Major clinical endpoints of general anesthesia, such as the alteration of consciousness, are achieved through effects of anesthetic agents on the central nervous system, and, more precisely, on the brain. Historically, clinicians and researchers have always been interested in quantifying and characterizing those effects through recordings of surface brain electrical activity, namely electroencephalography (EEG). Over decades of research, the complex signal has been dissected to extract its core substance, with significant advances in the interpretation of the information it may contain. Methodological, engineering, statistical, mathematical, and computer progress now furnishes advanced tools that not only allow quantification of the effects of anesthesia, but also shed light on some aspects of anesthetic mechanisms. In this article, we will review how advanced EEG serves the anesthesiologist in that respect, but will not review other intraoperative utilities that have no direct relationship with consciousness, such as monitoring of brain and spinal cord integrity. We will start with a reminder of anesthestic effects on raw EEG and its time and frequency domain components, as well as a summary of the EEG analysis techniques of use for the anesthesiologist. This will introduce the description of the use of EEG to assess the depth of the hypnotic and anti-nociceptive components of anesthesia, and its clinical utility. The last part will describe the use of EEG for the understanding of mechanisms of anesthesia-induced alteration of consciousness. We will see how, eventually in association with transcranial magnetic stimulation, it allows exploring functional cerebral networks during anesthesia. We will also see how EEG recordings during anesthesia, and their sophisticated analysis, may help corroborate current theories of mental content generation.

Humans excel at causal reasoning, yet at the same time consistently fail to respect its basic axioms. They seemingly fail to recognize, for instance, that only the direct causes of an event can affect its probability (the Markov condition). How can one explain this paradox? Here we argue that standard normative analyses of causal reasoning mostly apply to the idealized case where the reasoner has perfect confidence in her knowledge of the underlying causal model. Given uncertainty about the correct representation of a causal system, it is not always rational for a reasoner to respect the Markov condition and other ‘normative’ principles. To test whether uncertainty can account for the apparent fallibility of human judgments, we formulate a simple computational model of a rational-but-uncertain causal reasoner. In a re-analysis of a recent causal reasoning study, the model fits the data significantly better than its standard normative counterpart.

Cottonseed diets provide animals with increased levels of protein and energy to support growth. Recently, it was suggested that although the gossypol content of cottonseed could result in adverse animal reproduction, it could have a potential anthelmintic property beneficial to small ruminant operations. In addition, gossypol is primarily cleared and excreted from the animal via liver glucuronidation, which is a primary pathway for steroid clearance in ruminants. The objective of this experiment was to determine the effect of a cottonseed diet and parasite load on the hepatic portal blood flow an indicator of hepatic clearance rates and metabolism. Forty Boer x Spanish cross does were assigned to of 4 treatments (n = 10 per treatment group) in a 2x2 factorial design consisting of cottonseed supplementation and no parasite infection (CNP), cottonseed supplementation plus artificial infection with Haemonchus contortus (CP), commercial pellets with no parasite infection (NCNP), or commercial pellets plus artificial infection with Haemonchus contortus (NCP). On week 8 post-treatment, hepatic portal blood flow measurements were collected via Doppler ultrasonography on the right side of the animal at the 10th intercostal space. Blood flow was then calculated using the following equation: blood flow (mL/min) = mean velocity (cm/s) x vessel area x 60 seconds. The mean velocity was calculated by the following formula: (systolic – diastolic)/pulsatility index. Hepatic portal blood flow and body weight of does were analyzed with a One-way ANOVA using the MIXED procedure of SAS with diet and parasite load as the main effects and their interactions. A diet by parasite interaction (P = 0.026) was observed for the mean velocity of the hepatic portal vein, which was decreased in CP versus CNP treatments. A diet by parasite interaction (P = 0.012) was observed for the diameter of the hepatic portal vein, which was increased in the CP treatment versus all other groups. However, absolute hepatic portal blood flow was not different (P > 0.12) amongst treatments. A tendency for the main effect (P = 0.087) of diet was observed for hepatic portal blood flow relative to body weight, which was an increase in cottonseed (27.8 ±.8 mL/min*kg) versus NCS (23.2 ±.8 mL/min*kg). Body weight was not different (P > 0.35) amongst treatments at the time of Doppler ultrasound examination. In conclusion, cottonseed interacted with parasites to decrease mean velocity and increase the diameter of the portal vein. In addition, cottonseed appears to increase liver blood flow relative to body weight. This change in relative liver blood flow could have implications for mediating hepatic metabolism and clearance.