Cerebral hypoxia

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Cerebral hypoxia
Arteries beneath brain Gray closer.jpg
Circle of Willis
Arteries beneath brain
Specialty Critical care medicine

Cerebral hypoxia is a form of hypoxia (reduced supply of oxygen), specifically involving the brain; when the brain is completely deprived of oxygen, it is called cerebral anoxia. There are four categories of cerebral hypoxia; they are, in order of increasing severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury. [1] [2]

Contents

Cases of total oxygen deprivation are termed "anoxia", which can be hypoxic in origin (reduced oxygen availability) or ischemic in origin (oxygen deprivation due to a disruption in blood flow). Brain injury as a result of oxygen deprivation either due to hypoxic or anoxic mechanisms are generally termed hypoxic/anoxic injuries (HAI). Hypoxic ischemic encephalopathy (HIE) is a condition that occurs when the entire brain is deprived of an adequate oxygen supply, but the deprivation is not total. While HIE is associated in most cases with oxygen deprivation in the neonate due to birth asphyxia, it can occur in all age groups, and is often a complication of cardiac arrest. [3] [4] [5]

Signs and symptoms

CT in a person after generalized hypoxia. CCT Hypoxie-12.jpg
CT in a person after generalized hypoxia.

The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered blood oxygen by redirecting blood to the brain and increasing cerebral blood flow. Blood flow may increase up to twice the normal flow but no more. If the increased blood flow is sufficient to supply the brain's oxygen needs then no symptoms will result. [6]

However, if blood flow cannot be increased or if doubled blood flow does not correct the problem, symptoms of cerebral hypoxia will begin to appear. Mild symptoms include difficulties with complex learning tasks and reductions in short-term memory. If oxygen deprivation continues, cognitive disturbances, and decreased motor control will result. [6] The skin may also appear bluish (cyanosis) and heart rate increases. Continued oxygen deprivation results in fainting, long-term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death. [7]

Objective measurements of the severity of cerebral hypoxia depend on the cause. Blood oxygen saturation may be used for hypoxic hypoxia, but is generally meaningless in other forms of hypoxia. In hypoxic hypoxia 95–100% saturation is considered normal; 91–94% is considered mild and 86–90% moderate. Anything below 86% is considered severe. [8]

Cerebral hypoxia refers to oxygen levels in brain tissue, not blood. Blood oxygenation will usually appear normal in cases of hypemic, ischemic, and hystoxic cerebral hypoxia. Even in hypoxic hypoxia blood measures are only an approximate guide; the oxygen level in the brain tissue will depend on how the body deals with the reduced oxygen content of the blood.[ citation needed ]

Causes

Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events such as choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock. [9] It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

Pre- and postnatal

Hypoxic-anoxic events may affect the fetus at various stages of fetal development, during labor and delivery and in the postnatal period. Sometimes, even an infant that is still in the womb may exhibit signs of HIE or other hypoxic ischemic injury. Fetal distress being one of the most common signs of HIE or other oxygen-depriving event. [16] Other problems during pregnancy may include preeclampsia, maternal diabetes with vascular disease, congenital fetal infections, substance/alcohol use, severe fetal anemia, cardiac disease, lung malformations, or problems with blood flow to the placenta.

Problems during labor and delivery can include umbilical cord occlusion, torsion or prolapse, rupture of the placenta or uterus, excessive bleeding from the placenta, abnormal fetal position such as the breech position, prolonged late stages of labor, or very low blood pressure in the mother. Problems after delivery can include severe prematurity, severe lung or heart disease, serious infections, trauma to the brain or skull, congenital malformations of the brain or very low blood pressure in the baby [17] and due to suffocation in cases of Münchausen syndrome by proxy. [18]

The severity of a neonatal hypoxic-ischaemic brain injury may be assessed using Sarnat staging, which is based on clinical presentation and EEG findings, and also using MRI. [19] Signs and symptoms of HIE may include:

Mechanism

Details of the mechanism of damage from cerebral hypoxia, along with anoxic depolarization, can be found here: Mechanism of anoxic depolarization in the brain

Diagnosis

Classification

Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain's oxygen deprivation: [20]

Aneurysm in a cerebral artery, one cause of hypoxic anoxic injury (HAI). Aneurysem.jpg
Aneurysm in a cerebral artery,
one cause of hypoxic anoxic injury (HAI).
  1. Diffuse cerebral hypoxia – A mild to moderate impairment of brain function due to low oxygen levels in the blood.
  2. Focal cerebral ischemia – A stroke occurring in a localized area that can either be acute or transient. This may be due to a variety of medical conditions such as an aneurysm that causes a hemorrhagic stroke, or an occlusion occurring in the affected blood vessels due to a thrombus (thrombotic stroke) or embolus (embolic stroke). [21] Focal cerebral ischemia constitutes a large majority of the clinical cases in stroke pathology with the infarct usually occurring in the middle cerebral artery (MCA). [22]
  3. Global cerebral ischemia – A complete stoppage of blood flow to the brain.
  4. Cerebral infarction – A "stroke", caused by complete oxygen deprivation due to an interference in cerebral blood flow which affects multiple areas of the brain.

Cerebral hypoxia can also be classified by the cause of the reduced brain oxygen: [23]

Treatment

For newborn infants starved of oxygen during birth there is now evidence that hypothermia therapy for neonatal encephalopathy applied within 6 hours of cerebral hypoxia effectively improves survival and neurological outcome. [25] [26] In adults, however, the evidence is less convincing and the first goal of treatment is to restore oxygen to the brain. The method of restoration depends on the cause of the hypoxia. For mild-to-moderate cases of hypoxia, removal of the cause of hypoxia may be sufficient. Inhaled oxygen may also be provided. In severe cases treatment may also involve life support and damage control measures.

A deep coma will interfere with the body's breathing reflexes even after the initial cause of hypoxia has been dealt with; mechanical ventilation may be required. Additionally, severe cerebral hypoxia causes an elevated heart rate, and in extreme cases the heart may tire and stop pumping. CPR, defibrilation, epinephrine, and atropine may all be tried in an effort to get the heart to resume pumping. [8] Severe cerebral hypoxia can also cause seizures, which put the patient at risk of self-injury, and various anti-convulsant drugs may need to be administered before treatment.

There has long been a debate over whether newborn infants with cerebral hypoxia should be resuscitated with 100% oxygen or normal air. [27] It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. [28] Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen. [29] [30]

Brain damage can occur both during and after oxygen deprivation. During oxygen deprivation, cells die due to an increasing acidity in the brain tissue (acidosis). Additionally, during the period of oxygen deprivation, materials that can easily create free radicals build up. When oxygen enters the tissue these materials interact with oxygen to create high levels of oxidants. Oxidants interfere with the normal brain chemistry and cause further damage (this is known as "reperfusion injury").

Techniques for preventing damage to brain cells are an area of ongoing research. Hypothermia therapy for neonatal encephalopathy is the only evidence-supported therapy, but antioxidant drugs, control of blood glucose levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation. [31] Hyperbaric oxygen therapy is being evaluated with the reduction in total and myocardial creatine phosphokinase levels showing a possible reduction in the overall systemic inflammatory process. [32]

In severe cases it is extremely important to act quickly. Brain cells are very sensitive to reduced oxygen levels. Once deprived of oxygen they will begin to die off within five minutes. [31]

Prognosis

Mild and moderate cerebral hypoxia may result in seizures and impaired memory going forward. The outcome of severe cerebral hypoxia will depend on the success of damage control, amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. A general consequence may be epilepsy. The long-term effects will depend on the purpose of that portion of the brain. Damage to the Broca's area and the Wernicke's area of the brain (left side) typically causes problems with speech and language. Damage to the right side of the brain may interfere with the ability to express emotions or interpret what one sees. Damage on either side can cause paralysis of the opposite side of the body.

The effects of certain kinds of severe generalized hypoxias may take time to develop. For example, the long-term effects of serious carbon monoxide poisoning usually may take several weeks to appear. Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin sheath surrounding neurons. [33]

If hypoxia results in coma, the length of unconsciousness is often indicative of long-term damage. In some cases coma can give the brain an opportunity to heal and regenerate, [34] but, in general, the longer a coma, the greater the likelihood that the person will remain in a vegetative state until death. [9] Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

Long-term comas can have a significant impact on a patient's family. [35] Families of coma patients often have idealized images of the outcome based on Hollywood movie depictions of coma. [36] Adjusting to the realities of ventilators, feeding tubes, bedsores, and muscle wasting may be difficult. [37] Treatment decisions often involve complex ethical choices and can strain family dynamics. [38]

See also

Related Research Articles

<span class="mw-page-title-main">Hypoxia (medical)</span> Medical condition of lack of oxygen in the tissues

Hypoxia is a condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level. Hypoxia may be classified as either generalized, affecting the whole body, or local, affecting a region of the body. Although hypoxia is often a pathological condition, variations in arterial oxygen concentrations can be part of the normal physiology, for example, during strenuous physical exercise.

A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. TIA causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

<span class="mw-page-title-main">Cerebral edema</span> Excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain

Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, death.

Encephalopathy means any disorder or disease of the brain, especially chronic degenerative conditions. In modern usage, encephalopathy does not refer to a single disease, but rather to a syndrome of overall brain dysfunction; this syndrome has many possible organic and inorganic causes.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction. Ischemia causes not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial or total blockage. The inadequate delivery of oxygenated blood to the organs must be resolved either by treating the cause of the inadequate delivery or reducing the oxygen demand of the system that needs it. For example, patients with myocardial ischemia have a decreased blood flow to the heart and are prescribed with medications that reduce chronotrophy and ionotrophy to meet the new level of blood delivery supplied by the stenosed vasculature so that it is adequate.

<span class="mw-page-title-main">Cerebral infarction</span> Medical condition

Cerebral infarction is the pathologic process that results in an area of necrotic tissue in the brain. It is caused by disrupted blood supply (ischemia) and restricted oxygen supply (hypoxia), most commonly due to thromboembolism, and manifests clinically as ischemic stroke. In response to ischemia, the brain degenerates by the process of liquefactive necrosis.

<span class="mw-page-title-main">Intrauterine hypoxia</span> Medical condition when the fetus is deprived of sufficient oxygen

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction, maternal diabetes and maternal smoking. Intrauterine growth restriction may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system. This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, attention deficit hyperactivity disorder, eating disorders and cerebral palsy.

<span class="mw-page-title-main">Brain ischemia</span> Medical condition

Brain ischemia is a condition in which there is insufficient bloodflow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.

Animal models of ischemic stroke are procedures inducing cerebral ischemia. The aim is the study of basic processes or potential therapeutic interventions in this disease, and the extension of the pathophysiological knowledge on and/or the improvement of medical treatment of human ischemic stroke. Ischemic stroke has a complex pathophysiology involving the interplay of many different cells and tissues such as neurons, glia, endothelium, and the immune system. These events cannot be mimicked satisfactorily in vitro yet. Thus a large portion of stroke research is conducted on animals.

Targeted temperature management (TTM) previously known as therapeutic hypothermia or protective hypothermia is an active treatment that tries to achieve and maintain a specific body temperature in a person for a specific duration of time in an effort to improve health outcomes during recovery after a period of stopped blood flow to the brain. This is done in an attempt to reduce the risk of tissue injury following lack of blood flow. Periods of poor blood flow may be due to cardiac arrest or the blockage of an artery by a clot as in the case of a stroke.

Neonatal encephalopathy (NE), previously known as neonatal hypoxic-ischemic encephalopathy, is defined as a encephalopathy syndrome with signs and symptoms of abnormal neurological function, in the first few days of life in an infant born after 35 weeks of gestation. In this condition there is difficulty initiating and maintaining respirations, a subnormal level of consciousness, and associated depression of tone, reflexes, and possibly seizures. Encephalopathy is a nonspecific response of the brain to injury which may occur via multiple methods, but is commonly caused by birth asphyxia, leading to cerebral hypoxia.

Mild total body hypothermia, induced by cooling a baby to 33-34°C for three days after birth, is nowadays a standardized treatment after moderate to severe hypoxic ischemic encephalopathy in full-term and near to fullterm neonates. It has recently been proven to be the only medical intervention which reduces brain damage, and improves an infant's chance of survival and reduced disability.

Leukostasis is a medical emergency most commonly seen in patients with acute myeloid leukemia. It is characterized by an extremely elevated blast cell count and symptoms of decreased tissue perfusion. The pathophysiology of leukostasis is not well understood, but inadequate delivery of oxygen to the body's cells is the result. Leukostasis is diagnosed when white cell plugs are seen in the microvasculature. The most common symptoms are dyspnea and hypoxia, usually accompanied by visual changes, headaches, dizziness, confusion, somnolence, and coma. Prompt treatment is required since, if left untreated, it has a very high mortality rate. Treatments aim to rapidly reduce white blood cell counts while also treating the underlying disorder.

<span class="mw-page-title-main">Athetoid cerebral palsy</span> Type of cerebral palsy associated with basal ganglia damage

Athetoid cerebral palsy, or dyskinetic cerebral palsy, is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

Grinker's myelinopathy, also known as anoxic leukoencephalopathy, is a rare disease of the central nervous system. The disease is characterized by a delayed leukoencephalopathy after a hypoxic episode. It is typically, though not necessarily, related to carbon monoxide poisoning or heroin overdose. It occurs in roughly 2.8% of those who experience an acute hypoxic/anoxic episode. Because of the wide range of symptoms and the delay in onset, it is often misdiagnosed as other neuropathologies. Grinker's myelinopathy was originally characterized by Roy R. Grinker in 1925 or 1926, depending on the source.

<span class="mw-page-title-main">Ulegyria</span> Type of cortical scarring deep in the sulci

Ulegyria is a diagnosis used to describe a specific type of cortical scarring in the deep regions of the sulcus that leads to distortion of the gyri. Ulegyria is identified by its characteristic "mushroom-shaped" gyri, in which scarring causes shrinkage and atrophy in the deep sulcal regions while the surface gyri are spared. This condition is most often caused by hypoxic-ischemic brain injury in the perinatal period. The effects of ulegyria can range in severity, although it is most commonly associated with cerebral palsy, mental retardation and epilepsy. N.C. Bresler was the first to view ulegyria in 1899 and described this abnormal morphology in the brain as “mushroom-gyri." Although ulegyria was first identified in 1899, there is still limited information known or reported about the condition.

Anoxic depolarization is a progressive and uncontrollable depolarization of neurons during stroke or brain ischemia in which there is an inadequate supply of blood to the brain. Anoxic depolarization is induced by the loss of neuronal selective membrane permeability and the ion gradients across the membrane that are needed to support neuronal activity. Normally, the Na+/K+-ATPase pump maintains the transmembrane gradients of K+ and Na+ ions, but with anoxic brain injury, the supply of energy to drive this pump is lost. The hallmarks of anoxic depolarization are increased concentrations of extracellular K+ ions, intracellular Na+ and Ca2+ ions, and extracellular glutamate and aspartate. Glutamate and aspartate are normally present as the brain's primary excitatory neurotransmitters, but high concentrations activate a number of downstream apoptotic and necrotic pathways. This results in neuronal dysfunction and death.

Perinatal stroke is a disease where an infant has a stroke between the 140th day of the gestation period and the 28th postpartum day, affecting up to 1 in 2300 live births. This disease is further divided into three subgroups, namely neonatal arterial ischemic stroke, neonatal cerebral sinovenous ischemic stroke, and presumed perinatal stroke. Several risk factors contribute to perinatal stroke including birth trauma, placental abruption, infections, and the mother's health.

A cerebroprotectant is a drug that is intended to protect the brain after the onset of acute ischemic stroke. As stroke is the second largest cause of death worldwide and a leading cause of adult disability, over 150 drugs tested in clinical trials to provide cerebroprotection.

References

  1. ↑ Malhotra R, et al. (Nov 2001). "Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose". American Journal of Physiology. Cell Physiology . 281 (5): C1596–C1603. doi:10.1152/ajpcell.2001.281.5.c1596. PMID   11600423. S2CID   10558756.
  2. ↑ Mattiesen W. R.; et al. (May 2009). "Increased neurogenesis after hypoxic-ischemic encephalopathy in humans is age related". Acta Neuropathol. 117 (5): 525–534. doi: 10.1007/s00401-009-0509-0 . PMID   19277687.
  3. ↑ Robinson, LR; Micklesen, PJ; Tirschwell, DL; Lew, HL (Mar 2003). "Predictive value of somatosensory evoked potentials for awakening from coma". Critical Care Medicine. 31 (3): 960–967. doi:10.1097/01.ccm.0000053643.21751.3b. PMID   12627012. S2CID   18080596.
  4. ↑ Geraghty M. C.; Torbey M. T. (2006). "Neuroimaging and serologic markers of neurologic injury after cardiac arrest". Neurol Clin. 24 (1): 107–121. doi:10.1016/j.ncl.2005.10.006. PMID   16443133.
  5. ↑ Busl K. M.; Greer D. M. (Jan 2010). "Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms". NeuroRehabilitation. 26 (1): 5–13. doi: 10.3233/NRE-2010-0531 . PMID   20130351.
  6. 1 2 Butterworth, Roger F. (1999). "Hypoxic Encephalopathy". In: Siegel, George J. et al. (eds.) Basic Neurochemistry: Molecular, Cellular and Medical Aspects, 6th edition, Philadelphia: Lippincott Williams & Wilkins. ISBN   0-397-51820-X. Freely available at NCBI Bookshelf. Retrieved on 2007-04-13.
  7. ↑ "Cerebral hypoxia". MedlinePlus Medical Encyclopedia . U.S. National Library of Medicine. 2007-04-05. Retrieved 2007-04-13.
  8. 1 2 "The Maryland Medical Protocols for Emergency Medical Services Providers" (PDF). (1.00  MiB). Maryland Institute for Emergency Medical Services Systems (2004). Retrieved on 2007-04-13.
  9. 1 2 National Institute of Neurological Disorders and Stroke (2018-03-08). "Cerebral Hypoxia Information Page". U.S. National Institutes of Health . Retrieved 2007-04-13.
  10. ↑ Ferro J. M.; et al. (Dec 1996). "Diagnosis of transient ischemic attack by the nonneurologist: A validation study". Stroke. 27 (12): 2225–2229. doi:10.1161/01.STR.27.12.2225. PMID   8969785.
  11. ↑ Easton JD, et al. (Jun 2009). "Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council". Stroke. 40 (6): 2276–2293. doi: 10.1161/STROKEAHA.108.192218 . PMID   19423857.
  12. ↑ Herderscheê D, et al. (Sep 1992). "Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group". Stroke. 23 (9): 1220–1224. doi: 10.1161/01.str.23.9.1220 . PMID   1519274.
  13. ↑ Leary M. C.; Saver J. L. (2003). "Annual incidence of first silent stroke in the United States: a preliminary estimate". Cerebrovasc Dis. 16 (3): 280–285. doi:10.1159/000071128. PMID   12865617. S2CID   33095581.
  14. ↑ Vermeer S. E.; et al. (Jan 2002). "Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study". Stroke. 33 (1): 21–25. doi: 10.1161/hs0102.101629 . PMID   11779883.
  15. ↑ Herderscheê D, et al. (Sep 1992). ""Silent stroke in patients with transient ischemic attack or minor ischemic stroke". The Dutch TIA Trial Study Group". Stroke. 23 (9): 1220–1224. doi: 10.1161/01.str.23.9.1220 . PMID   1519274.
  16. 1 2 "What You Need To Know About Hypoxic Ischemic Encephalopathy (HIE)". Birth Injury Guide. Retrieved 2021-10-05.
  17. ↑ "Parent Info". Florida Neonatal Neurologic Network. Retrieved 28 January 2012.
  18. ↑ Bellemare S (2006). "Child abuse by suffocation: A cause of apparent life-threatening events Info". Paediatr Child Health. 11 (8): 493–495. PMC   2528639 . PMID   19030315.
  19. ↑ Gardiner M, Eisen S, Murphy C. Training in paediatrics: the essential curriculum. Oxford University Press, Oxford 2009.[ page needed ]
  20. ↑ "Hypoxia". The Gale Encyclopedia of Neurological Disorders. The Gale Group, Inc. 2005. Retrieved on 2007-04-13 from Answers.com.
  21. ↑ Pressman B. D.; Tourje E. J.; Thompson J. R. (Sep 1987). "An early CT sign of ischemic infarction: increased density in a cerebral artery". AJR Am J Roentgenol. 149 (3): 583–56. doi:10.2214/ajr.149.3.583. PMID   3497548.
  22. ↑ Jun Chen, Zao C. Xu, Xiao-Ming Xu, Animal Models of Acute Neurological Injuries, Humana Press; 1 edition, ISBN   978-1-60327-184-4 [ page needed ]
  23. ↑ "What is Hypoxia?". Gray Laboratory Cancer Research Trust. 1999-08-01. Archived from the original on 2003-09-21. Retrieved on 2007-04-13 from Archive.org.
  24. ↑ Brooks, Kevin E. (May–June 2005). "Are you a hypoxia expert?". Approach. United States Navy Naval Safety Center. Archived from the original on 2007-02-08. Retrieved 2007-04-13. This website provides hypoxia related safety tips for aviators working for the United States Navy aviators.
  25. ↑ Laurance, Jeremy (October 1, 2009). "Cooling 'cure' averts infant brain damage", The Independent .
  26. ↑ Jacobs, Susan E; Berg, Marie; Hunt, Rod; Tarnow-Mordi, William O; Inder, Terrie E; Davis, Peter G (2013-01-31). "Cooling for newborns with hypoxic ischaemic encephalopathy". Cochrane Database of Systematic Reviews. 2013 (1): CD003311. doi:10.1002/14651858.cd003311.pub3. ISSN   1465-1858. PMC   7003568 . PMID   23440789.
  27. ↑ Davis, PG; Tan, A; O'Donnell, CPF; Schulze, A (2004). "Resuscitation of newborn infants with 100% oxygen or air: a systematic review and meta-analysis". The Lancet . 364 (9442): 1329–1333. doi:10.1016/S0140-6736(04)17189-4. PMID   15474135. S2CID   24825982.
  28. ↑ Kutzsche, S; Ilves, P; Kirkeby, OJ; Saugstad, OD (2001). "Hydrogen peroxide production in leukocytes during cerebral hypoxia and reoxygenation with 100% or 21% oxygen in newborn piglets". Pediatric Research . 49 (6): 834–842. doi: 10.1203/00006450-200106000-00020 . PMID   11385146.
  29. ↑ ILCOR Neonatal Resuscitation Guidelines 2010
  30. ↑ Norwegian paediatrician honoured by University of Athens, Norway.gr
  31. 1 2 Richmond, T. S. (May 1997). "Cerebral Resuscitation after Global Brain Ischemia", AACN Clinical Issues 8 (2). Retrieved on 2007-04-13. Free full text Archived September 27, 2007, at the Wayback Machine at the American Association of Critical-Care Nurses website.
  32. ↑ Orozco-Gutierrez A, Rojas-Cerda L, Estrada RM, Gil-Rosales C (December 2010). "Hyperbaric oxygen in the treatment of asphyxia in two newborn infants". Diving and Hyperbaric Medicine. 40 (4): 218–220. PMID   23111939. Archived from the original on September 6, 2013. Retrieved 2013-06-06.{{cite journal}}: CS1 maint: unfit URL (link)
  33. ↑ University of Pennsylvania Medical Center (2004-09-06). "Long-Term Effects of Carbon Monoxide Poisoning Are an Autoimmune Reaction". ScienceDaily. Retrieved 2007-04-13.
  34. ↑ Phillips, Helen (2006-07-03). "'Rewired brain' revives patient after 19 years". New Scientist . Retrieved 2007-04-13.[ permanent dead link ]
  35. ↑ Mayo Clinic staff (2006-05-17). "Coma: Coping skills". Mayo Clinic . Retrieved 2007-04-13.
  36. ↑ Wijdicks E. F. M.; Wijdicks C. A. (2006). "The portrayal of coma in contemporary motion pictures". Neurology. 66 (9): 1300–1303. doi:10.1212/01.wnl.0000210497.62202.e9. PMID   16682658. S2CID   43411074.
  37. ↑ Konig P, et al. (1992). "Psychological counseling of the family of patients with craniocerebral injuries (psychological family counseling of severely ill patients)"". Zentralbl Neurochir. 53 (2): 78–84. PMID   1636327.
  38. ↑ Montgomery V, et al. (2002). "The effect of severe traumatic brain injury on the family". Journal of Trauma. 52 (6): 1121–1124. doi:10.1097/00005373-200206000-00016. PMID   12045640.
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