Despite major advances, emesis remains a major problem in the context of cancer chemotherapy and in the postoperative period. A better understanding of the relevant neurocircuitry, especially the central pattern generator responsible for emesis and the central role of substance P, led to the development of a new class of antiemetics: the neurokinin-1 (NK1) receptor antagonists. Aprepitant is the first NK1 receptor antagonist approved for use in postoperative nausea and vomiting, but several other compounds are currently being investigated for their potential as antiemetics in the postoperative and cancer chemotherapy settings.

SummaryWe describe the target-controlled administration of propofol and remifentanil, combined with monitoring of the bispectral index, during an awake craniotomy for removal of a left temporoparietal tumour near the motor speech centre. Target concentrations of the two drugs were adjusted according to the patient's responses to painful stimuli and surgical events, and the need for speech testing. Allowing the effect-site concentrations of propofol and remifentanil to decrease during surgery allowed the performance of cortical speech mapping and the testing of the patient's ability to speak. Although the bispectral index was not used as a guide for the administration of the drugs, its value correlated better with the patient's responsiveness than did the predicted effect-site concentrations of propofol. Side-effects, comprising hypotension, respiratory depression and airway obstruction, were related to rapid increases in drug infusion rates and were easily managed.

Rocuronium alters the RE-SE gradient and the RE and RE-SE responses to laryngoscopy. Muscle relaxation may confound interpretation of entropy monitoring.

1. Paralysis of the diaphragm in the dog is known to cause a compensatory increase in activation of the inspiratory intercostal muscles (parasternal intercostals, external intercostals, and levator costae). The present studies were designed to assess the mechanism(s) of that compensation. 2. Complete, selective diaphragmatic paralysis was induced by injecting local anaesthetic into small silicone cuffs placed around the phrenic nerve roots in the neck. 3. Paralysis produced a decrease in tidal volume and an increase in arterial P(CO2) (P(a,CO2)). The increased hypercapnic drive was a primary determinant of the increased inspiratory intercostal activity. 4. However, paralysis also produced an increased inspiratory cranial displacement of the ribs. When this increased rib displacement was reduced to that seen before paralysis, it appeared that the increase in external intercostal and levator costae inspiratory activity was commonly greater than anticipated on the basis of the increased P(a,CO2). 5. Diaphragmatic paralysis after bilateral vagotomy also elicited disproportionate increases in inspiratory intercostal activity, thus indicating that these increases are not caused by vagal afferent inputs. 6. These observations are consistent with the idea that the intercostal muscle compensation for diaphragmatic paralysis is, in part, due to the release of an inhibition originating from the contracting diaphragm. This inhibition might arise in the diaphragmatic tendon organs.

EudraCT 2011-000999-33.