Δευτέρα 15 Ιανουαρίου 2018
Neurological prognosis of 6 cases after chest compression during general anesthesia
Abstract
Introduction
Data on the outcomes after chest compression (CC) of patients who are under general anesthesia (GA) are limited. The present study aimed to evaluate the neurological outcomes in patients who received CC while under GA.
Methods
The patients who received CC while under GA, between 2010 and 2015, in Kyoto Medical Center were surveyed retrospectively. The primary outcome was poor neurologic function or death, as defined by a cerebral performance category score (CPC) score of 3–5 on day 28.
Results
Six patients received CC while under GA, and four patients had poor neurological outcomes with a CPC score of 4 or 5 on day 28. All these patients required emergency operation because of their primary disease.
Conclusion
Even if the patients were monitored and immediately managed under GA, ineffective management of preoperative conditions tended to result in the poor neurological prognosis.
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Ether-à-go-go K+ channels: effective modulators of neuronal excitability
Abstract
Mammalian EAG (ether-à-go-go) channels are voltage-gated K+ channels. They are encoded by the KCNH gene family and divided into three subfamilies, eag (Kv10), erg (eag-related gene; Kv11) and elk (eag-like; Kv12). All EAG channel subtypes are expressed in the brain where they effectively modulate neuronal excitability. This Topical Review describes the biophysical properties of each of the EAG channel subtypes, their function in neurons and the neurological diseases induced by EAG channel mutations. In contrast to the function of erg currents in the heart where they contribute to repolarization of the cardiac action potential, erg currents in neurons are involved in the maintenance of the resting potential, setting of action potential threshold and frequency accommodation. They can even support high frequency firing by preventing a depolarization-induced Na+ channel block. EAG channels are modulated differentially, e.g. eag channels by intracellular Ca2+, erg channels by extracellular K+ and GPCRs, and elk channels by changes in pH. So far, only currents mediated by erg channels have been recorded in neurons with the help of selective blockers. Neuronal eag and elk currents have not been isolated due to the lack of suitable channel blockers. However, findings in KO mice indicate a physiological role of eag1 currents in synaptic transmission and an involvement of elk2 currents in cognitive performance. Human eag1 and eag2 gain-of-function mutations underlie syndromes associated with epileptic seizures.
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Κυριακή 14 Ιανουαρίου 2018
Parvalbumin fast-spiking interneurons are selectively altered by pediatric traumatic brain injury
Abstract
Pediatric traumatic brain injury (TBI) is a leading cause of death and disability in children. Traditionally, ongoing neurodevelopment and neuroplasticity have thought to confer children with an advantage following TBI. However, recent findings indicate that the pediatric brain may be more sensitive to brain injury. Inhibitory interneurons are essential for proper cortical function and implicated in the pathophysiology of TBI, yet few studies have directly examined for TBI induced changes to interneurons themselves. To address this, we examine how inhibitory neurons are altered following controlled cortical impact (CCI) in juvenile mice with targeted Cre-dependent fluorescent labelling of interneurons (Vgat:Cre/Ai9 and PV:Cre/Ai6). While CCI failed to alter the number of excitatory neurons or somatostatin-expressing interneurons in the peri-injury zone it significantly decreased the density of parvalbumin (PV) immunoreactive cells by 71%. However, PV:Cre/Ai6 mice subjected to CCI showed a lesser extent of fluorescently labelled cell loss. PV interneurons are predominantly of a fast-spiking (FS) phenotype and when recorded electrophysiologically from the peri-injury zone exhibited similar intrinsic properties as control neurons. Synaptically, CCI induced a decrease in inhibitory drive onto FS interneurons combined with an increase in the strength of excitatory events. Our results indicate that CCI induced both a loss of PV interneurons and an even greater loss of PV expression. This suggests caution in interpreting changes in PV immunoreactivity alone as direct evidence of interneuronal loss. Further, in contrast with reports in adults TBI in the pediatric brain selectively alter PV-FS interneurons resulting in primarily a loss of interneuronal inhibition.
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