Evidence of traumatic brain injury in headbutting bovids

Traumatic brain injury (TBI) is a leading cause of neurologic impairment and death that remains poorly understood. Rodent models have yet to produce clinical therapies, and the exploration of larger and more diverse models remains relatively scarce. We investigated the potential for brain injury after headbutting in two combative bovid species by assessing neuromorphology and neuropathology through immunohistochemistry and stereological quantification. Postmortem brains of muskoxen (Ovibos moschatus,n = 3) and bighorn sheep (Ovis canadensis,n = 4) were analyzed by high-resolution MRI and processed histologically for evidence of TBI. Exploratory histological protocols investigated potential abnormalities in neurons, microglia, and astrocytes in the prefrontal and parietal cortex. Phosphorylated tau protein, a TBI biomarker found in the cerebrospinal fluid and in neurodegenerative lesions, was used to detect possible cellular consequences of chronic or acute TBI. MRI revealed no abnormal neuropathological changes; however, high amounts of tau-immunoreactive neuritic thread clusters, neurites, and neurons were concentrated in the superficial layers of the neocortex, preferentially at the bottom of the sulci in the muskoxen and occasionally around blood vessels. Tau-immunoreactive lesions were rare in the bighorn sheep. Additionally, microglia and astrocytes showed no grouping around tau-immunoreactive cells in either species. Our preliminary findings indicate that muskoxen and possibly other headbutting bovids suffer from chronic or acute brain trauma and that the males’ thicker skulls may protect them to a certain extent

Depth-dependent intracortical myelin organization in the living human brain determined by in vivo ultra-high field magnetic resonance imaging

Background: Intracortical myelin is a key determinant of neuronal synchrony and plasticity that underpin optimal brain function. Magnetic resonance imaging (MRI) facilitates the examination of intracortical myelin but presents with methodological challenges. Here we describe a whole-brain approach for the in vivo investigation of intracortical myelin in the human brain using ultra-high field MRI. Methods: Twenty-five healthy adults were imaged in a 7 Tesla MRI scanner using diffusion-weighted imaging and a T 1 -weighted sequence optimized for intracortical myelin contrast. Using an automated pipeline, T 1 values were extracted at 20 depth-levels from each of 148 cortical regions. In each cortical region, T 1 values were used to infer myelin concentration and to construct a non-linearity index as a measure the spatial distribution of myelin across the cortical ribbon. The relationship of myelin concentration and the non-linearity index with other neuroanatomical properties were investigated. Five patients with multiple sclerosis were also assessed using the same protocol as positive controls. Results: Intracortical T 1 values decreased between the outer brain surface and the gray-white matter boundary following a slope that showed a slight leveling between 50% and 75% of cortical depth. Higher-order regions in the prefrontal, cingulate and insular cortices, displayed higher non-linearity indices than sensorimotor regions. Across all regions, there was a positive association between T 1 values and non-linearity indices (P < 10 125 ). Both T 1 values (P < 10 125 ) and non-linearity indices (P < 10 1215 ) were associated with cortical thickness. Higher myelin concentration but only in the deepest cortical levels was associated with increased subcortical fractional anisotropy (P = 0.05). Conclusions: We demonstrate the usefulness of an automatic, whole-brain method to perform depth-dependent examination of intracortical myelin organization. The extracted metrics, T 1 values and the non-linearity index, have characteristic patterns across cortical regions, and are associated with thickness and underlying white matter microstructure

Seven-tesla magnetic resonance imaging of the nervus terminalis, olfactory tracts, and olfactory bulbs in COVID-19 patients with anosmia and hypogeusia

Introduction: Linking olfactory epithelium to the central nervous system are cranial nerve 1, the olfactory nerve, and cranial nerve “0,” and the nervus terminalis (NT). Since there is minimal expression of angiotensin-converting enzyme-2 (ACE-2) in the olfactory nerve, it is unclear how SARS-CoV-2 causes anosmia (loss of smell) and hypogeusia (reduction of taste). In animal models, NT expresses ACE-2 receptors, suggesting a possible SARS-CoV-2 viral entry site in humans. The purpose of this study was to determine whether ultra-high-field 7 T magnetic resonance imaging (MRI) could visualize the NT, olfactory bulbs (OB), and olfactory tract (OT) in healthy controls and COVID-19 anosmia or hypogeusia and to qualitatively assess for volume loss and T2 alterations. Methods: In this study, 7 T MRI was used to evaluate the brain and olfactory regions in 45 COVID-19 patients and 29 healthy controls. Neuroimaging was qualitatively assessed by four board-certified neuroradiologists who were blinded to outcome assignments: for the presence or absence of NT; for OB, OT, and brain volume loss; and altered T2 signal, white matter T2 hyperintensities, microhemorrhages, enlarged perivascular spaces, and brainstem involvement. Results: NT was identifiable in all COVID-19 patients and controls. T2 hyperintensity in the NT, OB, and OT in COVID-19 patients with anosmia or hypogeusia was statistically significant compared to controls and COVID-19 patients without anosmia or hypogeusia. Discussion: On 7 T MRI, NT was radiographically identifiable, adjacent to OB and OT. In COVID-19 anosmia and hypogeusia, T2 hyperintensity of NT, OB, and OT was statistically significant compared to COVID-19 patients without anosmia or hypogeusia and controls. The NT may be a potential entry site for SARs-CoV-2 and may play a role in the pathophysiology of COVID-19 anosmia

MASE-sLASER, a short-TE, matched chemical shift displacement error sequence for single-voxel spectroscopy at ultrahigh field

Contains fulltext : 192702.pdf (publisher's version ) (Closed access)15 p

Case Report: An MRI Traumatic Brain Injury Longitudinal Case Study at 7 Tesla: Pre- and Post-injury Structural Network and Volumetric Reorganization and Recovery

Importance: A significant limitation of many neuroimaging studies examining mild traumatic brain injury (mTBI) is the unavailability of pre-injury data.Objective: We therefore aimed to utilize pre-injury ultra-high field brain MRI and compare a collection of neuroimaging metrics pre- and post-injury to determine mTBI related changes and evaluate the enhanced sensitivity of high-resolution MRI.Design: In the present case study, we leveraged multi-modal 7 Tesla MRI data acquired at two timepoints prior to mTBI (23 and 12 months prior to injury), and at two timepoints post-injury (2 weeks and 8 months after injury) to examine how a right parietal bone impact affects gross brain structure, subcortical volumetrics, microstructural order, and connectivity.Setting: This research was carried out as a case investigation at a single primary care site.Participants: The case participant was a 38-year-old female selected for inclusion based on a mTBI where a right parietal impact was sustained.Main outcomes: The main outcome measurements of this investigation were high spatial resolution structural brain metrics including volumetric assessment and connection density of the white matter connectome.Results: At the first scan timepoint post-injury, the cortical gray matter and cerebral white matter in both hemispheres appeared to be volumetrically reduced compared to the pre-injury and subsequent post-injury scans. Connectomes produced from whole-brain diffusion-weighted probabilistic tractography showed a widespread decrease in connectivity after trauma when comparing mean post-injury and mean pre-injury connection densities. Findings of reduced fractional anisotropy in the cerebral white matter of both hemispheres at post-injury time point 1 supports reduced connection density at a microstructural level. Trauma-related alterations to whole-brain connection density were markedly reduced at the final scan timepoint, consistent with symptom resolution.Conclusions and Relevance: This case study investigates the structural effects of traumatic brain injury for the first time using pre-injury and post-injury 7 Tesla MRI longitudinal data. We report findings of initial volumetric changes, decreased structural connectivity and reduced microstructural order that appear to return to baseline 8 months post-injury, demonstrating in-depth metrics of physiological recovery. Default mode, salience, occipital, and executive function network alterations reflect patient-reported hypersomnolence, reduced cognitive processing speed and dizziness.</jats:p

Altered hippocampus and amygdala subregion connectome hierarchy in major depressive disorder

AbstractThe hippocampus and amygdala limbic structures are critical to the etiology of major depressive disorder (MDD). However, there are no high-resolution characterizations of the role of their subregions in the whole brain network (connectome). Connectomic examination of these subregions can uncover disorder-related patterns that are otherwise missed when treated as single structures. 38 MDD patients and 40 healthy controls (HC) underwent anatomical and diffusion imaging using 7-Tesla MRI. Whole-brain segmentation was performed along with hippocampus and amygdala subregion segmentation, each representing a node in the connectome. Graph theory analysis was applied to examine the importance of the limbic subregions within the brain network using centrality features measured by node strength (sum of weights of the node’s connections), Betweenness (number of shortest paths that traverse the node), and clustering coefficient (how connected the node’s neighbors are to one another and forming a cluster). Compared to HC, MDD patients showed decreased node strength of the right hippocampus cornu ammonis (CA) 3/4, indicating decreased connectivity to the rest of the brain, and decreased clustering coefficient of the right dentate gyrus, implying it is less embedded in a cluster. Additionally, within the MDD group, the greater the embedding of the right amygdala central nucleus (CeA) in a cluster, the greater the severity of depressive symptoms. The altered role of these limbic subregions in the whole-brain connectome is related to diagnosis and depression severity, contributing to our understanding of the limbic system involvement in MDD and may elucidate the underlying mechanisms of depression.</jats:p

Sleep Problems, Anxiety, and Global Self-Rated Health Among Hospice Family Caregivers

Background: Although research has linked sleep problems, anxiety, and poor health outcomes among patients’ family members in nonhospice settings, little is known about these often interrelated issues among hospice family caregivers. Objectives: We sought to examine the relationships between sleep problems, anxiety, and global self-rated health among hospice family caregivers. Methods, Setting, and Patients: We conducted a secondary analysis of quantitative data from 395 family caregivers of hospice patients in the Midwest and Southeastern United States. Results: Nearly one-third of the hospice family caregivers who participated in this study experienced clinically noteworthy levels of sleep problems and/or anxiety. Caregivers’ symptoms of anxiety and sleep problems were strongly correlated. Caregivers who reported more frequent sleep problems and higher levels of anxiety reported poorer overall health. Conclusion: Hospice providers, who are charged with attending to the needs of both patients and their family caregivers, may improve their practice by regularly assessing for sleep problems and anxiety among family caregivers and providing appropriate interventions or referrals. </jats:sec