Degree Of Neurological Deficit Research Articles

Correlation Analysis between Platelet Aggregation and Neurological Outcomes in Ischemic Stroke Patients

Ischemic stroke is a condition triggered by cerebral perfusion disorders with the risk factor of blood clotting disorders that can cause neurological deficits through a complex pathophysiological process of thrombus formation. The role of platelet aggregation as a blood clotting parameter has the potential to be used as a marker for the level of neurological deficit in patients with ischemic stroke in conjunction with the National Institutes of Health Stroke Scale (NIHSS). The study aimed to observe the correlation between platelet aggregation and the degree of neurological deficit calculated using NIHSS. The study utilized a cross-sectional design with 51 research subjects diagnosed with ischemic stroke based on CT Scan results, followed by platelet aggregation testing. Patients with a diagnosis of hemorrhagic stroke and cardiogenic ischemic stroke were excluded from this study. This study found variations in platelet aggregation among groups with different degrees of stroke severity. However, it was not statistically significant (p=0.427). Correlation analysis showed a mild positive correlation between platelet aggregation and the degree of neurological deficit (r=0.157), although it was not statistically significant (p=0.270). There are variations in platelet aggregation in assessing neurological deficits using NIHSS. There is a positive correlation between the percentage of platelet aggregation and the level of neurological deficit in patients with ischemic stroke.

MiRNA506 Activates Sphk1 Binding with Sirt1 to Inhibit Brain Injury After Intracerebral Hemorrhage via PI3K/AKT Signaling Pathway.

Intracerebral hemorrhage (ICH) is an acute neurological disorder characterized by high mortality and disability rates. Previous studies have shown that 75% of patients who survive ICH experience varying degrees of neurological deficits. Sphk1 has been implicated in a multitude of phylogenetic processes, including innate immunity and cell proliferation. An in vivo rat model of ICH and an in vitro model of neuronal oxyhemoglobin (OxyHb) were constructed. The expression level of Sphk1 was assessed using western blotting and immunofluorescence, whereas cell death following ICH was evaluated using fluoro-Jade B and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Immunofluorescence facilitated the examination of microglial phenotypic alterations, while enzyme-linked immunosorbent assays were used to determine the concentrations of inflammatory markers. Behavioral assays were employed to assess the overall behavioral modifications of animals. Neuronal Sphk1/Sirt1 protein levels gradually increased following the induction of ICH. Elevated Sphk1 expression resulted in increased levels of anti-inflammatory microglia and reduced levels of pro-inflammatory factors. In contrast, suppression of Sphk1 expression resulted in an increased number of dead cells, thereby exacerbating neurological deficits. In vitro findings indicated that the levels of phosphorylated PI3K and AKT proteins increased in conjunction with Sphk1 expression. This study established that after ICH, Sphk1 interacts with Sirt1 to mitigate neuroinflammation, cell death, oxidative stress, and brain edema via the PI3K/AKT signaling pathway. Augmenting expression of Sphk1 significantly can ameliorate neurological impairments induced by ICH, offering novel targets and perspectives for therapeutic interventions in ICH treatment.

Are Sirtuins 1 and 2 Relevant Players in Relapsing-Remitting Multiple Sclerosis?

A total of 115 patients with RRMS (78 women, 37 men, mean age 43 ± 9.9) and 39 healthy controls were included in the study. SIRT1 and SIRT2 were detected in the serum using the enzyme-linked immunoassay (ELISA) method. In the RRMS group, relationships were investigated between the SIRT 1 and 2 levels and the demographic data, MS-related clinical variables, and the results of tests evaluating fatigue, sleep problems, cognitive performance, autonomic dysfunction, and depression. The levels of SIRT1 and SIRT2 in RRMS patients were significantly lower than in the controls (11.14 vs. 14. 23, p = 0.04; 8.62 vs. 14.2, p < 0.01). In the RRMS group, the level of both SIRTs was higher in men than in women (15.7 vs. 9.0; 11.3 vs. 7.3, p = 0.002) and showed a significant correlation with the degree of disability (R = -0.25, p = 0.018). No other relationships were found between SIRT levels and the analyzed data. The serum levels of SIRT1 and 2 were decreased in the RRMS patients (especially in the female ones) and correlated with the degree of neurological deficit. The role of SIRTs as biomarkers of disease activity or mediators relevant for "invisible disability" in MS warrants further investigation.

Intramedullary pediatric low-grade glioma of the spine.

Pediatric intramedullary spinal cord low-grade gliomas (pLGGs) are rare diagnoses among central nervous system (CNS) tumors in the pediatric population. The classic presentation of the patients includes some degree of neurologic deficit, although many times the symptoms are vague which leads to delayed diagnosis. The first step in the diagnosis includes special parameters in spinal imaging, particularly magnetic resonance imaging (MRI), and surgical resection remains the cornerstone for both diagnosis and treatment. Yet, recent years advancement in molecular and genetic understanding of CNS tumors allows for better adjustment of the treatment and follow-up regimens. Based on postoperative status, adjuvant therapy may provide additional therapeutic advantage for some types of tumors. Ultimately, patients have a very promising prognosis when treated appropriately in most of the cases of pediatric spinal cord LGG with continued advances arising. This manuscript summarizes the most contemporary evidence regarding clinical and treatment features of intramedullary pLGGs.

Positional neuropathies in surgical oncology

Aim. To evaluate the frequency and clinical characteristics of positional neuropathies in patients with cancer who underwent surgery.Materials and methods. A retrospective study of medical records of patients undergoing surgical treatment in 2023, who showed signs of secondary neuropathy of the upper and/or lower extremities in the postoperative period. The main analyzed parameter was the frequency of postoperative neuropathies among patients who underwent surgery; additional parameters were the degree of neurological deficit according to the neurological deficit assessment scale, the median regression of neurological deficit. Results. The study included 29 patients who underwent surgery at the National Medical Research Center of Oncology named after N. N. Blokhin in 2023, who developed a clinical picture of positional neuropathy in the postoperative period. The overall incidence of positional neuropathies was 0.28 %. Neuropathies of the brachial plexus were predominant (96 %). A severe degree of neurological deficit was noted in 35 %, medium – in 45 %, mild – in 20 % of patients. 27.5 % of patients continued to have varying degrees of neurological deficit over a 10-month period.Conclusion. Positional neuropathies can persist for a long time; it is necessary to develop methods for their prevention.

Can We Rely on Prophylactic Two-Level Vertebral Cement Augmentation in Long-Segment Adult Spinal Deformity Surgery to Reduce the Incidence of Proximal Junctional Complications?

Background and Objectives: Proximal junctional kyphosis (PJK) and failure (PJF), the most prevalent complications following long-segment thoracolumbar fusions for adult spinal deformity (ASD), remain lacking in defined preventive measures. We studied whether one of the previously reported strategies with successful results-a prophylactic augmentation of the uppermost instrumented vertebra (UIV) and supra-adjacent vertebra to the UIV (UIV + 1) with polymethylmethacrylate (PMMA)-could also serve as a preventive measure of PJK/PJF in minimally invasive surgery (MIS). Materials and Methods: The study included 29 ASD patients who underwent a combination of minimally invasive lateral lumbar interbody fusion (MIS-LLIF) at L1-2 through L4-5, all-pedicle-screw instrumentation from the lower thoracic spine to the sacrum, S2-alar-iliac fixation, and two-level balloon-assisted PMMA vertebroplasty at the UIV and UIV + 1. Results: With a minimum 3-year follow-up, non-PJK/PJF group accounted for fifteen patients (52%), PJK for eight patients (28%), and PJF requiring surgical revision for six patients (21%). We had a total of seven patients with proximal junctional fracture, even though no patients showed implant/bone interface failure with screw pullout, probably through the effect of PMMA. In contrast to the PJK cohort, six PJF patients all had varying degrees of neurologic deficits from modified Frankel grade C to D3, which recovered to grades D3 and to grade D2 in three patients each, after a revision operation of proximal extension of instrumented fusion with or without neural decompression. None of the possible demographic and radiologic risk factors showed statistical differences between the non-PJK/PJF, PJK, and PJF groups. Conclusions: Compared with the traditional open surgical approach used in the previous studies with a positive result for the prophylactic two-level cement augmentation, the MIS procedures with substantial benefits to patients in terms of less access-related morbidity and less blood loss also provide a greater segmental stability, which, however, may have a negative effect on the development of PJK/PJF.

Maresin1 alleviates neuroinflammation by inhibiting caspase-3/ GSDME-mediated pyroptosis in mice cerebral ischemia-reperfusion model

ObjectiveTo explore the mechanism of Maresin1 in reducing cerebral ischemia-reperfusion injury. Materials and methodsMale C57BL/6 mice were randomly divided (n = 5 in each group), and focal middle cerebral artery occlusion (MCAO) model was used to simulate cerebral ischemia/reperfusion injury. TTC and the Longa score were used to detect the degree of neurological deficits. Western blot was used to detect the expression levels of GSDME, GSDME-N, caspase-3 and cleaved caspase-3 in cerebral ischemic penumbra tissue, and immunofluorescence was used to detect the expression levels of GSDME-N. The mRNA expression levels of GSDME and pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) were detected by RT-PCR. ResultsCompared with sham group, GSDME mRNA levels in MCAO group were significantly increased at 12 h and 24 h after reperfusion, and GSDME and GSDME-N significantly increased at 6–48 h after reperfusion. Compared with sham group, the percentage of infarct size, the Longa score, the mRNA expression levels of IL-1β, IL-6 and TNF-α, and GSDME, GSDME-N, caspase-3 and cleaved caspase-3 in MCAO group was significantly increased. Then, the percentage of infarct size and the Longa score significantly decreased after MaR1 administration, the mRNA expression levels of IL-1β and IL-6 downregulated, and GSDME, GSDME-N, caspase-3 and cleaved caspase-3 were also reduced. After administration of Z-DEVD-FMK(ZDF), the expression of caspase-3, cleaved caspase-3 and GSDME-N was decreased, which in MCAO+MaR1+ZDF group was not statistically significant compared with MCAO+ ZDF group. ConclusionMaresin1 alleviates cerebral ischemia/reperfusion injury by inhibiting pyroptosis mediated by caspase-3/GSDME pathway and alleviating neuroinflammation.

Tuberculous Paraplegia: Outcome of Operative Intervention.

Tuberculosis of the spine, a common manifestation of extra-pulmonary tuberculosis is characterized by vertebral destruction, paradiscal involvement, abscess collection and varying degrees of neurologic affectation. The primary disease caused by mycobacterium tuberculosis complex infects the lungs, lymph nodes of the mediastinum and gastrointestinal tract/ viscera with spinal involvement being secondary and caused by haematogenous spread. Tuberculous paraplegia arises as a complication of spinal involvement. To determine the outcome of operative intervention in tuberculous paraplegia. Methodology: This was a retrospective study involving 10 patients with tuberculous spinal involvement with varying degrees of neurological deficit as defined by both Tuli and ASIA grading. The VAS score, ESR, ASIA grade (both pre-op and post op), Tuli's grade (pre-op and post op) were used to analyze the therapeutic effects of the surgery. The mean pre-operative VAS score was 5.9 ±1.8, which significantly decreased to 2.2 ±1.3 six weeks post operatively. The mean pre-operative ESR and CRP was 78.9 ± 11.3mm/hr and 83 ± 13.5 respectively; which both showed a statistically significant decrease post-operatively, p<0.05. All cases achieved an increase of more than one ASIA grade post-operatively. Early surgical intervention is beneficial in patients with tuberculous spinal disease with neurologic involvement.

The extended post spinal surgery syndrome (EPSS)

Pain can occur after any spinal surgery. Despite this, there are other many signs and symptoms of neurological deficits that can occur in patients with varying severity. Our aim is to find some of the main neurological deficits that can occur after any spinal surgery. We searched the literature based on some of the important keywords like neurological deficits after spine surgery, foot drops, cauda equina syndrome, epidural hematoma, and nerve and dural injury. Based on this we analyzed the most important and widely read articles. The problems associated with spine surgery have been published in the literature but are much more than the failed back surgery syndrome and cause more discomfort to patients with varying degrees of neurological deficits. We have coined a new term “Extended Post-spinal Surgery Syndrome (EPSS)” for these conditions. We propose this to include the other complications after lumbar surgery including nerve injury, dural injury, cauda equina syndrome and epidural haematoma.

Differential diagnosis and treatment of nosocomial spinal infections in patients after open microdiscectomy (brief literature review)

Surgical site infections (SSI) occur in 0.7‒16.1 % of cases and are one of the most frequent nosocomial complications in spinal neurosurgery. The frequency of SSI after open microdiscectomies varies from 1.9 % to 5.5 % depending on several factors and requires clarification. The causative agents of spinal SSI are most often Staphylococcus aureus, S. epidermidis, methicillin-resistant S. aureus, less frequently anaerobic strains, and Mycobacterium tuberculosis.Symptoms of deep SSI caused by the most common Gram-positive and Gram-negative microflora are usually nonspecific and include fever, back pain, and limited movement. Anaerobic spondylodiscitis is characterized by long-lasting back pain, mainly without an increase in temperature, and a high frequency of epidural abscess formation. The most significant factors in the occurrence of SSI are surgical access, type and duration of surgical intervention, the number of levels operated on at once, the duration of hospitalization, the presence of diabetes, and the patient’s high body mass index. However, the importance of each of these and other factors in the development of SSI after surgical interventions for clinically manifest discogenic pathology continues to be studied. In several studies, open microdiscectomies were statistically significantly associated with a higher frequency of SSI formation. Posterior spondylodesis and implants in the spine increase the risk of SSI development. Prevention of SSI should include preoperative, intraoperative, and postoperative stages, compliance with which can contribute to reducing the risk of SSI. Treatment of purulent spondylodiscitis involves antibiotic therapy and long-term dynamic observation. Indications for surgical intervention are the effectiveness of antibiotic therapy, deterioration of neurological symptoms, and violation of the integrity of the vertebrae with the formation of instability. The issue of choosing the optimal access and volume of surgical intervention for postoperative spondylodiscitis is analyzed in many studies and, first of all, is determined by: localization, the nature of structural changes, the presence of accompanying abscesses, the degree of neurological deficit, the presence or absence of vertebral compression fractures and signs of spondylolisthesis.Postoperative SSI worsens patients’ quality of life and disease prognosis in patients with discogenic pathology. A clear understanding of the individual risk factors of SSI, timely diagnosis, and differentiated treatment can prevent the formation of these dangerous complications and minimize their manifestations.

Literature review of spinal hematoma case reports: causes and outcomes in pediatric, obstetric, neuraxial and pain medicine cases

BackgroundThe risk of spinal epidural hematoma (SEH) has been described in the literature but the impact in various patient populations has not been assessed in the same study. We identified...

Epidemiology of amyotrophic lateral sclerosis in the Krasnoyarsk region

Background. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that causes paralysis of muscles due to degeneration of motor neurons. According to available data, the incidence of ALS in different regions of the world is from 0.6 to 3.8 per 100,000 population per year. Data obtained during the study of the epidemiology of ALS at the regional level can be used in planning medical resources, in particular, calculating the necessary respiratory equipment and funds for nutritional support.Aim. Clinical and epidemiological analysis of ALS cases registered in the Krasnoyarsk region for the period 2018–2022.Materials and methods. A clinical and epidemiological analysis of ALS cases registered in the Krasnoyarsk region from 2018 to 2022 was conducted. To do this, we used data from the specialized office of neuromuscular pathology of the Regional Clinical Hospital in Krasnoyarsk and the Krasnoyarsk Regional Medical Information and Analytical Center. Diagnosis verification was carried out in accordance with the generally accepted El Escorial and Gold Coast criteria. The functional state and degree of neurological deficit were assessed using the ALS-FRS-R scale.Results. Over the period from 2018 to 2022, 78 cases of ALS were registered. The incidence rate was 0.54 cases per 100,000 population per year. In 2022, the prevalence rate was 1.16 cases per 100 thousand population. The time from symptom onset to diagnosis of the disease ranged from 4 to 57 months, with the average time to diagnosis being 17 months. Most patients were diagnosed with ALS when their ALS-FRS-R score decreased by 7–11 points. The division of patients into groups of rapid, moderate, and slow diagnostic correlates with life expectancy. Patients who are diagnosed quickly have a higher rate of disease progression, which results in a low life expectancy.Conclusion. The creation of specialized centers will improve the diagnosis and management of patients with ALS and plan the costs of palliative care. The increase in the incidence and detection of ALS emphasizes the need to develop new approaches to the treatment and rehabilitation of patients with ALS.

Delayed presentation of lower cervical facet dislocations: What to learn from past reports?

Delayed presentation of lower cervical facet dislocations is uncommon, and there is no standardized way to approach these neglected injuries. The literature on neglected lower cervical facet dislocations is limited to case reports and few retrospective studies. This justifies the need for a comprehensive review of this condition. Our purpose was to elaborate a review on the epidemiology, clinical and radiological presentation, and treatment techniques and approach to these neglected injuries. Middle-aged adults from 30 to 50 represent 73.8% of reported cases, and most of them are males (72.0%). The most affected level is C5-C6 (43.0%). While most delays are due to missed injuries (52.1%) and ineffective non-operative treatment (36.2%), the other reason for delay is negligence in seeking medical care (11.7%). Patients present with variable degrees of neurological deficit, persistent neck pain, and neck stiffness. Reported approaches and techniques to reduce and stabilize these injuries are highly variable and depend on the surgeon's judgment, experience, and preference. Fibrotic tissues and bony fusion around the dislocated facet joint contribute to the reduction challenge, and 77.0% of closed reduction attempts fail. Anterior and posterior approaches to the cervical spine are used selectively or in combination for surgical release, reduction, and stabilization. Despite the lack of standardized treatment guidelines and different approaches, most of the authors reported improvement in pain, balance, and neurology post-surgery. Starting with the posterior surgical approach aims to achieve reduction compared to the anterior approach which largely aims at spinal decompression. Given the existing controversies, the need for quality prospective studies to determine the best treatment approach for lower cervical facet dislocations presenting with delay is evident.

PSD-95 inhibitor Tat-NR2B9c (NA-1) protects the integrity of the blood-brain barrier after transient middle artery occlusion in rats by downregulating matrix metalloprotease-9 and upregulating endothelial nitric oxide synthase

BackgroundProtection against ischemic stroke may be most effective when multiple components of the neurovascular unit are protected, yet current treatments target mainly neurons. Here we explored whether the PSD-95 inhibitor Tat-NR2B9c (NA-1) can protect not only neurons but also the blood-brain barrier. MethodsAdult male Sprague-Dawley rats were randomly divided into three groups, which were subjected to either sham surgery or transient cerebral ischemia-reperfusion, after which some animals were treated with Tat-NR2B9c. The therapeutic efficacy of Tat-NR2B9c was assessed in terms of the degree of neurological deficit and cerebral infarction, integrity of the blood-brain barrier, cerebral water content, as well as expression of PSD-95, nitric oxide synthase, and matrix metalloprotease-9. ResultsTat-NR2B9c (NA-1) ameliorated neurofunctional deficit, reduced cerebral infarction, mitigated blood-brain barrier injury and improved its integrity following ischemia-reperfusion, leading to less cerebral edema. These improvements were associated with upregulation of tight junction proteins in the blood-brain barrier. At the same time, Tat-NR2B9c (NA-1) downregulated neuronal nitric oxide synthase and matrix metalloprotease-9, while reversing the ischemia-induced downregulation of endothelial nitric oxide synthase in brain. We report here the first evidence that PSD-95 is expressed in vascular endothelial cells in the brain. ConclusionOur experiments in a rat model of transient occlusion of the middle cerebral artery suggest that Tat-NR2B9c (NA-1) can mitigate ischemic injury to the blood-brain barrier, and that it may do so by downregulating matrix metalloprotease-9 and upregulating endothelial nitric oxide synthase.

Definition, prediction, prevention and management of patients with severe ischemic stroke and large infarction.

Severe ischemic stroke carries a high rate of disability and death. The severity of stroke is often assessed by the degree of neurological deficits or the extent of brain infarct, defined as severe stroke and large infarction, respectively. Critically severe stroke is a life-threatening condition that requires neurocritical care or neurosurgical intervention, which includes stroke with malignant brain edema, a leading cause of death during the acute phase, and stroke with severe complications of other vital systems. Early prediction of high-risk patients with critically severe stroke would inform early prevention and treatment to interrupt the malignant course to fatal status. Selected patients with severe stroke could benefit from intravenous thrombolysis and endovascular treatment in improving functional outcome. There is insufficient evidence to inform dual antiplatelet therapy and the timing of anticoagulation initiation after severe stroke. Decompressive hemicraniectomy (DHC) <48 h improves survival in patients aged <60 years with large hemispheric infarction. Studies are ongoing to provide evidence to inform more precise prediction of malignant brain edema, optimal indications for acute reperfusion therapies and neurosurgery, and the individualized management of complications and secondary prevention. We present an evidence-based review for severe ischemic stroke, with the aims of proposing operational definitions, emphasizing the importance of early prediction and prevention of the evolution to critically severe status, summarizing specialized treatment for severe stroke, and proposing directions for future research.

Intracerebral Hemorrhage Leads to Anemia By Disrupting Erythropoiesis and Erythromyeloblastic Islands

Intracerebral hemorrhage (ICH), caused by the rupture of a cerebral vessel and subsequent entry of blood into the brain parenchyma, is a major form of acquired brain injury and contributes a remarkable proportion of stroke-related morbidity and mortality. Due to the few proven effective emergency and preventive treatments, patients who survived suffer varying degrees of poor prognosis that affect their quality of life. There is an urgent need to explore the cellular and molecular basis of the differences in the severity and prognosis of ICH. Anemia is a common manifestation of ICH. However, the mechanisms underlying ICH-induced anemia as we as the correlation between anemia and ICH progression/prognosis remain unclear. In this study, we found that approximately 35.1% (39 of 111) of ICH patients exhibited anemia and that decreased hemoglobin levels were positively associated with higher scores on the National Institutes of Health Stroke Scale, which quantifies the degree of neurological deficit, at admission. Furthermore, patients with decreased hemoglobin levels at admission showed higher modified Rankin scale scores at 3 months, which reflect the global disability of daily living at this time, suggesting that anemia was associated with a more severe progression and poor patient prognosis. To investigate the effects of ICH on bone marrow (BM) erythropoiesis, we conducted experiments in 12-month-old mice with collagenase-induced striatal ICH. Our results showed that ICH caused apparent anemia on day 3, associated with larger hematomas in the striatum and more severe neurologic deficits. We first evaluated the phenotype of hematopoietic progenitors and found that mice suffering ICH exhibited increased granulocyte monocyte progenitors but a significant decrease in common myeloid progenitors and megakaryocyte erythrocyte progenitors compared to control mice, suggesting a reduced source of erythroid progenitors. Further analysis revealed that the colony-forming ability of erythroid progenitors and subsequent terminal differentiation was significantly suppressed after ICH. To assess whether ICH-induced suppression of erythropoiesis is associated with erythromyeloblastic islands (EMBIs), the niche for erythropoiesis/myelopoiesis, we performed ICH using 12-month-old EpoR-tdTomato-Cre mice and found that the number of BM EMBIs and EpoR + macrophages decreased significantly. Moreover, the number and proportion of developing erythroid cells surrounding EMBIs decreased while LY6G + cells representing granulocytes increased prominently, indicating an altered microenvironment, with EMBI favoring granulopoiesis over erythropoiesis after ICH. Studies have shown that inflammation plays a crucial role in secondary brain injury after ICH. We hypothesize that inflammatory cytokines may contribute to the suppression of erythropoiesis observed in ICH mouse models. To test this, we measured inflammatory factors in both peripheral blood and BM fluid using Quantibody Mouse Inflammation Array. In particular, IL-6 concentrations in peripheral blood and BM fluid in ICH mice were significantly higher than controls. Treatment with MR16-1, an IL-6 antagonist, alleviated ICH-induced anemia and improved BM erythropoiesis in ICH mice, as evidenced by increased peripheral red blood cells and hemoglobin levels, elevated numbers of erythroid progenitors and terminal erythroblast. MR16-1 treatment also improved BM EMBI formation and increased EpoR + macrophages. In addition, MR16-1 treatment effectively improved neurologic deficits and reduced brain hematoma after ICH. Administration of recombinant IL-6 to wild-type mice resulted in decreased levels of red blood cells and hemoglobin along with suppression of erythropoiesis in the BM. Collectively, these results suggest that ICH modulates erythropoiesis and erythromyeloblastic islands function to ultimately lead to anemia and reveal a possible therapeutic opportunity to reverse ICH-induced anemia and improve ICH prognosis by targeting IL-6.

S100B PROTEIN CONTENT IN ISCHEMIC STROKE AND ITS PROGNOSTIC VALUE IN PATIENTS SUBJECTED TO INVASIVE INTERVENTIONS

The aim of the study is to determine the levels of the S100B protein in patients with ischemic stroke and evaluate its relationship with the size of brain tissue damage, stroke severity, and clinical outcomes. Materials and methods.The study included 113 patients with acute ischemic stroke, hospitalized within the first day after its onset and subjected to invasive treatment. 101 men and 12 women were examined, including 32 at the age of 50-60, 64 at the age of 61-70, 17 at the age of 71-80. parameters and degree of functional deviations according to the NIHSS scale. Results. The content of S100B during the initial determination on average for the group significantly exceeded the level determined in the control by 3.22 times (p=0.025). There was a direct dependence of the content of S100B on the size of the stroke. A moderate increase in the indicator on the 3rd day relative to the determined one on the 1st day and a decrease on the 7th day after the development of the stroke were revealed. There was no significant dependence of S100B content on the presence of comorbidities. The influence of the studied parameter on the degree of neurological deficit was determined only in patients with a large stroke size.

Inter-Rater Reliability of Collateral Status Assessment Based on CT Angiography: A Retrospective Study of Middle Cerebral Artery Ischaemic Stroke.

The importance of assessing the collateral status (CS) in patients with ischaemic stroke (IS) has repeatedly been emphasised in clinical guidelines. Various publications offer qualitative or semiquantitative scales with gradations corresponding to the different extents of the collaterals, visualised mostly on the basis of CTA images. However, information on their inter-rater reliability is limited. Therefore, the aim of this study is to investigate the inter-rater reliability of the scales for collateral assessment. CTA images of 158 patients in the acute period of IS were used in the study. The assessment of CS was performed by two experts using three methodologies: the modified Tan scale, the Miteff scale, and the Rosenthal scale. Cohen's kappa, weighted kappa and Krippendorff's alpha were used as reliability measures. For the modified Tan scale and the Miteff and Rosenthal scales, the weighted kappa values were 0.72, 0.49 and 0.59, respectively. Although the best measure of consistency was found for the modified Tan scale, no statistically significant differences were revealed among the scales. The impact of the CS on the degree of neurological deficit at discharge was shown for the modified Tan and Rosenthal scales. In conclusion, the analysis showed a moderate inter-rater reliability of the three scales, but was not able to distinguish the best one among them.

INVESTIGATION OF THE EFFECTS OF CX3CL1 ON IMMUNOPATHOGENESIS AND COGNITIVE FUNCTIONS IN RELAPSING REMITTINGAND SECONDARY PROGRESSIVE MULTIPLE SCLEROSIS PATIENTS IN TERMS OF THE POSSIBILITY OF A BIOMARKER

Objectives. CX3CL1 is a unique chemokine with direct relationship with its receptor to reduce expression of proinflammatory genes inactivated microglia.It is constitutively expressed by healty neurons and defined as neuroimmune regulatory protein.CX3CL1/CX3CR1signaling has been linked to human neurodegeneration. Under physiological conditions, disruption of this signaling leads to impairments inmotor learning, cognitive function, and synaptic plasticity. CX3CR1 also plays a role in the regulation of hippocampal-dependent memoryformation.Our aim in this study is to evaluate the role of CX3CL1 on immunopathogenesis and cognitive functions in Relapsing Remitting (RRMS) and Secondary Progressive Multiple Sclerosis (SPMS) patients in terms of biomarker possibility. Methods. Eight RRMS, 24 SPMS and 30 healty controls have been participated in this study. RRMS and SPMS were diagnosed according toMc Donald 2017 criteria. The degree of neurological deficits were assessed by EDSS.Serum levels of CX3CL1 were measured by ELISAmethod.The severity of cognitive impairment in patients were evaluate with MoCA test.Statistical analysis were performed using the IBMSPSS21. Results. When the RRMS, SPMS and control groups were compared,it was observed that the serum CX3CL1 levels in the SPMS groupwere decreased statistically significant.In addition,there was a positive correlation between MoCA score and serum CX3CL1 level in thepatients with RRMS and SPMS. Conclusion. Cytokines and chemokines play an important role in the immunopathogenesis of multiple sclerosis.Amongchemokines, serum levels of CX3CL1 was reported to be elevated in RRMS patients. However, it has not been observed in patients SPMS. CX3CL1 is an intrinsic neuroprotective chemokine and inhibitor against neurotoxicity. According to the results of our study, thedecrease in serum CX3CL1 levels serum CX3CL1 supports the development of neurodegeneration related neuroinflammation. In addition, thepositive correlation of MoCA test with CX3CL1 levels suggests that it has an important role in cognition. As a result, our study shows that CX3CL1 can be used as an early biomarker associated with disease progression and cognition, additionally it will be promising newtherapeutic target.

Fracture Dislocation in the Cervical Spine – A Case Series Analysis of 32 Cases and Review of Literature

Abstract Complex cervical spine injuries result from road traffic accidents, fall from height, diving in the swimming pool, fall along with the ladder etc. This is a major cause of disability, morbidity and mortality and dependence. Most of these injuries are preventable by proper care, social reforms, teaching civic sense to students at an early age, adoption of safety measures while climbing heights, enforcement of traffic rules, building up of infrastructure, educating the people and mandatory emergency room service for the offenders. Fracture dislocations of the cervical spine mostly flexion distraction injuries. Dislocations can range from perched facets, unilateral facet dislocations to bilateral facet dislocations and spondyloptosis. These result in varying degrees of neurological deficit. The recovery of these patients depend on the initial magnitude of the injury, the safe transport of the victim to the trauma centre, careful management of the injuries and rehabilitation. Here a case series of 32 patients with varying degrees of fracture dislocations of the cervical spine are analyzed retrospectively.