The external hip adduction moment during walking is greater in individuals with gluteal tendinopathy (GT) than pain‐free controls. Although this likely represents a greater demand on the hip abductor ...muscles implicated in GT, no study has investigated activation of these muscles in GT. For this purpose, fine wire electrodes were inserted into the segments of the gluteus minimus and medius muscles, and surface electrodes placed on the tensor fascia lata, upper gluteus maximus, and vastus lateralis muscles of eight individuals with, and eight without, GT. Participants underwent six walking trials. Individual muscle patterns were compared between groups using a wavelet‐based linear effects model and muscle synergy analysis performed using non‐negative matrix factorization to evaluate muscle activation patterns, within‐ and between‐participant variability. Compared to controls, individuals with GT exhibited a more sustained initial burst of the posterior gluteus minimus and middle gluteus medius muscle segments. Two muscle synergies were identified; Synergy‐1 activated in early‐mid stance and Synergy‐2 in early stance. In GT participants, posterior gluteus minimus and posterior gluteus medius and tensor fascia lata contributed more to Synergy‐1 active during the period of single leg support. Participants with GT exhibited reduced within‐participant variability of posterior gluteus medius and reduced between‐participant variability of anterior gluteus minimus and medius and upper gluteus maximus. In conclusion, individuals with GT exhibit modified muscle activation patterns of the hip abductor muscles during walking, with potential relevance for gluteal tendon loading.
Altered brain activity and functional reorganization patterns during self-initiated movements have been reported in early pre-motor and motor stages of Parkinson's disease. The aim of this study was ...to investigate whether similar alterations can be observed in patients with idiopathic REM-sleep behavior disorder (RBD).
13 polysomnography-confirmed male and right-handed RBD patients and 13 healthy controls underwent a bilateral hand-movement fMRI task including internally selected (INT) and externally-guided (EXT) movement conditions for each hand. We examined functional activity and connectivity differences between groups and task-conditions, structural differences using voxel-based morphometry, as well as associations between functional activity and clinical variables.
No group differences were observed in fMRI-task performance or in voxel-based morphometry. Both groups showed faster reaction times and exhibited greater neural activation when movements were internally selected compared to externally-guided tasks. Compared to controls, RBD patients displayed stronger activation in the dorsolateral prefrontal cortex and primary somatosensory cortex during INT-tasks, and in the right fronto-insular cortex during EXT-tasks performed with the non-dominant hand. Stronger activation in RBD patients was associated with cognitive and olfactory impairment. Connectivity analysis demonstrated overall less interregional coupling in patients compared to controls. In particular, patients showed reduced temporo-cerebellar, occipito-cerebellar and intra-cerebellar connectivity, but stronger connectivity in fronto-cerebellar and fronto-occipital pathways.
The observed stronger activation during hand-movement tasks and connectivity changes in RBD may reflect early compensatory and reorganization patterns in order to preserve motor functioning. Our findings may contribute to a better understanding and prognosis of prodromal stages of α-synucleinopathies.
•RBD patients vs. controls showed increased brain activation in hand movement tasks.•Greater brain activation in RBD correlated with cognitive and olfactory impairment.•Patients showed reduced task-based connectivity, but increased long-range coupling.•Our findings indicate compensation strategies in RBD similar to Parkinson's disease.•This study provides new insight into prodromal stages of α-synucleinopathies.
To report outer retinal structural changes associated with macular capillary nonperfusion at the level of deep capillary plexus (DCP) in diabetic patients.
Prospective observational cross-sectional ...study.
The study included 14 eyes of 10 patients who were diagnosed as having diabetic retinopathy. To study the outer retina and localize areas of capillary nonperfusion at the superficial (SCP) or DCP, we used the spectral-domain optical coherence tomography (SDOCT) device (RTVue-XR Avanti; Optovue Inc, Fremont, California, USA) with split-spectrum amplitude-decorrelation angiography (SSADA) software for optical coherence tomography angiography (OCTA). Two independent masked graders (F.S. and A.A.F.) qualitatively evaluated SDOCT scans as either normal or having outer retina disruption. The angiographic images were examined to define the presence and location of capillary nonperfusion.
Eight eyes showed outer retinal disruption on SDOCT that co-localized to areas of enlarged foveal avascular zone, areas of no flow between capillaries, and capillary nonperfusion of the DCP. Six eyes without outer retinal changes on SDOCT showed robust perfusion of the DCP.
Using OCTA, this study shows that macular photoreceptor disruption on SDOCT in patients with diabetic retinopathy corresponds to areas of capillary nonperfusion at the level of the DCP. This is important in highlighting the contribution of the DCP to the oxygen requirements of the photoreceptors as well as the outer retina in diabetic macular ischemia.
Some individuals with functional neurological disorder (FND) exhibit motor and affective disturbances, along with limbic hyper-reactivity and enhanced motor-limbic connectivity. Given that the ...multimodal integration network (insula, dorsal cingulate, temporoparietal junction (TPJ)) is implicated in convergent sensorimotor, affective and interoceptive processing, we hypothesised that patients with FND would exhibit altered motor and amygdalar resting-state propagation to this network. Patient-reported symptom severity and clinical outcome were also hypothesised to map onto multimodal integration areas.
Between-group differences in primary motor and amygdalar nuclei (laterobasal, centromedial) were examined using graph-theory stepwise functional connectivity (SFC) in 30 patients with motor FND compared with 30 healthy controls. Within-group analyses correlated functional propagation profiles with symptom severity and prospectively collected 6-month outcomes as measured by the Screening for Somatoform Symptoms Conversion Disorder subscale and Patient Health Questionnaire-15 composite score. Findings were clusterwise corrected for multiple comparisons.
Compared with controls, patients with FND exhibited increased SFC from motor regions to the bilateral posterior insula, TPJ, middle cingulate cortex and putamen. From the right laterobasal amygdala, the FND cohort showed enhanced connectivity to the left anterior insula, periaqueductal grey and hypothalamus among other areas. In within-group analyses, symptom severity correlated with enhanced SFC from the left anterior insula to the right anterior insula and TPJ; increased SFC from the left centromedial amygdala to the right anterior insula correlated with clinical improvement. Within-group associations held controlling for depression, anxiety and antidepressant use.
These neuroimaging findings suggest potential candidate neurocircuit pathways in the pathophysiology of FND.
To describe the prevalence, nature and risk factors for the main clinical sequelae in coronavirus disease 2019 (COVID-19) survivors who have been discharged from the hospital for more than 3 months.
...This longitudinal study was based on a telephone follow-up survey of COVID-19 patients hospitalized and discharged from Renmin Hospital of Wuhan University, Wuhan, China before 1 March 2020. Demographic and clinical characteristics and self-reported clinical sequelae of the survivors were described and analysed. A cohort of volunteers who were free of COVID-19 and lived in the urban area of Wuhan during the outbreak were also selected as the comparison group.
Among 538 survivors (293, 54.5% female), the median (interquartile range) age was 52.0 (41.0–62.0) years, and the time from discharge from hospital to first follow-up was 97.0 (95.0–102.0) days. Clinical sequelae were common, including general symptoms (n = 267, 49.6%), respiratory symptoms (n = 210, 39%), cardiovascular-related symptoms (n = 70, 13%), psychosocial symptoms (n = 122, 22.7%) and alopecia (n = 154, 28.6%). We found that physical decline/fatigue (p < 0.01), postactivity polypnoea (p= 0.04) and alopecia (p < 0.01) were more common in female than in male subjects. Dyspnoea during hospitalization was associated with subsequent physical decline/fatigue, postactivity polypnoea and resting heart rate increases but not specifically with alopecia. A history of asthma during hospitalization was associated with subsequent postactivity polypnoea sequela. A history of pulse ≥90 bpm during hospitalization was associated with resting heart rate increase in convalescence. The duration of virus shedding after COVID-19 onset and hospital length of stay were longer in survivors with physical decline/fatigue or postactivity polypnoea than in those without.
Clinical sequelae during early COVID-19 convalescence were common; some of these sequelae might be related to gender, age and clinical characteristics during hospitalization.
Rapidly emerging evidence continues to describe an intimate and causal relationship between sleep and emotional brain function. These findings are mirrored by long-standing clinical observations ...demonstrating that nearly all mood and anxiety disorders co-occur with one or more sleep abnormalities. This review aims to (a) provide a synthesis of recent findings describing the emotional brain and behavioral benefits triggered by sleep, and conversely, the detrimental impairments following a lack of sleep; (b) outline a proposed framework in which sleep, and specifically rapid-eye movement (REM) sleep, supports a process of affective brain homeostasis, optimally preparing the organism for next-day social and emotional functioning; and (c) describe how this hypothesized framework can explain the prevalent relationships between sleep and psychiatric disorders, with a particular focus on posttraumatic stress disorder and major depression.
Sleep abnormalities are clearly recognized as a distinct clinical symptom of concern in neurodegenerative disorders. Appropriate management of sleep-related symptoms has a positive impact on quality ...of life in patients with neurodegenerative disorders. This review provides an overview of mechanisms that are currently being considered that tie sleep with neurodegeneration. It appraises the literature regarding specific sleep changes seen in common neurodegenerative diseases, with a focus on Alzheimer disease and synucleinopathies (ie, Parkinson disease, dementia with Lewy bodies, multiple system atrophy), that have been better studied. Sleep changes may also serve as markers to identify patients in the preclinical stage of some neurodegenerative disorders. A hypothetical model is postulated founded on the conjecture that specific sleep abnormalities, when noted to increase in severity beyond that expected for age, could be a surrogate marker reflecting pathophysiological processes related to neurodegenerative disorders. This provides a clinical strategy for screening patients in the preclinical stages of neurodegenerative disorders to enable therapeutic trials to establish the efficacy of neuroprotective agents to prevent or delay the development of symptoms and functional decline. It is unclear if sleep disturbance directly impacts neurodegenerative processes or is a secondary outcome of neurodegeneration; this is an active area of research. The clinical importance of recognizing and managing sleep changes in neurodegenerative disorders is beyond doubt.
Abstract Background Convergent studies have highlighted the dysfunction of default mode network (DMN) in major depressive disorder (MDD). The altered connectivity in posterior cingulate cortex (PCC) ...and medial prefrontal cortex (mPFC) was especially found to be of interest in the resting state functional connectivity analysis. Recently, more attention has turned to the internal functional connectivity within the DMN. However, the internal connection patterns within the DMN remain unclear at the initial onset of MDD. Methods Resting-state fMRI was performed on 38 first-episode, treatment-naïve MDD patients along with 38 matched healthy controls. Seed-based analysis was used to define the DMN and then a region-to-region connectivity analysis was performed to inspect the functional connectivity within the DMN. Spearman׳s rank correlation analysis was performed between significantly abnormal connectivities in MDD patients and clinical measurements. Results Decreased region-to-region connectivities within DMN were found between the PCC and dorsal medial prefrontal cortex (dmPFC), between PCC and the right inferior parietal gyrus/angular, as well as between the left thalamus and cerebellar tonsil. No significant increase in connectivity was found. Moreover, functional connectivity between the left thalamus and cerebellar tonsil revealed a marginal significant negative correlation with clinical Hamilton Depression Rating Scale (HDRS) scores. Limitations Noteworthiness in morbidity, a high risk of mortality, and a high rate of medical service utilization of MDD make the current results uncertain to apply to the more complicated situations. Conclusions Each region within DMN may have a specific, individual functional role. The reason to identify the pathological mechanism of MDD may not lie in the abnormal DMN functional connectivity, but rather in the abnormal functional connectivity within DMN.
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