Behavioral studies in rodents and humans have demonstrated deficits of spatial memory and orientation in bilateral vestibular failure (BVF). Our aim was to explore the functional consequences of chronic vestibular failure on different cognitive domains including spatial as well as non-spatial cognitive abilities. Sixteen patients with a unilateral vestibular failure (UVF), 18 patients with a BVF, and 17 healthy controls (HC) participated in the study. To assess the cognitive domains of short-term memory, executive function, processing speed and visuospatial abilities the following tests were used: Theory of Visual Attention (TVA), TAP Alertness and Visual Scanning, the Stroop Color-Word, and the Corsi Block Tapping Test. The cognitive scores were correlated with the degree of vestibular dysfunction and the duration of the disease, respectively. Groups did not differ significantly in age, sex, or handedness. BVF patients were significantly impaired in all of the examined cognitive domains but not in all tests of the particular domain, whereas UVF patients exhibited significant impairments in their visuospatial abilities and in one of the two processing speed tasks when compared independently with HC. The degree of vestibular dysfunction significantly correlated with some of the cognitive scores. Neither the side of the lesion nor the duration of disease influenced cognitive performance. The results demonstrate that vestibular failure can lead to cognitive impairments beyond the spatial navigation deficits described earlier. These cognitive impairments are more significant in BVF patients, suggesting that the input from one labyrinth which is distributed into bilateral vestibular circuits is sufficient to maintain most of the cognitive functions. These results raise the question whether BVF patients may profit from specific cognitive training in addition to physiotherapy.

ObjectiveFunctional dizziness syndromes are among the most common diagnoses made in patients with chronic dizziness, but their underlying neural characteristics are largely unknown. The aim of this neuroimaging study was to analyze the disease‐specific brain changes in patients with phobic postural vertigo (PPV).MethodsWe measured brain morphology, task response, and functional connectivity in 44 patients with PPV and 44 healthy controls.ResultsThe analyses revealed a relative structural increase in regions of the prefrontal cortex and the associated thalamic projection zones as well as in the primary motor cortex. Morphological increases in the ventrolateral prefrontal cortex positively correlated with disease duration, whereas increases in dorsolateral, medial, and ventromedial prefrontal areas positively correlated with the Beck depression index. Visual motion stimulation caused an increased task‐dependent activity in the subgenual anterior cingulum and a significantly longer duration of the motion aftereffect in the patients. Task‐based functional connectivity analyses revealed aberrant involvement of interoceptive, fear generalization, and orbitofrontal networks.InterpretationOur findings agree with some of the typical characteristics of functional dizziness syndromes, for example, excessive self‐awareness, anxious appraisal, and obsessive controlling of posture. This first evidence indicates that the disease‐specific mechanisms underlying PPV are related to networks involved in mood regulation, fear generalization, interoception, and cognitive control. They do not seem to be the result of aberrant processing in cortical visual, visual motion, or vestibular regions.

Ocean acidification is a major threat to calcifying marine organisms such as deep-sea cold-water corals (CWCs), but related knowledge is scarce. The aragonite saturation threshold (Ω a ) for calcification, respiration and organic matter fluxes were investigated experimentally in the Mediterranean Madrepora oculata. Over 10 weeks, colonies were maintained under two feeding regimes (uptake of 36.75 and 7.46 µmol C polyp) and exposed in 2 week intervals to a consecutively changing air-CO 2 mix ( pCO 2 ) of 400, 1600, 800, 2000 and 400 ppm. There was a significant effect of feeding on calcification at initial ambient pCO 2 , while with consecutive pCO 2 treatments, feeding had no effect on calcification. Respiration was not significantly affected by feeding or pCO 2 levels. Coral skeletons started to dissolve at an average Ω a threshold of 0.92, but recovered and started to calcify again at Ω a ≥1. The surplus energy required to counteract dissolution at elevated pCO 2 (≥1600 µatm) was twice that at ambient pCO 2 . Yet, feeding had no mitigating effect at increasing pCO 2 levels. This could be due to the fact that the energy required for calcification is a small fraction (1-3%) of the total metabolic energy demand and corals even under low food conditions might therefore still be able to allocate this small portion of energy to calcification. The response and resistance to ocean acidification are consequently not controlled by feeding in this species, but more likely by chemical reactions at the site of calcification and exchange processes between the calicoblastic layer and ambient seawater.