We presented two cases of COVID-19 associated SARS-CoV-2 infection during third trimester of pregnancy. Both mothers and newborns had excellent outcomes. We failed to identify SARS-CoV-2 in all the products of conception and the newborns. This report provided evidence of low risk of intrauterine infection by vertical transmission of SARS-CoV-2.
Background Idiopathic rapid eye movement sleep behavior disorder is an early sign of neurodegenerative disease. This study aimed to quantitatively evaluate iron content in idiopathic rapid eye movement sleep behavior disorder patients using quantitative susceptibility mapping and to examine the potential of this technique to identify the prodromal stage of α‐synucleinopathies. Methods Twenty‐five idiopathic rapid eye movement sleep behavior disorder patients, 32 Parkinson's disease patients, and 50 healthy controls underwent quantitative susceptibility mapping. The mean magnetic susceptibility values within the bilateral substantia nigra, globus pallidus, red nucleus, head of the caudate nucleus, and putamen were calculated and compared among groups. The relationships between the values and the clinical features of idiopathic rapid eye movement sleep behavior disorder and Parkinson's disease were measured using correlation analysis. Results Idiopathic rapid eye movement sleep behavior disorder patients had elevated iron in the bilateral substantia nigra compared with healthy controls. Parkinson's disease patients had increased iron in the bilateral substantia nigra, globus pallidus, and left red nucleus compared with healthy controls and had elevated iron levels in the bilateral substantia nigra compared with idiopathic rapid eye movement sleep behavior disorder patients. Mean magnetic susceptibility values were positively correlated with disease duration in the left substantia nigra in idiopathic rapid eye movement sleep behavior disorder patients. Conclusions Quantitative susceptibility mapping can detect increased iron in the substantia nigra in idiopathic rapid eye movement sleep behavior disorder, which becomes more significant as the disorder progresses. This technique has the potential to be an early objective neuroimaging marker for detecting α‐synucleinopathies. © 2019 International Parkinson and Movement Disorder Society
The brain has long been known to be the regulation center of itch, but the neuropathology of chronic itch, such as chronic spontaneous urticaria (CSU), remains unclear. Thus, we aimed to explore the brain areas involved in the pathophysiology of CSU in hopes that our results may provide valuable insights into the treatment of chronic itch conditions. 40 CSU patients and 40 healthy controls (HCs) were recruited. Urticaria activity scores 7 (UAS7) were collected to evaluate patient's clinical symptoms. Amplitude of low frequency fluctuations (ALFF), voxel-based morphometry (VBM), and seed-based resting-state functional connectivity (rs-FC) analysis were used to assess brain activity and related plasticity. Compared with HCs, CSU patients exhibited 1) higher ALFF values in the right ventral striatum / putamen, which were positively associated with clinical symptoms as measured by UAS7; 2) gray matter volume (GMV) increase in the right ventral striatum and putamen; and 3) decreased rs-FC between the right ventral striatum and the right occipital cortex and between the right putamen and the left precentral gyrus. Using multiple-modality brain imaging tools, we demonstrated the dysfunction of the striatum in CSU. Our results may provide valuable insights into the neuropathology and development of chronic itch.Chronic spontaneous urticaria (CSU) is a common disorder characterized by the spontaneous eruption of short-lived (<24 h) itchy wheals, with or without angioedema, for a period longer than 6 weeks 1 . CSU affects 0.5-1.0% of the population at any given time and severely diminishes the quality of life of patients 2,3 . Despite its prevalence, there is a lack of understanding of the pathology of CSU and consequently, limited treatment options. Standard therapy with regular doses of non-sedating second-generation H1 antihistamines (H1AH) are ineffective for more than 50% of patients with CSU 2 .Accumulating evidence suggests that the skin and brain are functionally connected 4,5 . For instance, the brain shares numerous mediators with skin through the hypothalamic-pituitary-adrenal axis (HPA axis) 4 . Studies have shown that the HPA axis may be altered in stress-related skin diseases, resulting in the activation of mast cells 6,7 , which are the primary effector cells in CSU 8 .The most common clinical manifestation of CSU is repeated itching and scratching. Studies suggest that the brain plays a key role in the itch-scratch cycle 9 . Functional brain imaging studies have identified brain regions associated with the itch-scratch cycle, such as the primary somatosensory cortex (SI), secondary somatosensory cortex (SII), primary motor cortex (MI), premotor cortex (PM), supplementary motor area (SMA), cerebellum, the prefrontal cortex (PFC), the striatum, and thalamus [10][11][12][13][14] .In recent years, resting-state functional magnetic resonance imaging (rs-fMRI) has been applied to investigate the intrinsic functional organization of the brain [15][16][17] . There are many resting-state fMRI data analysis methods,...
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