
An anaesthetic/sedative agent will proceed to evaluation of neuroprotective efficacy in a clinical trial when two major prerequisites are fulfilled: first, a body of preclinical evidence for its neuroprotective effects is necessary, second, circumstantial information from human use must be available. While testing of many promising drugs does not proceed past the stage of demonstrating neuroprotection in the physiology laboratory, in 1999, the FDA approved the α2-adrenoceptor agonist dexmedetomidine (DEX) for use in humans for analgesia and sedation [1]. However, although DEX is increasingly being used in the care of neurosurgical patients [1]–[3], its neuroprotective effects were not evaluated in a patient trial. In the present article, we will therefore outline the current understanding of DEX-mediated neuroprotection, and compare this state of knowledge with key criteria for the design of a clinical trial by experts in the field of anaesthetic neuroprotection [4], [5].
| citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 1 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Average | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Average | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Average |
