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Clin Neurol Neurosurg · Aug 2014
Median-evoked somatosensory potentials in severe brain injury: does initial loss of cortical potentials exclude recovery?
In patients with severe brain injury (SBI) median-evoked somatosensory potentials (M-SSEP) serve as a prognostic tool. Bilateral loss of cortical responses (BLCR) is usually thought to be a reliable marker of poor prognosis. Prognostic accuracy to predict a poor outcome depends on the cause of coma and is best in hypoxic-ischemic encephalopathy (HIE) reaching almost 100% which is in contrast to patients with other etiologies of coma, especially traumatic brain injury (TBI). Only little evidence exists on the possibility of electrophysiological recovery of BLCR in repeated or serial SSEP-examinations and detailed functional outcome in these cases. ⋯ Electrophysiological recovery from primarily BLCR seems possible and is accompanied by good functional outcome in a relevant number of patients. Thus caution is warranted in predicting a poor prognosis based predominantly on SSEP, especially in patients with TBI. Focusing SSEP-examination on the early days after severe brain injury and performing only one examination in the case of BLCR may lead to systematic underestimation of the possibility of recovery.
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Although early accelerated rehabilitation is recommended for the treatment of acute Achilles tendon rupture, most traditional rehabilitation techniques require some type of brace. ⋯ Level IV, retrospective case series.
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Remifentanil is a 4-anilidopiperidine mu-opioid analgesic which is rapidly metabolized by unspecific blood and tissue esterases. According to its unique pharmacokinetic profile, remifentanil-based anaesthesia combines high-dosage opioid analgesia intraoperatively with a rapid and predictable postoperative awakening. ⋯ The present paper was designed to review the current knowledge on remifentanil and all aspects of its use in anaesthesiology. In addition, present data on the use of remifentanil for analgesia and sedation of the critically ill patient are summarized.
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Journal of neurochemistry · Mar 2006
Interaction between interferon gamma and insulin-like growth factor-1 in hippocampus impacts on the ability of rats to sustain long-term potentiation.
There is compelling evidence to suggest that inflammation significantly contributes to neurodegenerative changes. Consistent with this is the observation that several neurodegenerative disorders are accompanied by an increase in the concentration of interleukin (IL)-1beta. IL-1beta has a negative impact on synaptic plasticity and therefore an increased concentration of IL-1beta, such as that in the hippocampus of the aged rat, is associated with a deficit in long-term potentiation (LTP). ⋯ Intracerebroventricular injection of IFNgamma inhibited LTP, and increased microglial activation was observed in both IFNgamma-injected and aged rats. The age-related increase in IFNgamma was accompanied by a decrease in the hippocampal concentration of insulin-like growth factor (IGF)-1. The evidence presented suggests that IGF-1 acts to antagonize the IFNgamma-induced microglial activation, the accompanying increase in IL-1beta concentration and the consequent deficit in LTP.