Tackling Insomnia Symptoms through Vestibular Stimulation in Patients with Breast Cancer: A Perspective Paper.

Insomnia symptoms are common among patients with breast cancer (BC; 20-70%) and are predictors of cancer progression and quality of life. Studies have highlighted sleep structure modifications, including increased awakenings and reduced sleep efficiency and total sleep time. Such modifications may result from circadian rhythm alterations consistently reported in this pathology and known as carcinogenic factors, including lower melatonin levels, a flattened diurnal cortisol pattern, and lower rest-activity rhythm amplitude and robustness. Cognitive behavioral therapy and physical activity are the most commonly used non-pharmacological interventions to counter insomnia difficulties in patients with BC. However, their effects on sleep structure remain unclear. Moreover, such approaches may be difficult to implement shortly after chemotherapy. Innovatively, vestibular stimulation would be particularly suited to tackling insomnia symptoms. Indeed, recent reports have shown that vestibular stimulation could resynchronize circadian rhythms and improve deep sleep in healthy volunteers. Moreover, vestibular dysfunction has been reported following chemotherapy. This perspective paper aims to support the evidence of using galvanic vestibular stimulation to resynchronize circadian rhythms and reduce insomnia symptoms in patients with BC, with beneficial effects on quality of life and, potentially, survival.

Effect of sleep deprivation after a night shift duty on simulated crisis management by residents in anaesthesia. A randomised crossover study.

BACKGROUND: Sleep deprivation has been associated with an increased incidence of medical errors and can jeopardise patients' safety during medical crisis management. The aim of the study was to assess the effect of sleep deprivation on the management of simulated anaesthesia crisis by residents in anaesthesiology. METHODS: A randomised, comparative, monocentric crossover study involving 48 residents in anaesthesia was performed on a high fidelity patient simulator. Each resident was evaluated in a sleep-deprived state (deprived group, after a night shift duty) and control state (control group, after a night of sleep). Performance was assessed through points obtained during crisis scenario 1 (oesophageal intubation followed by anaphylactic shock) and scenario 2 (anaesthesia-related bronchospasm followed by ventricular tachycardia). Sleep periods were recorded by actigraphy. Two independent observers assessed the performances. The primary endpoint of the study was the score obtained for each scenario. RESULTS: Resident's crisis management performance is associated with sleep deprivation (scenario 1: control=39 [33-42] points vs. deprived=26 [19-40] points, P=0.02; scenario 2: control=21 [17-24] vs. deprived=14 [12-19], P=0.01). The main errors observed were: error in drug administration and dose, delay in identification of hypotension, and missing communication with the surgical team about situation. CONCLUSIONS: The present study showed that sleep deprivation is associated with impairment of performance to manage crisis situations by residents in anaesthesia.

Does COMT val158met polymorphism influence P50 sensory gating, eye tracking or saccadic inhibition dysfunctions in schizophrenia?

Three electrophysiological endophenotypes are routinely studied in schizophrenia (SCZ): smooth pursuit eye movement (SPEM) dysfunction, deficits in P50 auditory-evoked potential inhibition, and saccadic inhibition deficits. The current study aimed to investigate the relationship between the COMT val158met polymorphism and these three endophenotypes. One hundred four SCZ patients (DSM-IV-R criteria) and 89 healthy controls were included in this study. P50 auditory-evoked potential inhibition, antisaccade paradigm and SPEM were analyzed. All individuals were genotyped for the COMT val158met. SCZ patients showed a higher rate of deficits measured by the SPEM, antisaccade and P50 inhibition paradigms without association with COMT val158met. However, in our control group, we have found an association between the Val polymorphism and the smoking status. More importantly, we have found a higher accuracy of saccades during the predictive pursuit task associated to the Met polymorphism in controls but not in SCZ patients who were receiving antidopaminergic medications. This result is in line with the hypothesis of the relationship between the Met polymorphism of the COMT gene, a higher level of dopamine in the prefrontal cortex and the role of the fronto-cerebellar loop in smooth predictive pursuit.

Vestibular loss promotes procedural response during a spatial task in rats.

Declarative memory refers to a spatial strategy using numerous sources of sensory input information in which visual and vestibular inputs are assimilated in the hippocampus. In contrast, procedural memory refers to a response strategy based on motor skills and familiar gestures and involves the striatum. Even if vestibular loss impairs hippocampal activity and spatial memory, vestibular-lesioned rats remain able to find food rewards during complex spatial memory task. Since hippocampal lesions induce a switch from declarative memory to procedural memory, we hypothesize that vestibular-lesioned rats use a strategy other than that of hippocampal spatial response to complete the task and to counterbalance the loss of vestibular information. We test, in a reverse T-maze paradigm, the types of strategy vestibular-lesioned rats preferentially uses in a spatial task. We clearly demonstrate that all vestibular-lesioned rats shift to a response strategy to solve the spatial task, while control rats use spatial and response strategies equally. We conclude that the loss of vestibular informations leading to spatial learning impairments is not offset at the hippocampus level by integration process of other sense mainly visual informations; but favors a response strategy through procedural memory most likely involving the striatum, cerebellum, and motor learning.

Differential respiratory control of the upper airway and diaphragm muscles induced by 5-HT1A receptor ligands.

BACKGROUND: Serotonin (5-HT) has a role in respiratory function and dysfunction. Although 5-HT affects respiratory drive to both phrenic and cranial motoneurons, relatively little is known about the role of 5-HT receptor subtypes in the control of upper airway muscle (UAM) respiratory activity. MATERIALS AND METHODS: Here, we performed central injections of 5-HT1A agonist (8-OHDPAT) or antagonist (WAY100635) in anesthetized rats and analyzed changes in the electromyographic activity of several UAM and other cardiorespiratory parameters. We also compared the pattern of Fos expression induced after central injection of a control solution or 8-OHDPAT. RESULTS: Results showed that 8-OHDPAT induced a robust increase in UAM activity, associated with either tachypnea under volatile anesthesia or bradypnea under liquid anesthesia. Injection of WAY100635 switched off UAM respiratory activity and led to bradypnea, suggesting a tonic excitatory role of endogenous 5-HT1A receptor activation. Co-injection of the agonist and the antagonist blocked the effects produced by each drug alone. Besides drug-induced changes in respiratory frequency, only slight increases in surface of diaphragm bursts were observed. Significant increases in Fos expression after 5-HT1A receptor activation were seen in the nucleus tractus solitarius, nucleus raphe pallidus, parapyramidal region, retrotrapezoid nucleus, lateral parabrachial, and Kölliker-Fuse nuclei. This restricted pattern of Fos expression likely identified the neural substrate responsible for the enhancement of UAM respiratory activity observed after 8-OHDPAT injection. CONCLUSIONS: These findings suggest an important role for the 5-HT1A receptors in the neural control of upper airway patency and may be relevant to counteract pharyngeal atonia during obstructive sleep apneas.

Vestibular decompensation in labyrinthectomized rats placed in weightlessness during parabolic flight.

The purpose of this study was to determine whether the absence of gravitational cues during weightlessness could alter the posture and static eye deviation of Earth compensated rats with peripheral vestibular lesions. The responses of bilaterally (BL) and unilaterally (UL) labyrinthectomized rats at a compensated stage (40-43 days after lesion) during parabolic flight were compared with those at an acute stage (2-7 h after lesion) on Earth. When free-floating in 0 g, UL animals showed the same postural pattern as during water immersion just after surgery. The most striking observation was a continuous roll body motion at about 4 Hz, and a skewed asymmetric posture. When restrained in 0 g, static eye deviation was also comparable to that observed at an acute stage. A return to a compensated posture and gaze was observed within a few seconds following the end of the weightlessness conditions. BL animals were less affected. These results suggest that vestibular compensation after unilateral lesion can be disrupted momentarily and is a fragile state during which the otolith system in the remaining vestibular apparatus presumably plays a continuous role.