Using non-invasive neuroimaging to enhance the care, well-being and experimental outcomes of laboratory non-human primates (monkeys).

Over the past 10-20 years, neuroscience witnessed an explosion in the use of non-invasive imaging methods, particularly magnetic resonance imaging (MRI), to study brain structure and function. Simultaneously, with access to MRI in many research institutions, MRI has become an indispensable tool for researchers and veterinarians to guide improvements in surgical procedures and implants and thus, experimental as well as clinical outcomes, given that access to MRI also allows for improved diagnosis and monitoring for brain disease. As part of the PRIMEatE Data Exchange, we gathered expert scientists, veterinarians, and clinicians who treat humans, to provide an overview of the use of non-invasive imaging tools, primarily MRI, to enhance experimental and welfare outcomes for laboratory non-human primates engaged in neuroscientific experiments. We aimed to provide guidance for other researchers, scientists and veterinarians in the use of this powerful imaging technology as well as to foster a larger conversation and community of scientists and veterinarians with a shared goal of improving the well-being and experimental outcomes for laboratory animals.

Bispectral index transiently decreased to "0" during per-embolization rupture of an intracranial aneurysm.

Interpreting a Bispectral Index (BIS) of "0", corresponding to an isolelectric electroencephalography, can be difficult. After ruling out technical issues, such as leads disconnection, several possible causes for a decrease in the BIS persists, including deep anesthesia, hypothermia, decrease in the cerebral perfusion pressure and cerebral ischemia. We report a sudden transient decrease of the BIS to "0" in a patient that underwent a coil embolization of a ruptured intracranial aneurysm and suggest that the change in BIS values could provide useful information about the cerebral hemodynamic during aneurysm treatment and might provide indications of a serious cerebral event.

Cerebral mechanisms of general anesthesia.

How does general anesthesia (GA) work? Anesthetics are pharmacological agents that target specific central nervous system receptors. Once they bind to their brain receptors, anesthetics modulate remote brain areas and end up interfering with global neuronal networks, leading to a controlled and reversible loss of consciousness. This remarkable manipulation of consciousness allows millions of people every year to undergo surgery safely most of the time. However, despite all the progress that has been made, we still lack a clear and comprehensive insight into the specific neurophysiological mechanisms of GA, from the molecular level to the global brain propagation. During the last decade, the exponential progress in neuroscience and neuro-imaging led to a significant step in the understanding of the neural correlates of consciousness, with direct consequences for clinical anesthesia. Far from shutting down all brain activity, anesthetics lead to a shift in the brain state to a distinct, highly specific and complex state, which is being increasingly characterized by modern neuro-imaging techniques. There are several clinical consequences and challenges that are arising from the current efforts to dissect GA mechanisms: the improvement of anesthetic depth monitoring, the characterization and avoidance of intra-operative awareness and post-anesthesia cognitive disorders, and the development of future generations of anesthetics.

Brain tissue water comes in two pools: evidence from diffusion and R2' measurements with USPIOs in non human primates.

Diffusion-weighted MRI of non-human primates revealed that USPIO Bulk Magnetic Susceptibility (BMS) T2' effects of Ultrasmall Superparamagnetic Particles with Iron Oxide (USPIO) in the brain cannot be explained by a single compartment model, as diffusion and T2' effects appear coupled: Apparent Diffusion Coefficient (ADC) values depend on USPIO concentration and relaxivity effects of USPIO decrease with the b value. On the other hand, USPIO and diffusion effects could be well uncoupled using a model consisting in a fast and a slow diffusion pool with different relaxivities. Diffusion-weighting acts as a filter which emphasizes the contribution of the slow pool when increasing b values (apparent decrease in ADC and R2'). Those results have implications for human studies using BMS contrast agents, as well as BOLD and diffusion fMRI.

Lithium carbonate therapy for granulocytopenia in a patient with myelofibrosis and septic arthritis.

We report a patient with myelofibrosis, granulocytopenia, and septic arthritis, in whom lithium carbonate induced a more appropriate granulocyte count. Further evaluation of the use of lithium carbonate in granulocytopenic states seems warranted.