Cerebral Function Research Articles

Neurocognitive correlates of cerebral mitochondrial function and energy metabolism using phosphorus magnetic resonance spectroscopy in older adults.

The goal of the current study was to learn about the role of cerebral mitochondrial function on cognition. Based on established cognitive neuroscience, clinical neuropsychology, and cognitive aging literature, we hypothesized mitochondrial function within a focal brain region would map onto cognitive behaviors linked to that brain region. To test this hypothesis, we used phosphorous (31P) magnetic resonance spectroscopy (MRS) to derive indirect markers of mitochondrial function and energy metabolism across two regions of the brain (bifrontal, left temporal). We administered cognitive tasks sensitive to frontal-executive or temporal-hippocampal systems to a sample of 70 cognitively unimpaired older adults with subjective memory complaints and a first-degree family history of Alzheimer's disease and predicted better executive function and recent memory performance would be related to greater frontal and temporal 31P MRS indirect markers, respectively. Results of separate hierarchical linear regressions indicated better recent memory scores were related to 31P MRS indirect markers of lower static energy and higher energy reserve within the left temporal voxel; these findings were associated with moderate effect sizes. Contrary to predictions, executive function performance was unrelated to 31P MRS indirect markers within the bilateral frontal voxel, which may reflect a combination of theoretical and/or methodological issues. Findings represent a snapshot of the relationship between cognition and 31P MRS indirect markers of mitochondrial function, providing potential avenues for future work investigating mitochondrial underpinnings of cognition. 31P MRS may provide a sensitive neuroimaging marker for differences in aspects of memory among persons at-risk for mild cognitive impairment or dementia.

The impact of neurological impairment and tone on hip joint development

Purpose: The purpose of this study was to define how different force environments by neuromuscular diagnosis (hypertonic versus hypotonic) impact the growth and morphology of the proximal femoral and acetabular regions relative to typically developing children. Methods: Children with cerebral palsy and spinal muscular atrophy were compared with typically developing children aged 6 months to 11 years. Routine pelvic radiographs were evaluated using measures of hip geometry for the proximal femur and acetabulum. The data were analyzed using general linear models to estimate the developmental patterns according to age and diagnosis. Results: One hundred eighty-four children met the inclusion criteria: 58 spastic cerebral palsy Gross Motor Function Classification System I–V (263 hips), 32 spinal muscular atrophy (79 hips)), and 94 typically developing (187 hips) were included with a mean age of 4.9 ± 3.1 years. Using spinal muscular atrophy as a reference, significant differences in proximal femoral development included long thin versus short neck ( p < 0.01) and round versus flat epiphysis ( p = 0.001). A thin neck-wide epiphysis was found in spinal muscular atrophy versus thick neck-small epiphysis for typically developing ( p < 0.05). The ratio of acetabular width to proximal femoral epiphysis width differed significantly for typically developing ( p = 0.001) compared with cerebral palsy and spinal muscular atrophy. There was a negative correlation between migration percentage and acetabular width to epiphysis width in children with cerebral palsy, but no correlation in children with spinal muscular atrophy. Conclusion: Hip geometry was impacted by the force environment experienced during growth. These findings emphasize the crucial roles of gross motor function, muscle tone, and strength differences in determining hip morphology. Level of Evidence: III, retrospective case control.

Cerebral Vasomotor Reactivity to Carbon Dioxide Using the Rebreathe Technique: Assessment of Within-day and Between-day Repeatability.

The cerebral vasodilator response to increased arterial carbon dioxide (CO2) concentration, termed cerebral vasomotor reactivity (CVMR), is used to assess cerebral vascular function. We sought to assess the within-day and between-day repeatability of CVMR to rebreathing-induced hypercapnia. Twelve healthy adults performed a within-day short interval protocol (17±2 minutes between trials), ten performed a within-day long interval protocol (145±16 minutes between trials), and seventeen performed a between-day protocol (5±2 days between visits). Repeatability of the slope of the percent change in middle cerebral artery mean blood velocity (%MCAvmean) and cerebral vascular conductance index (%CVCi), to the change in partial pressure of end-tidal CO2 (PETCO2) between the two trials/days was assessed. Within-day short interval %MCAvmean slope demonstrated fair to excellent repeatability (intraclass correlation, ICC=0.92 [95% confidence interval 0.72-0.98]; p<0.001) while %CVCi slope showed more variability (ICC=0.84 [0.47-0.95]; p=0.002]). Within-day long interval, %MCAvmean (ICC=0.95 [0.80-0.99]) and %CVCi (ICC=0.94 [0.71-0.99]) slopes showed good to excellent and fair to excellent repeatability respectively (p<0.001 for both). For between-day trials, better repeatability was observed for %CVCi (ICC=0.85 [0.57-0.95]; p<0.001) compared to %MCAvmean (ICC=0.76 [0.33-0.91]; p=0.004) slope. These findings indicate repeatable within- and between-day CVMR responses to rebreathe induced hypercapnia. However, a longer interval may be better for within-day repeat trials, particularly for CVCi measures.

T2 MRI visible Perivascular Spaces in Parkinson`s Disease: clinical significance and association with polysomnography measured sleep.

Poor sleep quality might contribute to the risk and progression of neurodegenerative disorders via deficient cerebral waste clearance functions during sleep. In this retrospective cross-sectional study, we explore the link between enlarged perivascular spaces (PVS), a putative marker of sleep-dependent glymphatic clearance, with sleep quality and motor symptoms in Parkinson`s disease (PD) patients. T2-weighted MRI images of 20 patients and 17 healthy control subjects were estimated visually for PVS in the basal ganglia (BG) and centrum semiovale (CSO). The patient group additionally underwent a single-night polysomnography. Readouts included polsyomnographic sleep features and slow-wave activity (SWA), a quantitative EEG marker of sleep depth. Associations between PVS counts, PD symptoms (MDS-UPDRS scores) and sleep parameters were evaluated using correlation and regression analyses. Intra- and inter-rater reproducibility was assessed with weighted Cohen`s kappa coefficient. BG and CSO PVS counts in both patients and controls did not differ significantly between groups. In patients, PVS in both brain regions were negatively associated with SWA (1-2Hz) (BG: r(15)=-0.58, padj=0.015 and CSO: r(15)=-0.6, padj=0.015). Basal ganglia PVS counts were positively associated with motor symptoms of daily living (IRR=1.05, CI [1.01, 1.09], p=0.007, padj=0.026) and antidepressant use (IRR=1.37, CI [1.05, 1.80], p=0.021, padj=0.043) after controlling for age. Centrum Semiovale PVS counts in patients were positively associated with a diagnosis of REM sleep behaviour disorder (IRR=1.39, CI [1.06 , 1.84]), p=0.018, padj=0.11). These results add evidence that sleep deterioration may play a role in impairing glymphatic clearance via altered perivascular function, potentially contributing to disease severity in PD patients.

Quantitative Electroencephalography Monitoring in Type A Aortic Dissection Surgery: A Clinical Case Review and Prospective Applications.

This review explores advanced methods for assessing perioperative cerebral function in Type A aortic dissection (TAAD) patients, with a focus on quantitative electroencephalography (QEEG). It highlights the critical issue of cerebral malperfusion, which is associated with higher mortality and poor prognosis during the perioperative phase in TAAD patients. The review centers on the utilization of QEEG as a pivotal tool for the extensive monitoring of brain function at various stages: preoperatively, intraoperatively, and postoperatively. It elaborates on the foundational principles of QEEG, including the mathematical and computational analysis of electroencephalographic signals, enriched with intuitive graphical representations of cerebral functional states. QEEG is presented as an innovative approach for the real-time, noninvasive, and reliable assessment of cerebral function. The review details the application of QEEG in monitoring conditions such as preoperative cerebral malperfusion, intraoperative deep hypothermic circulatory arrest, and postoperative recovery of cerebral function in patients undergoing TAAD treatment. Although QEEG is still in an exploratory phase for TAAD patients, it has shown efficacy in other domains, suggesting its potential in multimodal brain function monitoring. However, its broader application requires further research and technological advancements.

Neuroimaging Findings From Cerebral Structure and Function in Coronary Artery Disease.

An increasing number of evidence suggests that bidirectional communication between the cardiovascular system and the central nervous system (CNS), known as the heart-brain interaction, is crucial in understanding the impact of coronary artery disease (CAD) on brain health. The multifactorial role of CAD in the brain involves processes such as inflammation, oxidative stress, neuronal activity, neuroendocrine imbalances, and reduced cerebral perfusion, leading to various cerebral abnormalities. The mechanisms underlying the relationship between CAD and brain injury are complex and involve parallel pathways in the CNS, endocrine system, and immune system. Although the exact mechanisms remain partially understood, neuroimaging techniques offer valuable insights into subtle cerebral abnormalities in CAD patients. Neuroimaging techniques, including assessment of neural function, brain metabolism, white matter microstructure, and brain volume, provide information on the evolving nature of CAD-related cerebral abnormalities over time. This review provides an overview of the pathophysiological mechanisms of CAD in the heart-brain interaction and summarizes recent neuroimaging studies utilizing multiparametric techniques to investigate brain abnormalities associated with CAD. The application of advanced neuroimaging, particularly functional, diffusion, and perfusion advanced techniques, offers high resolution, multiparametric capabilities, and high contrast, thereby allowing for the early detection of changes in brain structure and function, facilitating further exploration of the intricate relationship between CAD and brain health. LEVEL OF EVIDENCE: 5 TECHNICAL EFFICACY: Stage 3.

Maternal Diabetes and Neurodevelopmental Outcomes of Infants Born Before 29 Weeks’ Gestation

To compare the neurodevelopmental outcomes of infants born at <29weeks' gestation and exposed to diabetes in pregnancy with those unexposed. This was a retrospective cohort study using the Canadian Neonatal Network and Canadian Neonatal Follow-Up Network databases. Infants born <29weeks' gestation and admitted to a level 3 neonatal intensive care unit from 2009 through 2018 who had neurodevelopmental assessments at 18-24months corrected age were eligible. The 2 primary outcomes were as follows: (1) Neurodevelopmental impairment (NDI) (≥1 of Bayley-III scores < 85 in any domain, cerebral palsy, or vision or hearing impairment); and (2) significant NDI (sNDI) (≥1 of Bayley-III scores < 70 in any domain, cerebral palsy Gross Motor Function Classification System ≥ 3, bilateral blindness, or need for hearing aids or cochlear implants). Secondary outcomes were the individual components of NDI and sNDI. Adjusted odds ratios with 95% CIs were calculated to determine outcomes between groups. Of 13 988 eligible infants, 55% attended neurodevelopmental follow-up assessments. Infants exposed to diabetes had increased odds of NDI compared with those unexposed (aOR 1.09 (95% CI 1.08-1.54); there was no difference in sNDI (aOR 1.07 (95% CI 0.84-1.36). Language and motor delays were more common in those exposed to maternal diabetes. Higher rates of NDI, language, or motor delays were present in infants born at <29weeks' gestation exposed to diabetes in utero. Future research is needed to determine the etiology and clinical significance of these findings.

Advances in retinal imaging biomarkers for the diagnosis of cerebrovascular disease.

The increasing incidence and mortality rates of cerebrovascular disease impose a heavy burden on both patients and society. Retinal imaging techniques, such as fundus photography, optical coherence tomography, and optical coherence tomography angiography, can be used for rapid, non-invasive evaluation of cerebral microcirculation and brain function since the retina and the central nervous system share similar embryonic origin characteristics and physiological features. This article aimed to review retinal imaging biomarkers related to cerebrovascular diseases and their applications in cerebrovascular diseases (stroke, cerebral small vessel disease [CSVD], and vascular cognitive impairment [VCI]), thus providing reference for early diagnosis and prevention of cerebrovascular diseases.

The Regulation of Cerebral Lymphatic Drainage in the Transverse Sinus Region of the Mouse Brain.

Cerebral lymphatic drainage is an important pathway for metabolic waste clearance in the brain, which plays a crucial role in the progression of central nervous system diseases. Recent studies have shown that norepinephrine (NE) is involved in the regulation of cerebral lymphatic drainage function, but the modulation mechanism remains unknown. In this study, we confirmed that NE rapidly reduced glymphatic influx and enhanced meningeal lymphatic clearance. Moreover, the transverse sinus (TS) was the vital region of cerebral lymphatic drainage regulation by NE. Further analysis revealed that NE inhibition could simultaneously enhance glymphatic drainage and dorsal meningeal lymphatic drainage, mainly acting on the TS region. This study demonstrated that the cerebral lymphatic drainage system can be regulated by NE, with the TS region serving as the primary modulating site. The findings provide a potential regulatory target for the amelioration of neurological diseases associated with cerebral lymphatic drainage function.

Targeting leptin/CCL3-CCL4 axes in NAFLD/MAFLD: A novel role for BPF in counteracting thalamic inflammation and white matter degeneration

Non-alcoholic fatty liver disease (NAFLD), redefined as Metabolic Associated Fatty Liver Disease (MAFLD), is characterized by an extensive multi-organ involvement. MAFLD-induced systemic inflammatory status and peripheral metabolic alteration lead to an impairment of cerebral function. Herein, we investigated a panel of leptin-related inflammatory mediators as predictive biomarkers of neuroinflammation and evaluated the possible role of Bergamot Polyphenolic Fraction (BPF) in counteracting this MAFLD-induced inflammatory cascade. Male DIAMOND mice were randomly assigned to fed chow diet and tap water or high fat diet with sugar water. Starting from week 16, mice were further divided and treated with vehicle or BPF (50 mg/kg/day), via gavage, until week 30. Magnetic resonance imaging was performed at the baseline and at week 30. Correlation and regression analyses were performed to discriminate the altered lipid metabolism in the onset of cerebral alterations. Steatohepatitis led to an increase in leptin levels, resulting in a higher expression of proinflammatory mediators. The inflammatory biomarkers involved in leptin/CCL3-CCL4 axes were correlated with the altered thalamus energetic metabolism and the white matter degeneration. BPF administration restored leptin level, improved glucose and lipid metabolism, and reduced chronic low-grade inflammatory mediators, resulting in a prevention of white matter degeneration, alterations of thalamus metabolism and brain atrophy. The highlighted positive effect of BPF, mediated by the downregulation of the inflammatory biomarkers involved in leptin/CCL3-CCL4 axes, affording novel elements to candidate BPF for the development of a therapeutic strategy aimed at counteracting MAFLD-related brain inflammation.

Neuromonitoring in the ICU: noninvasive and invasive modalities for critically ill children and neonates.

Critically ill children are at risk of neurologic dysfunction and acquiring primary and secondary brain injury. Close monitoring of cerebral function is crucial to prevent, detect, and treat these complications. A variety of neuromonitoring modalities are currently used in pediatric and neonatal ICUs. These include noninvasive modalities, such as electroencephalography, transcranial Doppler, and near-infrared spectroscopy, as well as invasive methods including intracranial pressure monitoring, brain tissue oxygen measurement, and cerebral microdialysis. Each modality offers unique insights into neurologic function, cerebral circulation, or metabolism to support individualized neurologic care based on a patient's own physiology. Utilization of these modalities in ICUs results in reduced neurologic injury and mortality and improved neurodevelopmental outcomes. Monitoring of neurologic function can significantly improve care of critically ill children. Additional research is needed to establish normative values in pediatric patients and to standardize the use of these modalities.

Pasienter innlagt ved en medisinsk intensivavdeling etter henging 2010–21

Hanging is one of the most common causes of death among young adults in Norway. Our aim was to study the hospital course and cerebral function on discharge in patients admitted to our Medical Intensive Care Unit after hanging without skeletal injury. Retrospective study based on the medical records of patients admitted to the Medical Intensive Care Unit at Oslo University Hospital (OUS), Ullevål after hanging, from January 2010 to December 2021. Cerebral function on discharge was classified according to Cerebral Performance Category (CPC) from grade 1 (normal cerebral function) to 5 (brain death). 135 patients were admitted to OUS after hanging during the period; 60 of these were admitted to the Medical Intensive Care Unit and were included in this study. There were 35 men and 25 women. Mental illness was documented in the medical records of 43 patients, somatic illness in 24, previous substance abuse in 19, and previous suicide attempts in 19. Upon admission, 34 patients had suffered cardiac arrest, and 39 had a Glasgow Coma Scale (GCS) score of 3. The most common complication was pneumonia (n=42). Twenty-seven patients (45%) died, all with a GCS score of 3 on admission, of which 25 had pre-hospital cardiac arrest. Ten became organ donors. Among the 33 survivors, 28 had a CPC score of 1 and five had a CPC score of 2 on discharge. The median lactate concentration at admission was 8.1 mmol/L among those who died versus 3.8 mmol/L among survivors. Hanging has a high mortality rate. Cardiac arrest, a GCS score of 3, and lactic acidosis were more common among those who died than among the survivors. The organ donation rate was high, and most survivors had a good cerebral function, assessed by CPC score.

Effects of Post-Hospital Arrival Factors on Out-of-Hospital Cardiac Arrest Outcomes During the COVID-19 Pandemic.

The relationship between post-hospital arrival factors and out-of-hospital cardiac arrest (OHCA) outcomes remains unclear. This study assessed the impact of post-hospital arrival factors on OHCA outcomes during the COVID-19 pandemic using a prediction model. In this cohort study, data from the All-Japan Utstein Registry, a nationwide population-based database, between 2015 and 2021 were used. A total of 541,781 patients older than 18 years old who experienced OHCA of cardiac origin were included. The primary exposure was trends in COVID-19 cases. The study compared the predicted proportion of favorable neurologic outcomes 1 month after resuscitation with the actual outcomes. Neurologic outcomes were categorized based on the Cerebral Performance Category score (1, good cerebral function; 2, moderate cerebral function). The prediction model, which had an area under the curve of 0.96, closely matched actual outcomes in 2019. However, a significant discrepancy emerged after the pandemic began in 2020, where outcomes continued to deteriorate as the virus spread, exacerbated by both pre- and post-hospital arrival factors. Post-hospital arrival factors were as important as pre-hospital factors in adversely affecting the prognosis of patients following OHCA during the COVID-19 pandemic. The results suggest that the overall response of the healthcare system needs to be improved during infectious disease outbreaks to improve outcomes.

Exploring the translational impact of type 1 diabetes on cerebral neurovascular function through ECoG-LSCI.

Type 1 diabetes mellitus (T1DM) can result in complications such as retinopathy, nephropathy, and peripheral neuropathy, which can lead to brain dysfunction. In this study, we investigated the effects of T1DM on cerebral neurovascular function in mice. Streptozotocin (STZ) is known to induce T1DM in animals; thus, we used an STZ-induced diabetes model to evaluate the effects of hyperglycemia on brain morphology and neurovascular tissue. Neurovascular coupling is the connection between neuronal activity and cerebral blood flow that maintains brain function. The ECoG-LSCI technique combines electrocorticography (ECoG) and laser speckle contrast imaging (LSCI) to detect cortical spreading depression (CSD) as a marker of neurovascular coupling and measure corresponding neurovascular function. Our results suggested that in the STZ group, hyperglycemia affected excitatory neurotransmission and metabolism, leading to reductions in intercellular signaling, somatosensory evoked potential (SSEP) amplitudes, and CSD transmission rates. Western blot data further revealed that brain-derived neurotrophic factor (BDNF) and neuronal nuclear antigen levels were reduced in the STZ group. Abnormalities in glucose metabolism in the brain and increased phosphorylation of AKT and GSK3 are hypothesized to be responsible for these decreases. Overall, this study highlights the importance of glucose metabolism in normal brain physiology and demonstrates that hyperglycemia disrupts neurovascular coupling and affects cerebral neurovascular function and that the degree of CSD is positively correlated with the extent of brain tissue damage. Further research is essential to gain a complete understanding of the related mechanisms and the implications of these findings.

Molecular and Functional Alterations in the Cerebral Microvasculature in an Optimized Mouse Model of Sepsis-Associated Cognitive Dysfunction.

Systemic inflammation has been implicated in the development and progression of neurodegenerative conditions such as cognitive impairment and dementia. Recent clinical studies indicate an association between sepsis, endothelial dysfunction, and cognitive decline. However, the investigations of the role and therapeutic potential of the cerebral microvasculature in sepsis-induced cognitive dysfunction have been limited by the lack of standardized experimental models for evaluating the alterations in the cerebral microvasculature and cognition induced by the systemic inflammatory response. Herein, we validated a mouse model of endotoxemia that recapitulates key pathophysiology related to sepsis-induced cognitive dysfunction, including the induction of an acute systemic hyperinflammatory response, blood-brain barrier (BBB) leakage, neurovascular inflammation, and memory impairment after recovery from the systemic inflammation. In the acute phase, we identified novel molecular (e.g., upregulation of plasmalemma vesicle-associated protein, PLVAP, a driver of endothelial permeability, and the procoagulant plasminogen activator inhibitor-1, PAI-1) and functional perturbations (i.e., albumin and small-molecule BBB leakage) in the cerebral microvasculature along with neuroinflammation. Remarkably, small-molecule BBB permeability, elevated levels of PAI-1, intra-/perivascular fibrin/fibrinogen deposition, and microglial activation persisted 1 month after recovery from sepsis. We also highlight molecular neuronal alterations of potential clinical relevance following systemic inflammation including changes in neurofilament phosphorylation and decreases in postsynaptic density protein 95 and brain-derived neurotrophic factor, suggesting diffuse axonal injury, synapse degeneration, and impaired neurotrophism. Our study serves as a standardized mouse model to support future mechanistic studies of sepsis-associated cognitive dysfunction and to identify novel endothelial therapeutic targets for this devastating condition.

Inhibition of Soluble Epoxide Hydrolase Ameliorates Cerebral Blood Flow Autoregulation and Cognition in Alzheimer's Disease and Diabetes-Related Dementia Rat Models.

Alzheimer's Disease and Alzheimer's Disease-related dementias (AD/ADRD) pose major global healthcare challenges, with diabetes mellitus (DM) being a key risk factor. Both AD and DM-related ADRD are characterized by reduced cerebral blood flow, although the exact mechanisms remain unclear. We previously identified compromised cerebral hemodynamics as early signs in TgF344-AD and type 2 DM-ADRD (T2DN) rat models. Genome-wide studies have linked AD/ADRD to SNPs in soluble epoxide hydrolase (sEH). This study explored the effects of sEH inhibition with TPPU on cerebral vascular function and cognition in AD and DM-ADRD models. Chronic TPPU treatment improved cognition in both AD and DM-ADRD rats without affecting body weight. In DM-ADRD rats, TPPU reduced plasma glucose and HbA1C levels. Transcriptomic analysis of primary cerebral vascular smooth muscle cells from AD rats treated with TPPU revealed enhanced pathways related to cell contraction, alongside decreased oxidative stress and inflammation. Both AD and DM-ADRD rats exhibited impaired myogenic responses and autoregulation in the cerebral circulation, which were normalized with chronic sEH inhibition. Additionally, TPPU improved acetylcholine-induced vasodilation in the middle cerebral arteries (MCA) of DM-ADRD rats. Acute TPPU administration unexpectedly caused vasoconstriction in the MCA of DM-ADRD rats at lower doses. In contrast, higher doses or longer durations were required to induce effective vasodilation at physiological perfusion pressure in both control and ADRD rats. Additionally, TPPU decreased reactive oxygen species production in cerebral vessels of AD and DM-ADRD rats. These findings provide novel evidence that chronic sEH inhibition can reverse cerebrovascular dysfunction and cognitive impairments in AD/ADRD, offering a promising avenue for therapeutic development.

Continuous Electroencephalographic Monitoring in Adult ICU Challenges and Potential Solutions: A Scoping Review

Background: Continuous electroencephalographic (cEEG) monitoring is continuous monitoring of brain activity that is often used in the intensive care unit (ICU). Recently, the usage of cEEG has grown in many institutions as it detects non-convulsive seizures better than routine EEG (rEEG). However, due to the aggressive environment of ICU, the application and the prolonged recording is challenging. The objectives of this scoping review are to evaluate the common challenges faced during cEEG in adult ICU and proper solutions for optimal implementation. Methods: A scoping review was conducted using Arksey and O’Malley framework. The included articles contain “continuous EEG in ICU settings” in their titles, written in English, and published between 2010 and 2022. That was by searching the databases: PubMed, Google Scholar, and Summon. Results: 14 articles were included as they meet the criteria of this review. (28.57 %) of the included studies mentioned the challenges regarding staff, (42.85 %) addressed the challenges of electrode application and the alternative techniques in ICU, and (42.85%) discussed the difficulties in interpretation and duration of the recording. Conclusion: Continuous EEG is increasingly recognized as valuable mean of monitoring cerebral function, but it is faced with numerous challenges: the difficult environment of ICU and the type of critical patient admitted requiring the optimal electrode application and maintenance, minimizing artifacts and adequate duration of recording to detect abnormalities, and sufficiently trained personnel including ICU staff, technologist and neurophysiologist to provide the optimal patient care as it is the main goal.

In-hospital mortality and its associated factors among hospitalized stroke patients at public hospitals of Eastern Ethiopia

BackgroundStroke is rapidly developing clinical signs of focal/ global disturbance of cerebral function, with symptoms lasting more than 24 h and leading to death. Data showed that stroke deaths in Ethiopia reached nearly seven percent of total deaths. Despite this report, there is a paucity of investigations about the problem.ObjectiveTo determine in-hospital mortality and its associated factors among hospitalized stroke patients in Hiwot Fana Comprehensive Specialized University Hospital and Jugal General Hospital, eastern Ethiopia from September 2016–August 2022 G.C.MethodsA retrospective cohort study was conducted among hospitalized stroke patients. A sample size of 395 medical records was selected from a total of 564 stroke patients by a simple random sampling technique. The data was analyzed by SPSS version 26 using bivariable and multivariable cox-regression models. A p-value of 0.05 and less at a 95% confidence interval was used to establish a statistically significant association.ResultsOf the total, 109 (27.6%) died in the hospital while 57.2% and 15.2% of them were discharged with improvement and against medical advice, respectively. Age greater than 65 (AHR = 4.71, 95% CI = 1.11–19.96), creatinine level > 1.2 mg/dl (AHR = 1.54, 95% CI = 1.0-2.39), and co-morbidity with atrial fibrillation (AHR = 1.48, 95% CI = 1.0-2.21) were significantly associated with in-hospital mortality.ConclusionIn-hospital mortality was found in more than a quarter of stroke patients. Mortality was more likely increased among the patients with age > 65, serum creatinine level > 1.2 mg/dl, and atrial fibrillation. Hence, these high-risk patients need to be monitored.

Vascular Function and Ion Channels in Alzheimer's Disease.

This review paper explores the critical role of vascular ion channels in the regulation of cerebral artery function and examines the impact of Alzheimer's disease (AD) on these processes. Vascular ion channels are fundamental in controlling vascular tone, blood flow, and endothelial function in cerebral arteries. Dysfunction of these channels can lead to impaired cerebral autoregulation, contributing to cerebrovascular pathologies. AD, characterized by the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles, has been increasingly linked to vascular abnormalities, including altered vascular ion channel activity. Here, we briefly review the role of vascular ion channels in cerebral blood flow control and neurovascular coupling. We then examine the vascular defects in AD, the current understanding of how AD pathology affects vascular ion channel function, and how these changes may lead to compromised cerebral blood flow and neurodegenerative processes. Finally, we provide future perspectives and conclusions. Understanding this topic is important as ion channels may be potential therapeutic targets for improving cerebrovascular health and mitigating AD progression.

Ginsenoside Rh2 Alleviate Sepsis-related Encephalopathy via Up-regulating Nrf2/HO-1 Pathway and Apoptosis Inhibition.

Sepsis patients are highly prone to sepsis-associated encephalopathy (SAE) complications, resulting in a high mortality rate. Recently, there has been no specific treatment for long-term improvement of cerebral function. Ginsenoside Rh2 is a form of steroidal saponins isolated from plant ginseng and has been shown to possess anti-inflammatory as well as neuroprotective characteristics; yet, the effect of ginsenoside Rh2 on SAE treatment is obscure. Accordingly, we proposed to investigate the effect of ginsenoside Rh2 in alleviating SAE damage. We established and utilized the SAE mouse model to determine the effect of Rh2 treatment on alleviating SAE. We determined the expression levels of Heme oxygenase-1(HO-1) and Nuclear factor erythroid 2-related factor 2 (Nrf2) as well as measured neural apoptosis by flow cytometry. Also, we quantified the levels of caspase-3, malondialdehyde (MDA), GSH-Px superoxide dismutase (SOD) and evaluated the animals' neural reflex function. First, used Rh2 to treat microglia BV2 and mouse neuron MN-c whether LPS exist or not, and then measured expression level of Iba-1, apoptotic rate, and ROS content applying flow cytometry. Also, we quantified the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). In comparison with the Sham group, the SAE model exhibited an elevated MDA content, caspase-3 activity, and cell apoptosis. On the other hand, the GSH-Px activity and SOD level were decreased along with a decreased neural reflex score. Our investigation concluded that Rh2 treatment significantly alleviated SAE damage and inhibited LPS-induced response via up-regulation of the Nrf2/HO-1 pathway to promote anti-oxidative stress capacity and inhibit neural cell apoptosis.