Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2010
ReviewNeuromodulation with pleiotropic and multimodal drugs -- future approaches to treatment of neurological disorders.
Neurologists are confronted with an ever-growing amount of new information regarding the intimate processes taking place in both normal and pathological brains. Concepts like neuroprotection, neurotrophicity, or anoikis and their clinical utility may be of dazzling complexity. ⋯ Since it is becoming more and more clear that using neuroprotective molecule with only one mechanism of action in disease treatment is a utopist idea, the research and use of multimodal drugs should be encouraged. It is not easy to find good therapeutic approaches to neurological disorders, especially if we do not have a deep understanding of all the basic endogenous biological processes, pathophysiological processes, and the links between them.
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Acta Neurochir. Suppl. · Jan 2010
Following brain trauma, copeptin, a stable peptide derived from the AVP precusor, does not reflect osmoregulation but correlates with injury severity.
The incidence of water and electrolyte disturbances following traumatic brain injury (TBI) is considerable and has been attributed to a dysregulation of the hypothalamic peptide arginine-vasopressin (AVP). Copeptin, the C-terminal part of the AVP prohormone, reflects AVP activity. In 71 TBI patients we measured copeptin in serum by a sandwich immunoassay. ⋯ Copeptin was significantly decreased following skullbase fracture (p = 0.016). Our data reveal a loss of hypothalamic osmoregulation following TBI. The measurement of Copeptin/AVP release reveals a significant predictive function for the severity of TBI.
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Acta Neurochir. Suppl. · Jan 2010
State-of-the-art management and monitoring of brain edema and intracranial hypertension in fulminant hepatic failure. A proposed algorithm.
Develop an evidence-based clinical algorithm integrating clinical decision making on intracranial pressure (ICP) monitoring and intracranial hypertension (ICH) management in the setting of fulminant hepatic failure (FHF). ⋯ State-of-the-art management of ICH due to brain edema in FHF includes Class I therapies such as mannitol and hypertonic saline. Bioartificial liver, hypothermia and hyperventilation are supported by Class II evidence. Indomethacin and sedation remain Class III. Monitoring ICP is supported by Class II and III evidence. A clinical algorithm was created based on the existing therapeutic armamentarium and corresponding evidence support.
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Acta Neurochir. Suppl. · Jan 2010
Randomized Controlled TrialEffects of magnesium sulfate infusion on cerebral perfusion in patients after aneurysmal SAH.
A meta-analysis of current data suggests that magnesium sulfate infusion improves the outcome after aneurysmal subarachnoid hemorrhage through a reduction in delayed ischemic neurological deficit. Two multi-center randomized controlled trials are currently underway to investigate this hypothesis. The possible pharmacological basis of this hypothesis includes neuroprotection and vasodilatation. We aim to investigate the cerebral hemodynamic effects of magnesium sulfate infusion in aneurysmal subarachnoid hemorrhage patients. ⋯ Magnesium sulfate infusion, in the dosage of current clinical trials, did not increase cerebral blood volume and cerebral blood flow, as postulated by dilation of small vessels and/or collateral pathways.
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Acta Neurochir. Suppl. · Jan 2010
Dynamics of S100B release into serum and cerebrospinal fluid following acute brain injury.
High S100B serum levels are considered to reflect brain injury severity. However, the dynamics of S100B passage from the cerebral compartment into the blood remain unclear. We examined the temporal profile of S100B release into the cerebrospinal fluid (CSF) and blood in acute brain injury. ⋯ Following brain injury, the S100B passage from the CSF to the blood was significantly impaired. Further, higher ratios were correlated with better neurological function (p = 0.002). Because stimulated active S100B release may serve as a repair mechanism, a higher S100B serum/CSF ratio may contribute to neurological recovery.