Articles: cations.
-
Treating neuroma pain is a clinical challenge. Identification of sex-specific nociceptive pathways allows a more individualized pain management. The Regenerative Peripheral Nerve Interface (RPNI) consists of a neurotized autologous free muscle using a severed peripheral nerve to provide physiological targets for the regenerating axons. ⋯ Prophylactic RPNI can prevent neuroma site pain in both sexes. However, attenuation of both cold allodynia and thermal allodynia occurred in males exclusively, potentially because of their sexually dimorphic effect on pathological changes of the central nervous system.
-
Directional leads have garnered widespread use in deep brain stimulation (DBS) because of the ability to steer current and maximize the therapeutic window. Accurate identification of lead orientation is critical to effective programming. Although directional markers are visible on 2-dimensional imaging, precise orientation may be difficult to interpret. Recent studies have suggested methods of determining lead orientation, but these involve advanced intraoperative imaging and/or complex computational algorithms. Our objective is to develop a precise and reliable method of determining orientation of directional leads using conventional imaging techniques and readily available software. ⋯ We propose a method to determine orientation of directional DBS leads in a precise manner on conventional imaging and readily available software. This method is reliable across DBS vendors, and it can simplify this process and aid in effective programming.
-
Objective: Neurological complications after myocardial ischemia/reperfusion (IR) injury remain high and seriously burden patients and their families. Dexmedetomidine (Dex), an α 2 agonist, is endowed with analgesic-sedative and anti-inflammatory effects. Therefore, our study aims to explore the mechanism and effect of Dex on brain damage after myocardial IR injury. ⋯ Results: Dex was capable of reducing myocardial IR-induced brain damage including inflammatory factor secretion, blood-brain barrier disruption, neuronal edema, microglial activation, and acute cognitive dysfunction. However, the protective role of Dex was attenuated in HIF-1α knockout mice. Conclusion: Dex protects against myocardial IR-induced brain injury, and the neuroprotection of Dex is at least partially dependent on the activation of the HIF-1 pathway.