Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jan 2016
Traumatic Brain Injury Patients With a Glasgow Coma Scale Score of ≤8, Cerebral Edema, and/or a Basal Skull Fracture are More Susceptible to Developing Hyponatremia.
Traumatic brain injury (TBI) is a common injury treated at the neurosurgery department. The incidence rate is approximately 3% in the general population and the mortality rate is 25%. The incidence of hyponatremia following TBI is 33%. Hyponatremia is one of the main causes of disability and/or death in TBI patients. This study investigated the epidemiology of hyponatremia following TBI. ⋯ TBI patients with a GCS score ≤8, cerebral edema, and/or a basal skull fracture are particularly prone to developing hyponatremia. These patients require additional treatment that should entail the normalization of serum sodium levels to prevent deterioration of their condition.
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J Neurosurg Anesthesiol · Jan 2016
CaMKII Phosphorylation in Primary Somatosensory Cortical Neurons is Involved in the Inhibition of Remifentanil-induced Hyperalgesia by Lidocaine in Male Sprague-Dawley Rats.
Previous clinical studies have shown that lidocaine can alleviate severe postoperative pain after remifentanil-based anesthesia. Experimental studies have also demonstrated that lidocaine can inhibit remifentanil-induced hyperalgesia, yet the mechanism remains unknown. The present study explored the role of the primary somatosensory (S1) cortex in remifentanil-induced hyperalgesia as well as its inhibition by lidocaine through evaluation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) phosphorylation and protein expression levels in S1 cortical neurons. ⋯ These results suggested that the phosphorylation of CaMKII in S1 cortical neurons increases significantly during the process of remifentanil-induced hyperalgesia. The increase of CaMKII phosphorylation could be inhibited by systemic application of lidocaine. This inhibition may play a role in the antihyperalgesia effects of lidocaine.
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J Neurosurg Anesthesiol · Jan 2016
Dexmedetomidine Attenuates Neurotoxicity Induced by Prenatal Propofol Exposure.
Anesthetic agents (eg, isoflurane, propofol) may cause neurodegeneration in the developing brains and impair animals' learning ability. Dexmedetomidine (DEX), a selective alpha 2-adrenoreceptor agonist, has antiapoptotic properties in several brain injury models. Here, we tested whether DEX can protect the brain from neurodegeneration in rats exposed to propofol in utero. ⋯ DEX attenuates neuronal injury induced by maternal propofol anesthesia in the fetal brains, providing neurocognitive protection in the offspring rats.
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J Neurosurg Anesthesiol · Jan 2016
Biography Historical ArticleIn Memoriam Prof. Dr Med. Thomas Pasch, FRCA.