Ischemic Stroke

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An Ischemic Stroke is a brain stroke that ...

References

2016

  • https://en.wikipedia.org/wiki/Brain_ischemia
    • Brain ischemia (aka cerebral ischemia, cerebrovascular ischemia) is a condition in which there is insufficient blood flow to the brain to meet metabolic demand.[1] This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke.[2] It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage.[3]

      Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis.[4]

      There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue.

      The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage.

      An interruption of blood flow to the brain for more than 10 seconds causes unconsciousness, and an interruption in flow for more than a few minutes generally results in irreversible brain damage.[5] In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. Accordingly, this discovery raised the possibility of intervening after brain ischemia before the damage becomes irreversible.[6]

  1. ↑ Template:Cite news
  2. ↑ Template:Cite news
  3. ↑ "UpToDate Inc.". http://www.uptodate.com/online/content/topic.do?topicKey=cva_dise/8834&linkTitle=Brain%20ischemia&source=preview&selectedTitle=4~132&anchor=5#5. 
  4. ↑ Vespa, Paul; Bergsneider, Marvin; Hattori, Nayoa; Wu, Hsiao-Ming; Huang, Sung-Cheng; Martin, Neil A; Glenn, Thomas C; McArthur, David L et al. (2005). "Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study". Journal of Cerebral Blood Flow & Metabolism 25 (6): 763–74. doi:10.1038/sj.jcbfm.9600073. PMC 4347944. PMID 15716852. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=4347944. 
  5. ↑ Template:Cite news
  6. ↑ Template:Cite news

2016

  • https://en.wikipedia.org/wiki/Stroke#Ischemic_2
    • Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade.[1] Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds[citation needed], and after approximately three hours will suffer irreversible injury possibly leading to the death of the tissue, i.e., infarction. (This is why fibrinolytics such as alteplase are given only until three hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques.[2] Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge in and block brain blood vessels. Since blood vessels in the brain are now blocked, the brain becomes low in energy, and thus it resorts into using anaerobic metabolism within the region of brain tissue affected by ischemia. Anaerobic metabolism produces less adenosine triphosphate (ATP) but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance in the brain. The ischemia area is referred to as the "ischemic penumbra”.[3]

      As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is the release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result, the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids, and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to programmed cell death.[4]

      Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the programmed cell death cascade by means of redox signaling.[5]

      These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has a little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.

      In addition to damaging effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.

  1. ↑ "Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis". Pathophysiology : the official journal of the International Society for Pathophysiology / ISP 17 (3): 197–218. June 2010. doi:10.1016/j.pathophys.2009.12.001. PMID 20074922. 
  2. ↑ Richard S. Snell (2006). Clinical neuroanatomy, 6. ed. Lippincott Williams & Wilkins, Philadelphia. pp. 478–485. ISBN 978-963-226-293-2. 
  3. ↑ Brunner and Suddarth's Textbook on Medical-Surgical Nursing, 11th Edition
  4. ↑ Kristián, T; Siesjö, BK (1996). "Calcium-related damage in ischemia.". Life Sciences 59 (5-6): 357–67. doi:10.1016/0024-3205(96)00314-1. PMID 8761323. 
  5. ↑ Chan, PH (January 2001). "Reactive oxygen radicals in signaling and damage in the ischemic brain.". Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 21 (1): 2–14. doi:10.1097/00004647-200101000-00002. PMID 11149664. 

2009

  • Kidd, Parris M. “Integrated brain restoration after ischemic stroke-medical management, risk factors, nutrients, and other interventions for managing inflammation and enhancing brain plasticity." Alternative Medicine Review 14, no. 1 (2009): 14-36.
    • ABSTRACT: Brain injury from ischemic stroke can be devastating, but full brain restoration is feasible. Time until treatment is critical; rapid rate of injury progression, logistical and personnel constraints on neurological and cardiovascular assessment, limitations of recombinant tissue plasminogen activator (rtPA) for thrombolysis, anticoagulation and antiplatelet interventions, and neuroprotection all affect outcome. Promising acute neuroprotectant measures include albumin, magnesium, and hypothermia. Long-term hyperbaric oxygen therapy (HBOT) is safe and holds great promise. Eicosanoid and cytokine down-regulation by omega-3 nutrients docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) may help quench stroke inflammation. C-reactive protein (CRP), an inflammatory biomarker and stroke-recurrence predictor, responds favorably to krill oil (a phospholipid-DHA/EPA-astaxanthin complex). High homocysteine (Hcy) is a proven predictor of stroke recurrence and responds to folic acid and vitamin [B.sub.12]. Vitamin E may lower recurrence for individuals experiencing high oxidative stress. Citicoline shows promise for acute neuroprotection. Glycerophosphocholine (GPC) is neuroprotective and supports neuroplasticity via nerve growth factor (NGF) receptors. Stem cells have shown promise for neuronal restoration in randomized trials. Endogenous brain stem cells can migrate to an ischemic injury zone; exogenous stem cells once transplanted can migrate ("home") to the stroke lesion and provide trophic support for cortical neuroplasticity. The hematopoietic growth factors erythropoietin (EPO) and granulocyte-colony stimulating factor (G-CSF) have shown promise in preliminary trials, with manageable adverse effects. Physical and mental exercises, including constraint-induced movement therapy (CIMT) and interactive learning aids, further support brain restoration following ischemic stroke. Brain plasticity underpins the function-driven brain restoration that can occur following stroke.
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