Articles: brain-injuries.
-
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.
-
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.
-
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.
-
To avoid ischaemic secondary insults after severe head injury (SHI) it would be helpful to know the relationship between cerebral perfusion pressure (CPP) and intracranial pressure (ICP). Static cerebrovascular autoregulation (AR) was tested in 14 patients after SHI. Mean arterial pressure (MAP) was varied to detect changes in intracranial pressure (ICP) indicative of intact AR. ⋯ Lower AR breakpoints were seen from 60 to 80 mmHg CPP, upper breakpoints were as high as 112. CPP monitoring achieves a twofold utility in targeted therapy: (1) defining the range of intact AR; and (2) lower AR breakpoint assessment to avoid secondary insults. Although the precise relationship between pAR breakpoints and the adequacy of cerebral perfusion to meet metabolic needs remains unclear, a technique such as described here is simple and has much to offer in targeting therapy toward specific pathophysiological processes in traumatic brain injury.