of ethanol. These changes may likely explain the neuroprotective effect of ethanol.