Neurological Injury Research Articles (Page 1)

Deep brain stimulation (DBS) is considered off-label and investigational in pediatric populations with some exceptions. There are limited data on the relative rates of complications after DBS across different indications and targets in children. This study aimed to evaluate the safety of DBS surgery for children with movement disorders (MDs; dystonia, chorea, or tic disorders), drug-resistant epilepsy (DRE), or neurodevelopmental disorders, namely, self-injurious behavior (SIB). Data were collected both prospectively and retrospectively from children implanted with DBS through the North American multicenter Child and Youth CompreHensIve Longitudinal Database for Deep Brain Stimulation and included demographic, clinical, operative, and postoperative variables. Complications included infection, noninfectious surgical site findings (dehiscence or seroma), hardware-related issues (disconnection or impedance change), intracranial injury, or other complications. The primary outcome was major complications, defined as any adverse event causing permanent neurologic injury or requiring surgical intervention. The secondary outcome was minor complications, defined as nonmajor complications. Generalized linear models were used to assess for any significant associations with complications. A total of 130 children and youth (mean age 12.2 ± 4.2; range 3-18) years and weighing 12.5-126.6 kg underwent DBS. The most common indication was MD (77, 59.2%), followed by DRE (47, 36.2%) and SIB (6, 4.6%). Major complications occurred in 11.5%, with a greater likelihood in MD (n = 12, 15.6%) compared with DRE (n = 2, 4.3%; odds ratio [OR] 3.55, 95% CI 2.66-4.73, p < 0.001) and significantly associated with lower weight at surgery (p < 0.001) and urgent intervention (p = 0.028). These included infection (6.2%), hardware malfunction (3.1%), and wound dehiscence (0.8%). Minor complications were also higher with MD compared with DRE (OR 1.83, 95% CI 1.16-2.89, p = 0.010) occurring in 22 participants (16.9%; 14 MD, 7 DRE, 1 SIB), including infection (6.2%), high impedance (1.5%), unrelated hydrocephalus (0.8%), perioperative worsening of symptoms (3.8%), incidental tract hemorrhage (2.3%), and noninfectious peri-electrode cystic changes (0.8%). DBS-associated complications were low across multiple pediatric indications and targets, with MD associated with higher risk of major complications. Limitations include a focus on surgical postoperative complications and not stimulation-related adverse outcomes. These findings demonstrate the safety profile of DBS in children in a large cohort.

Central venous catheterization (CVC) is a common procedure, yet it carries a risk of rare, preventable, and serious complications, such as guidewire loss, which can lead to severe morbidity and mortality. This case report aims to describe the occurrence, multidisciplinary management, and successful retrieval of a lost guidewire during an emergency CVC insertion. We report the case of a 63-year-old male with a subarachnoid hemorrhage. During CVC placement via the right femoral vein under ultrasound guidance, the guidewire was accidentally advanced into the central circulation and lost. A multidisciplinary team decided on endovascular retrieval. The retained guidewire was successfully retrieved three days later in the catheterization lab using a snaring technique, without any procedural complications. Unfortunately, the patient later died due to the progression of his primary neurological injury, underscoring that while the iatrogenic complication was resolved, the outcome was determined by the underlying critical illness. Guidewire loss is a preventable complication. Strict adherence to procedural protocols, especially in emergencies, early recognition, and prompt multidisciplinary coordination are crucial. Endovascular intervention is a safe and effective therapeutic option for managing this serious iatrogenic event.

Background: Supracondylar injuries of the humerus are the most prevalent elbow injury among pediatric patients. The conventional treatment of displaced fractures involves closing the reduction as well as percutaneous Kirchner wire pinning, using either lateral pin fixation or cross pin fixation. The objective of the study is to evaluate and contrast the results of lateral vs bilateral percutaneous pinning in pediatric patients with supracondylar humeral injuries. Methods: A comparative cross-sectional study was conducted at the National Institute of Traumatology and Orthopaedic Rehabilitation (NITOR) between July 2017 to June 2019. Children were classified into two groups according to the percutaneous pinning technique: Lateral pinning (n=15) and Crossed pinning (n=15). Both groups were comparable in terms of age, gender, injury duration, along with degree of fracture displacement. The chi-square test and t-tests for independence were employed. The results were reported as mean, frequency, along with percentage, with P &lt; 0.05 indicating statistical significance, using SPSS software. Result: The average age of patients was 6.86 ± 2.53 years for group I and 6.57 ± 2.41 years for group II overall. In the cohort with dual lateral K-wire fixation, 20% achieved exceptional outcomes, 66.67% obtained good outcomes, and 13.33% realized fair outcomes. In the medial-lateral K-wire fixation cohort, 20% achieved exceptional outcomes, 60% attained satisfactory results, and 20% exhibited acceptable results, with a P value of 0.881, signifying statistical insignificance. In the medial-lateral cross K-wire fixation group, the incidence of iatrogenic ulnar nerve injuries was 6.67%, while the two lateral K-wire fixation group reported no neurological injuries, yielding a P value of 0.664. Thus, the difference in the incidence of ulnar nerve injury between the two patient cohorts was not significant. Conclusion: Both fixation methods exhibit effectiveness; the application of two lateral K-wires offers stability akin to medial-lateral cross K-wire fixation while mitigating the danger of iatrogenic ulnar nerve injury. J Shaheed Suhrawardy Med Coll 2024; 16(1): 7-13

Survival following severe acute neurologic injury (SANI) is increasing. The complexities of caring for these patients are vast and gaps have been highlighted in post-acute care follow-up. While the development of post-ICU follow-up clinics have been increasing in popularity there is limited literature describing the landscape of post-neuroICU/NeuroRecovery clinics. We sought to describe the current landscape and identify benefits and barriers to clinic development in the United States. We developed a 19-question cross-sectional survey study. The survey was disseminated to clinicians working in neurocritical care units throughout the United States and open for completion from August 2023 to December 2023. Responses were characterized by descriptive statistics. None. Two hundred eighteen unique individuals responded to our survey. Post-neuroICU and/or NeuroRecovery clinics were uncommon and operational at only 69 of 215 respondents' institutions (32.1%). Forty-two percent reported an interest in engaging with a post-neuroICU clinic and an additional 39% showed interest but had identified other obligations preventing participation. Among the identified potential benefits of a clinic for survivors of SANI mitigating gaps in care, identifying differences between predicted and actual outcome, and reassessment of communication/prognosis ranked highest. Few post-neuroICU/NeuroRecovery clinics exist in the United States but interest in participating in this aspect of care is common within the neurocritical care community. The identification of gaps in care, obstacles to continued recovery, and potential to adjudicate differences between actual and predicted outcomes ranked among the most important potential benefits for extending the current neurocritical care paradigm to the clinic setting.

Tuberculous meningitis (TBM) is the most prevalent and severe manifestation of tuberculosis in CNS. The mechanisms of neurological injury caused by TBM are not well understood. Our study showed that overexpression of WTAP (Wilms tumor 1 associated protein) reduced inflammatory factors and Iba-1 expression induced in BV-2 by H37Rv. It also increased proliferation of neural stem/progenitor cells (NSPCs) and expression of the neuronal marker DCX in these cells. WTAP enhanced expression of high mobility group nucleosome-binding domain-containing protein 3 (HMGN3) by promoting m6A methylation of its mRNA. Reducing HMGN3 expression negated WTAP-induced anti-inflammatory and neuroprotective effects in TBM cell model. WTAP inhibited inflammation and microglia activation while promoting NSPC differentiation into neurons via elevation of HMGN3 expression. WTAP/HMGN3 proteins and the corresponding mRNA could be potential targets in the treatment of TBM.

Background: Nitric oxide signaling can mediate ischemia-reperfusion injury by altering vascular resistance and inflammatory responses, including the production and degradation of reactive oxygen species (ROS). Excess ROS contributes to oxidative stress and can impair mitochondrial energy synthesis via oxidative phosphorylation (OxPhos). We previously demonstrated that ROS and mitochondrial respiration in the neonatal brain can be adversely affected following deep hypothermic circulatory arrest (DHCA). It is unknown if inhaled nitric oxide (iNO) alters cerebral ROS and OxPhos capacity post-DHCA. Research Question: Does intraoperative iNO therapy affect cerebral ROS, OxPhos capacity, and neurologic injury or recovery after DHCA? Methods: Ten neonatal swine underwent DHCA (90min, 18 o C) prior to reperfusion and rewarming, of which half were randomized and blinded to receive iNO (40ppm) intraoperatively (DHCA 90min+iNO , N=5) and half did not (DHCA 90min , N=5). Five additional piglets underwent sham procedures without bypass, DHCA, or iNO. Upon study completion, brain tissue was analyzed using high-resolution mitochondrial respirometry. Immunohistochemistry assessed microglia- and neuron-specific inflammation using antibodies for ionized calcium-binding adaptor molecule 1 (IBA-1) and beta-amyloid precursor protein (β-APP), respectively. Results: Following DHCA 90min+iNO , cerebral ROS production did not decline compared to DHCA 90min animals ( P =0.210, Figure ), and OxPhos capacity via mitochondrial complex I was reduced compared to both sham ( P =0.041 ) and DHCA 90min animals ( P =0.078, Figure ). Rare and frequent β-APP staining was more common after DHCA 90min and DHCA 90min+iNO compared to sham animals ( P =0.055), and IBA-1 staining in subcortical white matter increased following DHCA 90min+iNO compared to both sham ( P =0.001 ) and DHCA 90min animals ( P =0.013 , Figure ). Conclusions iNO does not attenuate cerebral ROS following DHCA, and may even increase microglial inflammation and post-operative white matter injury by impairing energy synthesis via mitochondrial complex I. Further studies are warranted to elucidate how regional changes in the cerebral microcirculation may affect the delivery, efficacy, and toxicity of targeted therapeutics following DHCA. Improved insights into how microglial inflammation and mitochondrial energy synthesis mediate neurologic injury and recovery post-DHCA might ultimately help improve neurocognitive outcomes in congenital cardiac surgery.

Background: Cerebral edema after resuscitation from cardiac arrest (CA) may elevate intracranial pressure (ICP) and lower brain tissue oxygen (PbtO2) levels, causing secondary brain injury. We initiated a clinical protocol for invasive ICP and PbtO 2 monitoring and management in selected CA patients. Research Question: What specific radiographic and clinical criterial can be used to select post-resuscitation patients for invasive ICP and PbtO 2 monitoring, and does medical therapy mitigate high ICP (&gt;22mmHg) and low brain oxygen (&lt;20mHgHgHH)? Aim: Characterize the initial experience of selected post-CA patients with early radiographic edema managed with ICP/PbtO 2 monitoring. Approach: Right frontal Raumedic PTO catheters were placed in patients with abnormal head CT (loss of gray-white differentiation, narrowed cisternal spaces at the tentorium, diffuse loss of sulci), and early EEG suppression ratio &gt;70%. We excluded patients radiographically herniated, lacking cranial nerve reflexes, requiring systemic anticoagulation, or not desiring aggressive care. Monitors were placed during TTM, prior to rewarming, and elevated ICP and low PbtO 2 managed with a clinical algorithm. Results: Ten monitored patients included 6 women and 4 nonwhite people of mean age 40 (±13) years; 8/10 had noncardiac etiology of arrest. The ICP was elevated in 10/10 patients, requiring treatment with head positioning, sedation, cerebral perfusion pressure optimization, temperature management, osmotherapy, mild hyperventilation, and barbiturates. PbtO 2 was &lt;20mmHg in 8/8 patients, requiring treatment with increased FiO 2 or PEEP, fluids, vasopressors, inotropes, prone positioning, and ventilator changes. Of 10 patients with elevated ICP, 2 progressed to brain herniation, 2 rearrested and died, 6 were “successfully” managed with nonsurgical therapies, and 2 (20%) survived and made a good functional recovery. Prognostic MR imaging was often delayed due to monitoring, and temperature management often prolonged due to ICP elevation. No complications of ICP monitor insertion or maintenance were noted. Conclusions: All qualifying patients had dangerous elevations of ICP and low PbtO 2 . These abnormalities often responded to non-surgical therapy, and in 2/10 cases resulted in good functional outcomes. Intracranial hypertension and brain hypoxia after cardiac arrest are treatable, and might reduce secondary neurological injury leading to better outcomes.

Introduction: Early and accurate prediction of neurological injury during cardiopulmonary resuscitation (CPR) is vital for guiding clinical decisions and improving outcomes following cardiac arrest. Previous studies have shown the utility of non-invasive optical neuromonitoring as an indicator of CPR quality. This study further examines the utility of intra-arrest optical metrics of cerebral oxygenation, blood volume, and microvascular flow to predict post cardiac arrest cerebral metabolic injury. Hypothesis: Non-invasive optical neuromonitoring during CPR predicts cerebral microdialysis lactate-pyruvate ratio (LPR). Methods: A total of 46 pediatric swine ( Sus scrofa , 8–12 kg) underwent asphyxia-associated cardiac arrest followed by CPR. Continuous optical waveforms were recorded on the left forehead during CPR, including tissue oxygen saturation (StO 2 ), total hemoglobin concentration (THC), oxyhemoglobin concentration (HbO 2 ), and blood flow index (BFI) signals. Waveforms were block-averaged in non-overlapping 15-second windows. A cerebral microdialysis catheter was inserted in the contralateral hemisphere to a depth of 1-1.5cm. Microdialysis perfusate were obtained between ROSC time and 1h after ROSC, and peak LPR during this period was measured. To evaluate time dependency, we modeled multiple temporal CPR segments: 2–4, 2–6, 2–8, 2–10, 2–12, and 2–14 minutes. For each segment, the mean and slope (linear trend) of each optical feature were used to train extreme gradient boosting (XGB) regression models to predict post-ROSC peak LPR. Five-fold cross-validation was employed, and model performance was assessed using the coefficient of determination (R 2 ) from stacked predictions. Results: Mean StO 2 and HbO 2 were the most predictive univariate features (Table 1). Mean StO 2 explained 27–28% of the variance in the 2–8 and 2–10 minute segments, while mean HbO 2 explained 27–30% of LPR variance across all segments except 2–10 minutes. The best-performing multivariate model combined all optical features and achieved an R 2 of 0.40 using the 2–8 minute segment. Conclusion: Optical measurements during CPR, particularly indicators of cerebral oxygenation (StO 2 , HbO 2 ), show promise as non-invasive predictors of acute cerebral metabolic injury following cardiac arrest. These measures outperformed markers of blood volume (THC) and microvascular flow (BFI), supporting their potential role in real-time monitoring and decision-making during and following resuscitation.

Objective: This study aimed to investigate the relationship between serum inflammatory markers (TNF-α, IL-6, CRP) and cerebrospinal fluid (CSF) cytokine levels (AVP, OT, β-EP) with the severity of postoperative neurological injury and prognosis in patients with glioma. Methodology: In this retrospective study, 80 patients with glioma who underwent surgery (study group) and 80 non-glioma controls who underwent CSF sampling (control group) were enrolled from Baoding No.1 Hospital between May 2023 and December 2024. Serum inflammatory factors (TNF-α, IL-6, CRP) and CSF cytokines (AVP, OT, β-EP) were measured in both groups. Neurological impairment was assessed using the NIH Stroke Scale (NIHSS). Comparative analyses were performed between groups and across different pathological stages and neurological injury severities. Multivariate logistic regression was used to identify risk factors affecting 3-year survival. Results: The study group showed significantly elevated levels of serum TNF-α, IL-6, CRP and CSF AVP, OT, β-EP compared to controls (p &lt; 0.01). These markers increased with disease severity and higher pathological stage (III–IV vs. I–II, p &lt; 0.01). Multivariate analysis identified TNF-α, IL-6, AVP, β-EP, pathological stage, degree of neurological injury, and extent of resection as independent risk factors for three years survival (p &lt; 0.05). Conclusion: Elevated levels of serum inflammatory markers and CSF cytokines are associated with more severe neurological injury and worse prognosis in glioma patients. TNF-α, IL-6, AVP, and β-EP are independent risk factors for poor survival outcomes.

ABSTRACT Objective Anesthetic drugs have toxic effects on the central nervous system, leading to cognitive dysfunction. This study aimed to explore the potential protective effect of miR-672-3p against ketamine-induced neurological injury and its underlying molecular mechanism. Methods Reverse transcription quantitative polymerase chain reaction was employed to detect the expression of miR-672-3p in rat brain tissues and PC12 cells. The Morris water maze test was utilized to assess alterations in cognitive function in rats. Enzyme-linked immunosorbent assay kits were used to measure the levels of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6 and superoxide dismutase (SOD), malondialdehyde (MDA), lactate dehydrogenase (LDH) in rat brain tissues and cells. Cell viability was assessed via the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis levels were evaluated through Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Results MiR-672-3p was up-regulated in ketamine-induced brain tissues and cells. Ketamine-treated rats had a prolonged escape latency, a reduced number of platform crossings, and a reduced percentage of time spent in the target quadrant. Inhibition of miR-672-3p partially reversed these cognitive deficits. Ketamine increased tissue and cellular levels of TNF-α, IL-1β, IL-6, MDA, LDH and decreased SOD activity. Inhibition of miR-672-3p significantly attenuated inflammatory responses and oxidative stress injury. Ketamine decreased cell viability and increased apoptosis. Inhibition of miR-672-3p partially restored cell viability and reduced apoptosis. Conclusion Inhibition of miR-672-3p expression attenuates ketamine-induced nerve damage. This study provides potential molecular target and theoretical basis for the prevention and treatment of ketamine-induced neurological injuries and other anesthetic-related cognitive dysfunctions.

Traumatic brain injury (TBI) in childhood is a major global health concern and a leading cause of morbidity and mortality in the pediatric population. Its incidence is rising worldwide, with early childhood and adolescence representing the most vulnerable age groups. Beyond acute neurological injury, post-traumatic endocrine dysfunction has emerged as an underrecognized but clinically significant sequela, with potential long-term consequences for growth, puberty, metabolism, and overall quality of life. The hypothalamic–pituitary axis (HPA) is uniquely vulnerable due to its anatomical and vascular characteristics, making pituitary cells—particularly somatotrophs and gonadotrophs—susceptible to ischemic, traumatic, and inflammatory damage. Reported prevalence of post-TBI pituitary dysfunction in children ranges from 5 to 57%, reflecting a deep heterogeneity in injury severity, diagnostic methods, and timing of evaluations. Growth hormone deficiency (GHD) is the most frequently reported abnormality, with presentations varying from transient to persistent forms. Gonadal axis disturbances, including hypogonadotropic hypogonadism and, less commonly, central precocious puberty, highlight the impact of TBI on pubertal development. Adrenal dysfunctions, though less frequent, may be life-threatening if unrecognized, while posterior pituitary disorders, such as diabetes insipidus, usually revealed acutely, are often transient. Importantly, many endocrine sequelae manifest months to years after the initial trauma, complicating a timely diagnosis. Current evidence underscores the need for structured, longitudinal endocrine surveillance after pediatric TBI, with baseline and follow-up assessments at defined intervals. Early recognition and intervention, including hormone replacement when appropriate, may improve neurocognitive recovery and overall rehabilitation outcomes. Future multicenter studies and standardized screening protocols should be considered essential to clarify incidence, natural history, and optimal management strategies for post-traumatic endocrine dysfunction in children.

Peripheral nerve regeneration relies on repair Schwann cells (SCs) to support axonal regrowth and functional recovery. This study aimed to identify drugs that promote this repair phenotype, which is regulated by the expression of the transcription factor c-Jun. Purmorphamine (PUR) and Smoothened agonist (SAG) are both Sonic Hedgehog (SHH) agonists that have been implicated in promoting regeneration after neurological injury in animal models. Here, we have demonstrated that SHH agonists significantly increased c-Jun expression in rat primary SCs and promoted morphological and functional changes consistent with the repair SC phenotype, including an elongated bipolar morphology and increased secretion of neurotrophic factors. Notably, PUR consistently demonstrated a greater potency in driving these effects compared with SAG at the same concentrations. We also identified 2.5 µM PUR as an effective dosage producing these measurable effects in vitro. Coculturing dorsal root ganglion (DRG) neurons with PUR-treated SCs resulted in a marked increase in neurite elongation, suggesting that cell-based or contact-dependent features of repair SCs contribute to axon growth. These findings demonstrate that SHH agonists effectively reprogram SCs into a repair phenotype, which constitutes a potential therapeutic strategy for enhancing nerve regeneration and functional recovery in peripheral nerve injury treatment.

Assessment of a painful shoulder arthroplasty.

miR-23b-5p: A potential biomarker in fluoride-induced neurological injury.

Caveat Emptor: Characterizing Water Bead Consumer and Safety Reporting.

Exploratory Comparison of Autoregulation Indices in Severe Neurological Injury using Near-Infrared Spectroscopy and Pressure Reactivity Index

Hinge craniotomy versus decompressive craniectomy for the neurosurgical management of traumatic brain injury and stroke: A systematic review and meta-analysis.

Study DesignHybrid retrospective and prospective observational study.ObjectivesTo evaluate the safety and clinical utility of Functional Dynamic Cervical Spine Radiographs (FDCSR) under supervision in assessing instability of subaxial cervical spine in non-obtunded cervical spine trauma patients with incomplete or no neurological deficits.MethodsWe reviewed records and radiographs of patients with traumatic cervical spine injury from January 2014 to December 2017 (retrospectively) and January 2018 to December 2018 (prospectively). Inclusion criteria: (1) Patients with intact neurology and stable injuries on static radiographs (<11° angulation, <3.5mm translation) who underwent FDCSR; (2) Patients with neurological deficits and degenerative/congenital canal stenosis without discernible injuries on static radiographs, suggestive of hyperextension injuries. Outcomes assessed included X-ray adequacy, pre- and post-procedure neurological status, pain/spasm during imaging, and evidence of instability.ResultsOf 6890 patients evaluated, 364 met inclusion criteria (258 retrospective, 86 prospective). Pre-FDCSR neurological status was AIS-B (1.1%), AIS-C (8%), AIS-D (12.6%), and normal (78.3%). No neurological deterioration occurred post-FDCSR. X-rays were adequate in 202 cases (55.5%) and inadequate in 162. Instability was detected in 4.95% of adequate (n = 10) and 11.7% of inadequate (n = 19) FDCSR studies, with an overall instability rate of 7.97% (n = 29).ConclusionsFDCSR, when performed under appropriate supervision, is a safe and effective adjunct for detecting cervical spine instability in select trauma patients. It can identify occult instability even in suboptimal studies, supporting its utility in the evaluation of patients with equivocal findings on static imaging.

Background: Neonatal hypoxic-ischemic encephalopathy (HIE) due to perinatal hypoxia carries high risk of permanent neurological injury. Therapeutic hypothermia offers partial protection; complementary regenerative therapies are needed.

Background/Objectives: Calcified thoracic disc herniations are a formidable surgical challenge due to their proximity to the spinal cord and the heightened risk of iatrogenic neurological injury. Traditional anterior and posterolateral approaches, while effective in select scenarios, may not provide adequate exposure for large, centrally located calcified discs. Methods: We performed a narrative review of the literature and retrospective case series of seven patients who underwent transpedicular–transdural thoracic discectomy for central or centrolateral calcified disc herniations at our institution in recent years. All patients were followed clinically for a minimum of three months postoperatively. Surgical technique and intraoperative nuances were also documented. Results: The transdural approach enabled direct access to the ventral thoracic spine, allowing for the effective decompression of calcified herniations in all cases. Six out of seven patients (86%) demonstrated clinical improvement or neurological stability at three-month follow-up, while one out of seven patients (14%) who presented with severe preoperative neurological deficits had persisting neurological deterioration postoperatively. The technical aspects of the microsurgical approach were critical to minimizing risk. Conclusions: The transpedicular–transdural approach is a viable and effective surgical option for select cases of central or centrolateral calcified thoracic disc herniation. When executed with a precise microsurgical technique, it offers safe decompression with favourable short-term outcomes.