Permanent Neurological Damage Research Articles

A Study to Find Out Correlation of Depression with The Level of Disability in Stroke Patients

BACKGROUND: Stroke is a medical emergency, and can cause permanent neurological damage, complications, and even death. Depressive disorders and diminished functional capabilities have been recognized as common consequences of stroke More than one half of all stroke survivors are left with disabilities that prevent them from returning to their prestroke level of health and productivity. Poststroke depression is considered as the most frequent and important neuro-psychiatric consequence of stroke. As both depressive disorders and disability occurs after stroke, the purpose of the study is to correlate and find the relationship of depression with the level of disability in stroke patients. METHOD: A total of 100 stroke patients of both sexes in the age group of 30 to 60 years within a given time duration of 6 months after stroke were assessed for their depression and disability level. Depression was measured using Hamilton Depression Rating Scale (HDRS) with scores ranging from 0 to 54 and Disability was measured using modified Rankin Scale (mRS) with scores ranging from 0 to 6. OUTCOME MEASURE: The following outcome measures were measured: 1. Depression was measured using Hamilton Depression Rating Scale (HDRS) 2. Disability was measured using modified Rankin Scale (mRS) STATISTICAL ANALYSIS: • Karl Pearson’s correlation • P value <0.05 is taken up for statistical significance RESULTS: The r- value is 0.836, p- value is 0.000 and the result is highly significant with p<0.05 significance. In this study, r is between -1 and 1. Since it is a positive value (0.836), we can conclude that there exist a significant positive correlation between depression (HDRS) and level of disability (mRS) in stroke patients. CONCLUSION: Depression had a strong positive correlation with Disability in stroke patients Keywords: Stroke, Depression, Disability, Hamilton Depression Rating Scale (HDRS), Modified Rankin Scale (mRS).

Diagnostic evaluation of autoimmune encephalitis

Autoimmune encephalitis (AIE) is a complex neurological condition characterized by brain inflammation caused by autoantibodies targeting neuronal surface antigens or synaptic receptors resulting in direct antibody-mediated neuronal dysfunction. The aetiology of AIE includes malignancies and viral infections. However, significant proportion of these patients have no identifiable trigger.The clinical presentation of AIE is varied, ranging from memory deficits and psychiatric symptoms to seizures and movement disorders. The diagnosis is typically based on a combination of supportive clinical features and diagnostic tools such as EEG, MRI, and CSF findings. The detection of antibodies confirms diagnosis of specific autoimmune encephalitis syndromes.Early recognition and prompt treatment of AIE are crucial, as delayed intervention can result in permanent neurological damage. The primary treatment approach is immunotherapy, along with screening for underlying malignancies. With the evolving knowledge on different antibodies and their associated syndromes, it is important for clinicians to have a high degree of suspicion and rule out other differentials to ensure timely and appropriate diagnosis. Furthermore, the use of appropriate diagnostic criteria can help minimize delays in starting treatment.This review provides an overview of the current understanding of AIE, with a focus on pathophysiology, clinical presentation, diagnostics, and treatment modalities, specifically for the most commonly encountered types of AIE associated with cell surface and synaptic antibodies.

Clinical and surgical outcome in patients with cervical spondylodiscitis-a single-center retrospective case series of 24 patients.

Cervical spondylodiscitis is a rare pathology, with an incidence of 0.5-2.5 per 100,000 population, posing significant potential risks. This type of infection can lead to neurological impairment in up to 29% of patients. Radical surgical debridement of the infected segment, fusion, and an intravenous antibiotic regimen remains the gold standard in most spine centers. This study aimed to analyze the surgical outcome in a tertiary spine center based on disease severity. In this study, we retrospectively included all patients diagnosed with cervical spondylodiscitis and treated at the University Hospital Augsburg between January 2017 and May 2022. We collected and analyzed baseline parameters on clinical presentation with symptoms, laboratory parameters, radiological appearance, and surgical parameters such as type of approach and implant, as well as neurological and radiological outcomes. Descriptive statistics were performed using SPSS, and relevant correlations were examined using the t-test for independent samples and the chi-square test. Twenty-four patients (9%) with cervical spondylodiscitis were identified. Twenty-two (92%) surgically treated patients were subdivided into the complicated discitis group (n = 14, 64%) and the uncomplicated discitis group (n = 8, 36%). Seventeen patients (71%) presented with sepsis on admission, 17 patients (71%) were diagnosed with epidural abscess on primary imaging, and 5 patients (21%) had more than one discitis lesion at a distant spinal segment. The presence of epidural abscess was significantly associated with systemic sepsis (OR = 6.2; p = 0.03) and myelopathy symptoms (OR = 14.4; p = 0.00). The most frequently detected specimen was a multisensitive Staphylococcus aureus (10 patients, 42%). Six patients (25%) died after a median of 20 days despite antibiogram-accurate therapy, five of whom were diagnosed with a complicated type of discitis. The follow-up data of 15 patients (63%) revealed permanent neurological damage in 9 patients (38%). Notably, the surgical approach was a significant factor for revision surgery (p = 0.008), as three out of five (60%) ventrodorsal cases with complicated discitis were revised. Cervical spondylodiscitis represents a severe infectious disease that is often associated with permanent neurological damage or a fatal outcome, despite adequate surgical and antibiotic treatments. Complicated types of discitis may require a more challenging surgical and clinical course.

Bridge-layered decompression technique for vertebral artery-involved hemifacial spasm: technical note

BackgroundHemifacial spasm (HFS) is most effectively treated with microvascular decompression (MVD). However, there are certain challenges in performing MVD for HFS when the vertebral artery (VA) is involved in compressing the facial nerve (VA-involved). This study aimed to introduce a “bridge-layered” decompression technique for treating patients with VA-involved HFS and to evaluate its efficacy and safety to treat patients with HFS.MethodsA single-center retrospective analysis was conducted on the clinical data of 62 patients with VA-involved HFS. The tortuous trunk of VA was lifted by a multi-point “bridge” decompression technique to avoid excessive traction of the cerebellum and reduce the risk of damage to the facial-acoustic nerve complex. To fully decompress all the responsible vessels, the branch vessels of VA were then isolated using the “layered” decompression technique.ResultsAmong the 62 patients, 59 patients were cured immediately after the surgery, two patients were delayed cured after two months, and one had occasional facial muscle twitching after the surgery. Patients were followed up for an average of 19.5 months. The long-term follow-up results showed that all patients had no recurrence of HFS during the follow-up period, and no patients developed hearing loss, facial paralysis, or other permanent neurological damage complications. Only two patients developed tinnitus after the surgery.ConclusionThe “bridge-layered” decompression technique could effectively treat VA-involved HFS with satisfactory safety and a low risk of hearing loss. The technique could be used as a reference for decompression surgery for VA-involved HFS.

Direct aortic cannulation, a safe alternative to femoral artery cannulation - 17 years of type A dissection surgery experience

Aim: Optimal cannulation strategy for acute type A aortic dissection (ATAAD) surgery remains debated. Recent guidelines have advocated antegrade systemic perfusion through right axillary artery (RAX) cannulation, instead of femoral artery (FA) cannulation. However, RAX cannulation can be technically challenging and time-consuming. On the other hand, direct (ascending) aorta (DA) cannulation is a swift procedure that also ensures downstream antegrade flow. In this regard, we assessed whether DA cannulation is a safe alternative to FA cannulation. Methods: Records of all patients undergoing ATAAD surgery between 2006-2022 at the Radboud University Medical Center were retrospectively reviewed. Results: In total, 281 patients underwent surgery for ATAAD during the investigated period. Three patients were excluded due to death before the start of extracorporeal circulation and four because of RAX cannulation. Of the remaining 274 patients, 53% (N = 145) received primary FA and 47% (N = 129) DA cannulation, with a success rate of 98% for both approaches. Surgical mortality (combined in-hospital and 30-day) was 9.9% (7.8% DA group vs. 11.7% FA group, P = 0.271). New permanent neurological damage was seen in 10.9% vs. 6.9% (P = 0.248), respectively. In multivariate analysis, cannulation strategies were not significantly associated with surgical mortality nor postoperative new permanent neurological damage. Conclusion: DA cannulation offers a safe and fast alternative to FA cannulation in ATAAD surgery. There were no significant differences in mortality and neurological complications. Future studies should focus on the differences between RAX and DA cannulation strategies on postoperative outcomes in ATAAD surgery.

Poūmės kombinuotos nugaros smegenų degeneracijos, sukeltos diazoto monoksido („linksminančių dujų”) vartojimo, klinikinio atvejo aprašymas

Although nitrous oxide (N2O) has long been used as an anesthetic, it’s use as a recreational drug has recently increased. As N2O abuse is associated with a number of adverse health effects, it has become a significant public health issue. Chronic abuse can lead to a number of neurological complications, most commonly related to functional vitamin B12 deficiency. One of the most encountered forms of N2O neurotoxicity is a subacute combined degeneration, which can cause permanent neurological damage. The medical community should therefore be aware of the increasing scale of recreational N2O exposure and the possible complications of this drug abuse. Early recognition and treatment of N2O toxicity are crucial. We present the case of an 18-year-old male who was diagnosed with subacute combined spinal cord degeneration related to N2O abuse.

Nitrous oxide tank cold burn to the forearm: a case study and discussion of the literature.

Nitrous oxide (N 2 O) has become one of the most popular recreational drugs in Europe. While N 2 O is often used in medical settings as an analgesic and anaesthetic agent, its recreational use was documented many years before its introduction into clinical practice. The desired effects from inhaling N 2 O for recreational purposes include rapid feelings of relaxation, calmness and euphoria, which can be accompanied by giddiness and laughter. There are various adverse effects associated with N 2 O use, including headache, nausea, vomiting, drowsiness and the development of permanent neurological damage. Furthermore, its use is associated with cold burns and road accidents. This article details the case of a patient who sustained an N 2 O tank burn to his forearm from recreational use. It also discusses the prevalence, legal status and adverse effects of N 2 O use as well as the pathophysiology and management of cold burn injuries.

Gene expression variation underlying tissue-specific responses to copper stress in Drosophila melanogaster.

Copper is one of a handful of biologically necessary heavy metals that is also a common environmental pollutant. Under normal conditions, copper ions are required for many key physiological processes. However, in excess, copper results in cell and tissue damage ranging in severity from temporary injury to permanent neurological damage. Because of its biological relevance, and because many conserved copper-responsive genes respond to nonessential heavy metal pollutants, copper resistance in Drosophila melanogaster is a useful model system with which to investigate the genetic control of the heavy metal stress response. Because heavy metal toxicity has the potential to differently impact specific tissues, we genetically characterized the control of the gene expression response to copper stress in a tissue-specific manner in this study. We assessed the copper stress response in head and gut tissue of 96 inbred strains from the Drosophila Synthetic Population Resource using a combination of differential expression analysis and expression quantitative trait locus mapping. Differential expression analysis revealed clear patterns of tissue-specific expression. Tissue and treatment specific responses to copper stress were also detected using expression quantitative trait locus mapping. Expression quantitative trait locus associated with MtnA, Mdr49, Mdr50, and Sod3 exhibited both genotype-by-tissue and genotype-by-treatment effects on gene expression under copper stress, illuminating tissue- and treatment-specific patterns of gene expression control. Together, our data build a nuanced description of the roles and interactions between allelic and expression variation in copper-responsive genes, provide valuable insight into the genomic architecture of susceptibility to metal toxicity, and highlight candidate genes for future functional characterization.

Loss of Gucy1a3 causes poor post-stroke recovery by reducing angiogenesis via the HIF-1α/VEGFA signaling pathway in mice

ObjectivesIschemic stroke is a common and debilitating disease that can cause permanent neurological damage. Gucy1a3, which encodes the α1 subunit of soluble guanylyl cyclase, has been reported to be associated with functional recovery after ischemic stroke. However, the mechanism is still not well understood. In the present study, we investigated the effects of Gucy1a3 on (i) post-stroke recovery; (ii) vascular endothelial growth factor A (VEGFA) and hypoxia inducible factor 1 alpha (HIF-1α) expression; and (iii) angiogenesis after ischemic stroke. Materials and methodsWild-type and Gucy1a3 knockout C57BL/6J male mice were respectively used to establish the models of permanent middle cerebral artery occlusion (pMCAO). Neurological deficit scores were evaluated at 24 h and 96 h after pMCAO. Cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. For determining microvessel density, immunohistochemical analysis was performed with CD31. The expression of VEGFA and HIF-1α was detected by western blotting. ResultsOur results suggest that loss of Gucy1a3 increased the infarct volume and aggravated neurological deficits after pMCAO. In addition, the Gucy1a3 knockout brains exhibited significantly lower microvessel densities and VEGFA and HIF-1α expression levels than the wild-type brains at 96 h post-pMCAO. ConclusionsOur study indicates that GUCY1A3 might be involved in angiogenesis after ischemic stroke. Further investigation of GUCY1A3 will provide a new therapeutic target for stroke.

HGF secreted by hUC-MSCs mitigates neuronal apoptosis to repair the injured spinal cord via phosphorylation of Akt/FoxO3a pathway

Spinal cord injury (SCI) can cause severe and permanent neurological damage, and neuronal apoptosis could inhibit functional recovery of damaged spinal cord greatly. Human umbilical cord mesenchymal stem cells (hUC-MSCs) have great potential to repair SCI because of a series of advantages, including inhibition of neuronal apoptosis and multiple differentiation. The former may play an important role. However, the detailed regulatory mechanism associated with the inhibition of neuronal apoptosis after hUC-MSCs administration has not been elucidated. In this study, proteomics analysis of precious human cerebrospinal fluid (CSF) samples collected from SCI subjects receiving hUC-MSCs delivery indicated that hepatocyte growth factor (HGF) is largely involved in SCI repair. Furthermore, overexpression of HGF derived from hUC-MSCs could decrease reactive oxygen species to prevent neuron apoptosis to the maximum, and thus lead to significant recovery of spinal cord dysfunction. Moreover, HGF could promote phosphorylation of Akt/FoxO3a pathway to decrease reactive oxygen species to reduce neuron apoptosis. For the first time, our research revealed that HGF secreted by hUC-MSCs inhibits neuron apoptosis by phosphorylation of Akt/FoxO3a to repair SCI. This study provides important clues associated with drug selection for the effective treatment of SCI in humans.

Class A ventral spinal epidural hematoma as a rare complication of hypertensive crisis

Spinal epidural hematoma is a rare but severe medical condition that can cause neurological deficits and disability. In this case report, a 53-year-old man with poorly controlled hypertension and end-stage renal disease presented with hypertensive crisis and a one-week history of symptoms including back pain, abdominal pain, and pain radiating down his legs. Despite aggressive blood pressure control, the patient was found to have a 21mm ventral epidural hematoma at T10 causing thoracic cord compression and paraplegia. The patient underwent surgical hematoma evacuation but remained paraplegic with minimal motor and sensory recovery. Spinal epidural hematoma as a complication of hypertensive crisis is rare. Clinicians should be aware of the potential development of spinal epidural hematoma in patients with hypertensive crisis, even in cases with no obvious risk factors. Prompt diagnosis and treatment are crucial for preventing permanent neurological damage and improving patient outcomes. Further research is needed to better understand the underlying mechanisms and risk factors for spinal epidural hematoma in patients with hypertensive crisis.

THU213 Posterior Reversible Encephalopathy Syndrome As A Rare Presentation Of ACTH-dependent Cushing Syndrome In A Pediatric Patient

Abstract Disclosure: E.E. Bell-Sambataro: None. C. Tatsi: None. P. Chittiboina: None. S.A. Bowden: None. Background: Cushing disease (CD), caused by ACTH-secreting pituitary adenoma, is the most common cause of Cushing Syndrome (CS) in children > 5 years of age. Hypertension is reported in up to 50% of pediatric cases with CS. We report a challenging pediatric case with a rare presentation of hypertensive emergency associated with CD. Clinical Case: A 6-year-old female with 3 month-history of rapid weight gain (8 kg), round face, and hypertrichosis presented to emergency department for abdominal pain from nephrolithiasis and was noted to have severe hypertension. While in ED, she developed status epilepticus and altered mental status. Brain MRI findings were consistent with posterior reversible encephalopathy syndrome (PRES). Her hypertensive encephalopathy gradually improved with aggressive anti-hypertensive and anti-epileptic therapy. Further studies confirmed hypercortisolism with markedly elevated urine free cortisol of 1288 ug/day (<18 ug/day) and lack of diurnal variation of serum cortisol (8 AM cortisol of 47.9 ug/dL, midnight cortisol of 20.3 ug/dL). ACTH level of 23 pg/mL suggested ACTH-dependent CS. Low dose (1 mg) dexamethasone suppression test (DST) failed to suppress 8 am cortisol (31.4 ug/dL). High dose DST (120 mcg/kg) suppressed serum cortisol to 67%- borderline threshold for CD, likely due to increased dexamethasone clearance by anticonvulsant. Pituitary MRI did not reveal a visible lesion. Desmopressin stimulation test showed stimulation of ACTH by 700% and cortisol by 160% suggesting pituitary source. Inferior petrosal sinus sampling showed a mildly increased gradient in central to peripheral plasma ACTH of 1.7 at baseline (>2) and post-stimulation of 2.5 (>3). ACTH gradient did not reach cutoffs for pituitary source, likely due to insufficient catheterization of petrosal sinus from anatomically small blood vessels. Given her severity, she underwent surgical pituitary exploration. Postoperative morning cortisol was <5 mcg/dL, with decreased midnight salivary cortisol level obtained 2 months after surgery. She developed post-operative central hypothyroidism but did not have diabetes insipidus. She had a 4 kg weight loss with increased height percentile 5 months after surgery and remains under close monitoring. Conclusion: PRES is a clinical-radiographic disorder characterized by seizures, encephalopathy with neuroimaging findings of reversible cortical and subcortical vasogenic edema. Hypertension induced by marked hypercortisolism precipitated by pain is likely the etiologic factor. Prompt recognition and treatment of PRES are crucial to prevent further life-threatening complications and permanent neurological damage. Early diagnosis and treatment of CD are critical to prevent associated morbidities. Pituitary exploration by expert neurosurgery team should be considered in patients with MRI-negative CD. Presentation: Thursday, June 15, 2023

Cauda Equina Syndrome and the Adolescent Patient with Low Back Pain: A Case Report

Low back pain is a common complaint in adults of all ages, and is being increasingly seen in children and adolescents. The lifetime occurrence of low back pain is around 59%.1 Mechanical low back pain is globally one of the most common presentations seen by the Emergency Physician.14 Most cases of low back pain treated in the Emergency Department (ED) are not true emergencies, a notable exception being the Cauda Equina Syndrome (CES). Owing to the low occurrence and low index of suspicion in the pediatric/adolescent age group, there may be a significant delay in diagnosis of Cauda Equina Syndrome. This is concerning, because delay in diagnosis and there by treatment, runs the risk of permanent neurological damage and disability. Unequivocally, the most common predictor of a favourable outcome in CES is early diagnosis. We present the case of a 16-year-old male who presented to the ED on three separate occasions complaining of low back pain. The patient had red flag signs during the second visit; however, the relevant history and clinical findings were not elicited at the time. On the third ED visit, a clinical diagnosis of CES was made and urgent magnetic resonance imaging of the lumbo-sacral spine revealed a large right para-central herniation of the L4-L5 disc indenting the right L5 nerve root. Our aim in highlighting this case is two fold: 1. To make the Emergency Physician aware of the rare diagnosis of CES in this uncommon age group. 2. To stress the importance of early recognition of red flag signs in CES which will lead to an early diagnosis, and thereby a favourable outcome.

Spread of the Zoonotic Nematode Baylisascaris procyonis into a Naive Raccoon Population

The raccoon roundworm (Baylisascaris procyonis), a gastrointestinal nematode of the raccoon (Procyon lotor), may cause a severe form of larva migrans in humans, which can lead to death or permanent neurological damage. Although roundworms were inadvertently introduced to Europe alongside their raccoon hosts, the parasite is not present in every raccoon population. It is important to understand the geographic distribution of B. procyonis, as early and rapid treatment can prevent severe pathologies in humans. We present evidence for the roundworm spreading into a naive raccoon population through natural dispersal of infected raccoons. We sampled 181 raccoons from Saxony-Anhalt, a German federal state containing contact zones of different raccoon populations, two of which were previously free of the parasite. We screened the raccoons for roundworms and used microsatellite-based assignment tests to determine the genetic origin of the raccoons and their parasites. We detected roundworms in 16 of 45 raccoons sampled in a previously roundworm-free area in the northern part of the state. The largest proportion of the genetic ancestry (≥ 0.5) of the 16 raccoon hosts was assigned to the previously naive raccoon population. Conversely, the genetic ancestry of almost all the roundworms was assigned to the nearest roundworm population in the southern part of the state. Infected raccoons have, therefore, spread to the north of the state, where they interbred with and infected local raccoons. It seems likely that the roundworms will continue to spread. Health authorities should consider continuous surveillance programmes of naive populations and raise public awareness.

A selected case series of idiopathic hypertrophic pachymeningitis in a single center: Pathological characteristics and case-oriented review

Hypertrophic pachymeningitis (HP) is a relatively rare disease of the central nervous system characterized by local or diffuse fibrous thickening of the dura mater. At present, there is still insufficient research on the pathogenesis and treatment strategies of this disease. We reported a continuous case series of seven patients with idiopathic HP (IHP), and also details one case of immunoglobulin G4-related HP requiring surgical intervention. Early diagnosis and appropriate surgical intervention for IHP could prevent the progression of permanent neurological damage and spinal cord paraplegia.

Autoimmune gastritis as an unexpected cause of diarrhea in a young adult with type I diabetes: a case report

BackgroundType 1 diabetes mellitus (T1DM) is a lifelong diagnosis that involves immune-mediated damage of pancreatic beta cells and subsequent hyperglycemia, manifesting as: polyuria, polydipsia, polyphagia, and weight loss. Treatment of type 1 diabetes centers on insulin administration to replace or supplement the body's own insulin with the goal of achieving euglycemia and preventing or minimizing complications. Patients with T1DM are at risk for developing other autoimmune conditions, most commonly thyroid or celiac disease.Case presentationA 20-year-old African American female with T1DM was referred by her endocrinologist to pediatric gastroenterology for 2 months of nocturnal, non-bloody diarrhea, left lower quadrant pain, and nausea; she was also being followed by neurology for complaints of lower extremity paresthesias and pain. The patient’s initial lab-workup was remarkable for a low total Immunoglobulin A (IgA) level of < 6.7 mg/dL. As IgA deficiency is associated with an increased risk of celiac disease, the patient underwent upper and lower endoscopy, which was grossly unremarkable; however, histology revealed a pattern consistent with autoimmune gastritis. Subsequent serum evaluation was remarkable for an elevated fasting gastrin level and an elevated parietal cell antibody level without macrocytic anemia, iron deficiency, or vitamin B12 depletion. The patient was diagnosed with autoimmune gastritis (AIG) and subsequently initiated on parenteral B12 supplementation therapy with improvement in her neurologic and gastrointestinal symptoms.ConclusionThis case illustrates the importance of recognition of red flag findings in a patient with known autoimmune disease. Following well-established health maintenance recommendations for individuals with T1DM ensures that common comorbidities will be detected. Autoimmune gastritis, while a rarer pathology in the pediatric population, deserves consideration in patients with pre-existing autoimmune conditions and new gastrointestinal or neurologic symptoms, as AIG can be associated with poor outcomes and risk of malignancy. Initial lab findings associated with an eventual diagnosis of AIG typically include anemia, iron deficiency, or Vitamin B12 deficiency. However, as demonstrated in this case, symptoms of AIG can rarely present before anemia or Vitamin B12 deficiency develops. To prevent permanent neurological damage, parenteral Vitamin B12 therapy must be considered even in the absence of Vitamin B12 deficiency, especially in those patients already experiencing neurological symptoms.

A Triple-Targeted Rutin-Based Self-Assembled Delivery Vector for Treating Ischemic Stroke by Vascular Normalization and Anti-Inflammation via ACE2/Ang1-7 Signaling.

Changes in the cerebral microenvironment caused by acute ischemic stroke-reperfusion are the main obstacle to the recovery of neurological function and an important cause of stroke recurrence after thrombolytic therapy. The intracerebral microenvironment after ischemia-reperfusion reduces the neuroplasticity of the penumbra and ultimately leads to permanent neurological damage. To overcome this challenge, we developed a triple-targeted self-assembled nanodelivery system, which combines the neuroprotective drug rutin with hyaluronic acid through esterification to form a conjugate, and then connected SS-31, a small peptide that can penetrate the blood brain barrier and target mitochondria. Brain targeting, CD44-mediated endocytosis, hyaluronidase 1-mediated degradation, and the acidic environment synergistically promoted the enrichment of nanoparticles and drug release in the injured area. Results demonstrate that rutin has a high affinity for ACE2 receptors on the cell membrane and can directly activate ACE2/Ang1-7 signaling, maintain neuroinflammation, and promote penumbra angiogenesis and normal neovascularization. Importantly, this delivery system enhanced the overall plasticity of the injured area and significantly reduced neurological damage after stroke. The relevant mechanism was expounded from the aspects of behavior, histology, and molecular cytology. All results suggest that our delivery system may be an effective and safe strategy for the treatment of acute ischemic stroke-reperfusion injury.

CO155 Modelling the Long-Term Effectiveness of Inebilizumab in the Current Treatment Landscape of NMOSD

Neuromyelitis Optica Spectrum Disorder (NMOSD) is characterized by recurrent attacks, permanent neurological damage and cumulative disability impacting health-related quality of life (HRQoL). Due to the chronic nature of NMOSD, understanding the long-term relative effectiveness of immunotherapies is vital. We developed a model simulating long-term outcomes to evaluate the effects of inebilizumab compared with eculizumab, satralizumab and rituximab.

ID: 207794 Hematoma Complications After Spinal Cord Stimulation Trials and Implantations: A Meta-Analysis

Spinal cord stimulation (SCS) has been successful in the treatment of many chronic pain disorders, including failed back surgery syndrome, angina pectoris, complex regional pain syndrome, peripheral vascular disease, diabetic neuropathy, and nonsurgical low back pain. Although major complications are rare, the consequences can be devastating. For example, epidural hematomas can result in paralysis and typically require urgent surgery to prevent permanent neurologic damage. The aim of this study was to perform a meta-analysis to identify the incidence of neuraxial and non-neuraxial hematomas after SCS trials and implantations.

Targeted temperature management in brain edema

Background: Targeted temperature management is a treatment strategy to lower core body temperature to achieve neuroprotection or reduce elevated intracranial pressure. Therefore, it has been increasingly used in the neurointensive care unit to manage various types of acute neurologic injuries.Current Concepts: Targeted temperature management can be divided into three distinct phases, including induction, maintenance, and rewarming, and each phase has risks and predictable complications. In patients with acute neurocritical illnesses, including traumatic brain injury, subarachnoid hemorrhage, intracranial hemorrhage, and ischemic stroke, brain edema is a potentially life-threatening complication as it raises the intracranial pressure, leading to brain herniation and permanent neurological damage. In this sense, targeted temperature management can be considered the final strategy for medical treatment for controlling an intracranial pressure crisis in patients with severe brain injury.Discussion and Conclusion: In the neurointensive care unit, applying targeted temperature management to patients with severe brain injuries may be challenging. Targeted temperature management in critically ill neurological patients is associated with an increased risk of systemic complications, as hypothermia is prolonged, requiring a comprehensive patient-by-patient assessment of the advantages and disadvantages of treatment. Except for cerebral pressure management, analyses of targeted temperature management in patients with traumatic brain injury and subarachnoid hemorrhage remain controversial regarding its effect on prognosis. Targeted temperature management should be reserved for selective patients, and further studies are needed to improve the efficacy of hypothermia for individual conditions, including intracerebral hemorrhage and ischemic stroke.