Hypoxic Brain Injury
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Wildland Firefighter Smoke Exposure
❑ United States Department of Agriculture Wildland Firefighter Smoke Exposure EST SERVIC FOR E Forest National Technology & 1351 1803 October 2013 D E E P R A U RTMENT OF AGRICULT Service Development Program 5100—Fire Management Wildland Firefighter Smoke Exposure By George Broyles Fire Project Leader Information contained in this document has been developed for the guidance of employees of the U.S. Department of Agriculture (USDA) Forest Service, its contractors, and cooperating Federal and State agencies. The USDA Forest Service assumes no responsibility for the interpretation or use of this information by other than its own employees. The use of trade, firm, or corporation names is for the information and convenience of the reader. Such use does not constitute an official evaluation, conclusion, recommendation, endorsement, or approval of any product or service to the exclusion of others that may be suitable. The U.S. Department of Agriculture (USDA) prohibits discrimination in all its programs and activities on the basis of race, color, national origin, age, disability, and where applicable, sex, marital status, familial status, parental status, religion, sexual orientation, genetic information, political beliefs, reprisal, or because all or part of an individual’s income is derived from any public assistance program. (Not all prohibited bases apply to all programs.) Persons with disabilities who require alternative means for communication of program information (Braille, large print, audiotape, etc.) should contact USDA’s TARGET Center at (202) 720-2600 (voice and TDD). To file a complaint of discrimination, write USDA, Director, Office of Civil Rights, 1400 Independence Avenue, S.W., Washington, D.C. -
Electroencephalography (EEG) Technology Applications and Available Devices
applied sciences Review Electroencephalography (EEG) Technology Applications and Available Devices Mahsa Soufineyestani , Dale Dowling and Arshia Khan * Department of Computer Science, University of Minnesota Duluth, Duluth, MN 55812, USA; soufi[email protected] (M.S.); [email protected] (D.D.) * Correspondence: [email protected] Received: 18 September 2020; Accepted: 21 October 2020; Published: 23 October 2020 Abstract: The electroencephalography (EEG) sensor has become a prominent sensor in the study of brain activity. Its applications extend from research studies to medical applications. This review paper explores various types of EEG sensors and their applications. This paper is for an audience that comprises engineers, scientists and clinicians who are interested in learning more about the EEG sensors, the various types, their applications and which EEG sensor would suit a specific task. The paper also lists the details of each of the sensors currently available in the market, their technical specs, battery life, and where they have been used and what their limitations are. Keywords: EEG; EEG headset; EEG Cap 1. Introduction An electroencephalography (EEG) sensor is an electronic device that can measure electrical signals of the brain. EEG sensors typically measure the varying electrical signals created by the activity of large groups of neurons near the surface of the brain over a period of time. They work by measuring the small fluctuations in electrical current between the skin and the sensor electrode, amplifying the electrical current, and performing any filtering, such as bandpass filtering [1]. Innovations in the field of medicine began in the early 1900s, prior to which there was little innovation due to the uncollaborative nature of the field of medicine. -
10 Dangerous Drugs That Attack Your Brain and Body (PDF)
ALCOHOL Legal but dangerous. Causes changes in behavior, impairs judgement and coordination required to drive a car safely. Moderate to high doses severely alters a person's ability to learn and remember. Very high doses cause death. 10 Dangerous Drugs: Long term consumption of large quantities, combined with poor nutrition, can lead to permanent damage to brain. liver, pancreas and stomach. That attack your Brain and AMPHETAMINES Body Illegal. Users may experience sweating, headaches, blurred vision, dizziness, sleeplessness and anxiety. High doses can cause irregular heartbeat, loss of coordination, and collapse. Injection creates a sudden increase in blood pressure that can result in very high fever, or heart failure and death. BARBITURATES Illegal. Effects are similar of those of alcohol: slurred speech, staggering walk. Very large doses can cause coma and death. Combination of barbiturates and alcohol multiplies risks. COCAINE Illegal. Stimulates the central nervous system. Immediate effects include dilated pupils, elevated blood pressure, heart and respiratory problems, and stuffy nose. Crack, or freebase rock, is extremely addictive, and effects are felt within 10 seconds! Causes dilated pupils, increased pulse rate, elevated blood pressure, insomnia, loss of appetite, hallucinations, paranoia, and seizures. Use of cocaine can cause death by cardiac arrest. HALLUCINOGENS Lysergic acid. (LSD) Commonly causes sensations and feelings to change rapidly. Causes illusions (being deceived by the normal) and hallucinations (a false or mistaken idea) dilated pupils, elevated body temperature, increased heart rate and blood pressure, loss of appetite, sleeplessness and tremors. The user may experience panic, confusion, suspicions, anxiety and loss of control. Delayed effects (flashbacks), can occur even after use has ceased. -
Function and Biomarkers of the Blood-Brain Barrier in a Neonatal Germinal Matrix Haemorrhage Model
cells Article Function and Biomarkers of the Blood-Brain Barrier in a Neonatal Germinal Matrix Haemorrhage Model Erik Axel Andersson 1 , Eridan Rocha-Ferreira 2 , Henrik Hagberg 2, Carina Mallard 1 and Carl Joakim Ek 1,* 1 Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Medicinaregatan 11, 413 90 Gothenburg, Sweden; [email protected] (E.A.A.); [email protected] (C.M.) 2 Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, 413 90 Gothenburg, Sweden; [email protected] (E.R.-F.); [email protected] (H.H.) * Correspondence: [email protected] Abstract: Germinal matrix haemorrhage (GMH), caused by rupturing blood vessels in the germinal matrix, is a prevalent driver of preterm brain injuries and death. Our group recently developed a model simulating GMH using intrastriatal injections of collagenase in 5-day-old rats, which corresponds to the brain development of human preterm infants. This study aimed to define changes to the blood-brain barrier (BBB) and to evaluate BBB proteins as biomarkers in this GMH model. Regional BBB functions were investigated using blood to brain 14C-sucrose uptake as well as using biotinylated BBB tracers. Blood plasma and cerebrospinal fluids were collected at various times after GMH and analysed with ELISA for OCLN and CLDN5. The immunoreactivity of BBB proteins was assessed in brain sections. Tracer experiments showed that GMH produced a defined region surrounding the hematoma where many vessels lost their integrity. This region expanded for at least 6 h following GMH, thereafter resolution of both hematoma and re-establishment of BBB Citation: Andersson, E.A.; Rocha- Ferreira, E.; Hagberg, H.; Mallard, C.; function occurred. -
Hypoxia in Alzheimer's Disease: Effects of Hypoxia Inducible Factors
Perspective associated virus-HIF-1α inhibits neuronal Hypoxia in Alzheimer’s disease: apoptosis of the hippocampus induced by Aβ peptides. HIF-1 increases glycolysis and the hexose monophosphate shunt, maintains effects of hypoxia inducible factors the mitochondrial membrane potential and cytosolic accumulation of cytochrome C, thereby inactivating caspase-9 and caspase-3, * Halimatu Hassan, Ruoli Chen and thus prevents neuronal death in the AD brain. Oxidative damage, caused by Aβ peptide Alzheimer’s disease (AD), a common (Lall et al., 2019). Neuroinflammation plays induces mitochondrial dysfunction, which is neurodegenerative disease, afflicts 26 million a detrimental role in AD pathogenesis, as a major characteristic of neuronal apoptosis. people worldwide currently with projection of a microglia depletion by colony stimulating factor Additional pathological features of AD are fourfold increase in this figure by the year 2050 receptor 1 inhibitors improves AD symptoms in astrocyte activation and reduced glucose (Brookmeyer et al., 2018). The majority of AD in vivo (Rawlinson et al., 2020). metabolism in some selected brain areas. cases (95%) are sporadic, having the late-onset Cells respond to hypoxia by stabilizing hypoxia Maintenance of HIF-1α levels reverses Aβ affecting those over 65 years old. About 15% inducible factor (HIF), a key transcription factor peptide-induced glial activation and glycolytic among those 65 years and older suffer from regulating oxygen homeostasis. The HIF levels changes, thus mediating a neuroprotective AD, and the incidence of AD is close to 50% for in cells are directly regulated by four oxygen- response to Aβ peptide by maintaining those aged over 85 years (Brookmeyer et al., sensitive hydroxylases: 3 prolyl hydroxylases metabolic integrity. -
Hypoxic Brain Injury
Hypoxic brain injury Headway’s publications are all available to freely download from the information library on the charity’s website, while individuals and families can request hard copies of the booklets via the helpline. Please help us to continue to provide free information to people affected by brain injury by making a donation at www.headway.org.uk/donate. Thank you. Acknowledgements: Many thanks to Dr Steven White, Consultant Neurophysiologist at St. Mary’s Hospital, London, and Great Ormond Street Hospital, London, for co-authoring this factsheet. Introduction The brain needs a constant supply of oxygen to survive and function. Any interruption in this supply leads to a condition called hypoxia, which can cause brain injury. Hypoxic brain injuries can sometimes be overlooked due to the fact that the primary illness was unrelated to the brain, for example, a heart attack or smoke inhalation. This is especially true if the primary condition is successfully treated and the impact on the brain was relatively mild. It is very important to seek specialist support for the effects of the brain injury as soon as possible and to be aware that changes in functioning and behaviour after such an event may be related to brain injury. This factsheet is intended as an overview of the causes, effects, treatment and rehabilitation of hypoxic brain injury. The information will be particularly useful for the family members of people who have sustained such an injury and also provides a useful starting point for professionals who wish to improve their knowledge of the subject. What is hypoxic brain injury? The brain needs a continuous supply of oxygen to survive and it uses 20% of the body’s oxygen intake. -
Neuro Anesthesia for Trauma Patients
Neuro Anesthesia for Traumatic Brain Injury A Review of The Basics Michele Kolowitz CRNA, MHS October 2014 Introduction CDC • 1.7 Million sustained TBI • 52,000 Deaths • 275,000 Hospitalizations • 80% treated & released from ER (~1.3 million) • Those ≥ 75 highest rates of TBI-related hospitalization & death The Brain Trauma Foundation • TBI affects 2% of the population annually • Major cause of death & severe disability among young people • Most important complication—intracranial hematoma CDC 2002-2006 The BTF 2007 Objectives • Review Cerebral Anatomy, Physiology, & Circulation • Explore The 2007 Brain Trauma Foundation Guidelines for Management of Severe TBI • Discuss Sodium & Water Balance after TBI • Central Neurogenic Diabetes Insipidus • Syndrome of Inappropriate Secretion of Antidiuretic Hormone • Cerebral Salt-Wasting Syndrome Cerebral Anatomy Cranial Vault Brain 80% Blood 12% CSF 8% Brain 1300 grams (3lbs) ~20% Cardiac Output High metabolic rate Absence of O2 stores Cerebral Metabolism—CMRO2 Oxygen Consumption 3-3.8mL/100g/min Average adult ~50ml/min 60% generate ATP neuronal electrical activity *ABSENCE of significant O2 reserves when O2 tension <30 mm/Hg 3-8 min before ATP depletedirreversible cellular injury Cerebral Metabolism & Glucose Glucose 5mg/100g/min Average Adult ~65-70mg/min • 90% aerobic metabolism • CMRO2 parallels glucose consumption • Can metabolize some lactate *Acute Sustained HYPOglycemia is equally as devastating as hypoxia Aerobic vs. Anaerobic Metabolism Cerebral Blood Flow Normal CBF 40-50ml/100g/min Average adult ~750 ml/min • Global BF & metabolic rate remain fairly stable • Regional BF & metabolic rate can change dramatically As metabolic rate goes up, BF goes up—Coupling Increase [K+ & H+] in ECF arteriole dilation & BF Barash 2006 Manipulating CO2 CO2 causes vasodilation & Blood Flow CO2 from 40 to 80 mm/Hg—DOUBLE BF CO2 from 40 to 20 mm/Hg—HALVES BF *Changes are transcient lasting ~6-8hours. -
Health Concerns from Smoke Released by Fires
Health Concerns from Smoke Released by Fires Key Points The materials released by a fire vary from one fire to another, depending on the items burning, the availability of oxygen and fresh air, and the temperature of the fire itself. Even within a fire covering a large area, the materials released may vary from location to location. Inhaling the smoke from a fire can cause injury from the heat of the smoke, the chemicals within the smoke, and the particles of soot. " The heat can cause burns to the nasal passages, airways and lungs. " The chemicals can poison the body, depending on the amount of carbon monoxide, cyanide, and other chemicals produced by the burning. " Soot particles and other substances can irritate the airways. Inhaling smoke can cause asthma and other lung conditions to worsen for hours to days after breathing the smoky air. The best course of action is to leave the smoky air as soon as possible. Staying indoors with closed windows is better than being outdoors when smoke is widespread. If symptoms occur after smoke inhalation, seek medical care for further evaluation and treatment as needed. Fire Chemistry and Toxicology The products of combustion from a fire are a complex mixture. Carbon monoxide is produced in every fire. In general, more carbon monoxide is produced from fires occurring indoors. Carbon monoxide is important to health because it interferes with a person’s ability to use oxygen to maintain body functions. As carbon monoxide levels rise, the amount of impairment also rises. Carbon monoxide levels above 10% typically cause symptoms. -
The Role of Metabolism in Migraine Pathophysiology and Susceptibility
life Review The Role of Metabolism in Migraine Pathophysiology and Susceptibility Olivia Grech 1,2 , Susan P. Mollan 3 , Benjamin R. Wakerley 1,4, Daniel Fulton 5 , Gareth G. Lavery 1,2 and Alexandra J. Sinclair 1,2,4,* 1 Metabolic Neurology, Institute of Metabolism and Systems Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK; [email protected] (O.G.); [email protected] (B.R.W.); [email protected] (G.G.L.) 2 Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham B15 2TH, UK 3 Birmingham Neuro-Ophthalmology Unit, University Hospitals Birmingham NHS Foundation Trust, Birmingham B15 2TH, UK; [email protected] 4 Department of Neurology, Queen Elizabeth Hospital, University Hospitals Birmingham NHS Trust, Birmingham B15 2TH, UK 5 Institute of Inflammation and Ageing, University of Birmingham, Birmingham B15 2TT, UK; [email protected] * Correspondence: [email protected] Abstract: Migraine is a highly prevalent and disabling primary headache disorder, however its patho- physiology remains unclear, hindering successful treatment. A number of key secondary headache disorders have headaches that mimic migraine. Evidence has suggested a role of mitochondrial dysfunction and an imbalance between energetic supply and demand that may contribute towards Citation: Grech, O.; Mollan, S.P.; migraine susceptibility. Targeting these deficits with nutraceutical supplementation may provide an Wakerley, B.R.; Fulton, D.; Lavery, additional adjunctive therapy. Neuroimaging techniques have demonstrated a metabolic phenotype G.G.; Sinclair, A.J. The Role of in migraine similar to mitochondrial cytopathies, featuring reduced free energy availability and Metabolism in Migraine increased metabolic rate. -
Guidelines for the Management of Severe Traumatic Brain Injury 4Th Edition
Guidelines for the Management of Severe Traumatic Brain Injury 4th Edition Nancy Carney, PhD Oregon Health & Science University, Portland, OR Annette M. Totten, PhD Oregon Health & Science University, Portland, OR Cindy O'Reilly, BS Oregon Health & Science University, Portland, OR Jamie S. Ullman, MD Hofstra North Shore-LIJ School of Medicine, Hempstead, NY Gregory W. J. Hawryluk, MD, PhD University of Utah, Salt Lake City, UT Michael J. Bell, MD University of Pittsburgh, Pittsburgh, PA Susan L. Bratton, MD University of Utah, Salt Lake City, UT Randall Chesnut, MD University of Washington, Seattle, WA Odette A. Harris, MD, MPH Stanford University, Stanford, CA Niranjan Kissoon, MD University of British Columbia, Vancouver, BC Andres M. Rubiano, MD El Bosque University, Bogota, Colombia; MEDITECH Foundation, Neiva, Colombia Lori Shutter, MD University of Pittsburgh, Pittsburgh, PA Robert C. Tasker, MBBS, MD Harvard Medical School & Boston Children’s Hospital, Boston, MA Monica S. Vavilala, MD University of Washington, Seattle, WA Jack Wilberger, MD Drexel University, Pittsburgh, PA David W. Wright, MD Emory University, Atlanta, GA Jamshid Ghajar, MD, PhD Stanford University, Stanford, CA Reviewed for evidence-based integrity and endorsed by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. September 2016 TABLE OF CONTENTS PREFACE ...................................................................................................................................... 5 ACKNOWLEDGEMENTS ............................................................................................................................................. -
Studies on the Intracerebral Toxicity of Ammonia
Studies on the Intracerebral Toxicity of Ammonia Steven Schenker, … , Edward Brophy, Michael S. Lewis J Clin Invest. 1967;46(5):838-848. https://doi.org/10.1172/JCI105583. Research Article Interference with cerebral energy metabolism due to excess ammonia has been postulated as a cause of hepatic encephalopathy. Furthermore, consideration of the neurologic basis of such features of hepatic encephalopathy as asterixis, decerebrate rigidity, hyperpnea, and coma suggests a malfunction of structures in the base of the brain and their cortical connections. The three major sources of intracerebral energy, adenosine triphosphate (ATP), phosphocreatine, and glucose, as well as glycogen, were assayed in brain cortex and base of rats given ammonium acetate with resultant drowsiness at 5 minutes and subsequent coma lasting at least 30 minutes. Cortical ATP and phosphocreatine remained unaltered during induction of coma. By contrast, basilar ATP, initially 1.28 ± 0.15 μmoles per g, was unchanged at 2.5 minutes but fell by 28.1, 27.3, and 26.6% (p < 0.001) at 5, 15, and 30 minutes after NH4Ac. At comparable times, basilar phosphocreatine fell more strikingly by 62.2, 96, 77.1, and 71.6% (p < 0.001) from a control level of 1.02 ± 0.38 μmoles per g. These basilar changes could not be induced by anesthesia, psychomotor stimulation, or moderate hypoxia and were not due to increased accumulation of ammonia in the base. Glucose and glycogen concentrations in both cortex and base fell significantly but comparably during development of stupor, and prevention of the cerebral glucose decline by pretreatment with […] Find the latest version: https://jci.me/105583/pdf Journal of Clinical Investigation Vol. -
Inhalation Injury
Emergency Files Inhalation injury Bryan Wise MD CCFP Zachary Levine MD CCFP(EM) Case description mask, and starting intravenous fluids as indicated by the Mr B. is a 46-year-old man who is brought to your patient’s circulatory status.2 emergency department one night after being rescued Once that is complete, a brief history should be from a fire in his apartment complex. He thinks he obtained from the patient or any witnesses. Details of might have briefly lost consciousness while he was the exposure, including the type and location of the fire, trapped in a smoke-filled room before firefighters the duration of smoke exposure, any loss of conscious- were able to free him. He is fully awake and breathing ness, and the condition of any other victims, can provide comfortably upon arrival. Measurement of his vital information about potential inhalation injury.3,4 signs reveals the following: heart rate of 85 beats/min, A targeted physical examination should evaluate for blood pressure of 124/76 mm Hg, respiratory rate of any signs suggestive of inhalation injury, such as face 20 breaths/min, oxygen saturation of 100% on room and neck burns, singed nasal hairs, carbonaceous spu- air, temperature of 36.8°C, and a glucose level of tum, soot in the upper airways, voice changes, or wheez- 6.5 mmol/L. A brief examination reveals only superfi- ing.3,4 It is important to note that the absence of these cial burns to his face and neck. He says that he feels signs does not rule out inhalation injury.2 Additionally, fine now and he wants to return home.