What is ischemic injury

For example, the availability of transgenic mice generated by the laboratory of Dr. V Gallo at the Children's National Medical Centre, Washington DC, in which green fluorescent protein expression is under the control of the astrocyte specific GFAP promoter, should provide investigators with the means of assessing astrocyte injury more thoroughly in an in situ environment.

Astrocytes have long been ascribed a housekeeping function and ischaemia-induced alterations of the many functions they perform are capable of influencing the outcome of surrounding cells. For example, numerous studies of energy deprivation in the perinatal brain have reported astrocytic activation 59 — Astrocytes may become "activated" by inflammatory mediators in a range of circumstances such as ischaemia and trauma leading to a characteristic up-regulation of GFAP, cellular hypertrophy, astrocyte proliferation and process extension The consequences of astrocytic activation are not well understood and may be both beneficial and detrimental.

For example, free radicals and inflammatory mediators such as TNFa may be released with the potential to cause injury while trophic factors such as TGFd and brain derived neurotrophic factor are also released and, remarkably, free radical scavenging is possible 64 — Banker and Larroche's description of PVL noted the presence of "retraction balls and clubs", that is, the presence of swollen axon cylinders and such injury will undoubtedly contribute to the phenotype of the ensuing disorder.

Recently amyloid precursor protein, a marker of the integrity of fast axonal transport and therefore axon injury, has been detected in the brains of infants with WM injury 59 , 72 — Furthermore, in a developmental study on axon conduction during acute energy deprivation, a rapid decrease in the ability of RONs to recover electrical activity following OGD was noted around the onset of myelination Although papers on the mechanisms of injury to myelinating axons have not been forthcoming, the response of myelinated central axons to energy deprivation has been extensively studied, primarily using the hypoxic rat optic nerve model 76 — Following on from these initial studies, investigators are now beginning to look at the mechanisms behind the injury sustained following both oxygen and glucose withdrawal; perhaps a more clinically relevant model given that the cessation of blood flow that occurs during stroke will decrease the availability of both oxygen and glucose.

The authors speculated that the underlying reasons for this might include myelin damage, an increase in tissue energy use or the loss of trophic support Similar protection of optic nerve axons following OGD withdrawal has been reported in abstract form raising the possibility that in the event of a more severe metabolic insult, excitotoxicity may play an important role in acute axonal injury 82 , Ouardouz et al.

Such evidence indicates that ischemia-induced axon injury in the developing brain is likely to be the result of numerous pathways operating together leading to a catastrophic loss of function. Although the developing brain is relatively resistant to ischemia, severe insults can result in a characteristically cortical-sparring pathology associated with both mental and physical disability. Numerous models for studying the effects of energy deprivation upon the developing brain are now available and have resulted in an ever growing body of literature on the subject.

An understanding of the Byzantine pathophysiology of ischemia-induced white matter injury is steadily leading researchers towards the development of effective therapeutic interventions in the near future. Coronal section of cerebrum. The focal black circles and diffuse grey shading components of PVL are shown in one hemisphere and the cerebral vascular supply in the other.

The long and short penetrating arteries supply the cerebral WM, as shown. From 9. Oligodendrocyte injury during ischemia. In addition, a developmental lag in anti-oxidant defences can lead to the build up of lethal free radicals such as the hydroxyl radical 3. Diagram illustrating mechanisms of ischemic injury to CNS axons. National Center for Biotechnology Information , U.

Journal List Mcgill J Med v. Mcgill J Med. James J. Author information Copyright and License information Disclaimer. His research interests lie within the field of developmental neurobiology, with a particular emphasis on perinatal brain injury.

This article has been cited by other articles in PMC. Open in a separate window. Figure 1. Figure 2. Figure 3. Selective vulnerability of late oligodendrocyte progenitors to hypoxia-ischemia. J Neurosci. Carbohydrate and energy metabolism in perinatal rat brain: relation to survival in anoxia.

J Neurochem. Kabat H. The greater resistance of very young animals to arrest of the brain circulation. Am J Physiol. Volpe JJ. Neurobiology of periventricular leukomalacia in the premature infant. Pediatr Res. Report of the National Institute of Neurological Disorders and Stroke workshop on perinatal and childhood stroke. Epidemiology of perinatal stroke. Curr Opin Pediatr. Virchow R. Zur pathologischen Anatomie des Gehirns I.

Congenitale Encephalitis und Myelitis. Periventricular leukomalacia of infancy. A form of neonatal anoxic encephalopathy. Arch Neurol. Volpe, J. Maternal infection, fetal inflammatory response, and brain damage in very low birth weight infants. Developmental Epidemiology Network Investigators. NBQX attenuates excitotoxic injury in developing white matter. The vulnerability of the fetal sheep brain to hypoxemia at mid-gestation.

Brain Res Dev Brain Res. Rat model of perinatal hypoxic-ischemic brain damage. J Neurosci Res. Apoptosis and necrosis in the newborn piglet brain following transient cerebral hypoxia-ischaemia.

Neuropathol Appl Neurobiol. Emerging concepts in periventricular white matter injury. Semin Perinatol. Rorke LB. Anatomical features of the developing brain implicated in pathogenesis of hypoxic-ischemic injury. Brain Pathol. Cerebral blood flow requirement for brain viability in newborn infants is lower than in adults.

Ann Neurol. A mechanical clot removal can be performed up to 24 hours after the onset of stroke symptoms. Long-term treatments include aspirin Bayer or an anticoagulant to prevent further clots.

For example, your doctor may recommend a stent to open an artery narrowed by plaque or statins to lower blood pressure. If the stroke caused paralysis or severe weaknes s, you may also need rehabilitation afterward to regain function.

Rehabilitation is often necessary to regain motor skills and coordination. Occupational, physical, and speech therapy might also be useful to help regain other lost function. Younger people and people who start improving quickly are likely to recover more function.

Having one ischemic stroke puts you at a higher risk for having another. Taking steps to reduce your risk, such as quitting smoking , are an important part of long-term recovery. Learn more about stroke recovery. Ischemic stroke is a serious condition and requires prompt treatment. However, with the correct treatment, most people with ischemic stroke can recover or maintain enough function to take care of their basic needs. Knowing the signs of ischemic stroke can help save your life or the life of someone else.

Stroke recovery can be a lengthy process that requires patience, hard work, and commitment. Recovery from stroke can take place in a range of…. A stroke happens when the blood flow to your brain is interrupted. Some see acupuncture as a complement to traditional rehabilitation methods.

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If the brain becomes damaged irreversibly and tissue death occurs, the symptoms may be permanent. Cerebral ischemia is linked to many diseases or irregularities. Patients with compressed blood vessels, plaque buildup in the arteries, blood clots, very low blood pressure as a result of heart attack, congenital heart defects and even sickle cell anemia have a higher tendency to cerebral ischemia in comparison to their healthy counterparts.

Sickle cell anemia may cause cerebral ischemia linked with the irregularly shaped blood cells. Sickle shaped blood cells clot more easily than normal blood cells, obstructing blood flow to the brain. Compression of blood vessels may also lead to cerebral ischemia, by obstructing the arteries that bring oxygen to the brain. Tumors can be a cause of blood vessel compression.

Plaque buildup in the arteries may also result in ischemia. Even the slightest amount of plaque buildup can cause the narrowing of passageways, affecting that area to become more prone to blood clots. Bigger blood clots can also cause ischemia by blocking blood flow.

A heart attack can also lead to cerebral ischemia due to the association that exists between heart attack and low blood pressure. Extremely low blood pressure usually characterizes the insufficient oxygenation of tissues. Untreated heart attacks slow blood flow enough that blood may start to clot and stop the flow of blood to the brain or other major organs. Cerebral ischemia can result from events other than heart attacks.