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The National Aeronautics and Space Administration (NASA) recommends using promethazine to prevent and treat space motion sickness, but pharmacologic responses in space and on Earth are different. Twelve volunteers were [...]

We investigated the alteration in flow-dependent-dilatation in the orthostatic intolerance occurring after bed-rest deconditioning. Eight men [aged mean (SEM) 32 (2) years] underwent two consecutive periods of 7 days of head-down-tilt (HDT, –6°) during bed rest. A control age and sex matched group [n=8, 30 (2) years], maintained its usual physical activity. Blood flow velocity (BFV) and diameter (Doppler and echotracking systems) were measured in the brachial artery, under basal conditions and during the post ischaemic hyperaemia following occlusion. The increase in BFV post-ischaemia did not change before, during and after HDT but the relative increase in the diameter was greater on the 7th day of the HDT period than before HDT [+8.8 (1.6)% compared to +3.7 (1.0)%, P<0.001]. After HDT, 11 of 16 standing tests (comprising eight subjects in the two HDT periods) had to be stopped because of orthostatic intolerance. The flow-dependent-dilatation measured at the end of HDT was negatively correlated with the post-bed-rest duration of orthostatic tolerance (r=0.78, P<0.01). After the sublingual administration of glyceryl trinitrate, there was no change in the increase in diameter. No significant changes were observed in the control group. Bed-rest deconditioning enhances the flow-dependent vasodilatation of large arteries and might contribute to the orthostatic intolerance observed following bed-rest. [ABSTRACT FROM AUTHOR]

Severe aortic arch atheroma (AAA) is a strong risk factor for ischaemic stroke, but it is unclear whether AAA is a source of cerebral emboli or simply a marker of cerebral atherosclerosis. The purpose of this study was to find out the prevalence of asymptomatic cerebral embolic signals (ES) in patients with acute cerebral ischaemia, AAA and no other potential source of cerebral embolism. Forty patients with anterior circulation ischaemic stroke or transient ischaemic attack (TIA) were prospectively studied using transesophageal echocardiography (TEE) and transcranial Doppler (TCD) scanning within seven days of symptom onset. Patients with a cardiac source of embolism or carotid stenosis > 50 % were excluded. ES were detected in 14.3 % (2/14) of patients with AAA ≥ 4 mm and in no patients with AAA < 4 mm or no AAA (p=0.14). The findings suggest that ES may be associated with severe AAA but their prevalence is low in this setting. [ABSTRACT FROM AUTHOR]

Disease-modifying treatments are currently being trialled in multiple system atrophy. Approaches based solely on clinical measures are challenged by heterogeneity of phenotype and pathogenic complexity. Neurofilament light chain protein has been explored as a reliable biomarker in several neurodegenerative disorders but data on multiple system atrophy have been limited. Therefore, neurofilament light chain is not yet routinely used as an outcome measure in multiple system atrophy. We aimed to comprehensively investigate the role and dynamics of neurofilament light chain in multiple system atrophy combined with cross-sectional and longitudinal clinical and imaging scales and for subject trial selection. In this cohort study, we recruited cross-sectional and longitudinal cases in a multicentre European set-up. Plasma and CSF neurofilament light chain concentrations were measured at baseline from 212 multiple system atrophy cases, annually for a mean period of 2 years in 44 multiple system atrophy patients in conjunction with clinical, neuropsychological and MRI brain assessments. Baseline neurofilament light chain characteristics were compared between groups. Cox regression was used to assess survival; receiver operating characteristic analysis to assess the ability of neurofilament light chain to distinguish between multiple system atrophy patients and healthy controls. Multivariate linear mixed-effects models were used to analyse longitudinal neurofilament light chain changes and correlated with clinical and imaging parameters. Polynomial models were used to determine the differential trajectories of neurofilament light chain in multiple system atrophy. We estimated sample sizes for trials aiming to decrease neurofilament light chain levels. We show that in multiple system atrophy, baseline plasma neurofilament light chain levels were better predictors of clinical progression, survival and degree of brain atrophy than the neurofilament light chain rate of change. Comparative analysis of multiple system atrophy progression over the course of disease, using plasma neurofilament light chain and clinical rating scales, indicated that neurofilament light chain levels rise as the motor symptoms progress, followed by deceleration in advanced stages. Sample size prediction suggested that significantly lower trial participant numbers would be needed to demonstrate treatment effects when incorporating plasma neurofilament light chain values into multiple system atrophy clinical trials in comparison to clinical measures alone. In conclusion, neurofilament light chain correlates with clinical disease severity, progression and prognosis in multiple system atrophy. Combined with clinical and imaging analysis, neurofilament light chain can inform patient stratification and serve as a reliable biomarker of treatment response in future multiple system atrophy trials of putative disease-modifying agents., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain.)

Purpose: To determine the change in intraocular pressure (IOP) due to postural changes in young healthy volunteers., Materials and Methods: Intraocular pressure was measured using a calibrated Pulsair noncontact tonometer in both eyes of 25 female volunteers in a sitting position and after 1, 3, and 10 minutes in a supine position. In the second part of the experiment (a 7-day -6 degrees head-down tilt [HDT]), IOP (at 8 am, 12 am and 6 pm) and corneal thickness (12 am) were monitored in 8 female volunteers before, during, and after the HDT period. Blood pressure, hematocrit, plasma volume and osmolality, and plasma catecholamines concentrations were also measured., Results: Intraocular pressure was significantly higher in the supine position (16.1 +/- 3.6 mm Hg) than in the sitting position, with a mean pressure difference of 2.23 +/- 2.9 mm Hg after 1 minute, 0.9 +/- 3 mm Hg after 3 minutes, and 1.9 +/- 3.8 mm Hg after 10 minutes in a supine position (P < 0.001). During the period of HDT, IOP values decreased significantly on the fifth day (13.3 +/- 1.6 mm Hg, P = 0.03) and the seventh day (12.7 +/- 1.7 mm Hg, P = 0.02) when compared with IOP in the supine position (14.26 +/- 2 mm Hg). The corneal thickness increased significantly (P < 0.0001) at day 5 (549.25 +/- 48.7 microm) and day 7 (540.31 +/- 46.9 microm) compared with baseline (532.45 +/- 38.6 microm). Two days after the end of the HDT bedrest, the mean supine IOP significantly increased (14.1 +/- 1.8 mm Hg, P = 0.003) and corneal thickness was similar to that found at baseline. The mean decrease of IOP was positively correlated with that of the plasma volume (-10%, r = 0.61, P = 0.02) and negatively correlated with the mean rise of hematocrit (r = -0.5, P = 0.07), variables that are considered to be indirect measures of plasma dehydration., Conclusions: During a 7-day HDT bedrest experiment in healthy women, eyes seemed to compensate the moderate rise of IOP described between a sitting and a supine position, and exhibited a slight and progressive average decrease of 1.3 mm Hg. These physiological modifications could be related to an ocular dehydration or to systemic cardiovascular and hormonal variations during bedrest.