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high-altitude cerebral edema

Jose V Lafuente, G Bermudez, L Camargo-Arce, S Bulnes
Cerebral syndromes related to high altitude exposure are becoming more frequent as the number of trips to high altitudes has increased in the last decade. The commonest symptom is headache, followed by acute mountain sickness (AMS) and high-altitude cerebral edema (HACE), which can be fatal. The pathophysiology of these syndromes is not fully comprehended. The classical "tight-fit hypothesis" defends the fact that there are some anatomical variations that would obstruct the sinovenous outflow and worsen the vasogenic edema and intracranial hypertension reactive to hypoxia...
September 20, 2016: CNS & Neurological Disorders Drug Targets
Roberta Rosas Petrocinio, Elga Dias Gomes
BACKGROUND: High altitude retinopathy (HAR) includes a number of diseases related to high altitude such as acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). High altitude retinopathy is mainly characterized by retinal hemorrhages, usually sparing the macular region, a condition specifically known as high altitude retinal hemorrhages (HARH). The pathogenesis of HARH is unclear. Many studies show that lack of oxygen causes an inadequate autoregulation of retinal circulation, causing vascular incompetence...
2016: Aerospace Medicine and Human Performance
Samuel Verges, Thomas Rupp, Marjorie Villien, Laurent Lamalle, Irène Troprés, Camille Poquet, Jan M Warnking, François Estève, Pierre Bouzat, Alexandre Krainik
OBJECTIVE: Hypoxic exposure in healthy subjects can induce acute mountain sickness including headache, lethargy, cerebral dysfunction, and substantial cerebral structural alterations which, in worst case, can lead to potentially fatal high altitude cerebral edema. Within this context, the relationships between high altitude-induced cerebral edema, changes in cerebral perfusion, increased brain parenchyma volume, increased intracranial pressure, and symptoms remain unclear. METHODS: In 11 subjects before and after 6 days at 4350 m, we performed multiparametric magnetic resonance investigations including anatomical, apparent diffusion coefficient and arterial spin labeling sequences...
2016: Frontiers in Physiology
Martin J MacInnis, Michael S Koehle
MacInnis, Martin J., and Michael S. Koehle. Evidence for and against genetic predispositions to acute and chronic altitude illnesses. High Alt Med Biol 00:000-000, 2016.-Humans exhibit marked variation in their responses to hypoxia, with susceptibility to acute and chronic altitude illnesses being a prominent and medically important example. Many have hypothesized that genetic differences are the cause of these variable responses to hypoxia; however, until recently, these hypotheses were based primarily on small (and sometimes anecdotal) reports pertaining to apparent differences in altitude illness susceptibility between populations, the notion that a history of altitude illness is indicative of subsequent risk, the heritability of hypoxia-related traits, and candidate gene association studies...
August 8, 2016: High Altitude Medicine & Biology
Yu Sh Khalimov, O V Vetryakov, R G Makiev, V G Kuzmich
The authors present an analysis of adverse climatic factors mid- and high mountains, which have a significant negative impact on fighting facility and capacity for work in military servicemen that may cause an acute mountain sickness and severe complications (high altitude pulmonary edema and high-altitude cerebral edema). Complicated mechanisms of organism disorder are shown. Sophisticated medical and tactical factors of mountain theatre of war, defining the nature of actions of troops, require special approaches to organisation of medical support...
January 2016: Voenno-medit︠s︡inskiĭ Zhurnal
Chris Imray
Rapid ascent to high altitude commonly results in acute mountain sickness, and on occasion potentially fatal high-altitude cerebral edema. The exact pathophysiological mechanisms behind these syndromes remain to be determined. One of the main theories to explain the development of Acute Mountain Sickness (AMS) is an increase in intracranial pressure (ICP). Vasogenic (extracellular water accumulation due to increased permeability of the blood- brain barrier) and cytotoxic (intracellular) oedema have also been postulated as the mechanisms that underlie High Altitude Cerebral Edema (HACE)...
April 8, 2016: Experimental Physiology
L J Wu
The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar...
2016: Genetics and Molecular Research: GMR
Nasiruddin Jamal, Mubina Rajhy, Mustaafa Bapumia
An individual experiencing dyspnoea or syncope at high altitude is commonly diagnosed to have high-altitude pulmonary edema or cerebral edema. Acute myocardial infarction (AMI) is generally not considered in the differential diagnosis. There have been very rare cases of AMI reported only from Mount Everest. We report a case of painless ST segment elevation myocardial infarction (STEMI) that occurred while climbing Mount Kilimanjaro. A 51-year-old man suffered dyspnoea and loss of consciousness near the mountain peak, at about 5600 m...
2016: BMJ Case Reports
Ting-Ting Song, Yan-Hua Bi, Yu-Qi Gao, Rui Huang, Ke Hao, Gang Xu, Jia-Wei Tang, Zhi-Qiang Ma, Fan-Ping Kong, John H Coote, Xue-Qun Chen, Ji-Zeng Du
BACKGROUND: High-altitude cerebral edema (HACE) is the severe type of acute mountain sickness (AMS) and life threatening. A subclinical inflammation has been speculated, but the exact mechanisms underlying the HACE are not fully understood. METHODS: Human volunteers ascended to high altitude (3860 m, 2 days), and rats were exposed to hypoxia in a hypobaric chamber (5000 m, 2 days). Human acute mountain sickness was evaluated by the Lake Louise Score (LLS), and plasma corticotrophin-releasing hormone (CRH) and cytokines TNF-α, IL-1β, and IL-6 were measured in rats and humans...
2016: Journal of Neuroinflammation
Neetu Kushwah, Vishal Jain, Satayanarayan Deep, Dipti Prasad, Shashi Bala Singh, Nilofar Khan
Hypoxic exposure results in several pathophysiological conditions associated with nervous system, these include acute and chronic mountain sickness, loss of memory, and high altitude cerebral edema. Previous reports have also suggested the role of hypoxia in pathogenesis of depression and related psychological conditions. On the other hand, sub lethal intermittent hypoxic exposure induces protection against future lethal hypoxia and may have beneficial effect. Therefore, the present study was designed to explore the neuroprotective role of intermittent hypobaric hypoxia (IHH) in Unpredictable Chronic Mild Stress (UCMS) induced depression like behaviour in rats...
2016: PloS One
Ian Quigley, Ken Zafren
High altitude cerebral edema (HACE) is a life-threatening condition that can affect people who ascend to altitudes above 2500 m. Altered mental status and the presence of ataxia distinguishes HACE from acute mountain sickness (AMS). We describe a patient with subtle cognitive dysfunction, likely due to HACE that had not fully resolved. When he initially presented, the patient appeared to have normal mental status and was not ataxic. The diagnosis of HACE was missed initially but was made when further history became available...
June 2016: Wilderness & Environmental Medicine
Morteza Khodaee, Heather L Grothe, Jonathan H Seyfert, Karin VanBaak
CONTEXT: Athletes at different skill levels perform strenuous physical activity at high altitude for a variety of reasons. Multiple team and endurance events are held at high altitude and may place athletes at increased risk for developing acute high altitude illness (AHAI). Training at high altitude has been a routine part of preparation for some of the high level athletes for a long time. There is a general belief that altitude training improves athletic performance for competitive and recreational athletes...
March 2016: Sports Health
Angelika Hoffmann, Reiner Kunze, Xavier Helluy, David Milford, Sabine Heiland, Martin Bendszus, Mirko Pham, Hugo H Marti
Human pathophysiology of high altitude hypoxic brain injury is not well understood and research on the underlying mechanisms is hampered by the lack of well-characterized animal models. In this study, we explored the evolution of brain injury by magnetic resonance imaging (MRI) and histological methods in mice exposed to normobaric hypoxia at 8% oxygen for 48 hours followed by rapid reoxygenation and incubation for further 24 h under normoxic conditions. T2*-, diffusion-weighted and T2-relaxometry MRI was performed before exposure, immediately after 48 hours of hypoxia and 24 hours after reoxygenation...
2016: PloS One
Ravjit S Sagoo, Charles E Hutchinson, Alex Wright, Charles Handford, Helen Parsons, Victoria Sherwood, Sarah Wayte, Sanjoy Nagaraja, Eddie Ng'Andwe, Mark H Wilson, Christopher He Imray
Rapid ascent to high altitude commonly results in acute mountain sickness, and on occasion potentially fatal high-altitude cerebral edema. The exact pathophysiological mechanisms behind these syndromes remain to be determined. We report a study in which 12 subjects were exposed to a FiO2 = 0.12 for 22 h and underwent serial magnetic resonance imaging sequences to enable measurement of middle cerebral artery velocity, flow and diameter, and brain parenchymal, cerebrospinal fluid and cerebral venous volumes...
January 8, 2016: Journal of Cerebral Blood Flow and Metabolism
Deependra Pratap Singh, Charu Nimker, Piyush Paliwal, Anju Bansal
Sudden exposure to altitude hypoxia is responsible for acute mountain sickness (AMS) in un-acclimatized persons. If not treated in time, AMS can worsen and leads to high altitude cerebral edema, which can be fatal. Present study explores the efficacy of ethyl 3,4-dihydroxybenzoate (EDHB), a prolyl hydroxylase enzyme inhibitor, in modulating adaptive responses to hypobaric hypoxia (HH) in rat brain. Male Sprague-Dawley rats treated with EDHB (75 mg/kg for 3 days), were subjected to acute HH exposure at 9144 m (30,000 ft) for 5 h...
July 2016: Journal of Physiological Sciences: JPS
Justin S Lawley, Benjamin D Levine, Michael A Williams, Jon Malm, Anders Eklund, David M Polaner, Andrew W Subudhi, Peter H Hackett, Robert C Roach
The pathophysiology of acute mountain sickness and high-altitude cerebral edema, the cerebral forms of high-altitude illness, remain uncertain and controversial. Persistently elevated or pathological fluctuations in intracranial pressure are thought to cause symptoms similar to those reported by individuals suffering cerebral forms of high-altitude illness. This review first focuses on the basic physiology of the craniospinal system, including a detailed discussion of the long-term and dynamic regulation of intracranial pressure...
January 15, 2016: Journal of Applied Physiology
Harvey V Lankford
Dull and hypoxic brains have been a frequent subject in the medical and mountaineering literature. Deterioration of cognitive and other neurological function occurs at high altitude, with or without high altitude cerebral edema. This historical essay explores a 2014 first-ever English translation of cerebral blood flow studies by nineteenth century physiologist Angelo Mosso. Some of the medical history and physiology of brain function is discussed, but much of the style focuses on quotations from the writings of mountaineers and mountaineering physicians to provide color commentary about dull brains at high altitude...
December 2015: High Altitude Medicine & Biology
Mark H Wilson, Christopher H E Imray
Most hypobaric hypoxia studies have focused on oxygen delivery and therefore cerebral blood inflow. Few have studied venous outflow. However, the volume of blood entering and leaving the skull (∼700 ml/min) is considerably greater than cerebrospinal fluid production (0.35 ml/min) or edema formation rates and slight imbalances of in- and outflow have considerable effects on intracranial pressure. This dynamic phenomenon is not necessarily appreciated in the currently taught static "Monro-Kellie" doctrine, which forms the basis of the "Tight-Fit" hypothesis thought to underlie high altitude headache, acute mountain sickness, and high altitude cerebral edema...
January 15, 2016: Journal of Applied Physiology
Tatiana Havryliuk, Bhuwan Acharya, Emily Caruso, Tracy Cushing
We surveyed Nepali porters and guides as well as English- and non-English-speaking trekkers on their knowledge of altitude illness and its treatment during trekking expeditions to the Annapurna region of Nepal. From March 15 to April 15, 2014, Nepali porters and visiting trekkers were surveyed regarding their ability to recognize and treat altitude illness in Manang, Nepal (3540 m). Their personal use of medications and home remedies and presence of acute mountain sickness (AMS) symptoms were also assessed...
September 2015: High Altitude Medicine & Biology
Jing Jing Pan, You-Yan Zhao, Chao Lu, Yu-Hua Hu, Yang Yang
The aim of this study was to explore the clinical characteristics and etiology of mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) in China by retrospectively analyzing five MERS cases from the Jiangsu Provincial Hospital within a total of 27 reported MERS cases from available Chinese literature. Most of the 27 cases originated near the eastern and southern parts of China. Ages for 23 MERS cases were under 30 years and the female-to-male ratio was 1:1.25. The major causes of MERS included infection, antiepileptic drug withdrawal, high-altitude cerebral edema, and cesarean section (C-section)...
November 2015: Neurological Sciences
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