Progress in brain research
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Brain-computer interfaces (BCIs) include stimulators, infusion devices, and neuroprostheses. They all belong to functional neurosurgery. Deep brain stimulators (DBS) are widely used for therapy and are in need of innovative evolutions. Robotized exoskeletons require BCIs able to drive up to 26 degrees of freedom (DoF). We report the nanomicrotechnology development of prototypes for new 3D DBS and for motor neuroprostheses. For this complex project, all compounds have been designed and are being tested. Experiments were performed in rats and primates for proof of concepts and development of the electroencephalogram (EEG) recognition algorithm. ⋯ We have designed multielectrodes wireless implants to open the way for BCI ECoG-driven effectors. These technologies are also used to develop new generations of brain stimulators, either cortical or for deep targets. This chapter is aimed at illustrating that BCIs are actually the daily background of DBS, that the evolution of the method involves a growing multiplicity of targets and indications, that new technologies make possible and simpler than before to design innovative solutions to improve DBS methodology, and that the coming out of BCI-driven neuroprostheses for compensation of motor and sensory deficits is a natural evolution of functional neurosurgery.
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Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a common sleep disorder that is characterized by repeated episodes of complete or partial cessation of breathing while sleeping. These recurrent breathing events result in fragmented sleep and recurrent hypoxemia. Distressing daytime sequelae reported by OSAHS patients include excessive daytime sleepiness, self-reported changes in mood, and cognitive problems. ⋯ Current studies examining cognitive recovery with positive airway pressure treatment are presented. It appears that the cognitive dysfunction of OSAHS is not likely to be due to a single mediating mechanism, nor is it pervasive across all patients. Future research should attempt to identify these moderators for cognitive dysfunction in OSAHS and to highlight the mechanisms of dysfunction by cognitive domain.
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The past decade of neuroscience research has provided considerable evidence that the adult brain can undergo substantial reorganization following injury. For example, following an ischemic lesion, such as occurs following a stroke, there is a cascade of molecular, genetic, physiological and anatomical events that allows the remaining structures in the brain to reorganize. Often, these events are associated with recovery, suggesting that they contribute to it. ⋯ But more recently, efforts have been made to differentiate beneficial from detrimental changes. These notions are timely now that neurorehabilitative research is developing novel treatments to modulate, increase, or inhibit plasticity in targeted brain regions. We will review basic principles of plasticity and some of the new and exciting approaches that are currently being investigated to shape plasticity following injury in the central nervous system.
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The Göttingen minipig has been established as a translational research animal for neurological and neurosurgical disorders. This animal has a large gyrencephalic brain suited for examination at sufficient resolution with conventional clinical scanning modalities. The large brain, further, allows use of standard neurosurgical techniques and can accommodate clinical neuromodulatory devises such as deep brain stimulation (DBS) electrodes and encapsulated cell biodelivery devices making the animal ideal for basic scientific studies on neuromodulation mechanisms and preclinical tests of new neuromodulation technology for human use. The use of the Göttingen minipig is economical and does not have the concerns of the public associated with the experimental use of primates, cats, and dogs, thus providing a cost-effective research model for translation of rodent data before clinical trials are initiated.
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Sleep and cognition are temporally regulated by a homeostatic process generating pressure for sleep as a function of sleep/wake history, and a circadian process generating pressure for wakefulness as a function of time of day. Under normal nocturnal sleep conditions, these two processes are aligned in such a manner as to provide optimal daytime performance and consolidated nighttime sleep. Under conditions of sleep deprivation, shift work or transmeridian travel, the two processes are misaligned, resulting in fatigue and cognitive deficits. ⋯ Accident risk increases as a function of fatigue severity as well as the duration of exposure to fatigue. Work schedule and accident rate information from an operational setting can thus be used to calibrate a mathematical model of fatigue and performance to predict accident risk. This provides a fatigue risk management tool that helps to direct mitigation resources to where they would have the greatest mitigating effect.