Neurophysiologic Monitoring and Neuroprotection

2017 ◽  
Author(s):  
Aws Alawi ◽  
Michael Reznik ◽  
Jan Claassen
Keyword(s):  
Early Detection ◽  
Brain Injuries ◽  
Cerebral Injury ◽  
Secondary Brain Injury ◽  
Neurophysiologic Monitoring ◽  
Permanent Damage ◽  
Injured Brain ◽  
Physiological Assessment ◽  
Physiologic Parameters ◽  
Sedation Monitoring

One of the main goals of monitoring neurologically ill patients is detection of secondary brain injury early enough to intervene to prevent permanent damage. In some patients with impaired levels of consciousness and those who require sedation, monitoring various brain physiologic parameters by invasive and noninvasive means has become an essential tool in the care of critically ill patients. Integration of multiple physiological parameters provides a more comprehensive physiological assessment of the injured brain and allows real-time, early detection of secondary cerebral injury and intervention to prevent permanent damage. Importantly, these modalities should be interpreted collectively and not in isolation in order to manage acute brain injuries, which are often complex and dynamic at the same time.

scholarly journals Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Depeng Feng ◽  
Dezhe Chen ◽  
Tuanzhi Chen ◽  
Xiaoqian Sun
Keyword(s):  
Matrix Metalloproteinase ◽  
Test Scores ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Cerebral Injury ◽  
Control Group ◽  
Secondary Brain Injury ◽  
Walking Test ◽  
Matrix Metalloproteinase 3 ◽  
Injured Brain

Objective. This study is aimed at exploring the possible neuroprotective mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. Methods. We established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, the injured brain area, and the beam walking test were used to estimate the degree of cerebral injury among the rats. Immunohistochemistry and immunofluorescence were used to detect activated microglia, matrix metalloproteinase-3 (MMP-3), and osteopontin (OPN). Results. The injured brain area and mortality were dramatically reduced ( p < 0.01 ), and the beam walking test scores were elevated ( p < 0.01 ) in the acetylsalicylic acid (ASA) group compared to the control group. The number of microglia-, MMP-3-, and OPN-positive cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group. After LPS stimulation, the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. In the ASA group, the number of microglia was significantly smaller ( p < 0.05 ), especially at 24 h ( p < 0.01 ), compared to the LPS group. Moreover, the injured brain area and the mortality were dramatically increased and the beam walking test scores were reduced ( p < 0.01 ) after LPS simulation following CIRP. The degree of injury in the ASA group resembled that in the control group. However, the number of MMP-3-immunoreactive neurons or microglia was significantly larger than that of the control group ( p < 0.05 ). In the ASA group, the MMP-3 expression was also considerably decreased ( p < 0.05 ). Conclusions. After CIRP, microglia were rapidly activated and the expression of MMP-3 and OPN significantly increased. For rats injected with LPS at reperfusion, the injured brain area and mortality also dramatically increased and the neurologic impairment worsened. However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction after CIRP injury.

Multimodality Monitoring

2018 ◽  
pp. 155-164
Author(s):  
Maranatha Ayodele ◽  
Kristine O’Phelan
Keyword(s):  
Traumatic Brain Injury ◽  
Critical Care ◽  
Brain Injury ◽  
Early Recognition ◽  
Secondary Injury ◽  
Multimodality Monitoring ◽  
Injured Brain ◽  
Brain Injured ◽  
Physiologic Parameters ◽  
Injured Patients

Advancements in the critical care of patients with various forms of acute brain injury (traumatic brain injury, subarachnoid hemorrhage, stroke, etc.) in its current evolution recognizes that in addition to the initial insult, there is a secondary cascade of physiological events in the injured brain that contribute significantly to morbidity and mortality. Multimodality monitoring (MMM) in neurocritical care aims to recognize this secondary cascade in a timely manner. With early recognition, critical care of brain-injured patients may then be tailored to preventing and alleviating this secondary injury. MMM includes a variety of invasive and noninvasive techniques aimed at monitoring brain physiologic parameters such as intracranial pressure, perfusion, oxygenation, blood flow, metabolism, and electrical activity. This chapter provides an overview of these techniques and offers a practical guide to their integration and use in the intensive care setting.

scholarly journals HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

2018 ◽  
Vol 46 (6) ◽  
pp. 2532-2542 ◽  
Author(s):  
Lijun Yang ◽  
Feng Wang ◽  
Liang Yang ◽  
Yunchao Yuan ◽  
Yan Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Therapeutic Potential ◽  
High Mobility ◽  
Neurological Injury ◽  
Secondary Brain Injury ◽  
Cell Degeneration ◽  
Injured Brain ◽  
Walking Tests

Background/Aims: Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. Methods: TBI was induced by controlled cortical impact (CCI) in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan’s blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. Results: HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Conclusion: Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI.

scholarly journals Sports-related brain injuries: connecting pathology to diagnosis

2016 ◽  
Vol 40 (4) ◽  
pp. E14 ◽  
Author(s):  
James Pan ◽  
Ian D. Connolly ◽  
Sean Dangelmajer ◽  
James Kintzing ◽  
Allen L. Ho ◽  
...  
Keyword(s):  
Early Detection ◽  
Disease Burden ◽  
Brain Injuries ◽  
Biomarker Discovery ◽  
Chronic Traumatic Encephalopathy ◽  
Traumatic Brain Injuries ◽  
Postmortem Examination ◽  
High Impact ◽  
Diagnostic Challenge ◽  
Mild Traumatic Brain Injuries

Brain injuries are becoming increasingly common in athletes and represent an important diagnostic challenge. Early detection and management of brain injuries in sports are of utmost importance in preventing chronic neurological and psychiatric decline. These types of injuries incurred during sports are referred to as mild traumatic brain injuries, which represent a heterogeneous spectrum of disease. The most dramatic manifestation of chronic mild traumatic brain injuries is termed chronic traumatic encephalopathy, which is associated with profound neuropsychiatric deficits. Because chronic traumatic encephalopathy can only be diagnosed by postmortem examination, new diagnostic methodologies are needed for early detection and amelioration of disease burden. This review examines the pathology driving changes in athletes participating in high-impact sports and how this understanding can lead to innovations in neuroimaging and biomarker discovery.

scholarly journals Heparin-Induced Fever in Neurointensive Care Unit: A Rarity Yet a Possibility

2021 ◽  
Author(s):  
Mathangi Krishnakumar ◽  
Shweta S. Naik ◽  
Venkatapura J. Ramesh ◽  
S Mouleeswaran
Keyword(s):  
Care Setting ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Protective Response ◽  
Inflammatory Cascade ◽  
Persistent Fever ◽  
Neurointensive Care Unit ◽  
Injured Tissue ◽  
Injured Brain ◽  
Resistance To Infection

AbstractFever is considered a protective response having multitude of benefits in terms of enhancing resistance to infection, recruiting cytokines to the injured tissue, and promoting healing. In terms of an injured brain, this becomes a double-edged sword triggering an inflammatory cascade resulting in secondary brain injury. It is important to identify the etiology so that corrective measures can be taken. Here we report a case of persistent fever in a patient with Guillain-Barré syndrome, which was probably due to heparin. This is the first report of heparin-induced fever in a neurocritical care setting and third report overall.

scholarly journals A case report: use of cerebral oximetry in the early detection of cerebral hypoperfusion in a post-cardiac arrest patient during targeted temperature management

2019 ◽  
Vol 3 (3) ◽  
Author(s):  
Shonda Ng ◽  
Yew Woon Chia
Keyword(s):  
Cardiac Arrest ◽  
Early Detection ◽  
Respiratory Acidosis ◽  
Targeted Temperature Management ◽  
Cerebral Oximetry ◽  
Cerebral Hypoperfusion ◽  
Temperature Management ◽  
Secondary Brain Injury ◽  
Arterial Blood ◽  
Ventilator Settings

Abstract Background We present a patient who received cerebral oximetry monitoring during targeted temperature management (TTM) post-cardiac arrest and discuss its potential in the early detection of cerebral hypoperfusion and implications on haemodynamics and ventilatory management. Case summary A 60-year-old Chinese male was admitted for acute pulmonary oedema with Type 2 respiratory failure. He failed an initial trial of non-invasive ventilation and was planned for intubation and mechanical ventilation. However, the patient suffered a pulseless electrical activity cardiac arrest peri-intubation. He was started on our institution’s protocolized post-cardiac arrest care bundle, which included cerebral regional oxygen saturation (rSO2) monitoring and TTM. Initial arterial blood gas (ABG) post-return of spontaneous circulation showed severe respiratory acidosis, and the patient was sedated, paralyzed, and ventilator settings optimized. Repeat ABG showed resolution of respiratory acidosis. However, a drop in rSO2 to 35% was subsequently noted. Ventilator settings were quickly adjusted, and dobutamine was started to improve global and cerebral perfusion. These measures improved cerebral rSO2 to more than 50%. Patient was cooled for 24 h and gradually rewarmed. He was later extubated with a cerebral performance category of 1 and is now on outpatient follow-up. Discussion During post-cardiac arrest care, there are many factors which can contribute to a decrease in cerebral blood flow. Therapeutic hypothermia and ventilation strategies, including the use of neuromuscular blocking agents, can both reduce pCO2 which is a major regulator of cerebrovascular tone. Accidental hypocapnia can lead to adverse cerebral vasoconstriction and hypoperfusion. Without cerebral oximetry, cerebral ischaemia may not be detected early and can potentially result in secondary brain injury.

Early detection of cerebral injury

1952 ◽  
Vol 40 (5) ◽  
pp. 606-620 ◽  
Author(s):  
James G. Hughes ◽  
Billie Camp Davis
Keyword(s):  
Early Detection ◽  
Cerebral Injury

scholarly journals An Optimized Method Using CNN, RF, Cuckoo Search and HOG for Early Detection of Eye Disease in Humans

2020 ◽  
Vol 4 (2) ◽  
Author(s):  
Tian Jipeng ◽  
Manasa S. ◽  
T. C. Manjunath
Keyword(s):  
Neural Network ◽  
Early Detection ◽  
Hybrid Algorithm ◽  
Cuckoo Search ◽  
Eye Diseases ◽  
Image Texture ◽  
Eye Disease ◽  
Advanced Stage ◽  
Permanent Damage ◽  
Unique Method

Glaucoma is a group of eye diseases that cause damage to the optic nerve, causing the successive narrowing of the visual field in affected patients due to increased intraocular pressure, which can lead the patient, at an advanced stage, to blindness without clinical reversal. As we have heard and seen from generations across that Glaucoma has been and is still one of the leading diseases that has permanent damage if untreated. As per the current research it says that 79 Million are affected BY 2020 which are untreated. So, to make it easy for us humans, early detection is one of the best way to create awareness and treat the diseased. After having gone through the majority of the literatures, have seen that when LBP is given to HOG has accurate results for better feature extraction than other methods, also application of Cuckoo search (CS) algorithm, Random forest (for classifying) and Conventional Neural Network (for segmentation) have better outcome compared to the previously used hybrid algorithm methods to detected the diseased from the normal eye. So, to achieve this I will be using Matlab tool as it produces more accurate results than any other platform. In one of the paper LBP algorithm has been extensively used to obtain the desired results but when learnt about HOG, it looked as it has better properties to enhance the required results when combined along with LBP. CS is another unique method to analyze on aggregation of the image texture.

scholarly journals Analysis of Neuron Specific Enolase Serum Levels in Traumatic Brain Injury

2021 ◽  
Vol 5 (4) ◽  
pp. 1218-1222
Author(s):  
Yuliarni Syafrita ◽  
Nora Fitri
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Injuries ◽  
Neuron Specific Enolase ◽  
Serum Levels ◽  
Pathological Process ◽  
P Value ◽  
Secondary Brain Injury ◽  
Post Injury ◽  
The Brain

Background : Traumatic brain injury is still the main cause of death and disability in productive age. Assessment the level of consciousness and imaging examinations after a brain injury can not always describe the severity of damage in the brain, this is because the pathological process is still ongoing due to secondary brain injury. Therefore, it is necessary to examine biomarkers that can describe the severity of the pathological process that occurs. The purpose of this study was to assess serum neuron-specific enolase (NSE) levels and their relationship to the severity and outcome of a traumatic brain injury. Methods : A cross sectional design was conducted in the emergency department of DR M Djamil Hospital, Padang. There were 72 patients who met the inclusion criteria. A Glasgow Coma Scale examination was performed to assess the severity of brain injury and examination of NSE serum levels at 48 hours post- injury using ELISA technique and assess the Glasgow outcome scale (GOS) at 6 weeks post-injury. Data analysis using SPSS 22 program, the results are significance if the p value <0.05  Results : The average NSE level was higher in severe brain injuries than moderate and mild brain injuries and this difference was statistically significant (p<0.05).  The NSE serum levels were higher in poor outcomes than in good outcomes and this difference was statistically significant (p<0.05).  Conclusion : High NSE serum levels in the acute phase were associated with the severity of the brain injury and poor outcome 6 weeks after the brain injury. 

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