Subacute Stage Research Articles

A case report of Budd-Chiari syndrome with cardiac complications and low SpO2 successfully managed by an Integrated-approach

Budd-Chiari syndrome [BCS] is a rare, potentially life-threatening condition characterized by the triad of abdominal pain, ascites, and hepatomegaly (with or without jaundice). There will be an underlying disorder in most cases. The diagnosis, as well as management of the case, requires a multidisciplinary approach. The treatment should aim at reducing the presenting symptoms as well as removing the underlying pathology. Here we explain a case report of a 21-year-old male patient in the subacute stage of BCS with its complications and considered as a candidate for liver transplantation. His liver enzymes, PT/INR, D- dimer, and homocysteine values were above normal levels. The arterial oxygen saturation level was subnormal, and he was on supportive oxygen supplement. Inferior venacava [IVC] Doppler revealed a non-obstructive intrahepatic thrombus. The patient was treated with Homoeopathic medicine Arsenicum album and Arnica montana, given as an adjuvant to conventional treatment.

Recurrent Transient Ischemic Attack Induces Neural Cytoskeleton Modification and Gliosis in an Experimental Model.

Transient ischemic attack (TIA) presents a high risk for subsequent stroke, Alzheimer's disease (AD), and related dementia (ADRD). However, the neuropathophysiology of TIA has been rarely studied. By evaluating recurrent TIA-induced neuropathological changes, our study aimed to explore the potential mechanisms underlying the contribution of TIA to ADRD. In the current study, we established a recurrent TIA model by three times 10-min middle cerebral artery occlusion within a week in rat. Neither permanent neurological deficit nor apoptosis was observed following recurrent TIA. No increase of AD-related biomarkers was indicated after TIA, including increase of tau hyperphosphorylation and β-site APP cleaving enzyme 1 (BACE1). Neuronal cytoskeleton modification and neuroinflammation was found at 1, 3, and 7days after recurrent TIA, evidenced by the reduction of microtubule-associated protein 2 (MAP2), elevation of neurofilament-light chain (NFL), and increase of glial fibrillary acidic protein (GFAP)-positive astrocytes and ionized calcium binding adaptor molecule 1 (Iba1)-positive microglia at the TIA-affected cerebral cortex and basal ganglion. Similar NFL, GFAP and Iba1 alteration was found in the white matter of corpus callosum. In summary, the current study demonstrated that recurrent TIA may trigger neuronal cytoskeleton change, astrogliosis, and microgliosis without induction of cell death at the acute and subacute stage. Our study indicates that TIA-induced neuronal cytoskeleton modification and neuroinflammation may be involved in the vascular contribution to cognitive impairment and dementia.

Reversible cerebral artery constriction accompanied with stroke-like episode in MELAS: A case series

ObjectiveThe pathophysiology of stroke-like episode (SLE) in mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) was uncertain, though mitochondrial metabolic crisis of cortical neurons and mitochondrial proliferation in small vessels of brain have been considered. However, the involvement of major cerebral vessels was debated. We aimed to investigate whether major cerebral vessels participate in SLE. MethodsWe retrospectively collected the clinical and neuroimaging data of MELAS patients diagnosed in our center. Through follow-up, the cases harboring reversible cerebral artery constriction on brain magnetic resonance angiography (MRA) examination were included in this study. ResultsThere were 20 patients with intact brain MRA data at acute and non-acute phases. Only 3 cases with m.3243A > G mutation were enrolled. They suffered once or twice SLEs manifesting headache, blurred vision, seizures or mental and behavior disorder. New lesions were present in temporo-parietal and/or temporo-occipital regions. Segmental stenosis at middle cerebral artery and/or posterior cerebral artery, proximal portions in particular, was ipsilateral to the lesions at acute phase in all the 3 patients, which was resolved during the subacute or chronic stages. Moreover, the SLEs lesions were located within the stenotic arteries territory. In addition, dilation at distal portions of the stenotic arteries was observed at acute phase as well in 2 patients. ConclusionReversible constriction of cerebral arteries may contribute to SLE of MELAS. MELAS should be a differential diagnosis when stenosis of major cerebral vessels is present at acute phase of SLE.

Subacute and chronic proteomic and phosphoproteomic analyses of a mouse model of traumatic brain injury at two timepoints and comparison with chronic traumatic encephalopathy in human samples

Repetitive mild traumatic brain injury (r-mTBI) is the most widespread type of brain trauma worldwide. The cumulative injury effect triggers long-lasting pathological and molecular changes that may increase risk of chronic neurodegenerative diseases. R-mTBI is also characterized by changes in the brain proteome, where the majority of molecules altered early post-TBI are different from those altered at more chronic phases. This differentiation may contribute to the heterogeneity of available data on potential therapeutic targets and may present an obstacle in developing effective treatments. Here, we aimed to characterize a proteome profile of r-mTBI in a mouse model at two time points – 3 and 24 weeks post last TBI, as this may be a more relevant therapeutic window for individuals suffering negative consequences of r-mTBI. We identified a great number of proteins and phosphoproteins that remain continuously dysregulated from 3 to 24 weeks. These proteins may serve as effective therapeutic targets for sub-acute and chronic stages of post r-mTBI. We also compared canonical pathway activation associated with either total proteins or phosphoproteins and revealed that they both are upregulated at 24 weeks. However, at 3 weeks post-TBI, only pathways associated with total proteins are upregulated, while pathways driven by phosphoproteins are downregulated. Finally, to assess the translatability of our data, we compared proteomic changes in our mouse model with those reported in autopsied human samples of Chronic Traumatic Encephalopathy (CTE) patients compared to controls. We observed 39 common proteins that were upregulated in both species and 24 common pathways associated with these proteins. These findings support the translational relevance of our mouse model of r-mTBI for successful identification and translation of therapeutic targets.

White matter abnormalities characterize the acute stage of sports-related mild traumatic brain injury.

Sports-related concussion, a form of mild traumatic brain injury, is characterized by transient disturbances of brain function. There is increasing evidence that functional brain changes may be driven by subtle abnormalities in white matter microstructure, and diffusion MRI has been instrumental in demonstrating these white matter abnormalities in vivo. However, the reported location and direction of the observed white matter changes in mild traumatic brain injury are variable, likely attributable to the inherent limitations of the white matter models used. This cross-sectional study applies an advanced and robust technique known as fixel-based analysis to investigate fibre tract-specific abnormalities in professional Australian Football League players with a recent mild traumatic brain injury. We used the fixel-based analysis framework to identify common abnormalities found in specific fibre tracts in participants with an acute injury (≤12 days after injury; n = 14). We then assessed whether similar changes exist in subacute injury (>12 days and <3 months after injury; n = 15). The control group was 29 neurologically healthy control participants. We assessed microstructural differences in fibre density and fibre bundle morphology and performed whole-brain fixel-based analysis to compare groups. Subsequent tract-of-interest analyses were performed within five selected white matter tracts to investigate the relationship between the observed tract-specific abnormalities and days since injury and the relationship between these tract-specific changes with cognitive abnormalities. Our whole-brain analyses revealed significant increases in fibre density and bundle cross-section in the acute mild traumatic brain injury group when compared with controls. The acute mild traumatic brain injury group showed even more extensive differences when compared with the subacute injury group than with controls. The fibre structures affected in acute concussion included the corpus callosum, left prefrontal and left parahippocampal white matter. The fibre density and cross-sectional increases were independent of time since injury in the acute injury group, and were not associated with cognitive deficits. Overall, this study demonstrates that acute mild traumatic brain injury is characterized by specific white matter abnormalities, which are compatible with tract-specific cytotoxic oedema. These potential oedematous changes were absent in our subacute mild traumatic brain injury participants, suggesting that they may normalize within 12 days after injury, although subtle abnormalities may persist in the subacute stage. Future longitudinal studies are needed to elucidate individualized recovery after brain injury.

Post-Viral Polyarthritis

Background: Viral infection is the infection caused by a virus in the human body. The immune response to a virus infection is attacking the body’s own cells. This causes stress and inflammation of tissues in the body and damage to the cells. Polyarthritis is one of the most common complications caused by viral infection. Post viral polyarthritis mainly affects the large joint such as the knee, but can affect several joints such as ankle, wrist. The full recovery time is still not sure, some studies have shown that it usually takes six weeks or it can even last for months or years. Case Description: A 15-year-old male complains of fever with dry cough for 2 days followed by Multiple joint pain and soft tissue pain since 2 months. Swelling was also noticed in both wrist and knee for a week. For assessment outcome measures like VAS, MMT, ROM were taken prior to the treatment. Patient underwent a 4 weeks physiotherapy rehab program and showed marked improvement in the pain, range of motion, muscle strength and functional activities. Result: When the post-assessment was done, patient showed significant improvement in the pain relief, showed improvement in range of motion of the joints, increase in the muscle strength and noticeable improvement in functional capacity. Conclusion: This concluded that starting physiotherapy management in the sub-acute stage of the condition is effective in reducing pain increasing mobility and increasing the strength and endurance.

Predictive Validity of the Postural Assessment Scale for Stroke (PASS) to Classify the Functionality in Stroke Patients: A Retrospective Study.

The analysis of the predictive validity of a scale allows us to establish objectives in rehabilitation and to make decisions in the clinical setting. The objective of this study was to determine the validity of the Postural Assessment Scale for Stroke (PASS) to predict functionality at each stage of recovery in stroke patients. Methods: A retrospective study was carried out collecting data from patients admitted to a neurorehabilitation hospital. All patients having suffered a stroke less than two months before hospital admission were included in the study. The balance was measured with the PASS scale and the functionality with the Functional Independence Measure (FIM) scale. Simple linear regressions were performed to model the relationship between the PASS and FIM scores in the acute, subacute and chronic stages (6 and 12 months), as well as between the PASS scores at admission and the FIM values in the chronic stage. Results: The PASS scale showed a good predictive validity (R2 values from 0.54 to 0.87; β values from 1.99 to 2.62; p < 0.001) for FIM scores at acute, subacute and chronic stages, with lower goodness-of-fit for PASS scores at admission and FIM scores at 12 months (R2 = 0.383; β = 1.61 (0.96–2.26); p < 0.001). Cut-off points in the PASS scale to predict high functional level were 17.5 for the acute stage and 16.5 for the subacute and chronic stages. A score of 8.5 on the PASS scale measured in the acute phase predicted a high functional level at 12 months. Conclusion: The PASS scale is a useful tool to classify the functionality of stroke patients in the acute, subacute and chronic phases. The PASS score upon admission into the hospital can predict the functionality of the stroke patients after 12 months. However, future studies should be carried out to corroborate our findings with larger sample sizes.

The PI3K/AKT signalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities.

ObjectsTraumatic spinal cord injury (TSCI) causes neurological dysfunction below the injured segment of the spinal cord, which significantly impacts the quality of life in affected patients. The phosphoinositide 3kinase/serine‐threonine kinase (PI3K/AKT) signaling pathway offers a potential therapeutic target for the inhibition of secondary TSCI. This review summarizes updates concerning the role of the PI3K/AKT pathway in TSCI.Materials and MethodsBy searching articles related to the TSCI field and the PI3K/AKT signaling pathway, we summarized the mechanisms of secondary TSCI and the PI3K/AKT signaling pathway; we also discuss current and potential future treatment methods for TSCI based on the PI3K/AKT signaling pathway.ResultsEarly apoptosis and autophagy after TSCI protect the body against injury; a prolonged inflammatory response leads to the accumulation of pro‐inflammatory factors and excessive apoptosis, as well as excessive autophagy in the surrounding normal nerve cells, thus aggravating TSCI in the subacute stage of secondary injury. Initial glial scar formation in the subacute phase is a protective mechanism for TSCI, which limits the spread of damage and inflammation. However, mature scar tissue in the chronic phase hinders axon regeneration and prevents the recovery of nerve function. Activation of PI3K/AKT signaling pathway can inhibit the inflammatory response and apoptosis in the subacute phase after secondary TSCI; inhibiting this pathway in the chronic phase can reduce the formation of glial scar.ConclusionThe PI3K/AKT signaling pathway has an important role in the recovery of spinal cord function after secondary injury. Inducing the activation of PI3K/AKT signaling pathway in the subacute phase of secondary injury and inhibiting this pathway in the chronic phase may be one of the potential strategies for the treatment of TSCI.

Hyperglykämische Notfälle im Rettungsdienst

In prehospital acute care, an undefined disturbance of consciousness frequently occurs as an alarm diagnosis for rescue vehicles. This group of patients usually includes those affected by hyperglycemic emergencies; since in general practice such patients are often already identified in the subacute stage and can be admitted for inpatient treatment if necessary (e.g. by ambulance), an acute life-threatening hyperglycemic emergency rarely occurs. In acute care, however, in addition to ensuring vital functions—especially airway management in the case of impaired consciousness Glasgow Coma Scale (GCS) ≤ 8—the diagnostic differentiation from other acute clinical pictures, such as a central neurological deficit, is difficult, since most ambulances and physician-staffed emergency response vehicles do not have the diagnostic equipment for arterial blood gas (ABG) analysis or imaging. Especially the differentiation between ketoacidotic and hyperosmolar hyperglycemic emergency is difficult due to the lack of ABG; for causal therapy the patient is also referred to the clinical setting because insulin in its different dosage forms is also not part of the common drug equipment of rescue vehicles. This means that prehospital acute care is generally limited to rapid diagnosis, stabilization of vital functions (especially airway management, volume substitution), and transport to the nearest suitable hospital (with intensive care capacity if necessary). Nevertheless, development of the competence “clinical reasoning” is paramount because a successful clinical therapy course is already set preclinically.

The Translational Potential of Microglia and Monocyte-Derived Macrophages in Ischemic Stroke.

The immune response to ischemic stroke is an area of study that is at the forefront of stroke research and presents promising new avenues for treatment development. Upon cerebral vessel occlusion, the innate immune system is activated by danger-associated molecular signals from stressed and dying neurons. Microglia, an immune cell population within the central nervous system which phagocytose cell debris and modulate the immune response via cytokine signaling, are the first cell population to become activated. Soon after, monocytes arrive from the peripheral immune system, differentiate into macrophages, and further aid in the immune response. Upon activation, both microglia and monocyte-derived macrophages are capable of polarizing into phenotypes which can either promote or attenuate the inflammatory response. Phenotypes which promote the inflammatory response are hypothesized to increase neuronal damage and impair recovery of neuronal function during the later phases of ischemic stroke. Therefore, modulating neuroimmune cells to adopt an anti-inflammatory response post ischemic stroke is an area of current research interest and potential treatment development. In this review, we outline the biology of microglia and monocyte-derived macrophages, further explain their roles in the acute, subacute, and chronic stages of ischemic stroke, and highlight current treatment development efforts which target these cells in the context of ischemic stroke.

Bringing rehabilitation home with an e-health platform to treat stroke patients: study protocol of a randomized clinical trial (RGS@home)

BackgroundThere is a pressing need for scalable healthcare solutions and a shift in the rehabilitation paradigm from hospitals to homes to tackle the increase in stroke incidence while reducing the practical and economic burden for patients, hospitals, and society. Digital health technologies can contribute to addressing this challenge; however, little is known about their effectiveness in at-home settings. In response, we have designed the RGS@home study to investigate the effectiveness, acceptance, and cost of a deep tech solution called the Rehabilitation Gaming System (RGS). RGS is a cloud-based system for delivering AI-enhanced rehabilitation using virtual reality, motion capture, and wearables that can be used in the hospital and at home. The core principles of the brain theory-based RGS intervention are to deliver rehabilitation exercises in the form of embodied, goal-oriented, and task-specific action.MethodsThe RGS@home study is a randomized longitudinal clinical trial designed to assess whether the combination of the RGS intervention with standard care is superior to standard care alone for the functional recovery of stroke patients at the hospital and at home. The study is conducted in collaboration with hospitals in Spain, Sweden, and France and includes inpatients and outpatients at subacute and chronic stages post-stroke. The intervention duration is 3 months with assessment at baseline and after 3, 6, and 12 months. The impact of RGS is evaluated in terms of quality of life measurements, usability, and acceptance using standardized clinical scales, together with health economic analysis. So far, one-third of the patients expected to participate in the study have been recruited (N = 90, mean age 60, days after stroke ≥ 30 days). The trial will end in July 2023.DiscussionWe predict an improvement in the patients’ recovery, high acceptance, and reduced costs due to a soft landing from the clinic to home rehabilitation. In addition, the data provided will allow us to assess whether the prescription of therapy at home can counteract deterioration and improve quality of life while also identifying new standards for online and remote assessment, diagnostics, and intervention across European hospitals.Trial registrationClinicalTrials.gov NCT04620707. Registered on November 3, 2020

The dynamic cellular and molecular features during the development of radiation proctitis revealed by transcriptomic profiling in mice

BackgroundRadiation proctitis (RP) is the most common complication of radiotherapy for pelvic tumor. Currently there is a lack of effective clinical treatment and its underlying mechanism is poorly understood. In this study, we aimed to dynamically reveal the mechanism of RP progression from the perspective of RNomics using a mouse model, so as to help develop reasonable therapeutic strategies for RP.ResultsMice were delivered a single dose of 25 Gy rectal irradiation, and the rectal tissues were removed at 4 h, 1 day, 3 days, 2 weeks and 8 weeks post-irradiation (PI) for both histopathological assessment and RNA-seq analysis. According to the histopathological characteristics, we divided the development process of our RP animal model into three stages: acute (4 h, 1 day and 3 days PI), subacute (2 weeks PI) and chronic (8 weeks PI), which could recapitulate the features of different stages of human RP. Bioinformatics analysis of the RNA-seq data showed that in the acute injury period after radiation, the altered genes were mainly enriched in DNA damage response, p53 signaling pathway and metabolic changes; while in the subacute and chronic stages of tissue reconstruction, genes involved in the biological processes of vessel development, extracellular matrix organization, inflammatory and immune responses were dysregulated. We further identified the hub genes in the most significant biological process at each time point using protein-protein interaction analysis and verified the differential expression of these genes by quantitative real-time-PCR analysis.ConclusionsOur study reveals the molecular events sequentially occurred during the course of RP development and might provide molecular basis for designing drugs targeting different stages of RP development.

Widespread white matter oedema in subacute COVID-19 patients with neurological symptoms.

While neuropathological examinations in patients who died from COVID-19 revealed inflammatory changes in cerebral white matter, cerebral MRI frequently fails to detect abnormalities even in the presence of neurological symptoms. Application of multi-compartment diffusion microstructure imaging (DMI), that detects even small volume shifts between the compartments (intra-axonal, extra-axonal and free water/CSF) of a white matter model, is a promising approach to overcome this discrepancy.In this monocentric prospective study, a cohort of 20 COVID-19 inpatients (57.3 ± 17.1 years) with neurological symptoms (e.g. delirium, cranial nerve palsies) and cognitive impairments measured by the Montreal Cognitive Assessment (MoCA test; 22.4 ± 4.9; 70% below the cut-off value <26/30 points) underwent DMI in the subacute stage of the disease (29.3 ± 14.8 days after positive PCR). A comparison of whole-brain white matter DMI parameters with a matched healthy control group (n = 35) revealed a volume shift from the intra- and extra-axonal space into the free water fraction (V-CSF). This widespread COVID-related V-CSF increase affected the entire supratentorial white matter with maxima in frontal and parietal regions. Streamline-wise comparisons between COVID-19 patients and controls further revealed a network of most affected white matter fibres connecting widespread cortical regions in all cerebral lobes. The magnitude of these white matter changes (V-CSF) was associated with cognitive impairment measured by the MoCA test (r = −0.64, P = 0.006) but not with olfactory performance (r = 0.29, P = 0.12). Furthermore, a non-significant trend for an association between V-CSF and interleukin-6 emerged (r = 0.48, P = 0.068), a prominent marker of the COVID-19 related inflammatory response. In 14/20 patients who also received cerebral 18F-FDG PET, V-CSF increase was associated with the expression of the previously defined COVID-19-related metabolic spatial covariance pattern (r = 0.57; P = 0.039). In addition, the frontoparietal-dominant pattern of neocortical glucose hypometabolism matched well to the frontal and parietal focus of V-CSF increase.In summary, DMI in subacute COVID-19 patients revealed widespread volume shifts compatible with vasogenic oedema, affecting various supratentorial white matter tracts. These changes were associated with cognitive impairment and COVID-19 related changes in 18F-FDG PET imaging.

Elevation of neutrophil carcinoembryonic antigen-related cell adhesion molecule 1 associated with multiple inflammatory mediators was related to different clinical stages in ischemic stroke patients.

BackgroundWe aimed to analyze the level of carcinoembryonic antigen‐related cell adhesion molecule 1 (CEACAM1) in neutrophils of ischemic stroke (IS) patients at different stages, together with its roles in neutrophils.Patients and methodsSixty‐seven patients were classified into acute phase group (n = 19), subacute phase group (n = 28), and stable phase group (n = 20), and 20 healthy individuals who had received physical examination at the same time period as healthy control. We then analyzed the expression level of CEACAM1 and cell viability in CEACAM1 positive and CEACAM1 negative neutrophils by flow cytometry and the content of plasma CEACAM1, neutrophil gelatinase‐associated lipocalin (NGAL), matrix metalloproteinases‐9 (MMP‐9) was measured using enzyme‐linked immunosorbent assay (ELISA), while that of interleukin‐10 (IL‐10) and tumor necrosis factor (TNF) was determined using a Human Enhanced Sensitivity Flex set.ResultsCompared with healthy control, the percentage of CEACAM1 positive neutrophils in IS patients showed a significant increase, and a significant increase was also noticed in the content of plasma CEACAM1 at the subacute stage. Reduction in cell viability was observed in CEACAM1 positive neutrophils compared with CEACAM1 negative counterparts. There was a positive correlation between CEACAM1 expression rate in neutrophils and plasma CEACAM1 and IL‐10 content in the subacute group. Compared with acute group and healthy control group, there was an instinct increase in the level of plasma MMP‐9 and NGAL in subacute group.ConclusionsOur data showed that there was a rapid increase of CEACAM1 in neutrophils at the acute stage of IS. We speculated that CEACAM1 may serve as an inhibitory regulator involving in the progression of IS.

Impaired Duration Perception in Patients With Unilateral Vestibulopathy During Whole-Body Rotation.

This study aimed to evaluate vestibular perception in patients with unilateral vestibulopathy. We recruited 14 patients (9 women, mean age = 59.3 ± 14.3) with unilateral vestibulopathy during the subacute or chronic stage (disease duration = 6 days to 25 years). For the evaluation of position perception, the patients had to estimate the position after whole-body rotation in the yaw plane. The velocity/acceleration perception was evaluated by acquiring decisions of patients regarding which direction would be the faster rotation after a pair of ipsi- and contra-lesional rotations at various velocity/acceleration settings. The duration perception was assessed by collecting decisions of patients for longer rotation directions at each pair of ipsi- and contra-lesional rotations with various velocities and amplitudes. Patients with unilateral vestibulopathy showed position estimates and velocity/acceleration discriminations comparable to healthy controls. However, in duration discrimination, patients had a contralesional bias such that they had a longer perception period for the healthy side during the equal duration and same amplitude rotations. For the complex duration task, where a longer duration was assigned to a smaller rotation amplitude, the precision was significantly lower in the patient group than in the control group. These results indicate persistent impairments of duration perception in unilateral vestibulopathy and favor the intrinsic and distributed timing mechanism of the vestibular system. Complex perceptual tasks may be helpful to disclose hidden perceptual disturbances in unilateral vestibular hypofunction.

Association between Sleep Disturbances at Subacute Stage of Mild Traumatic Brain Injury and Long-Term Outcomes.

Mild (mTBI) traumatic brain injury (TBI) accounts for the majority of all TBI cases. Evidence has suggested that patients with mTBI can suffer from long-lasting cognitive deficits, persistent symptoms, and decreased quality of life. Sleep disorders are commonly observed after TBI, with the prevalence rate of sleep disturbances in persons with TBI being much higher than that in the general population. Poor sleep quality can impair cognitive functions in the general population. This effect of sleep disturbances may impede the recovery processes in the population with TBI. The objective of this study is to add to our understanding of the relationship between self-reported sleep problems and other post-concussion symptoms and look at the association between early sleep problems and long-term outcomes in mTBI. Post-concussion symptoms, neurocognitive functions, level of global outcomes, and rating of satisfaction of life were assessed in 64 patients with mTBI. The results revealed that the presence of sleep disturbances co-occur with an increased level of overall post-concussion symptoms at the subacute stage of mTBI, particularly with symptoms including poor concentration, memory problems, and irritability. In addition, sleep disturbance at the subacute stage is associated with persistent poor concentration and memory problems, as well as worse neurocognitive function, slower overall recovery, and lower satisfactory of life at the long term. Our findings suggest that sleep disturbance can be a prognostic factor of long-term outcomes after mTBI. Early interventions to improve sleep quality can have potential benefits to facilitate the recovery process from mTBI.

Neurobiological Links between Stress, Brain Injury, and Disease.

Stress, which refers to a combination of physiological, neuroendocrine, behavioral, and emotional responses to novel or threatening stimuli, is essentially a defensive adaptation under physiological conditions. However, strong and long-lasting stress can lead to psychological and pathological damage. Growing evidence suggests that patients suffering from mild and moderate brain injuries and diseases often show severe neurological dysfunction and experience severe and persistent stressful events or environmental stimuli, whether in the acute, subacute, or recovery stage. Previous studies have shown that stress has a remarkable influence on key brain regions and brain diseases. The mechanisms through which stress affects the brain are diverse, including activation of endoplasmic reticulum stress (ERS), apoptosis, oxidative stress, and excitatory/inhibitory neuron imbalance, and may lead to behavioral and cognitive deficits. The impact of stress on brain diseases is complex and involves impediment of recovery, aggravation of cognitive impairment, and neurodegeneration. This review summarizes various stress models and their applications and then discusses the effects and mechanisms of stress on key brain regions—including the hippocampus, hypothalamus, amygdala, and prefrontal cortex—and in brain injuries and diseases—including Alzheimer's disease, stroke, traumatic brain injury, and epilepsy. Lastly, this review highlights psychological interventions and potential therapeutic targets for patients with brain injuries and diseases who experience severe and persistent stressful events.

Combination of fecal calprotectin and initial coronary dimensions to predict coronary artery lesions persistence in Kawasaki disease

Kawasaki Disease (KD) is systemic vasculitis involving medium-sized vessels in children. The aim of our study is to determine if fecal calprotectin (FC) could be useful in predicting the development or persistence of coronary artery lesions (CALs) in KD. We conducted a prospective monocentric study including all consecutive diagnoses of. Clinical, laboratory, echocardiographic data were recorded during the acute and subacute phase, including FC. Correlations among laboratory values, FC, clinical manifestations, IVIG-responsiveness and CALs development were investigated. We enrolled 26 children (76.9% boys; median age 34.5 months). The combination of FC > 250 microg/g and z-score > 2 during the acute phase was associated with the persistence of CALs (p = 0.022). A z-score > 2 alone during the acute phase was not related to CALs during the subacute stage (p > 0.05). A neutrophil percentage > 70% and WBC > 15,000/mmc during the acute phase significantly correlated with the presence of CALs during the subacute phase (p = 0.008). C-reactive protein (CRP) > 13 mg/dL at KD onset was significantly associated with the presence of CALs during the acute (p = 0.017) and subacute phase (p = 0.001). The combination of FC > 250 microg/g and a z-score > 2 during the acute phase of KD may be used as a predictor of CALs persistence. It can be useful especially in children with an initial CRP < 13 mg/dl.

Development and feasibility testing of action observation training videos in acute stroke survivors.

Background: Action observation training (AOT) is used for lower limb (LL) stroke rehabilitation in subacute and chronic stages, but concise information regarding the types of activities to be used and the feasibility of administration in the acute stroke population is unknown. The aim of this study was to develop and validate videos of appropriate activities for LL AOT and test administrative feasibility in acute stroke. Method: A video inventory of LL activities was created after a literature survey and expert scrutiny. Five stroke rehabilitation experts validated the videos per domains of relevance, comprehension, clarity, camera position and brightness. LL AOT was then tested on ten individuals with acute stroke for uncovering barriers for clinical use in a feasibility study. Participants watched the activities and attempted imitation of the same. Determination of administrative feasibility was undertaken via participant interviews. Results: Suitable LL activities for stroke rehabilitation were identified. Content validation of videos led to improvements in selected activities and video quality. Expert scrutiny led to further video processing to include different perspectives of view and speeds of projected movements. Barriers identified included inability to imitate actions shown in videos and increased distractibility for some participants. Conclusion: A video catalogue of LL activities was developed and validated. AOT was deemed safe and feasible for acute stroke rehabilitation and may be used in future research and clinical practice.

Dynamic Relationship Between Interhemispheric Functional Connectivity and Corticospinal Tract Changing Pattern After Subcortical Stroke

Background and PurposeIncreased interhemispheric resting-state functional connectivity (rsFC) between the bilateral primary motor cortex (M1) compensates for corticospinal tract (CST) impairment, which facilitates motor recovery in chronic subcortical stroke. However, there is a lack of data on the evolution patterns and correlations between M1–M1 rsFC and diffusion indices of CSTs with different origins after subcortical stroke and their relations with long-term motor outcomes.MethodsA total of 44 patients with subcortical stroke underwent longitudinal structural and functional magnetic resonance imaging (MRI) examinations and clinical assessments at four time points. Diffusion tensor imaging was used to extract fractional anisotropy (FA) values of the affected CSTs with different origins. Resting-state functional MRI was used to calculate the M1–M1 rsFC. Longitudinal patterns of functional and anatomic changes in connections were explored using a linear mixed-effects model. Dynamic relationships between M1–M1 rsFC and FA values of the affected specific CSTs and the impact of these variations on the long-term motor outcomes were analyzed in patients with subcortical stroke.ResultsStroke patients showed a significantly decreased FA in the affected specific CSTs and a gradually increasing M1–M1 rsFC from the acute to the chronic stage. The FA of the affected M1 fiber was negatively correlated with the M1–M1 rsFC from the subacute to the chronic stage, FA of the affected supplementary motor area fiber was negatively correlated with the M1–M1 rsFC in the subacute stage, and FA of the affected M1 fiber in the acute stage was correlated with the long-term motor recovery after subcortical stroke.ConclusionOur findings show that the FA of the affected M1 fiber in the acute stage had the most significant correlation with long-term motor recovery and may be used as an imaging biomarker for predicting motor outcomes after stroke. The compensatory role of the M1–M1 rsFC enhancement may start from the subacute stage in stroke patients with CST impairment.