Acute Brain Research Articles

Dysfunctional Brain Dynamics of Parkinson's Disease and the Effect of Acute Deep Brain Stimulation.

Background: Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease, and deep brain stimulation (DBS) can effectively alleviate PD symptoms. Although previous studies have detected network features of PD and DBS, few studies have considered their dynamic characteristics.Objective: We tested two hypotheses. (1) Reduced brain dynamics, as evidenced by slowed microstate dynamic change, is a characteristic of PD and is related to the movement disorders of patients with PD. (2) Therapeutic acute DBS can partially reverse slow brain dynamics in PD to healthy levels.Methods: We used electroencephalography (EEG) microstate analysis based on high density (256-channel) EEG to detect the effects of PD and DBS on brain dynamic changes on a sub-second timescale. We compared 21 healthy controls (HCs) with 20 patients with PD who were in either DBS-OFF or DBS-ON states. Assessment of movement disorder using the Unified Parkinson's Disease Rating Scale III was correlated with microstate parameters.Results: Compared with HCs, patients with PD displayed a longer mean microstate duration with reduced occurrence per second, which were significantly associated with movement disorders. In patients with PD, some parameters of microstate analysis were restored toward healthy levels after DBS.Conclusions: Resting-state EEG microstate analysis is an important tool for investigating brain dynamic changes in PD and DBS. PD can slow down brain dynamic change, and therapeutic acute DBS can partially reverse this change toward a healthy level.

Association between serum metal element levels and the severity of acute traumatic brain injury following traffic accidents

Association between serum metal element levels and the severity of acute traumatic brain injury following traffic accidents

Endothelial-specific insulin receptor substrate-1 overexpression worsens neonatal hypoxic-ischemic brain injury via mTOR-mediated tight junction disassembly

Hypoxic-ischemic (HI) encephalopathy is the major cause of mortality and disability in newborns. The neurovascular unit is a major target of acute and chronic brain injury, and therapies that protect simultaneously both neurons and vascular endothelial cells from neonatal HI injury are in demand. Insulin receptors and its key downstream molecule-insulin receptor substrate −1 (IRS-1) are potential neuroprotective targets and expressed both in neuron and endothelial cells. To investigate whether IRS-1 can act similarly in neurons and vascular endothelial cells in protecting neurovascular units and brain form HI injury, we found that neuron-specific IRS-1 transgenic rats showed reduced neurovascular injury and infarct volumes, whereas endothelial-specific IRS-1 transgenic rats showed increased blood-brain barrier (BBB) disruption and exaggerated neurovascular injury after neonatal HI brain injury. Endothelial-specific IRS-1 overexpression increased vascular permeability and disassembled the tight junction protein (zonula occludens-1) complex. Inhibition of mammalian target of rapamycin (mTOR) by rapamycin preserved tight junction proteins and attenuated BBB leakage and neuronal apoptosis after HI in the endothelial-specific IRS-1 transgenic pups. Together, our findings suggested that neuronal and endothelial IRS-1 had opposite effects on the neurovascular integrity and damage after neonatal HI brain injury and that endothelial IRS-1 worsens neurovascular integrity after HI via mTOR-mediated tight junction protein disassembly.

Neuritin improves the neurological functional recovery after experimental intracerebral hemorrhage in mice

Stroke is one of the leading causes of death worldwide, with intracerebral hemorrhage (ICH) being the most lethal subtype. Neuritin (Nrn) is a neurotropic factor that has been reported to have neuroprotective effects in acute brain and spinal cord injury. However, whether Nrn has a protective role in ICH has not been investigated. In this study, ICH was induced in C57BL/6 J mice by injection of collagenase VII, while the overexpression of Nrn in the striatum was induced by an adeno-associated virus serotype 9 (AAV9) vector. We found that compared with GFP-ICH mice, Nrn-ICH mice showed improved performance in the corner, cylinder and forelimb tests after ICH, and showed less weight loss and more rapid weight recovery. Overexpression of Nrn reduced brain lesions, edema, neuronal death and white matter and synaptic integrity dysfunction caused by ICH. Western blot results showed that phosphorylated PERK and ATF4 were significantly inhibited, while phosphorylation of Akt/mammalian target of rapamycin was increased in the Nrn-ICH group, compared with the GFP-ICH group. Whole cell recording from motor neurons indicated that overexpression of Nrn reversed the decrease of spontaneous excitatory postsynaptic currents (sEPSCs) and action potential frequencies induced by ICH. These data show that Nrn improves neurological deficits in mice with ICH by reducing brain lesions and edema, inhibiting neuronal death, and possibly by increasing neuronal connections.

OTULIN is a new target of EA treatment in the alleviation of brain injury and glial cell activation via suppression of the NF-\u03baB signalling pathway in acute ischaemic stroke rats

ObjectiveOvarian tumour domain deubiquitinase with linear linkage specificity (OTULIN) is a potent negative regulator of the nuclear factor-κB (NF-κB) signalling pathway, and it plays a strong neuroprotective role following acute ischemic stroke. Electroacupuncture (EA) is an effective adjuvant treatment for reducing brain injury and neuroinflammation via the inhibition of NF-κB p65 nuclear translocation, but the underlying mechanism is not clear. The present study investigated whether OTULIN was necessary for EA to mitigate brain injury and glial cell activation in a transient middle cerebral artery occlusion (tMCAO) model in rats.MethodsAn acute ischaemic stroke model was established via tMCAO surgery in Sprague–Dawley (SD) rats. EA was performed once daily at “Baihui (GV 20)”, “Hegu (LI 4)”, and “Taichong (LR 3)” acupoints. The effect of EA on the spatiotemporal expression of OTULIN in the ischaemic penumbra of the cerebral cortex was detected within 7 days after reperfusion. The effects of OTULIN gene silencing on EA neurological deficits, cerebral infarct volume, neuronal damage, the activation of microglia and astrocytes, the contents of tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6), and the expression of p-IκBa, IκBa and nucleus/cytoplasm NF-κB p65 protein were assessed.ResultsEA treatment increased endogenous OTULIN expression, which peaked at 48 h. Enhanced OTULIN was primarily located in neurons, but a small amount of OTULIN was detected in microglia. OTULIN silencing obviously reversed EA neuroprotection, which was demonstrated by worsened neurobehavioural performance, cerebral infarct volume and neuronal injury. The inhibitory effect of EA on the NF-κB pathway was also attenuated by enhanced IκBα phosphorylation and NF-κB p65 nuclear translocation. EA partially inhibited the transformation of microglia and astrocytes from resting states to activated states and reduced the secretion of TNF-α, IL-1β and IL-6. However, these preventive effects were reversed after the silencing of OTULIN expression.ConclusionsOTULIN provides a new potential therapeutic target for EA to alleviate acute ischaemic stroke-induced brain injury and the activation of glial cells, which are related to suppression of the NF-κB signalling pathway.

Neurological complications during veno-venous extracorporeal membrane oxygenation: Does the configuration matter? A retrospective analysis of the ELSO database

BackgroundSingle- (SL) and double-lumen (DL) catheters are used in clinical practice for veno-venous extracorporeal membrane oxygenation (V-V ECMO) therapy. However, information is lacking regarding the effects of the cannulation on neurological complications.MethodsA retrospective observational study based on data from the Extracorporeal Life Support Organization (ELSO) registry. All adult patients included in the ELSO registry from 2011 to 2018 submitted to a single run of V-V ECMO were analyzed. Propensity score (PS) inverse probability of treatment weighting estimation for multiple treatments was used. The average treatment effect (ATE) was chosen as the causal effect estimate of outcome. The aim of the study was to evaluate differences in the occurrence and the type of neurological complications in adult patients undergoing V-V ECMO when treated with SL or DL cannulas.ResultsFrom a population of 6834 patients, the weighted propensity score matching included 6245 patients (i.e., 91% of the total cohort; 4175 with SL and 20,270 with DL cannulation). The proportion of patients with at least one neurological complication was similar in the SL (306, 7.2%) and DL (189, 7.7%; odds ratio 1.10 [95% confidence intervals 0.91–1.32]; p = 0.33). After weighted propensity score, the ATE for the occurrence of least one neurological complication was 0.005 (95% CI − 0.009 to 0.018; p = 0.50). Also, the occurrence of specific neurological complications, including intracerebral hemorrhage, acute ischemic stroke, seizures or brain death, was similar between groups. Overall mortality was similar between patients with neurological complications in the two groups.ConclusionsIn this large registry, the occurrence of neurological complications was not related to the type of cannulation in patients undergoing V-V ECMO.

Abstract P148: Role of Endothelin B Receptors in Neuronal Progenitor Cell Differentiation and Mitochondrial Function in Ischemic Stroke

Neuronal progenitor cells (NPCs) and mitochondria are well known to play roles in regeneration and functions of the brain, respectively. However, stimulation of endothelin-B receptors (ETBR) using an agonist, sovateltide (IRL-1620) on their fate in the brain after stroke remains elusive. We evaluated the effect of sovateltide mediated ETBR stimulation on differentiation of NPCs and fate of mitochondria after stroke. Ischemic stroke was induced by performing permanent right middle cerebral artery occlusion (MCAO) in rats. Sovateltide (5 μg/kg) or saline (equal volume) was injected intravenously; neurological and motor function evaluation was done at 24 hrs and day 7 post MCAO. Brain tissues were analyzed for NPCs differentiation and mitochondrial fate using techniques such as western blots, immunofluorescence, transmission electron microscopy and in situ PCR. In vitro hypoxia experiment was carried out to confirm sovateltide mediated neuronal differentiation. Neurological and motor functions were significantly improved in sovateltide treated rats at 24 hrs and day 7 post MCAO. Differentiation of NPCs was evident with upregulation of neuronal differentiation markers Neuro D1 (p=0.00002) as well as HuC/HuD (p=0.0037) along with neuronal marker Doublecortin (DCX) (p=0.00011) at 24 hrs post MCAO. However, significant upregulation only in HuC/HuD (p=0.043) was observed at day 7. Better preserved mitochondrial fate was observed in sovateltide rat brains with downregulation of mitochondrial fission marker, DRP1 (p<0.001), increase in fusion marker, MFN2 (p<0.0001) and increase in cross-sectional area x number (p<0.05) as well as mitochondrial/tissue area (p<0.05) at 24 hrs and day 7 post MCAO. In situ PCR analysis showed increased mitochondrial DNA (p=0.0418), indicating better mitochondrial biogenesis at day 7 post MCAO. In vitro exposure of sovateltide and hypoxia to cultured NPCs showed higher NeuroD1 and NeuN (a mature neuronal marker) expression confirming NPCs differentiation. Sovateltide mediated ETBR stimulation promotes differentiation of NPCs and mitochondrial fusion as well as biogenesis and helps in neuronal regeneration and function restoration in acute ischemic brains.

Abstract P731: Genetic Knockout of Cd38 Protects Mice Against Ischemic Brain Injury

Introduction: CD38 is an ectoenzyme that is present on the cellular membranes of endothelial cells and subtypes of inflammatory cells. We have shown that ischemia/reperfusion (I/R) in the heart triggers CD38 activation that in turns leads to NADPH depletion and endothelial nitric oxide synthase (eNOS) impairment. This cascade results in worsening of ischemic injury secondary to endothelial dysfunction. We hypothesize that a similar paradigm exists in acute ischemic stroke and that loss of CD38 function is protective against cerebral I/R injury. Methods: Middle cerebral artery occlusion (MCAO) was performed for 60 minutes in 15 week-old CD38 knockout mice (KO) n=12 and wild type (WT) mice n=12. Stroke volume was calculated using T2 MRI sequences obtained at 48 hours post MCAO. Percentage of brain infarction volume compensated for swelling (IFV) was calculated by manual segmentation of the stroke area and non-affected cerebral hemisphere. Following brain MRI, H&E staining and immunohistochemistry assessment of superoxide radicals (DHE fluorescence) nitric oxide (NO) (DAF fluorescence), eNOS expression, CD38 expression and microglia activation (Iba1) were performed. (P<0.05) was considered significant in statistical testing. Results: CD38 KO mice had a smaller IFV as % of the normal contralateral hemisphere volume compared to WT (19.6±3 vs 33.5±9, P=0.001). Both western blotting and immunohistology confirmed lack of CD38 expression in CD38 KO mice. CD38 expression was 55% higher in the ipsilateral stroke side compared to the contralateral stroke side in WT mice (P=0.0105). Compared to WT mice, CD38 KO had 45% lower superoxide levels (P<0.001), 50% higher NO levels (P<0.05) and 46% lower Iba-1 expression with more significance in ipsilateral side (P<0.01) than contralateral side (P<0.05). While eNOS expression was 40% lower in WT vs CD38 KO, this did not reach statistical significance. Conclusions: Thus, genetic deletion of CD38 is protective against cerebral ischemia with reduced superoxide production and preserved NO production, likely through the protection conferred against NADPH depletion. These results suggest that inhibition of CD38 could serve as a potent therapeutic approach to protect against acute ischemic stroke and related brain I/R injury.

Safety and efficacy of normobaric oxygenation on rescuing acute intracerebral hemorrhage-mediated brain damage\u2014a protocol of randomized controlled trial

BackgroundAll of the existing medication and surgical therapies currently cannot completely inhibit intracerebral hemorrhage (ICH)-mediated brain damage, resulting in disability in different degrees in the involved patients. Normobaric oxygenation (NBO) was reported attenuating ischemic brain injury. Herein, we aimed to explore the safety and efficacy of NBO on rescuing the damaged brain tissues secondary to acute ICH, especially those in the perihematoma area being threatened by ischemia and hypoxia.MethodsA total of 150 patients confirmed as acute spontaneous ICH by computed tomography (CT) within 6 h after symptoms onset, will enroll in this study after signing the informed consent, and enter into the NBO group or control group randomly according to a random number. In the NBO group, patients will inhale high-flow oxygen (8 L/min, 1 h each time for 6 cycles daily) and intake low-flow oxygen (2 L/min) in intermittent periods by mask for a total of 7 days. While in the control group, patients will breathe in only low-flow oxygen (2 L/min) by mask for 7 consecutive days. Computed tomography and perfusion (CT/CTP) will be used to evaluate cerebral perfusion status and brain edema. CT and CTP maps in the two groups at baseline and day 7 and 14 after NBO or low-flow oxygen control will be compared. The primary endpoint is mRS at both Day14 post-ICH and the end of the 3rd month follow-up. The secondary endpoints include NIHSS and plasma biomarkers at baseline and Day-1, 7, and 14 after treatment, as well as the NIHSS at the end of the 3rd month post-ICH and the incidence of bleeding recurrence and the mortalities within 3 months post-ICH.DiscussionThis study will provide preliminary clinical evidence about the safety and efficacy of NBO on correcting acute ICH and explore some mechanisms accordingly, to offer reference for larger clinical trials in the future.Trial registrationClinicalTrials.gov NCT04144868. Retrospectively registered on October 29, 2019.

Comparative Characteristics of Structural and Functional Changes in the Hippocampal CA<sub>3</sub> Region in White Rats After Acute Ischemia and Brain Injury

The aimof the study was to study pyramidal neurons and astrocytes of the hippocampal CA3region in dynamics in white rats after acute ischemia and severe traumatic brain injury.Material and methods.Acute ischemia was simulated by 20-minute occlusion of the common carotid arteries (CCA), and severe traumatic brain injury (TBI) by a free-falling weight impact. The Nissl staining, hematoxylin and eosin staining, immunohistochemical reactions for NSE, MAP-2, p38, GFAP were used in the study. The proliferative activity of the cells was assessed using the Ki-67 response. The study was carried out on thin (4 μm) serial frontal sections in the animals of the control group (animals without pathological factors, n=5) in 1, 3, 7 and 14 days after the experimental modeling of CCA occlusion (n=20) and TBI (n=20). Morphometric analysis was performed using the ImageJ 1.52s software. The relative area of edema-swelling zones in the neuropil, the number density of pyramidal neurons, the content of dystrophic and necrobiotically altered neurons, the content of neurons with one or more nucleoli, proliferating cells, the density of large trunks of pyramidal neurons dendrites, the total number density and the relative area of giant synaptic terminals in stratum lucidum was detected. The distribution of variation series, the verification of statistical hypotheses, and the construction of graphs were assessed using the Statistica 8.0 software and the R.Results.Mortality between groups did not differ and did not exceed 7%. In a day after CCA occlusion and TBI, there was a statistically significant increase in the relative volume of edema-swelling, the content of dystrophic and necrobiotically altered neurons, the total number density and the relative area of the terminals decreased, but the total number density of neurons did not change. In 3, 7 and 14 days, the mechanisms of neuroglio- and synaptic plasticity were activated. The content of neurons with two or more nucleoli increased, the total number and content of hypertrophied astrocytes increased, the cytoskeleton of damaged neurons was restored, and the content of interneuronal synapses increased. During the period from 3 to 14 days, the total number density of neurons in CCA occlusion decreased by 16.3%, and in TBI – by 33.7% (p=0.001). Pathological and compensatory-restorative changes were of a diffuse-focal nature and were more pronounced after TBI.Conclusion.Thus, the same type of focal heterochronous and heteromorphic dystrophic, necrobiotic and compensatory-restorative changes in the nervous tissue were observed after CCA occlusion and TBI in the hippocampal CA3region. Structural and functional recovery occurred together with a decrease in the total numerical density of pyramidal neurons and edema-swelling of the nervous tissue. More pronounced dystrophic and necrobiotic changes in TBI were combined with more pronounced compensatory-restorative changes in astrocytes and giant interneuronal synapses of the hippocampal CA3region. The revealed changes were considered as the basis for the standard permanent compensatory-restorative reorganization of the nervous tissue of the hippocampus in the postischemic and post-traumatic periods.

The accuracy of initial diagnoses in coma: an observational study in 835 patients with non-traumatic disorder of consciousness

BackgroundManagement of patients with coma of unknown etiology (CUE) is a major challenge in most emergency departments (EDs). CUE is associated with a high mortality and a wide variety of pathologies that require differential therapies. A suspected diagnosis issued by pre-hospital emergency care providers often drives the first approach to these patients. We aim to determine the accuracy and value of the initial diagnostic hypothesis in patients with CUE.MethodsConsecutive ED patients presenting with CUE were prospectively enrolled. We obtained the suspected diagnoses or working hypotheses from standardized reports given by prehospital emergency care providers, both paramedics and emergency physicians. Suspected and final diagnoses were classified into I) acute primary brain lesions, II) primary brain pathologies without acute lesions and III) pathologies that affected the brain secondarily. We compared suspected and final diagnosis with percent agreement and Cohen’s Kappa including sub-group analyses for paramedics and physicians. Furthermore, we tested the value of suspected and final diagnoses as predictors for mortality with binary logistic regression models.ResultsOverall, suspected and final diagnoses matched in 62% of 835 enrolled patients. Cohen’s Kappa showed a value of κ = .415 (95% CI .361–.469, p < .005). There was no relevant difference in diagnostic accuracy between paramedics and physicians. Suspected diagnoses did not significantly interact with in-hospital mortality (e.g., suspected class I: OR .982, 95% CI .518–1.836) while final diagnoses interacted strongly (e.g., final class I: OR 5.425, 95% CI 3.409–8.633).ConclusionIn cases of CUE, the suspected diagnosis is unreliable, regardless of different pre-hospital care providers’ qualifications. It is not an appropriate decision-making tool as it neither sufficiently predicts the final diagnosis nor detects the especially critical comatose patient. To avoid the risk of mistriage and unnecessarily delayed therapy, we advocate for a standardized diagnostic work-up for all CUE patients that should be triggered by the emergency symptom alone and not by any suspected diagnosis.

Statistical analysis plan for the Prophylactic Melatonin for Delirium in Intensive Care (ProMEDIC): a randomised controlled trial

RationaleDelirium is defined as acute organic brain dysfunction characterised by inattention and disturbance of cognition. It is common in the intensive care unit and is associated with poorer outcomes. Good quality sleep is important in the prevention and management of delirium. Melatonin is a natural hormone secreted by the pineal gland which helps in the regulation of the sleep-wake cycle. It is possible that melatonin supplementation in intensive care improves sleep and prevents delirium.Methods and designThe ‘Prophylactic Melatonin for Delirium in Intensive Care’ study is a multi-centre, randomised, double-blinded, placebo-controlled trial. The primary objective of this study is to determine whether melatonin given prophylactically decreases delirium in critically ill patients. A total of 850 ICU patients have been randomised (1:1) to receive either melatonin or a placebo. Participants were monitored twice daily for symptoms of delirium.ResultsThis paper and the attached additional files describe the statistical analysis plan (SAP) for the trial. The SAP has been developed and submitted for publication before the database has been locked and before the treatment allocation has been unblinded. The SAP contains details of analyses to be undertaken, which will be reported in the primary and secondary publications.DiscussionThe SAP details the analyses that will be done to avoid bias coming from knowledge of the results in advance. This trial will determine whether prophylactic melatonin administered to intensive care unit patients helps decrease the rate and the severity of delirium.Trial registrationAustralian and New Zealand Clinical Trial Registry (ANZCTR) ACTRN1261600043647, registration date: 06 April 2016. WHO Trial Number – U1111-1175-1814

Extended Cranial Ultrasound Views in Infants with Acute Brain Stem/Infratentorial Lesions: Diagnosis of a Progressive Midline Glioma in a 6-Week-Old Infant

AbstractCentral nervous system (CNS) tumors are the most common solid tumors in children and adolescents. However, in neonates and children aged younger than a year, they are very rare. Clinical presentation in neonates is often subtle and nonspecific. When neurological symptoms are apparent at this age, cranial ultrasound (CUS) is often done as the initial evaluation, with a standard approach through the anterior fontanel (AF), followed by further imaging, such as magnetic resonance imaging (MRI), if necessary. We report the first neonatal case of a rapidly progressive diffuse midline glioma positive for histone H3 K27M mutation (World Health Organization [WHO] grade IV) in which using extended (transmastoid) CUS studies through the mastoid fontanelle (MF) in the second month of life defined the lesion in the brainstem.

Management of acute traumatic brain injury and acute spinal cord injury.

Management of acute traumatic brain injury and acute spinal cord injury.

Craniotomies following acute traumatic brain injury in Finland – a national study between 1997 and 2018

Craniotomies following acute traumatic brain injury in Finland – a national study between 1997 and 2018

Медицинский логопед в мультидисциплинарной реабилитационной команде. Практический опыт Клиники Института Мозга

Background. In domestic and foreign publications, there are no descriptions of the principles of interaction between a medical speech therapist (MST) and other members of a multidisciplinary rehabilitation team (MDRT). Aim. To analyze our own experience in organizing the work of the speech therapy service of the regional neurorehabilitation Center. Materials and methods. We conducted a retrospective analysis of the activities of the division of MST of the interterritorial Center for Neurorehabilitation “Clinic of the Brain Institute“ (CBI) for the period 2015–2019. In the structure of the CBI, there is a 24-hour hospital with 45 beds, including a 9-bed intensive care unit, an 8-bed day hospital, a polyclinic with 50 visits per shift, and a telemedicine center. The speech therapy team of the MDRT consists of 8 specialists with higher education in the specialty “speech pathologist-defectologist“. Speech therapy examination consists of key blocks of clinical diagnosis of speech therapy syndromes: dysphagia, dysarthria, aphasia and prosoparesis. Each block represents a complex of a basic score scale and additional instrumental, including neurophysiological methods. The basis of speech therapy is voice training, articulation and probe massage and other standard procedures, combined in the concept of “basic techniques” for speech therapy syndromes. Drug and non-drug modulations are used to enhance the basic techniques. Results. In the period from 2015 to 2019, 5243 patients were treated in CBI after acute cerebral circulatory disorders and traumatic brain injuries, of which 4273 (81%) needed the help of clinical speech therapists. The most common problem was dysarthria – 55%. Speech breakdown in the framework of aphasia syndrome was noted in 26% of all hospitalized patients. Dysphagia was diagnosed in 30% of all hospitalized patients. During the hospitalization period of 14 days, each patient receives at least 45 minutes of daily individual training with a specialist and group articulation exercises, including weekends. The lesson is preceded by a modulating drug or non-drug procedure. For 5 years, 4273 patients were treated with speech therapy team. In 154 (11.6%) patients, speech therapy syndromes completely regressed, in 28% the severity of their manifestations decreased by 1–2 levels. Conclusion. At the early stage of rehabilitation, the speech therapist is called upon to solve priority tasks: achieving the maximum possible level of independence of the patient, at least staying at home with a minimum level of dependence on the help of a guardian. This is a prerequisite for the implementation of an individual comprehensive rehabilitation program. Despite many methodological and organizational problems, the MST is a key member of the MDRT, without which an effective rehabilitation process is impossible.

Experimental modeling and pathomorphological picture of dosed acute traumatic brain injury

In recent decades, there has been a wide spread of open traumatic brain injury (TBI) closely associated with an increase in the pace of life, rise in the number of high-speed vehicles, industrialization, as well as such phenomena as terrorism and local military conflicts. The problem of diagnostics and effective treatment of traumatic brain injury is one of the most important for ambulance doctors, doctors of the Ministry of Emergency Situations, and neurosurgeons in providing timely qualified assistance, and is also of interest for modern medical science for further studying pathological processes and preventing the development of complications in this pathology.

Factors associated with silent cerebral events during catheter ablation for atrial fibrillation in the era of uninterrupted oral anticoagulation therapy

Abstract Background A silent cerebral event (SCE), detected by brain magnetic resonance imaging (MRI), is defined as an acute new brain lesion without clinically apparent neurological deficit, and is frequently observed after catheter ablation in atrial fibrillation (AF) patients. Although the small number of SCEs does not cause neurocognitive dysfunction, the greater volume and/or larger number of SCE lesions are reportedly related to neuropsychological decline; SCE incidence may be a surrogate marker for the potential thromboembolic risk. Thus, strategies to reduce SCEs would be beneficial. Uninterrupted oral anticoagulation strategy for peri-procedural period reportedly reduced the risk of SCEs, but the incidence hovers at 10% to 30%. We sought factors associated with SCEs during catheter ablation for AF in patients with peri-procedural uninterrupted oral anticoagulation (OAC) therapy. Methods AF patients undergoing catheter ablation were eligible (n=255). All patients took non-vitamin K antagonist oral anticoagulants (NOACs) or vitamin K antagonist (VKA) for peri-procedural OAC (&amp;gt;4 weeks) without interruption during the procedure. Brain MRI was performed within 2 days after the procedure to detect SCEs. Clinical characteristics and procedure-related parameters were compared between patients with and without SCEs. Results SCEs were detected in 59 patients (23%, SCE[+]) but not in 196 patients (77%, SCE[-]). Average age was higher in SCE[+] than SCE[-] (66±10 years vs. 62±12 years, p&amp;lt;0.05). Persistent AF prevalence, CHADS2/CHA2DS2-VASc scores, and serum NT-ProBNP levels increased in SCE[+] vs. SCE[-]. In transthoracic/transesophageal echocardiography, left-atrial dimension (LAD) was larger and AF rhythm/spontaneous echo contrast were more frequently observed in SCE[+] than SCE[-]. SCE[+] had lower initial activated clotting time (ACT) before unfractionated heparin (UFH) injection and longer time to reach optimal ACT (&amp;gt;300 sec) before trans-septal puncture than SCE [-]. In multivariate analysis, LAD, initial ACT before UFH injection, and time to reach optimal ACT were predictors for SCEs. Conclusions LAD and intra-procedural ACT kinetics affect SCEs during the procedure in patients with uninterrupted OAC for AF ablation. Shortening time to achieve optimal ACT during the procedure may reduce the risk of SCEs. Funding Acknowledgement Type of funding source: None

Gunshot wounds of the head in peacetime, with the formation of a delayed carotid-cavernous fistula (case report)

The objective of the article is to present the clinical observation of a gunshot wounds of the head in peacetime, with the formation of a delayed carotid-cavernous fistula.Clinical case. A patient aged 26 years received a penetrating parabasal single gunshot wound to the head. After transfer to the N.V. Sklifosovsky Research Institute of Emergency Medicine from a local hospital, intima dissection and occlusion of the left internal carotid artery (ICA) were diagnosed. Supraclinoid section of the left ICA, left anterior cerebral and middle cerebral arteries were filled from the right ICA through the anterior communicating artery. For prevention of suppurative-septic complications as well as decubitus of the left ICA and development of life-threatening hemorrhages, repeat surgery was performed. Acute subdural hematoma and brain detritus were removed. Using pterional approach, the chiasm and sellar region was accessed. Sequentially the ophthalmic, interpenducular, penducular cisterns, cisterna laminae terminalis and left carotid cistern were dissected. Sequentially the left ophthalmic nerve, left ICA, left choroid arteries were isolated. A metallic foreign object (bullet) located in the medial regions of the larger wing of the sphenoid bone and lateral wall of the cavernous sinus was found and removed. On day 14 after the second surgery, headache became worse, pulsing noise developed in the left part of the head, as well as moderate exophthalmos on the left. Left-hand type A (per the Barrow classification) carotid-cavernous anastomosis with retrograde inflow due to occlusion of the left ICA was diagnosed. Endovascular intervention was performed: separation of the carotid-cavernous anastomosis through retrograde occlusion of the supraclinoid segment of the left ICA with microcoils through contralateral ICA and anterior communicating artery. The patient was discharged at day 30 after hospitalization. Cerebral and meningeal symptoms regressed. Ptosis grade decreased, the left eye started to move.Conclusion. This abovementioned observation is of interest due to the rarity of such pathology and the possibilities of modern multidisciplinary centers for the diagnosis and treatment of such patients as of this date.

A mixed methods randomised feasibility trial investigating the management of benign paroxysmal positional vertigo in acute traumatic brain injury

BackgroundTraumatic brain injury (TBI) is the leading cause of long-term disability in working age adults. Recent studies show that most acute TBI patients demonstrate vestibular features of dizziness and imbalance, often from combined peripheral and central vestibular dysfunction. Effective treatment for vestibular impairments post-TBI is important given its significant adverse impact upon quality of life and employment prospects. The most frequent peripheral vestibular disorder in acute TBI is benign paroxysmal positional vertigo (BPPV), affecting approximately half of acute cases. Although there is effective treatment for idiopathic BPPV, there are no high-quality clinical data for post-TBI BPPV regarding its prevalence, natural history, which treatment is most effective and when is the best time to treat. In particular, observational studies suggest post-TBI BPPV may be recurrent, indicating that hyperacute treatment of BPPV may be futile. Given the potential hurdles and the lack of accurate post-TBI BPPV data, the current study was designed to provide information regarding the feasibility and optimal design of future large-scale prospective treatment studies that would compare different interventions and their timing for post-TBI BPPV.MethodA multi-centre randomised mixed methods feasibility study design was employed. We aim to recruit approximately 75 acute TBI patients across a range of clinical severities, from three major trauma centres in London. Patients will be randomised to one of three treatment arms: (1) therapist-led manoeuvres, (2) patient-led exercises and (3) advice. Participants will be re-assessed by blinded outcome assessors at 4 and 12 weeks. Acceptability of the intervention will be obtained by patient interviews at the end of their treatment and therapist interviews at the end of the study. Primary outcomes relate to feasibility parameters including recruitment and retention rates, adverse events and intervention fidelity. We will also aim to provide a more accurate estimate of the prevalence of BPPV in TBI cases on the trauma ward.DiscussionThe multi-centre nature of our feasibility study will inform the design of a future prospective treatment trial of BPPV in acute TBI. Important parameters we will obtain from this study, key for designing a future prospective treatment study, include estimating the prevalence of BPPV in TBI patients admitted to UK major trauma wards, and elucidating both patient and care-provider barriers in delivering BPPV treatment.Trial registrationISRCTN, ISRCTN91943864. Registered on 10 February 2020.