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Purpose: We aim to analyse and compare the efficacy of the excision of HO around the hip with and without CT-guided navigation. We also aim to compare the functional outcome between CT navigation guided versus conventional excision of HO. Patients and methods: This study is a retrospective analysis of prospectively collected data from 2015 to 2022. There were 23 patients (24 hips) in the final cohort. Intraoperative CT navigation guided excision was performed in 7 hips and conventional excision of HO was done in 17 hips. The HO was classified by Brooker's grading in radiographs. CT scan was taken preoperatively in all patients to exactly identify the volume, location and preoperative planning. The functional outcome was analysed according to Harris Hip Score (HHS) and International Hip Outcome Tool (iHOT) for self-ambulatory patients and improvement in the sitting or nursing care was assessed in patients mobilising with wheelchair or walker support. Any complications or recurrence noted postoperatively and in follow-up were recorded. Results: The mean follow-up was 41.2 months in the CT navigation-guided excision group and 55 months in the conventional excision group. According to Brooker's grading, grade IV was present in 20 hips and grade III in four hips. Twelve patients were self-ambulatory and the other 12 patients were requiring support for mobilisation. There was a significant improvement in the HHS from 21.3 ± 3.7, 18.3 ± 2.5 preoperatively to 75.2 ± 8.3, 72.2 ± 4.3 postoperatively in the CT navigation guided and conventional group respectively (p < 0.001) in the self-ambulatory group. There was one anterior wall and one partial posterior wall fracture in the conventional group. One patient in the conventional group had a deep infection and recurrence. One patient had a superficial infection and another had superficial vein thrombosis in the CT guided excision group. Conclusion: Intraoperative CT navigation helps to exactly localize the HO and facilitates safe excision. Functional excision of the HO leads to better nursing care and functional outcomes between both groups. [ABSTRACT FROM AUTHOR]

Background: Patients with neurologic injuries often receive neuromuscular blocking agents to facilitate airway management. The urgent nature of intubation may result in paralytic administration prior to neurologic examination, delaying clinical assessment, prognostication, and surgical interventions. Objective: In October 2018, an institutional guideline was implemented to extend institutional sugammadex use to include patients with uncertain neurologic examinations with recent rocuronium administration. The guideline allowed for a dose range of 2 mg/kg to 16 mg/kg. The objective of this continuous quality improvement project was to describe the use of sugammadex after implementation of an institutional guideline. Methods: Patient records between October 2018 and March 2020 were reviewed for guideline adherence and outcomes. Information assessed included patient weight, injury mechanism, the dosage and timing of rocuronium and sugammadex administration, and neurologic examination findings. Descriptive statistics were used to assess outcomes. Results: During the study period, eleven patients received sugammadex to facilitate neurologic examinations. The most common dose of sugammadex was 4 mg/kg with a mean total dose of 498.4 ± 333.5 mg. The mean time between rocuronium and sugammadex administration was 73.9 ± 41 minutes. Most patients (72.7%) had definitive changes in neurologic examination after sugammadex administration. Five patients had neurosurgical interventions offered and performed, with 1 of the patients surviving. Conclusions: This case series suggests that sugammadex is useful for reversing rocuronium induced paralysis to facilitate neurologic examination needed to determine management strategies for patients with a neurologic injury. [ABSTRACT FROM AUTHOR]

This review delves into the emerging field of the gut microbiota–brain axis, emphasizing its bidirectional communication and implications for neurological health, particularly in trauma and neurosurgery. While disruptions in this axis can lead to dysbiosis and hinder neurological recovery, recent studies have highlighted the therapeutic potential of interventions like probiotics in targeting this axis. This review aims to focus on the efficacy of probiotic supplementation to support the gut microbiota–brain axis in trauma, neurosurgery, or pain based on the current clinical trials to assess the complex interplays among probiotics, the gut microbiota, and the central nervous system (CNS). This comprehensive literature review identified 10 relevant publications on probiotic interventions for various neurosurgical conditions across multiple countries. These studies demonstrated diverse outcomes, with significant improvements observed in gastrointestinal mobility, inflammatory responses, and infection rates, particularly in post-traumatic brain injury and spinal surgery. Probiotics also showed promise in mitigating antibiotic-associated diarrhea and modulating inflammatory cytokines. Despite the promising findings, the complex interplays among probiotics, the gut microbiota, and the central nervous system (CNS) call for cautious interpretation. Conflicting outcomes emphasize the need for better-designed trials to understand strain-specific and disease-specific effects accurately. In conclusion, probiotics offer a promising adjuvant therapy for neurosurgical patients, traumatic brain injuries, and post-spinal surgery. However, further well-designed randomized controlled trials are essential to elucidate the intricate relationship between microbiome-modulating interventions and the CNS via the gut microbiota–brain axis. [ABSTRACT FROM AUTHOR]

Introduction: Swine exhibit cerebral cortex mitochondrial dysfunction and neuropathologic injury after hypoxic cardiac arrest treated with hemodynamic-directed CPR (HD-CPR) despite normal Cerebral Performance Category scores. We analyzed the temporal evolution of plasma protein biomarkers of brain injury and inflammatory cytokines, as well as cerebral cortical mitochondrial injury and neuropathology for five days following pediatric asphyxia-associated cardiac arrest treated with HD-CPR. Methods: One-month-old swine underwent asphyxia associated cardiac arrest, 10–20 min of HD-CPR (goal SBP 90 mmHg, coronary perfusion pressure 20 mmHg), and randomization to post-ROSC survival duration (24, 48, 72, 96, 120 h; n = 3 per group) with standardized post-resuscitation care. Plasma neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and cytokine levels were collected pre-injury and 1, 6, 24, 48, 72, 96, and 120 h post-ROSC. Cerebral cortical tissue was assessed for: mitochondrial respirometry, mass, and dynamic proteins; oxidative injury; and neuropathology. Results: Relative to pre-arrest baseline (9.4 pg/ml [6.7–12.6]), plasma NfL was increased at all post-ROSC time points. Each sequential NfL measurement through 48 h was greater than the previous value {1 h (12.7 pg/ml [8.4–14.6], p = 0.01), 6 h (30.9 pg/ml [17.7–44.0], p = 0.0004), 24 h (59.4 pg/ml [50.8–96.1], p = 0.0003) and 48 h (85.7 pg/ml [61.9–118.7], p = 0.046)}. Plasma GFAP, inflammatory cytokines or cerebral cortical tissue measurements were not demonstrably different between time points. Conclusions: In a swine model of pediatric cardiac arrest, plasma NfL had an upward trajectory until 48 h post-ROSC after which it remained elevated through five days, suggesting it may be a sensitive marker of neurologic injury following pediatric cardiac arrest.

This review delves into the emerging field of the gut microbiota–brain axis, emphasizing its bidirectional communication and implications for neurological health, particularly in trauma and neurosurgery. While disruptions in this axis can lead to dysbiosis and hinder neurological recovery, recent studies have highlighted the therapeutic potential of interventions like probiotics in targeting this axis. This review aims to focus on the efficacy of probiotic supplementation to support the gut microbiota–brain axis in trauma, neurosurgery, or pain based on the current clinical trials to assess the complex interplays among probiotics, the gut microbiota, and the central nervous system (CNS). This comprehensive literature review identified 10 relevant publications on probiotic interventions for various neurosurgical conditions across multiple countries. These studies demonstrated diverse outcomes, with significant improvements observed in gastrointestinal mobility, inflammatory responses, and infection rates, particularly in post-traumatic brain injury and spinal surgery. Probiotics also showed promise in mitigating antibiotic-associated diarrhea and modulating inflammatory cytokines. Despite the promising findings, the complex interplays among probiotics, the gut microbiota, and the central nervous system (CNS) call for cautious interpretation. Conflicting outcomes emphasize the need for better-designed trials to understand strain-specific and disease-specific effects accurately. In conclusion, probiotics offer a promising adjuvant therapy for neurosurgical patients, traumatic brain injuries, and post-spinal surgery. However, further well-designed randomized controlled trials are essential to elucidate the intricate relationship between microbiome-modulating interventions and the CNS via the gut microbiota–brain axis.

The present review aimed to identify the means through which neurologic injury can predispose individuals to Post-Traumatic Stress Disorder (PTSD). In recent years, comprehensive studies have helped to clarify which structures in the central nervous system can lead to distinct PTSD symptoms—namely, dissociative reactions or flashbacks—when damaged. Our review narrowed its focus to three common neurologic injuries, traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and stroke. We found that in each of the three cases, individuals may be at an increased risk of developing PTSD symptoms. Beyond discussing the potential mechanisms by which neurotrauma may lead to PTSD, we summarized our current understanding of the pathophysiology of the disorder and discussed predicted associations between the limbic system and PTSD. In particular, the effect of noradrenergic neuromodulatory signaling on the hypothalamic pituitary adrenal (HPA) axis as it pertains to fear memory recall needs to be further explored to better understand its effects on limbic structures in PTSD patients. At present, altered limbic activity can be found in both neurotrauma and PTSD patients, suggesting a potential causative link. Particularly, changes in the function of the limbic system may be associated with characteristic symptoms of PTSD such as intrusive memories and acute psychological distress. Despite evidence demonstrating the correlation between neurotrauma and PTSD, a lack of PTSD prognosis exists in TBI, SAH, and stroke patients who could benefit from early treatment. It should be noted that PTSD symptoms often compound with pre-existing issues, further deteriorating health outcomes for these patients. It is ultimately our goal to clarify the relationship between neurotrauma and PTSD so that earlier diagnoses and appropriate treatment are observed in clinic. [ABSTRACT FROM AUTHOR]

Medical research on neurologic ailments requires representative animal models to validate treatments before they are translated to human clinical trials. Rodents are the predominant animal model used in neurological research despite limited anatomic and physiologic similarities to humans. As a result, functional testing designed to assess locomotor recovery after neurologic impairment is well established in rodent models. Comparatively, larger, more clinically relevant models have not been as well studied. To achieve similar locomotor testing standardization in larger animals, the models must be accessible to a wide array of researchers. Non-human primates are the most relevant animal model for translational research, however ethical and financial barriers limit their accessibility. This review focuses on swine, sheep, and goats as large animal alternatives for transitional studies between rodents and non-human primates. The objective of this review is to compare motor testing and data collection methods used in swine, sheep, and goats to encourage testing standardization in these larger animal models. The PubMed database was analyzed by searching combinations of swine, sheep, and goats, neurologic injuries, and functional assessments. Findings were categorized by animal model, data collection method, and assessment design. Swine and sheep were used in the majority of the studies, while only two studies were found using goats. The functional assessments included open pen analysis, treadmill walking, and guided free walking. Data collection methods included subjective behavioral rating scales and objective tools such as pressure-sensitive mats and image-based analysis software. Overall, swine and sheep were well-suited for a variety of assessment designs, with treadmill walking and guided free walking offering the most consistency across multiple trials. Data collection methods varied, but image-based gait analysis software provided the most robust analysis. Future studies should be conducted to standardize functional testing methods after neurologic impairment in large animals.

Background: Traumatic spinopelvic dissociation is a rare injury pattern resulting in discontinuity between the spine and bony pelvis. This injury is associated with a known risk of neurologic compromise which can impact the clinical outcome of these patients. We sought to determine incidence and characteristics of neurologic injury, outcomes following treatment, and predictive factors for neurologic recovery.Methods: We reviewed the clinical documentation and imaging of 270 patients with spinopelvic dissociation from three Level-1 trauma centers treated over a 20-year period. From this cohort, 137 patients fulfilled inclusion criteria with appropriate follow-up. Details surrounding patient presentation, incidence of neurologic injury, and outcome variables were collected for each injury. Neurologic injuries were categorized using the Gibbons criteria. Multivariate analysis was performed to assess for patient and injury factors predictive of neurologic injury and recovery.Results: The overall incidence of neurologic injury in spinopelvic dissociation injuries was 33% (45/137), with bowel and/or bladder dysfunction (n=16) being the most common presentation. Complete neurologic recovery was seen in 26 cases (58%) and two patients (4%) improved at least one Gibbon stage in clinical follow-up. The most common long-term neurologic sequela at final follow-up was radiculopathy (n=12, 9%). Increased kyphosis was found to be associated with neurologic injury (p=0.002), while location of transverse limb and Roy-Camille type were not predictive of neurologic injury (p=0.31 and p=0.07, respectively). There were no factors found to be predictive of neurologic recovery in this cohort.Conclusion: Neurologic injury is commonly seen in patients with spinopelvic dissociation and complete neurologic recovery was seen in the majority of patients at final follow-up. When present, long term neurologic dysfunction is most commonly characterized by radiculopathy. While increasing kyphosis was shown to be associated with neurologic injury, no patient or injury factors were predictive of neurologic recovery. [ABSTRACT FROM AUTHOR]

Acute hyperinflammatory response (cytokine storm) and immunosuppression are responsible for critical illness in patients infected with coronavirus disease 2019 (COVID-19). It is a serious public health crisis that has affected millions of people worldwide. The main clinical manifestations are mostly by respiratory tract involvement and have been extensively researched. Increasing numbers of evidence from emerging studies point out the possibility of neurological involvement by COVID-19 highlighting the need for developing technology to diagnose, manage, and treat brain injury in such patients. Here, we aimed to discuss the rationale for the use of an emerging spectrum of blood biomarkers to guide future diagnostic strategies to mitigate brain injury-associated morbidity and mortality risks in COVID-19 patients, their use in clinical practice, and prediction of neurological outcomes.

The present review aimed to identify the means through which neurologic injury can predispose individuals to Post-Traumatic Stress Disorder (PTSD). In recent years, comprehensive studies have helped to clarify which structures in the central nervous system can lead to distinct PTSD symptoms—namely, dissociative reactions or flashbacks—when damaged. Our review narrowed its focus to three common neurologic injuries, traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and stroke. We found that in each of the three cases, individuals may be at an increased risk of developing PTSD symptoms. Beyond discussing the potential mechanisms by which neurotrauma may lead to PTSD, we summarized our current understanding of the pathophysiology of the disorder and discussed predicted associations between the limbic system and PTSD. In particular, the effect of noradrenergic neuromodulatory signaling on the hypothalamic pituitary adrenal (HPA) axis as it pertains to fear memory recall needs to be further explored to better understand its effects on limbic structures in PTSD patients. At present, altered limbic activity can be found in both neurotrauma and PTSD patients, suggesting a potential causative link. Particularly, changes in the function of the limbic system may be associated with characteristic symptoms of PTSD such as intrusive memories and acute psychological distress. Despite evidence demonstrating the correlation between neurotrauma and PTSD, a lack of PTSD prognosis exists in TBI, SAH, and stroke patients who could benefit from early treatment. It should be noted that PTSD symptoms often compound with pre-existing issues, further deteriorating health outcomes for these patients. It is ultimately our goal to clarify the relationship between neurotrauma and PTSD so that earlier diagnoses and appropriate treatment are observed in clinic.

Background: Ferritin is a protein that is critical for storing iron. Ferritin has recently been shown to play a role in iron homeostasis, immunomodulation, inflammation, and antioxidation. Previously, it was believed that ferritin was exclusively an intracellular peptide. However, there is significant evidence that ferritin is also in the serum, cerebral spinal fluid, and synovial fluid. Summary: Within the brain, ferritin can bind to oligodendrocytes adjacent to the blood-brain barrier to allow a docking point for ferritin to be engulfed by microglia in the brain parenchyma. When iron supplies in the brain are low, the lysosomal-autophagy pathway is activated to degrade ferritin and mobilize iron. Iron is critical in the brain for the formation of myelin and used during cellular respiration. If this sequestration and degradation of iron are impaired, the oxidative effects of iron may leave the brain vulnerable to neurotoxic effects. Subarachnoid hemorrhage (SAH) causes hemolysis of erythrocytes leading to the release of iron. Subsequently, a rise in ferritin is observed which promotes the neurologic insult following SAH. The degree to which ferritin is elevated post-SAH may correlate with the downstream neurotoxicity. Key Messages: The literature seems to point to a critical balance in ferritin levels. Ferritin is protective against further oxidative effects of iron, but ferritin also contributes to neurotoxic outcomes. In this review, we will discuss the role of ferritin in the brain. Specifically, we will address cerebral ferritin iron uptake and ferritin clearance. This homeostatic process influences the development and progression of SAH. [ABSTRACT FROM AUTHOR]

Background: Unrecognized intraoperative cerebral ischemia during neonatal aortic arch reconstruction may precede neurologic injury. Electroencephalogram (EEG) alpha:delta ratio (A:D) changes predict cerebral ischemia; however, if A:D differences can identify ischemia during neonatal antegrade cerebral perfusion (ACP) and aortic arch reconstruction is unknown. We hypothesized that A:D changes would precede neurologic injury. Methods: Simultaneous EEG derived left versus right: hemispheric and anterior cerebral A:Ds were retrospectively measured at baseline and every 5 min during arterial cannulation, cooling, ACP, and the rewarming phases of the operation. A paired left versus right A:D difference >25% was considered significant for ischemia, and the duration of a significant and continuous A:D difference was quantified in minutes. Neonates were divided into two groups: (1) new neurologic injury (stroke or seizure) and (2) no known neurologic injury. Results: From 72 neonates, there were no significant differences in the baseline A:Ds. Seven neonates (9.7%) developed a new neurologic injury (seizure = 3, stroke = 2, seizure and stroke = 2). Male gender and longer ACP times were significantly associated with neurologic injury. In neonates with a neurologic injury, the duration of a significant and continuous A:D difference was longer within the hemispheric and anterior regions. Multivariable analysis demonstrated that a significant and continuous anterior A:D difference (odds ratio: 1.345, 95% CI 1.058-1.712; P  = .01) was independently associated with neurologic injury. Conclusions: A longer continuous anterior A:D difference > 25% was independently associated with neurologic injury. Intraoperative EEG monitoring could be considered during neonatal arch reconstruction., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Abstract Background Subarachnoid hemorrhage accounts for more than 30,000 cases of stroke annually in North America and encompasses a 4.4% mortality rate. Since a vast number of subarachnoid hemorrhage cases present in a younger population and can range from benign to severe, an accurate diagnosis is imperative to avoid premature morbidity and mortality. Here, we present a straightforward approach to evaluating, risk stratifying, and managing subarachnoid hemorrhages in the emergency department for the emergency medicine physician. Discussion The diversities of symptom presentation should be considered before proceeding with diagnostic modalities for subarachnoid hemorrhage. Once a subarachnoid hemorrhage is suspected, a computed tomography of the head with the assistance of the Ottawa subarachnoid hemorrhage rule should be utilized as an initial diagnostic measure. If further investigation is needed, a CT angiography of the head or a lumbar puncture can be considered keeping risks and limitations in mind. Initiating timely treatment is essential following diagnosis to help mitigate future complications. Risk tools can be used to assess the complications for which the patient is at greatest. Conclusion Subarachnoid hemorrhages are frequently misdiagnosed; therefore, we believe it is imperative to address the diagnosis and initiation of early management in the emergency medicine department to minimize poor outcomes in the future.

Supracondylar humerus fractures (ScHF) account for 60% of fractures of the elbow region in children. We assessed the relationship between neurovascular complications and the degree of fracture displacement as rated on the basis of modified Gartland classification. Moreover, we aimed to evaluate predisposing factors, e.g., age and gender, and outcomes of neurovascular complications in ScHF. Between 2004 and 2019, we treated 329 patients with ScHF at the Department of Traumatology and Orthopedics of the Upper Silesian Child Centre, Katowice, Poland. Mean age of patients (189 boys and 140 girls) was 7.2 years (Confidence interval: 6.89, 7.45). Undisplaced fractures were treated conservatively with a cast. Displaced fractures were managed by closed reduction and percutaneous Kirschner wire fixation using two pins inserted laterally. We retrospectively assessed the number of neurovascular lesions at baseline and recorded any iatrogenic injury resulting from the surgical intervention. Acute neurovascular lesions occurred in 44 of 329 ScHF patients (13.4%). The incidence of accompanying neurovascular injuries was positively associated with the severity of fracture displacement characterized by Gartland score. Vascular injuries occurred mainly in Gartland type IV ScHF, while nerve lesions occurred in both Gartland type III and IV ScHF. We noted a significantly higher mean Gartland score and mean age at injury in the group of children suffering from neurovascular injuries when compared to those in the group without such injuries (p = 0.045 and p = 0.04, respectively). We observed no secondary nerve lesions after surgical treatment. For the treatment of ScHF in children, we recommend closed reduction and stabilization of displaced fractures with K-wires inserted percutaneously from the lateral aspect of the upper arm. We advocate vessel exploration in case of absent distal pulses after closed reduction but do not consider primary nerve exploration necessary, unless a complete primary sensomotoric nerve lesion is present. [ABSTRACT FROM AUTHOR]

Background: Globally, reverse shoulder arthroplasty (RSA) has moved away from the Grammont design to modern prosthesis designs. The purpose of this 2-part study was to systematically review each of the most common complications of RSA, limiting each search to publications in 2010 or later. In this part (part I), we examined (1) scapular notching (SN), (2) periprosthetic infection (PJI), (3) mechanical failure (glenoid or humeral component), and (4) neurologic injury (NI). Methods: Four separate PubMed database searches were performed following Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. Overall, 113 studies on SN, 62 on PJI, 34 on mechanical failure, and 48 on NI were included in our reviews. Univariate analysis was performed with the χ2 or Fisher exact test. Results: The Grammont design had a higher SN rate vs. all other designs combined (42.5% vs. 12.3%, P < .001). The onlay humeral design had a lower rate than the lateralized glenoid design (10.5% vs. 14.8%, P < .001). The PJI rate was 2.4% for primary RSA and 2.6% for revision RSA. The incidence of glenoid and humeral component loosening was 2.3% and 1.4%, respectively. The Grammont design had an increased NI rate vs. all other designs combined (0.9% vs. 0.1%, P = .04). Conclusions: Focused systematic reviews of the recent literature with a large volume of RSAs demonstrate that with the use of non-Grammont modern prosthesis designs, complications including SN, PJI, glenoid component loosening, and NI are significantly reduced compared with previous studies. As the indications for RSA continue to expand, it is imperative to accurately track the rates and types of complications to justify its cost and increased indications.

Introduction: Traumatic brain injury is a leading cause of injury-related death and morbidity. Multiple clinical and pre-clinical studies have reported various results regarding sex-based differences in TBI. Our accepted rodent model of traumatic brain injury was used to identify sex-based differences in the pathological features of TBI. Methods: Male and female Sprague-Dawley rats were subjected to either controlled-cortical impact (CCI) or sham injury; brain tissue was harvested at different time intervals depending on the specific study. Blood-brain barrier (BBB) analysis was performed using infrared imaging to measure fluorescence dye extravasation. Microglia and splenocytes were characterized with traditional flow cytometry; microglia markers such as CD45, P2Y12, CD32, and CD163 were analyzed with t-distributed stochastic neighbor embedding (t-SNE). Flow cytometry was used to study tissue cytokine levels, and supplemented with ELISAs of TNF-⍺, IL-17, and IL-1β of the ipsilateral hemisphere tissue. Results: CCI groups of both sexes recorded a higher BBB permeability at 72 hours post-injury than their respective sham groups. There was significant difference in the integrated density value of BBB permeability between the male CCI group and the female CCI group (female CCI mean = 3.08 x 108 ± 2.83 x 107, male CCI mean = 2.20 x 108 ± 4.05 x 106, p = 0.0210), but otherwise no differences were observed. Traditional flow cytometry did not distinguish any sex-based difference in regards to splenocyte cell population after CCI. t-SNE did not reveal any significant difference between the male and female injury groups in the activation of microglia. Cytokine analysis after injury by flow cytometry and ELISA was limited in differences at the time point of 6 hours post-injury. Conclusion: In our rodent model of traumatic brain injury, sex-based differences in pathology and neuroinflammation at specified time points are limited, and only noted in one specific analysis of BBB permeability. [ABSTRACT FROM AUTHOR]

Introduction: Continuous neurologic assessment in the pediatric intensive care unit is challenging. Current electroencephalography (EEG) guidelines support monitoring status epilepticus, vasospasm detection, and cardiac arrest prognostication, but the scope of brain dysfunction in critically ill patients is larger. We explore quantitative EEG in pediatric intensive care unit patients with neurologic emergencies to identify quantitative EEG changes preceding clinical detection. Methods: From 2017 to 2020, we identified pediatric intensive care unit patients at a single quaternary children's hospital with EEG recording near or during acute neurologic deterioration. Quantitative EEG analysis was performed using Persyst P14 (Persyst Development Corporation). Included features were fast Fourier transform, asymmetry, and rhythmicity spectrograms, "from-baseline" patient-specific versions of the above features, and quantitative suppression ratio. Timing of quantitative EEG changes was determined by expert review and prespecified quantitative EEG alert thresholds. Clinical detection of neurologic deterioration was defined pre hoc and determined through electronic medical record documentation of examination change or intervention. Results: Ten patients were identified, age 23 months to 27 years, and 50% were female. Of 10 patients, 6 died, 1 had new morbidity, and 3 had good recovery; the most common cause of death was cerebral edema and herniation. The fastest changes were on "from-baseline" fast Fourier transform spectrograms, whereas persistent changes on asymmetry spectrograms and suppression ratio were most associated with morbidity and mortality. Median time from first quantitative EEG change to clinical detection was 332 minutes (interquartile range: 201-456 minutes). Conclusion: Quantitative EEG is potentially useful in earlier detection of neurologic deterioration in critically ill pediatric intensive care unit patients. Further work is required to quantify the predictive value, measure improvement in outcome, and automate the process. [ABSTRACT FROM AUTHOR]

Acute hyperinflammatory response (cytokine storm) and immunosuppression are responsible for critical illness in patients infected with coronavirus disease 2019 (COVID-19). It is a serious public health crisis that has affected millions of people worldwide. The main clinical manifestations are mostly by respiratory tract involvement and have been extensively researched. Increasing numbers of evidence from emerging studies point out the possibility of neurological involvement by COVID-19 highlighting the need for developing technology to diagnose, manage, and treat brain injury in such patients. Here, we aimed to discuss the rationale for the use of an emerging spectrum of blood biomarkers to guide future diagnostic strategies to mitigate brain injury-associated morbidity and mortality risks in COVID-19 patients, their use in clinical practice, and prediction of neurological outcomes. [ABSTRACT FROM AUTHOR]

The purpose is to estimate the effectiveness of electrocardiograms during resting and active participation by the differentiation between the electrical activity of the heart while standing and sitting in a resting state. The concern is to identify the electrocardiogram parameters that did not show significant changes within these positions. The electrocardiogram parameters can be considered to be a standard marker for medically compromised patients. The electrocardiogram is recorded in the standing and sitting positions focusing on healthy participants using standard electrode placement of lead-I. Combined lead-I patterns (camel-hump or ST-segment prolongation) are usually seen in neurologic injury or hypothermia patients. The pairwise comparisons of a year data are about 454,400 cycles of sitting and 493,470 cycles of standing data. Thus, it is essential to quantify the nature and magnitude of changes seen in the electrocardiogram with a change of posture from sitting to standing in a healthy individual. This makes the findings of electrocardiogram analysis in this paper interesting in which some parameters (i.e., camel-hump patterns in lead-I) are helpful for clinical interpretations and could be suggestive of neurologic injury.

IntroductionTraumatic brain injury is a leading cause of injury-related death and morbidity. Multiple clinical and pre-clinical studies have reported various results regarding sex-based differences in TBI. Our accepted rodent model of traumatic brain injury was used to identify sex-based differences in the pathological features of TBI.MethodsMale and female Sprague-Dawley rats were subjected to either controlled-cortical impact (CCI) or sham injury; brain tissue was harvested at different time intervals depending on the specific study. Blood-brain barrier (BBB) analysis was performed using infrared imaging to measure fluorescence dye extravasation. Microglia and splenocytes were characterized with traditional flow cytometry; microglia markers such as CD45, P2Y12, CD32, and CD163 were analyzed with t-distributed stochastic neighbor embedding (t-SNE). Flow cytometry was used to study tissue cytokine levels, and supplemented with ELISAs of TNF-⍺, IL-17, and IL-1β of the ipsilateral hemisphere tissue.ResultsCCI groups of both sexes recorded a higher BBB permeability at 72 hours post-injury than their respective sham groups. There was significant difference in the integrated density value of BBB permeability between the male CCI group and the female CCI group (female CCI mean = 3.08 x 108 ± 2.83 x 107, male CCI mean = 2.20 x 108 ± 4.05 x 106, p = 0.0210), but otherwise no differences were observed. Traditional flow cytometry did not distinguish any sex-based difference in regards to splenocyte cell population after CCI. t-SNE did not reveal any significant difference between the male and female injury groups in the activation of microglia. Cytokine analysis after injury by flow cytometry and ELISA was limited in differences at the time point of 6 hours post-injury.ConclusionIn our rodent model of traumatic brain injury, sex-based differences in pathology and neuroinflammation at specified time points are limited, and only noted in one specific analysis of BBB permeability.

Introduction: Swine exhibit cerebral cortex mitochondrial dysfunction and neuropathologic injury after hypoxic cardiac arrest treated with hemodynamic-directed CPR (HD-CPR) despite normal Cerebral Performance Category scores. We analyzed the temporal evolution of plasma protein biomarkers of brain injury and inflammatory cytokines, as well as cerebral cortical mitochondrial injury and neuropathology for five days following pediatric asphyxia-associated cardiac arrest treated with HD-CPR., Methods: One-month-old swine underwent asphyxia associated cardiac arrest, 10-20 min of HD-CPR (goal SBP 90 mmHg, coronary perfusion pressure 20 mmHg), and randomization to post-ROSC survival duration (24, 48, 72, 96, 120 h; n = 3 per group) with standardized post-resuscitation care. Plasma neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), and cytokine levels were collected pre-injury and 1, 6, 24, 48, 72, 96, and 120 h post-ROSC. Cerebral cortical tissue was assessed for: mitochondrial respirometry, mass, and dynamic proteins; oxidative injury; and neuropathology., Results: Relative to pre-arrest baseline (9.4 pg/ml [6.7-12.6]), plasma NfL was increased at all post-ROSC time points. Each sequential NfL measurement through 48 h was greater than the previous value {1 h (12.7 pg/ml [8.4-14.6], p = 0.01), 6 h (30.9 pg/ml [17.7-44.0], p = 0.0004), 24 h (59.4 pg/ml [50.8-96.1], p = 0.0003) and 48 h (85.7 pg/ml [61.9-118.7], p = 0.046)}. Plasma GFAP, inflammatory cytokines or cerebral cortical tissue measurements were not demonstrably different between time points., Conclusions: In a swine model of pediatric cardiac arrest, plasma NfL had an upward trajectory until 48 h post-ROSC after which it remained elevated through five days, suggesting it may be a sensitive marker of neurologic injury following pediatric cardiac arrest., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Dr. Julia Slovis currently works for GalaxoSmithKline, but her employment began after completion of her contribution to this manuscript., (© 2024 The Authors.)

It is more common to perform non-invasive examination during general anaesthesia to ensure effective perioperative patient care. To achieve these results, researchers and clinicians are seeking out different technologies and developing new equipment. One such apparatus is a cerebral oximeter, which is used during cardiac surgery with cardiopulmonary bypass for neuroprotection management for reducing risk of postoperative neurological injury (cerebral stroke, neurocognitive dysfunction, and cerebral haemorrhage). A cerebral oximeter performs non-invasive transcutaneous measurements using near infrared radiation to assess the oxygenation of tissues. The objective of the study was to determine if the angle and thickness of a patient's skull affects measurements. Intralipid water solution, gelatine, and ink were used to make six phantoms with skull thickness ranging from 6 to 11 mm. All phantoms were bent froma0to20 degrees angle. The cerebral oximeter SOMETICS INVOS 5100C was used to perform regional oximetry measurements. For skull thickness of 11 mm, the rSO2 was 45.8% (SD 0.96); for skull thickness of 10 mm, the rSO2 was 45.25% (SD 2.22); for skull thickness of 9 mm, the rSO2 was 32% (SD 1.63); for skull thickness of 8 mm, the rSO2 was 17% (SD 1.83); for skull thickness of 7 mm, the rSO2 was 15% (SD 0); for skull thickness of 6 mm, the rSO2 was 15% (SD 0). No significant changes were observed regarding the angle of the skull phantom. The thickness of the bone layer of the skull phantom affected the regional oximetry results, whereas the angle of the skull did not affect it. [ABSTRACT FROM AUTHOR]

To investigate the frequency, predictors, and outcomes of neurologic injury in adults treated with postcardiotomy extracorporeal membrane oxygenation (PC-ECMO). A retrospective multicenter registry study. Twenty-one European institutions where cardiac surgery is performed. A total of 781 adult patients who required PC-ECMO during 2010 to 2018 were divided into patients with neurologic injury (NI) and patients without neurologic injury (NNI). Baseline and operative data, in-hospital outcomes, and long-term survival were compared between the NI and the NNI groups. Predictors of neurologic injury were identified. A subgroup analysis according to the type of neurologic injury was performed. Overall, NI occurred in 19% of patients in the overall series, but the proportion of patients with NI ranged from 0% to 65% among the centers. Ischemic stroke occurred in 84 patients and hemorrhagic stroke in 47 patients. Emergency procedure was the sole independent predictor of NI. In-hospital mortality was higher in the NI group than in the NNI group (79% v 61%, p < 0.001). The one-year survival was lower in the NI group (17%) compared with the NNI group (37%). Long-term survival did not differ between patients with ischemic stroke and those with hemorrhagic stroke. Neurologic injury during PC-ECMO is common and associated with a dismal prognosis. There is considerable interinstitutional variation in the proportion of neurologic injury in PC-ECMO-treated adults. Well-known risk factors for stroke are not associated with neurologic injury in this setting. [ABSTRACT FROM AUTHOR]

Hypothermic circulatory arrest (HCA) is a technique used for complex repair of the aorta, but it can be associated with neurologic morbidity. To better understand the molecular changes that underlie ischemic brain injury, we assessed gene expression and cytokine/chemokine polypeptide concentration in brain tissue and cerebrospinal fluid (CSF) of canines that underwent two hours of HCA. Materials and Methods: Adult male canines were cannulated peripherally for cardiopulmonary bypass, cooled to 18°C, and arrested for two hours. Animals were euthanized two, eight, or 24 hours post-HCA (n = 8 per group), and their brains were compared to brains from eight normal canines, using gene expression microarray analysis, cytokine assay, and histopathology. Two to eight hours after HCA, pro-inflammatory cytokine mRNAs increased markedly, and gene expression was enriched within signaling pathways related to neuroinflammation or ischemic injury. Concentrations of pro-inflammatory cytokine polypeptides IL-6, IL-8, IL-1β, and CCL2 were very low in normal canine brain, whereas anti-inflammatory IL-10 and TGF-β1 were expressed at moderate levels. Pro-inflammatory cytokine concentrations rose robustly in cerebral tissue and CSF after HCA. IL-6 and IL-8 peaked at eight hours and declined at 24 hours, while IL-1β and CCL2 remained elevated. Concentrations of anti-inflammatory IL-10 and TGF-β1 were maintained after HCA, with a significant increase in TGF-β1 at 24 hours. These cytokines represent potential diagnostic markers for ischemic neurologic injury that could be used to assess neurologic injury in patients undergoing HCA. The cellular mechanisms underlying this pro-inflammatory, ischemic-induced injury represent potential targets for neuroprotection in the future. [ABSTRACT FROM AUTHOR]

We aimed to study the clinical utility of serum lipoprotein-associated phospholipase A2 (Lp-PLA2) in acute ischemic stroke (AIS) with cerebral artery stenosis (CAS). We included 200 AIS patients and 90 healthy controls in this study. AIS patients were classified into three subgroups depending on the severity of CAS. They were also classified based on the stability of the carotid plaques. Spearman correlation analysis was performed to determine the correlation relationship between the level of Lp-PLA2 and neurologic injury. Binary logistic regression analysis was performed to determine the independent risk factors for AIS. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic value of Lp-PLA2 for AIS and for the degree of CAS. We found that the serum level of Lp-PLA2 in AIS patients was significantly higher than that in the control group. Lp-PLA2 was further identified as an independent risk factor for AIS (p = 0.001, OR = 1.057). In addition, serum Lp-PLA2 level was the highest in AIS patients with severe CAS or occlusion. Lp-PLA2 level was higher in AIS patients with unstable plaques and in AIS patients with moderate to severe neurological injury. Lp-PLA2 level was positively correlated with National Institutes of Health Stroke Scale (NIHSS) score (r = 0.335, p = 0.001). We found that the optimal cut-off value for Lp-PLA2 level was 123.365 ng/ml, at which the sensitivity and specificity for the diagnosis of ACI were 74.5 and 86.7%, respectively, and the area under ROC curve (AUC) was 0.892. Similarly, the optimal value for Lp-PLA2 level was 136.46 ng/ml, at which the sensitivity and specificity for the diagnosis of the presence of moderate to severe artery stenosis or occlusion were 79.6 and 95.2%, respectively, and the AUC was 0.938. The ROC curve indicated that serum Lp-PLA2 level has an excellent diagnostic value for AIS and severe stenosis. Based on these results we conclude that Lp-PLA2 could be a potential biomarker to complement the current imaging methods in the prediction and diagnosis of AIS. An elevated Lp-PLA2 level is also correlated with carotid plaque instability, severe neurological injury and cerebrovascular stenosis. Future longitudinal studies are needed to determine whether there is a causative relationship between Lp-PLA2 and AIS.

Background: Subarachnoid hemorrhage accounts for more than 30,000 cases of stroke annually in North America and encompasses a 4.4% mortality rate. Since a vast number of subarachnoid hemorrhage cases present in a younger population and can range from benign to severe, an accurate diagnosis is imperative to avoid premature morbidity and mortality. Here, we present a straightforward approach to evaluating, risk stratifying, and managing subarachnoid hemorrhages in the emergency department for the emergency medicine physician. Discussion: The diversities of symptom presentation should be considered before proceeding with diagnostic modalities for subarachnoid hemorrhage. Once a subarachnoid hemorrhage is suspected, a computed tomography of the head with the assistance of the Ottawa subarachnoid hemorrhage rule should be utilized as an initial diagnostic measure. If further investigation is needed, a CT angiography of the head or a lumbar puncture can be considered keeping risks and limitations in mind. Initiating timely treatment is essential following diagnosis to help mitigate future complications. Risk tools can be used to assess the complications for which the patient is at greatest. Conclusion: Subarachnoid hemorrhages are frequently misdiagnosed; therefore, we believe it is imperative to address the diagnosis and initiation of early management in the emergency medicine department to minimize poor outcomes in the future. [ABSTRACT FROM AUTHOR]

Children supported by extracorporeal membrane oxygenation present a high risk of neurological complications. Although carotid cannulation is known to be associated with neurologic injury, conflicting data exist with regard to the predominance of right- or left-sided lesions. We describe here two infants requiring veno-arterial extracorporeal membrane oxygenation for septic shock who encountered right watershed infarction ipsilateral to carotid artery cannulation. Hemodynamic failure seems to be the most probable underlying mechanism. The asymmetry of transcranial Doppler metrics in one case and the low right regional cerebral oxygen saturation value observed soon after right cannulation in both cases suggest an insufficient cerebral collateral flow compensation. The risk of ipsilateral watershed injury should be considered before cervical cannulation, notably in the context of sepsis and an evaluation of the cerebral collateral blood flow before and just after cannulation may be interesting in order to identify infants with higher risk of ipsilateral ischemic lesions. [ABSTRACT FROM AUTHOR]

We aimed to study the clinical utility of serum lipoprotein-associated phospholipase A2 (Lp-PLA2) in acute ischemic stroke (AIS) with cerebral artery stenosis (CAS). We included 200 AIS patients and 90 healthy controls in this study. AIS patients were classified into three subgroups depending on the severity of CAS. They were also classified based on the stability of the carotid plaques. Spearman correlation analysis was performed to determine the correlation relationship between the level of Lp-PLA2 and neurologic injury. Binary logistic regression analysis was performed to determine the independent risk factors for AIS. Receiver operating characteristic (ROC) analysis was performed to assess the diagnostic value of Lp-PLA2 for AIS and for the degree of CAS. We found that the serum level of Lp-PLA2 in AIS patients was significantly higher than that in the control group. Lp-PLA2 was further identified as an independent risk factor for AIS (p = 0.001, OR = 1.057). In addition, serum Lp-PLA2 level was the highest in AIS patients with severe CAS or occlusion. Lp-PLA2 level was higher in AIS patients with unstable plaques and in AIS patients with moderate to severe neurological injury. Lp-PLA2 level was positively correlated with National Institutes of Health Stroke Scale (NIHSS) score (r = 0.335, p = 0.001). We found that the optimal cut-off value for Lp-PLA2 level was 123.365 ng/ml, at which the sensitivity and specificity for the diagnosis of ACI were 74.5 and 86.7%, respectively, and the area under ROC curve (AUC) was 0.892. Similarly, the optimal value for Lp-PLA2 level was 136.46 ng/ml, at which the sensitivity and specificity for the diagnosis of the presence of moderate to severe artery stenosis or occlusion were 79.6 and 95.2%, respectively, and the AUC was 0.938. The ROC curve indicated that serum Lp-PLA2 level has an excellent diagnostic value for AIS and severe stenosis. Based on these results we conclude that Lp-PLA2 could be a potential biomarker to complement the current imaging methods in the prediction and diagnosis of AIS. An elevated Lp-PLA2 level is also correlated with carotid plaque instability, severe neurological injury and cerebrovascular stenosis. Future longitudinal studies are needed to determine whether there is a causative relationship between Lp-PLA2 and AIS. [ABSTRACT FROM AUTHOR]

PURPOSE OF THE STUDY Acute knee dislocation is a less common injury of the knee joint. It is, however, a serious injury with a high rate of nerve and vascular damage and it is considered a limb threatening injury with long-term functional disability, which can ultimately lead to amputation. Knee dislocations constitute less than 0.5% of all joint dislocations. Most of these injuries occur in highenergy traumas and careful diagnosis can identify the patient at risk of this injury. MATERIAL AND METHODS The total number of patients with knee dislocation was 37. The incidence of knee dislocation was 2.5 patients per year. The mean age of patients was 49 years. After the evaluation of blood supply to the limb and before the examination of the ligament injury, routine X-ray views of the affected joint were performed. It was necessary to confirm good blood supply of the limb, in which knee dislocation had been suspected. In patients with reduced knee joint and asymmetric pulses in the lower limb, CT angiography was indicated. The absence of peripheral pulses and the presence of serious clinical signs of peripheral blood supply disruption in case of the reduced knee or irreducible knee dislocation necessitated immediate revision by a vascular surgeon performed in the operating room. RESULTS Dislocation of the knee without TKA (a total of 34 cases) was caused by a high-energy trauma in 19 cases (56%) and in 7 cases (21%) it was a part of polytrauma. The most common was a motorcycle accident, namely in 7 cases (21%). In 12 cases (35%), it was a low-energy trauma, a fall or a slip while walking. In three cases (9%), the patients suffered an open knee dislocation. In 18 patients (47%), no knee surgery was performed. The knee ligament injury was treated non-operatively through knee brace fixation. An open revision with sutures of injured ligament structures and knee capsule was performed in 16 patients (42%). In two cases, above-the-knee amputation was done. External fixation was performed in two polytrauma patients. Three cases of infectious complications were reported. Nerve lesions were observed in 9 cases (25%). Vascular lesions were recorded in 9 cases (25%). Deep vein thrombosis was observed in three cases in our study group. The Lysholm knee questionnaire was used to assess subjective difficulties. DISCUSSION In agreement with the literature, these injuries occur most frequently when riding on motorcycle. The patients, in whom a vascular lesion was identified and revascularisation performed within 8 hours, showed a significantly lower incidence of amputations (11%) compared to those who underwent surgery after 8 hours (86%). Majority of vascular surgeons consider 6 hours to be the time limit for the performance of vascular reconstruction since a surgery performed after 6 hours is accompanied by a higher complication rate. Currently, the aim of the final treatment is to perform anatomic suture or reconstruction of knee ligaments and meniscus to achieve a stable, pain-free, functional knee and to prevent any complications. CONCLUSIONS Knee joint dislocation ranks among less common injuries that can be accompanied by a vascular injury in 20% on average and a nerve lesion in 10–40% (around 25% on average). A negative X-ray in spontaneous reduction of knee dislocation can be misleading for proper diagnosis. It is crucial to rule out a vascular injury that might be a limb threatening. In case of a vascular lesion, an early reconstruction of vascular supply is necessary within 6 hours after the injury. The revascularisation performed later is accompanied by a high risk of complications and can ultimately lead to above-the-knee amputation. It is most appropriate to refer such serious injuries to specialised trauma centres that avail of necessary equipment and experience with treating the patients who sustained such complicated orthopaedic injuries. As to the ligament reconstruction, most surgeons prefer to postpone the procedure in majority of cases by 10–14 days. [ABSTRACT FROM AUTHOR]

Communication between the enteric nervous system (ENS) of the gastrointestinal (GI) tract and the central nervous system (CNS) is vital for maintaining systemic homeostasis. Intrinsic and extrinsic neurological inputs of the gut regulate blood flow, peristalsis, hormone release, and immunological function. The health of the gut microbiome plays a vital role in regulating the overall function and well-being of the individual. Microbes release short-chain fatty acids (SCFAs) that regulate G-protein-coupled receptors to mediate hormone release, neurotransmitter release (i.e., serotonin, dopamine, noradrenaline, γ-aminobutyric acid (GABA), acetylcholine, and histamine), and regulate inflammation and mood. Further gaseous factors (i.e., nitric oxide) are important in regulating inflammation and have a response in injury. Neurologic injuries such as ischemic stroke, spinal cord injury, traumatic brain injury, and hemorrhagic cerebrovascular lesions can all lead to gut dysbiosis. Additionally, unfavorable alterations in the composition of the microbiota may be associated with increased risk for these neurologic injuries due to increased proinflammatory molecules and clotting factors. Interventions such as probiotics, fecal microbiota transplantation, and oral SCFAs have been shown to stabilize and improve the composition of the microbiome. However, the effect this has on neurologic injury prevention and recovery has not been studied extensively. The purpose of this review is to elaborate on the complex relationship between the nervous system and the microbiome and to report how neurologic injury modulates the status of the microbiome. Finally, we will propose various interventions that may be beneficial in the recovery from neurologic injury.

Supracondylar humerus fractures (ScHF) account for 60% of fractures of the elbow region in children. We assessed the relationship between neurovascular complications and the degree of fracture displacement as rated on the basis of modified Gartland classification. Moreover, we aimed to evaluate predisposing factors, e.g., age and gender, and outcomes of neurovascular complications in ScHF. Between 2004 and 2019, we treated 329 patients with ScHF at the Department of Traumatology and Orthopedics of the Upper Silesian Child Centre, Katowice, Poland. Mean age of patients (189 boys and 140 girls) was 7.2 years (Confidence interval: 6.89, 7.45). Undisplaced fractures were treated conservatively with a cast. Displaced fractures were managed by closed reduction and percutaneous Kirschner wire fixation using two pins inserted laterally. We retrospectively assessed the number of neurovascular lesions at baseline and recorded any iatrogenic injury resulting from the surgical intervention. Acute neurovascular lesions occurred in 44 of 329 ScHF patients (13.4%). The incidence of accompanying neurovascular injuries was positively associated with the severity of fracture displacement characterized by Gartland score. Vascular injuries occurred mainly in Gartland type IV ScHF, while nerve lesions occurred in both Gartland type III and IV ScHF. We noted a significantly higher mean Gartland score and mean age at injury in the group of children suffering from neurovascular injuries when compared to those in the group without such injuries (p = 0.045 and p = 0.04, respectively). We observed no secondary nerve lesions after surgical treatment. For the treatment of ScHF in children, we recommend closed reduction and stabilization of displaced fractures with K-wires inserted percutaneously from the lateral aspect of the upper arm. We advocate vessel exploration in case of absent distal pulses after closed reduction but do not consider primary nerve exploration necessary, unless a complete primary sensomotoric nerve lesion is present.

Neurologic injury remains the most important morbidity of prematurity. Those born at the earliest gestational ages can face a lifetime of major disability. Perinatal insults result in developmental delay, cerebral palsy, and other profound permanent neurologic impairments. The EXTracorporeal Environment for Neonatal Development (EXTEND) aims to transition premature neonates through this sensitive period, but it's impact on neurologic development requires analysis. Fetal sheep were maintained in a fluid-filled environment for up to 28 days. Physiologic parameters were measured continuously; tissues were subsequently fixed and preserved for myelin quantification, glial cell staining, and structural assessment via magnetic resonance. Surviving animals were functionally assessed. No evidence of fetal brain ischemia or white matter tract injury associated with the EXTEND system was detected, and the degree of myelination was regionally appropriate and consistent with age matched controls. No evidence of neurologic injury or immaturity was visible on magnetic resonance; animals that transitioned from the system had no persistent neurologic deficits. No evidence of major neurologic morbidity was found in animals supported on the EXTEND system, though more work needs to be done in order to verify its safety during critical periods of neurologic development. [ABSTRACT FROM AUTHOR]

Melatonin, a potent free radical scavenger, plays an important role in homeostasis of cell and organ physiology. The increased demand and synthesis from the pineal gland during times of oxidative stress suggests a potential benefit of melatonin supplementation during hospitalization for acute illness. Yet, the paucity of clinical studies for non‐anesthetic–associated indications in pediatric populations hampers the safe, effective, and consistent use of melatonin. The objective of this study was to systematically review published studies of melatonin use for non‐sedative and non‐analgesic indications in hospitalized pediatric patients. We conducted a search of PubMed, EMBASE, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Science, and Scopus databases for articles on the use of melatonin for pediatric patients in a hospital setting. Thirteen eligible studies, all in neonates, were identified. Data elements extracted included study design, number of study subjects, indication for melatonin therapy, and melatonin regimen (formulation, dosage, and duration). Because study methodologies were very heterogeneous, a quantitative synthesis of the published findings was not possible. The identified studies were therefore categorized by the indication of melatonin (adjuvant‐antioxidant or anti‐inflammatory therapy) in the following specific disease states: (i) acute infections, (ii) respiratory distress syndrome, (iii) neurologic injury, and (iv) jaundice. The current data suggest that melatonin is safe for use in hospitalized neonates. Melatonin may be beneficial for reducing inflammatory markers in neonatal patients with disease states and clinical sequelae that are associated with increased inflammation and oxidative stress. Melatonin, in conjunction with phototherapy, is not superior to use of vitamin D with phototherapy for treatment of neonatal jaundice. However, studies in other pediatric populations are needed given widespread use across clinical inpatient settings. [ABSTRACT FROM AUTHOR]

Background This study aimed to evaluate the significance of serum neuron-specific enolase (NSE) level as a predictor of neurologic injury in thoracic aortic surgery. Methods We neurologically assessed 60 consecutive patients who underwent thoracic aortic surgery for thoracic aortic aneurysm (n = 26) and aortic dissection (n = 34). Using moderate hypothermic circulatory arrest with antegrade cerebral perfusion, total arch replacement and hemiarch replacement were performed in 37 and 23 patients, respectively. Serum NSE levels in venous blood samples drawn before surgery and at 1 day after surgery were measured. Severity of neurologic injury was categorized as either uncomplicated (n = 48), temporary neurologic dysfunction (TND, n = 5), or permanent neurologic dysfunction (PND, n = 7). The extent of stroke was estimated on computed tomography or magnetic resonance imaging. Results The NSE level significantly differed among the three groups (PND > TND > uncomplicated) on the first postoperative day. Receiver-operating characteristic curve analysis showed that the cutoff value of NSE level was 34.14 ng/mL for neurologic injury (sensitivity, 0.769; specificity, 0.851) and 43.56 ng/mL for PND (sensitivity, 1.000; specificity, 0.963). The NSE level significantly correlated with the extent of stroke (r = 0.61, p < 0.001). Conclusion Serum NSE level is a significant predictor of adverse neurologic outcomes and extent of stroke after thoracic aortic surgery. [ABSTRACT FROM AUTHOR]

• Percutaneous sacroiliac (SI) screw fixation is a well-known method for fixing posterior pelvic ring injuries. • An understanding of the anatomical variations of sacral morphology, and proper reduction are both mandatory for accurate screw placement. • Despite the introduction of intraoperative navigation, SI screw misplacement still occurs. • The optimal technique for (SI) screw removal is controversial. • Percutaneous extraction of an intact SI screw resulted in complete neurologic recovery. Percutaneous sacroiliac fixation is an effective minimally invasive method for posterior pelvic ring stabilization. Screw misplacement, and subsequent neurologic injury are two well described complications. Managing those complications however is under-reported. A young female, sustained an unstable pelvic ring injury as a victim of motor vehicle collision. Following percutaneous sacroiliac screw fixation, she complained of L5 nerve root radiculopathy, and muscle weakness. Percutaneous removal of the screw after a wait period for fracture union resulted in immediate symptoms relief. Safe sacroiliac screw placement is technically demanding requiring good understanding of sacral complex morphology and its anatomic variants. Risk of screw misplacement, and potential neurologic injury increases in dysmorphic sacra, or with inaccurate fracture reduction. Advances in intraoperative imaging modalities have been introduced in an attempt to improve accurate screw insertion. Literature is scarce with reports discussing removal of sacroiliac screw. Technique of screw retrieval is also controversial. This case addresses management of an iatrogenic neurologic complication following percutaneous sacroiliac screw fixation. Our experience showed that, percutaneous retrieval of an intact misplaced sacroiliac screw is achievable, resulting in complete resolution of neurologic symptoms. [ABSTRACT FROM AUTHOR]