Is clonidine-induced neuronal activation in the spinal cord altered after peripheral nerve injury?
Previous studies suggest a shift in alpha 2 adrenoceptor subtype and the involvement of cholinergic interneurons in antinociception in the spinal cord after nerve injury. The current results suggest that intrathecal clonidine, by direct or indirect methods, increases neuronal activation in normal animals, presumably leading to net inhibition of pain signaling, whereas it reduces the increase in neuronal activity induced by nerve injury.
If using current radiotherapy practices and clinical recommendations based on dose surrogates computed globally on OARs and TVs, one does not need to take radiobiological effects into account while accumulating total dose as these lead to very small differences compared to a simple accumulation technique consisting of a linear sum of the dose fractions. However, care must be taken if other adaptive strategies, based on local rather than global information, are used.