A comparative study of four novel sleep apnoea episode prediction systems

The prediction of sleep apnoea and hypopnoea episodes could allow treatment to be applied before the event be-comes detrimental to the patients sleep, and for a more spe-cific form of treatment. It is proposed that features extracted from breaths preceding an apnoea and hypopnoea could be used in neural networks for the prediction of these events. Four different predictive systems were created, processing the nasal airflow signal using epoching, the inspiratory peak and expiratory trough values, principal component analysis (PCA) and empirical mode decomposition (EMD). The neu-ral networks were validated with naïve data from six over-night polysomnographic records, resulting in 83.50% sensi-tivity and 90.50% specificity. Reliable prediction of apnoea and hypopnoea is possible using the epoched flow and EMD of breaths preceding the event

Differences in neuroplasticity after spinal cord injury in varying animal models and humans

Rats have been the primary model to study the process and underlying mechanisms of recovery after spinal cord injury. Two weeks after a severe spinal cord contusion, rats can regain weight-bearing abilities without therapeutic interventions, as assessed by the Basso, Beattie and Bresnahan locomotor scale. However, many human patients suffer from permanent loss of motor function following spinal cord injury. While rats are the most understood animal model, major differences in sensorimotor pathways between quadrupeds and bipeds need to be considered. Understanding the major differences between the sensorimotor pathways of rats, non-human primates, and humans is a start to improving targets for treatments of human spinal cord injury. This review will discuss the neuroplasticity of the brain and spinal cord after spinal cord injury in rats, non-human primates, and humans. A brief overview of emerging interventions to induce plasticity in humans with spinal cord injury will also be discussed

Blocking human fear memory with the matrix metalloproteinase inhibitor doxycycline

Learning to predict threat is a fundamental ability of many biological organisms, and a laboratory model for anxiety disorders. Interfering with such memories in humans would be of high clinical relevance. On the basis of studies in cell cultures and slice preparations, it is hypothesised that synaptic remodelling required for threat learning involves the extracellular enzyme matrix metalloproteinase (MMP) 9. However, in vivo evidence for this proposal is lacking. Here we investigate human Pavlovian fear conditioning under the blood-brain barrier crossing MMP inhibitor doxycyline in a pre-registered, randomised, double-blind, placebo-controlled trial. We find that recall of threat memory, measured with fear-potentiated startle 7 days after acquisition, is attenuated by ~60% in individuals who were under doxycycline during acquisition. This threat memory impairment is also reflected in increased behavioural surprise signals to the conditioned stimulus during subsequent re-learning, and already late during initial acquisition. Our findings support an emerging view that extracellular signalling pathways are crucially required for threat memory formation. Furthermore, they suggest novel pharmacological methods for primary prevention and treatment of posttraumatic stress disorder.Molecular Psychiatry advance online publication, 4 April 2017; doi:10.1038/mp.2017.65

The effects of chronic ritanserin treatment on sleep and the neuroendocrine response to L-tryptophan.

A previous study has shown that acute administration of the 5-HT2 receptor antagonist ritanserin doubles Slow Wave Sleep (SWS) and increases the prolactin (PRL) response to L-tryptophan (LTP). The present study investigated the effect of repeated ritanserin treatment on sleep, neuroendocrine response to LTP and 5-HT2 platelet receptor binding. After 2 weeks, ritanserin administration SWS was persistently increased but the PRL response to LTP was unchanged. Platelet 5-HT receptor binding was undetectable at the end of ritanserin treatment but recovered 2 weeks after drug withdrawal. The results suggest that ritanserin causes a sustained effect on the 5-HT mechanisms mediating SWS and on platelet 5-HT2 receptors. However, adaptation occurs to its effect on 5-HT-mediated neuroendocrine responses