The Greater Omentum: Multifaceted Interactions in Neurological Recovery and Disease Progression.

The greater omentum, a unique anatomical structure composed of adipocytes, loose connective tissue, and a dense vascular network. Plays a pivotal role beyond its traditional understanding. It houses specialized immunological units known as 'Milky spots,' making it a key player in immune response. Moreover, the omentum's capacity to enhance tissue perfusion, absorb edema fluid, boost acetylcholine synthesis, and foster neuron repair have rendered it a topic of interest in the context of various diseases, especially neurological disorders. This review provides a comprehensive overview of the intricate anatomy and histology of the greater omentum, casting light on its multifaceted functions and its associations with a spectrum of diseases. With a specific focus on neurological ailments, we delineate the intricate relationship that the omentum shares with other pathologies like stroke and we underly its contribution to serving as a therapeutic agent in neurological disorders. By deciphering the underlying mechanisms and emphasizing areas that demand further investigation. This review aims to spark renewed interest and pave the way for comprehensive studies exploring the greater omentum's potential in neurology and broader medicine overall. Given these diverse interactions that yet remain elusive, we must investigate and understand the nuanced relationship between the greater omentum and pathologies, especially its role in stroke's pathophysiology and therapeutic interventions so as to enhance patient care.

A narrative review of retinal vascular parameters and the applications (Part II): Diagnosis in stroke.

The retina, as an external extension of the diencephalon, can be directly, noninvasively observed by ocular fundus photography. Therefore, it offers a convenient and feasible mode to study nervous system diseases. Caliber, tortuosity, and fractal dimension, as three commonly used retinal vascular parameters, are not only the reflection of structural changes in the retinal microcirculation but also capture the branching pattern or density changes of the retinal microvascular network. Therefore, it contributes to better reflecting the subclinical pathological changes (e.g., lacunar stroke and small cerebral vascular disease) and predicting the risk of incident stroke and recurrent stroke.

A narrative review of retinal vascular parameters and the applications (Part I): Measuring methods.

The retina is often used to evaluate the vascular health status of eyes and the whole body directly and noninvasively in vivo. Retinal vascular parameters included caliber, tortuosity and fractal dimension. These variables represent the density or geometric characteristics of the vascular network apart from reflecting structural changes in the retinal vessel system. Currently, these parameters are often used as indicators of retinal disease, cardiovascular and cerebrovascular disease. Advanced digital fundus photography apparatus and computer-assisted analysis techniques combined with artificial intelligence, make the quantitative calculation of these parameters easier, objective, and labor-saving.

Induced Inflammatory and Oxidative Markers in Cerebral Microvasculature by Mentally Depressive Stress.

Background: Cerebrovascular disease (CVD) is recognized as the leading cause of permanent disability worldwide. Depressive disorders are associated with increased incidence of CVD. The goal of this study was to establish a chronic restraint stress (CRS) model for mice and examine the effect of stress on cerebrovascular inflammation and oxidative stress responses. Methods: A total of forty 6-week-old male C57BL/6J mice were randomly divided into the CRS and control groups. In the CRS group (n = 20), mice were placed in a well-ventilated Plexiglas tube for 6 hours per day for 28 consecutive days. On day 29, open field tests (OFT) and sucrose preference tests (SPT) were performed to assess depressive-like behaviors for the two groups (n = 10/group). Macrophage infiltration into the brain tissue upon stress was analyzed by measuring expression of macrophage marker (CD68) with immunofluorescence in both the CRS and control groups (n = 10/group). Cerebral microvasculature was isolated from the CRS and controls (n = 10/group). mRNA and protein expressions of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1), and macrophage chemoattractant protein-1 (MCP-1) in the brain vessels were measured by real-time PCR and Western blot (n = 10/group). Reactive oxygen species (ROS), hydrogen peroxide (H2O2), and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) activities were quantified by ELISA to study the oxidative profile of the brain vessels (n = 10/group). Additionally, mRNA and protein expressions of NOX subunits (gp91phox, p47phox, p67phox, and p22phox) in the cerebrovascular endothelium were analyzed by real-time PCR and Western blot (n = 10/group). Results: CRS decreased the total distances (p < 0.05) and the time spent in the center zone in OFT (p < 0.001) and sucrose preference test ratio in SPT (p < 0.01). Positive ratio of CD68+ was increased with CRS in the entire region of the brain (p < 0.001), reflecting increased macrophage infiltration. CRS increased the expression of inflammatory factors and oxidative stress in the cerebral microvasculature, including TNF-α (p < 0.001), IL-1ß (p < 0.05), IL-6 (p < 0.05), VCAM-1 (p < 0.01), MCP-1 (p < 0.01), ROS (p < 0.001), and H2O2 (p < 0.001). NADPH oxidase (NOX) was activated by CRS (p < 0.01), and mRNA and protein expressions of NOX subunits (gp91phox, p47phox, p67phox, and p22phox) in brain microvasculature were found to be increased. Conclusions: To our knowledge, this is the first study to demonstrate that CRS induces depressive stress and causes inflammatory and oxidative stress responses in the brain microvasculature.

Clinical Characteristics and Outcomes of Multiple Sclerosis and Neuromyelitis Optica Spectrum Disorder With Brainstem Lesions as Heralding Prodrome.

Objective: The present study sought to differentiate multiple sclerosis and neuromyelitis optica spectrum disorder patients at their first attack by describing and distinguishing their clinical features, radiographic characteristics, and immunologic characteristics of serum and cerebrospinal fluid. Methods: We retrospectively studied 58 patients with multiple sclerosis (MS) and 52 patients with neuromyelitis optica spectrum disorder (NMOSD) by referencing brainstem lesions as the prodromal events. Their demographics and presentation at the time of the first attack was evaluated including their gender, age, clinical features of the first attack, the expanded disability status scale (EDSS), brainstem lesion(s) by head MRI, and immunological indices of serum and cerebrospinal fluid. Results: The NMOSD group had more female patients (4.8 vs. 1.9, p < 0.05), and was older than the MS group (37.81 ± 16.60 vs. 27.57 ± 11.17, p <0.001). NMOSD patients also had a significantly higher association with autoimmune diseases or positive autoimmune antibodies (p < 0.01). There was no significant difference in the EDSS scores between the two groups (p = 0.420). Central hiccups, vomiting, and pyramidal tract signs were more common in the NMOSD group than the MS group (p < 0.001, p < 0.001, p < 0.01), while eye movement abnormalities were more common with MS (p < 0.01). There were no significant differences in other clinical manifestations such as vertigo, diplopia, limb weakness, numbness, and eating difficulty. MS patients were more likely to have midbrain and pons imaging lesions (p < 0.001, p < 0.001), while NMOSD patients had more lesions in the medulla oblongata (p < 0.001). The lesions in the MS group were mostly located in the periphery, while those in the NMOSD group were centrally located (p < 0.001, p < 0.001). Patchy lesions were more common in MS patients (p < 0.001), while large lesions were more common in the NMOSD group (p < 0.001). Finally, serum AQP4 Ab was found only in the NMOSD group (p < 0.001). Conclusion: Patients with MS and NMOSD have differentiating clinical manifestations at the time of their first brainstem lesions which include central hiccups, vomiting, pyramidal tract signs, and abnormal eye movements. Additionally, distinct imaging manifestations such as lesion location(s) and morphology may also aid in the development of pathognomonic criteria leading to timely initial diagnosis of MS and NMOSD.

Factors influencing the outcome of cardiogenic cerebral embolism: a literature review.

OBJECTIVE: The onset of cardiogenic cerebral embolism is sudden, dangerous, and often has high morbidity and mortality. Improving understanding of factors contributing to outcomes of cardiogenic cerebral embolism will improve prognostic and therapeutic capabilities. METHODS: Through PubMed and Google Scholar, this paper examined and analyzed the factors implicated in the outcome of patients with cardiogenic cerebral embolism using the key terms 'cardiogenic cerebral embolism', 'atrial fibrillation', 'stroke related diseases', 'collateral circulation', 'emboli profile', 'epigenetic' up to 28 February 2021. Full texts of the retrieved articles were accessed. In general, in these literatures, National Institute Health of Stroke Scale (NIHSS) score ≥ 17, modified Rankin Scale (mRS) score ≥ 2, stroke recurrence, death caused by stroke are regarded as the criteria of poor prognosis. As long as one of these conditions occurs, it is judged as poor prognosis. RESULTS: Factors influencing patient outcomes including patient outcome include severity of neurological impairment, types and severity of combined heart diseases, establishment of cerebral collateral circulation, treatments, components of emboli causing cardiogenic cerebral embolism, existence and control of other system complications, distribution and expression of inflammatory immune cells and molecules in the course of cardiogenic cerebral embolism, and epigenetic changes related to disease prognosis. CONCLUSION: Regarding to prevention and treatment of cardiogenic cerebral embolism, the related factors, such as clinical setting, emboli pathological profile, and epigenetic changes should be emphasized so that outcomes and recurrence of cardiogenic cerebral embolism can be improvised.

Neuroplastic Effect of Exercise Through Astrocytes Activation and Cellular Crosstalk.

Physical exercise is an effective therapy for neurorehabilitation. Exercise has been shown to induce remodeling and proliferation of astrocyte. Astrocytes potentially affect the recruitment and function of neurons; they could intensify responses of neurons and bring more neurons for the process of neuroplasticity. Interactions between astrocytes, microglia and neurons modulate neuroplasticity and, subsequently, neural circuit function. These cellular interactions promote the number and function of synapses, neurogenesis, and cerebrovascular remodeling. However, the roles and crosstalk of astrocytes with neurons and microglia and any subsequent neuroplastic effects have not been studied extensively in exercise-induced settings. This article discusses the impact of physical exercise on astrocyte proliferation and highlights the interplay between astrocytes, microglia and neurons. The crosstalk between these cells may enhance neuroplasticity, leading to the neuroplastic effects of exercise.

Prophylactic Low-Molecular-Weight Heparin Versus Unfractionated Heparin in Spine Surgery (PLUSS): A Pilot Matched Cohort Study.

BACKGROUND: Despite a proven superior efficacy of prophylactic low-molecular-weight heparin (LMWH) over unfractionated heparin (UFH) in the majority of surgical specialties, chemoprophylactic techniques after spine surgery have not been established because of the fear of epidural hematomas with LMWH. OBJECTIVE: To determine the efficacy of LMWH vs UFH in the prevention of venous thromboembolism (VTE) events, balanced against the risk of epidural hematoma. METHODS: This is the first matched cohort design that directly compares prophylactic LMWH to UFH after spine surgery for degenerative/deformity pathologies at a tertiary academic center. Prospectively collected patients receiving prophylactic LMWH and a historical cohort of patients receiving prophylactic UFH (prior to 2017) were matched in 1:1 ratio based on age ±5 yr, American Society of Anesthesiologists classification, location in the spinal column, and type of surgery. RESULTS: Of 562 patients, VTE events equaled 1.4% (n = 8): 1.4% (n = 4) with LMWH was exactly equal to 1.4% (n = 4) with UFH. Epidural hematomas reached 0.8% (n = 5): 1.4% (n = 4) with UFH vs 0.3% (n = 1) with the LMWH (P = .178). Utilizing adjusted odds ratio (ORadj), the type of chemoprophylaxis after spine surgery failed to predict VTE events. Similarly, the chemoprophylactic technique failed to predict epidural hematoma in the multivariable regression analysis, although UFH trended toward a higher complication rate (ORadj = 3.15 [0.48-20.35], P = .227). CONCLUSION: Chemoprophylactic patterns failed to predict VTE. Although no differences in epidural hematoma rates were detected, our analysis does highlight a trend toward a safer profile with LMWH vs UFH. LMWH may be a safe alternative to UFH in spine surgery.

Geographic landscape of foreign medical graduates in US neurosurgery training programs from 2007 to 2017.

OBJECTIVE: Although foreign medical graduates (FMGs) have been essential to the US physician workforce, the increasing competitiveness has made it progressively challenging for FMGs to match in US neurosurgery programs. We describe geographic origins and characteristics associated with successful match into US neurosurgery training programs. METHODS: Retrospective review of AANS membership data (2007-2017). Scopus was used to collect bibliometrics. RESULTS: From 2009 neurosurgical residents, 165 (8.2%) were FMGs. Most were male (n = 148; 89.6%) with a median age of 34.0 years. Top six feeder countries (TFC) included India (13.9%; n = 23), Lebanon and Pakistan (9.1%; n = 15), Caribbean Region (7.2%; n = 12), Mexico (6.67%; n = 11), and Greece (3.6%; n = 6). Compared to FMGs from non-top feeder countries (NTFC), TFC FMGs had higher H-indices (2 vs 4, p = 0.049), greater number of publications (2 vs 5, p = 0.04), were more likely to have an MBBS/MBBCh (n = 38 vs n = 17, p = 0.03), and had twice as many candidates from major feeder medical schools that successfully matched into a US neurosurgery program (n = 43 vs NTFC = 20, p < 0.001). NTFC FMGs were almost 3-times more likely to match at an affiliated neurosurgery program (8 vs TFC = 3, p = 0.03), while TFC FMGs were 1.5-times more likely to match at an NIH Top-40 program (33 vs NTFC = 21, p = 0.03). CONCLUSIONS: TFC graduates have higher bibliometrics, frequently come from major feeder schools, and have greater match success at a broader selection of programs and NIH top-40 programs. Future studies characterizing FMG country and medical school origins may enable foreign students to geographically target institutions of interest and could allow US programs to better evaluate foreign training environments.

Expandable Cage Technology-Transforaminal, Anterior, and Lateral Lumbar Interbody Fusion.

This review of the literature will focus on the indications, surgical techniques, and outcomes for expandable transforaminal lumbar interbody fusion (TLIF), anterior lumbar interbody fusion (ALIF), and lateral lumbar interbody fusion (LLIF) operations. The expandable TLIF cage has become a workhorse for common degenerative pathology, whereas expandable ALIF cages carry the promise of greater lordotic correction while evading the diseased posterior elements. Expandable LLIF cages call upon minimally invasive techniques for a retroperitoneal, transpsoas approach to the disc space, obviating the need for an access surgeon and decreasing risk of injury to the critical neurovascular structures. Nuances between expandable and static cages for all 3 TLIF, ALIF, and LLIF operations are discussed in this review.

Impact of the COVID-19 Pandemic on Acute Stroke Care, Time Metrics, Outcomes, and Racial Disparities in a Southeast Michigan Health System.

BACKGROUND: COVID-19 has impacted acute stroke care with several reports showing worldwide drops in stroke caseload during the pandemic. We studied the impact of COVID-19 on acute stroke care in our health system serving Southeast Michigan as we rolled out a policy to limit admissions and transfers. METHODS: in this retrospective study conducted at two stroke centers, we included consecutive patients presenting to the ED for whom a stroke alert was activated during the period extending from 3/20/20 to 5/20/20 and a similar period in 2019. We compared demographics, time metrics, and discharge outcomes between the two groups. RESULTS: of 385 patients presented to the ED during the two time periods, 58% were African American. There was a significant decrease in the number of stroke patients presenting to the ED and admitted to the hospital between the two periods (p <0.001). In 2020, patients had higher presenting NIHSS (median: 2 vs 5, p = 0.012), discharge NIHSS (median: 2 vs 3, p = 0.004), and longer times from LKW to ED arrival (4.8 vs 9.4 h, p = 0.031) and stroke team activation (median: 10 vs 15 min, p = 0.006). In 2020, stroke mimics rates were lower among African Americans. There were fewer hospitalizations (p <0.001), and transfers from outside facilities (p = 0.015). CONCLUSION: a trend toward faster stroke care in the ED was observed during the pandemic along with dramatically reduced numbers of ED visits, hospitalizations and stroke mimics. Delayed ED presentations and higher stroke severity characterized the African American population, highlighting deepening of racial disparities during the pandemic.

Muscle BDNF improves synaptic and contractile muscle strength in Kennedy's disease mice in a muscle-type specific manner.

KEY POINTS: Muscle-derived neurotrophic factors may offer therapeutic promise for treating neuromuscular diseases. We report that a muscle-derived neurotrophic factor, BDNF, rescues synaptic and muscle function in a muscle-type specific manner in mice modelling Kennedy's disease (KD). We also find that BDNF rescues select molecular mechanisms in slow and fast muscle that may underlie the improved cellular function. We also report for the first time that expression of BDNF, but not other members of the neurotrophin family, is perturbed in muscle from patients with KD. Given that muscle BDNF had divergent therapeutic effects that depended on muscle type, a combination of neurotrophic factors may optimally rescue neuromuscular function via effects on both pre- and postsynaptic function, in the face of disease. ABSTRACT: Deficits in muscle brain-derived neurotrophic factor (BDNF) correlate with neuromuscular deficits in mouse models of Kennedy's disease (KD), suggesting that restoring muscle BDNF might restore function. To test this possibility, transgenic mice expressing human BDNF in skeletal muscle were crossed with '97Q' KD mice. We found that muscle BDNF slowed disease, doubling the time between symptom onset and endstage. BDNF also improved expression of genes in muscle known to play key roles in neuromuscular function, including counteracting the expression of neonatal isoforms induced by disease. Intriguingly, BDNF's ameliorative effects differed between muscle types: synaptic strength was rescued only in slow-twitch muscle, while contractile strength was improved only in fast-twitch muscle. In sum, muscle BDNF slows disease progression, rescuing select cellular and molecular mechanisms that depend on fibre type. Muscle BDNF expression was also affected in KD patients, reinforcing its translational and therapeutic potential for treating this disorder.