Ultrasound Measurements of Fetal Thyroid: Reference Ranges from a Cohort of Low-Risk Pregnant Women.

BACKGROUND: Adequate thyroid function is essential for normal growth and development of the fetus. Sonographic recognition of alterations in fetal thyroid dimensions may be the first sign of thyroid dysfunction, permitting early diagnosis and intervention. The main goal of this study was to build curves with reference values for ultrasound measurements of the fetal thyroid from 14 to 40 weeks of gestation. METHODS: This is a prospective longitudinal study of 90 Brazilian pregnant women, complementary to a cohort multicentre study named "WHO multicentre study for the development of growth standards from fetal life to childhood: the fetal component." Pregnant women without any pre-existing conditions that might affect fetal growth received antenatal care from the first trimester until childbirth, undergoing serial ultrasound evaluations of the fetus, including the thyroid. Longitudinal, anteroposterior, and transverse diameters of both thyroid lobes were measured in the fetus. Fetal thyroid lobe volume was also estimated. By quantile regression analysis, reference curves of measurements were fitted according to the gestational age. RESULTS: A reference standard of thyroid growth was defined during pregnancy by fitting curves of its measurements. Reference values for the 10th, 50th, and 90th centiles of fetal thyroid measurements (longitudinal, anteroposterior, transverse diameters, and lobe volume) were defined, from 14 to 40 weeks of gestation. CONCLUSION: We provided a reference curve of optimal thyroid development in a low-risk population that can be used as a standard of comparison to diagnose deviations from the norm. In addition, we demonstrated an alternative and simplified method for early recognition of thyroid morphological alterations by an individualized technique to evaluate the thyroid lobes.

Anatomical and Functional MRI Changes after One Year of Auditory Rehabilitation with Hearing Aids.

Hearing aids (HAs) are an effective strategy for auditory rehabilitation in patients with peripheral hearing deficits. Yet, the neurophysiological mechanisms behind HA use are still unclear. Thus far, most studies have focused on changes in the auditory system, although it is expected that hearing deficits affect a number of cognitive systems, notably speech. In the present study, we used audiometric evaluations in 14 patients with bilateral hearing loss before and after one year of continuous HA use and functional magnetic resonance imaging (fMRI) and cortical thickness analysis in 12 and 10 of them compared with a normal hearing control group. Prior to HA fitting, fMRI activity was found reduced in the auditory and language systems and increased in visual and frontal areas, expanding to multimodal integration cortices, such as the superior temporal gyrus, intraparietal sulcus, and insula. One year after rehabilitation with HA, significant audiometric improvement was observed, especially in free-field Speech Reception Threshold (SRT) test and functional gain, a measure of HA efficiency. HA use increased fMRI activity in the auditory and language cortices and multimodal integration areas. Individual fMRI signal changes from all these areas were positively correlated with individual SRT changes. Before rehabilitation, cortical thickness was increased in parts of the prefrontal cortex, precuneus, fusiform gyrus, and middle temporal gyrus. It was reduced in the insula, supramarginal gyrus, medial temporal gyrus, occipital cortex, posterior cingulate cortex, and claustrum. After HA use, increased cortical thickness was observed in multimodal integration regions, particularly the very caudal end of the superior temporal sulcus, the angular gyrus, and the inferior parietal gyrus/superior temporal gyrus/insula. Our data provide the first evidence that one year of HA use is related to functional and anatomical brain changes, notably in auditory and language systems, extending to multimodal cortices.

The neural correlates of negative prediction error signaling in human fear conditioning.

In a temporal difference (TD) learning approach to classical conditioning, a prediction error (PE) signal shifts from outcome deliverance to the onset of the conditioned stimulus. Omission of an expected outcome results in a negative PE signal, which is the initial step towards successful extinction. In order to visualize negative PE signaling during fear conditioning, we employed combined functional magnetic resonance (fMRI) and skin conductance response (SCR) measurements in a conditioning task with visual stimuli and mild electrical shocks. Positive PE signaling was associated with increased activation in the bilateral insula, supplementary motor area, brainstem, and visual cortices. Negative PE signaling was associated with increased activation in the ventromedial and dorsolateral prefrontal cortices, the left lateral orbital gyrus, the middle temporal gyri, angular gyri, and visual cortices. The involvement of the ventromedial prefrontal and orbitofrontal cortex in extinction learning has been well documented, and this study provides evidence for the notion that these regions are already involved in negative PE signaling during fear conditioning.

The neural correlates and temporal sequence of the relationship between shock exposure, disturbed sleep and impaired consolidation of fear extinction.

Consolidation of extinction learning is a primary mechanism disrupted in posttraumatic stress disorder (PTSD), associated with hypoactivity of the ventromedial prefrontal cortex and hippocampus. A role for rapid eye movement (REM) sleep disturbances in this failure to consolidate extinction learning has been proposed. We performed functional magnetic resonance imaging (fMRI) with simultaneous skin conductance response (SCR) measurements in 16 healthy participants during conditioning/extinction and later recall of extinction. The visual stimuli were basic geometric forms and electrical shocks functioned as the unconditioned stimulus. Between the conditioning/extinction and recall sessions, participants received a 90-min sleep window in the sleep laboratory. This daytime sleep was polysomnographically recorded and scored by professionals blind to the study design. Only seven out of 16 participants had REM sleep; participants without REM sleep had a significantly slower decline of both SCR and neural activity of the laterodorsal tegmentum in response to electrical shocks during conditioning. At recall of fear extinction, participants with preceding REM sleep had a reduced SCR and stronger activation of the left ventromedial prefrontal cortex and bilateral lingual gyrus in response to the extinguished stimulus than participants lacking REM sleep. This study indicates that trait-like differences in shock reactivity/habituation (mediated by the brainstem) are predictive of REM sleep disruption, which in turn is associated with impaired consolidation of extinction (mediated by the ventromedial prefrontal cortex). These findings help understand the neurobiological basis and the temporal sequence of the relationship between shock exposure, disturbed sleep and impaired consolidation of extinction, as observed in PTSD.

Quantitative evaluation of hemodynamic response after hypercapnia among different brain territories by fMRI.

The brain vascular system has an autoregulatory mechanism that maintains blood perfusion within normal limits at the capillary level. Partially due to its clinical importance, it is of interest to better understand the mechanisms involved in vascular regulation. Therefore, using functional magnetic resonance imaging (fMRI), we quantitatively investigated hemodynamic response characteristics of regions supplied by the main cerebral arteries, during two breath holding tests (BHT): after inspiration and after expiration. We used an auto-regressive method capable of estimating four signal parameters: onset delay, full width at half maximum (FWHM), time-to-peak and amplitude. The onset delay was significantly longer for the posterior cerebral artery (PCA) than for middle cerebral artery (MCA) and anterior arteries (ACA). FWHM and time-to-peak were larger in the ACA territory, indicating a slower blood flow in this region. Differences were also observed in the amplitude among the three areas, where MCA and PCA territories showed the smallest and the highest amplitudes, respectively. Moreover, differences were found in amplitude and onset when BHT was performed after inspiration as compared to BHT after expiration. Time-to-peak and FWHM showed no statistical differences between these two challenges. Such results are related to regional anatomical specificities and biochemical mechanisms responsible for vasodilation, such as those related to vascularity and vessel sizes.