Cerebral hypoxia

Cerebral hypoxia
Cerebral hypoxia
Classification and external resources

Circle of Willis
Arteries beneath brain
ICD-9 437.9
MeSH D002534

Cerebral hypoxia refers to a reduced supply of oxygen to the brain. Cerebral anoxia refers to a complete lack of oxygen to the brain. There are four separate categories of cerebral hypoxia; in order of severity they are; 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]

Cases of total oxygen deprivation are termed anoxia, which can be hypoxic in origin i.e. reduced oxygen availability, or ischemic in origin i.e., 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 isn't 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]



Cerebral hypoxia is typically grouped into four categories depending on the severity and location of the brain’s oxygen deprivation:[6]

Aneuyrsm 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; is a stroke occurring in a localized area that can either be acute (sudden onset)and/ or transient (of short duration). This may be due to a variety of medical conditions such as an aneuryrsm which causes a hemorrhagic stroke, or an occlusion occurring in the affected blood vessel/s due to a thrombus (thrombotic stroke) or embolus (embolic stroke).[7] 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).[8]
  3. Global cerebral ischemia. A complete stoppage of blood flow to the brain.
  4. Massive Cerebral infarction; is 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:[9]

  • Hypoxic hypoxia. Limited oxygen in the environment causes reduced brain function. Divers, aviators,[10] mountain climbers and fire fighters are all at risk for this kind of cerebral hypoxia. The term also includes oxygen deprivation due to obstructions in the lungs. Choking, strangulation, the crushing of the windpipe all cause this sort of hypoxia. Severe asthmatics may also experience symptoms of hypoxic hypoxia.
  • Hypemic hypoxia. Reduced brain function is caused by inadequate oxygen in the blood despite adequate environmental oxygen. Anemia and carbon monoxide poisoning are common causes of hypemic hypoxia.
  • Ischemic hypoxia (a.k.a. stagnant hypoxia). Reduced brain oxygen is caused by inadequate blood flow to the brain. Stroke, shock, and heart attacks are common causes of stagnant hypoxia. Ischemic hypoxia can also be created by pressure on the brain. Cerebral edema, brain hemorrhages and hydrocephalus exert pressure on brain tissue and impede their absorption of oxygen.
  • Histotoxic hypoxia. Oxygen is present in brain tissue but cannot be metabolized. Cyanide poisoning is a well known example.


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 work in nitrogen rich environments, ascent from a deep water dive, flying at high altitudes in an un-pressurized cabin, and intense exercise at high altitudes prior to acclimatization.

Severe cerebral hypoxia and anoxia is usually caused by traumatic events. Examples include choking, drowning, strangulation, smoke inhalation, drug overdoses, crushing of the trachea, status asthmaticus, and shock.[11] It is also recreationally self-induced in the fainting game and in erotic asphyxiation.

  • Transient ischemic attack (TIA), is often referred to as a "mini-stroke". The American Heart Association and American Stroke Association (AHA/ASA) refined the definition of transient ischemic attack. TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The symptoms of a TIA can resolve within a few minutes unlike a stroke. TIAs share the same underlying etiology as strokes; a disruption of cerebral blood flow. TIAs and strokes present with the same symptoms such as contralateral paralysis (opposite side of body from affected brain hemisphere), or sudden weakness or numbness. A TIA may cause sudden dimming or loss of vision, aphasia, slurred speech and mental confusion. The symptoms of a TIA typically resolve within 24 hours unlike a stroke. Brain injury may still occur in a TIA lasting only a few minutes. Having a TIA is a risk factor for eventually having a stroke.[12][13]
  • Silent stroke is a stroke which does not have any outward symptoms, and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms a silent stroke still causes damage to the brain, and places the patient at increased risk for a major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of theses strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as fMRI.[14][15] The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being predisposing factors.[16][17]

Signs and symptoms

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. [18]

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.[18] 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.[19]

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. 86-90% is considered moderate. Anything below 86% is considered severe.[20]

It should be noted that 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.


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[citation needed]. 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 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. 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.[20] Severe cerebral hypoxia can also cause seizures. Seizures put the patient at risk of self injury. If convulsions are sufficiently severe medical professionals may not be able to provide medical treatment. Various anti-convulsant drugs may need to be administered before treatment can continue.

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 called reperfusion injury.

Techniques for preventing damage to brain cells are an area of on-going research.Hypothermia therapy for neonatal encephalopathy is the only evidence-supported therapy, but anti-oxidant drugs, control of blood glucose levels, and hemodilution (thinning of the blood) coupled with drug-induced hypertension are some treatment techniques currently under investigation.[21]

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.[21]


Mild and moderate cerebral hypoxia generally has no impact beyond the episode of hypoxia. Severe cerebral hypoxia is another matter. Outcome will depend on the success of damage control measures, the amount of brain tissue deprived of oxygen, and the speed with which oxygen was restored to the brain.

If cerebral hypoxia was localized to a specific part of the brain, brain damage will be localized to that region. 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 CO induced changes in the myelin sheath surrounding neurons.[22]

If hypoxia results in coma, the length of unconsciousness is often used as an indication of long term damage. In some cases coma can give the brain an opportunity to heal and regenerate,[23] but, in general, the longer a coma continues the greater the likelihood that the person will remain in a vegetative state until death.[11] Even if the patient wakes up, brain damage is likely to be significant enough to prevent a return to normal functioning.

The effects of long term comas are not limited to the comatose person. Long term coma can have significant impact on their families.[24] Families of coma victims often have idealized images of the outcome based on Hollywood movie depictions of coma.[25] Adjusting to the realities of ventilators, feeding tubes, bedsores and muscle wasting may be difficult.[26] Treatment decision often involve complex ethical choices and can strain family dynamics.[27]

See also


  1. ^ Malhotra R. et al. Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose. Am J Physiol Cell Physiol. 2001 Nov;281(5):C1596-603.PMID 11600423
  2. ^ Mattiesen WR. et al.Increased neurogenesis after hypoxic-ischemic encephalopathy in humans is age related. Acta Neuropathol. 2009 May;117(5):525-34. PMID 19277687
  3. ^ Robinson LR. et al. Predictive value of somatosensory evoked potentials for awakening from coma.Crit Care Med. 2003 Mar;31(3):960-7. Predictive value of somatosensory evoked potentials for awakening from coma. PMID 12627012
  4. ^ Geraghty MC, Torbey MT. Neuroimaging and serologic markers of neurologic injury after cardiac arrest.Neurol Clin. 2006 Feb;24(1):107-21, vii.PMID 16443133
  5. ^ Busl KM, Greer DM. Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms.NeuroRehabilitation. 2010 Jan;26(1):5-13.PMID 20130351
  6. ^ "Hypoxia". The Gale Encyclopedia of Neurological Disorders. The Gale Group, Inc. 2005. http://www.answers.com/topic/hypoxia.  Retrieved on 2007-04-13 from Answers.com.
  7. ^ Pressman BD, Tourje EJ, Thompson JR. AJR Am J Roentgenol.An early CT sign of ischemic infarction: increased density in a cerebral artery. 1987 Sep;149(3):583-6.PMID 3497548
  8. ^ Animal Models of Acute Neurological Injuries By Jun Chen, Zao C. Xu, Xiao-Ming Xu. Publisher: Humana Press; 1 edition Language: English ISBN 978-1603271844
  9. ^ "What is Hypoxia?". Gray Laboratory Cancer Research Trust. 1999-08-01. Archived from the original on 2003-09-21. http://web.archive.org/web/20030921221421/http://www.graylab.ac.uk/groups/advtec/hypoxia/hypoxia2.html.  Retrieved on 2007-04-13 from Archive.org.
  10. ^ 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. http://web.archive.org/web/20070208102227/http://www.safetycenter.navy.mil/MEDIA/approach/issues/mayjun05/hypoxiaexpert.htm. Retrieved 2007-04-13.  This website provides hypoxia related safety tips for aviators working for the United States Navy aviators.
  11. ^ a b National Institute of Neurological Disorders and Stroke (2007-02-08). "Cerebral Hypoxia Information Page". U.S. National Institutes of Health. http://www.ninds.nih.gov/disorders/anoxia/anoxia.htm. Retrieved 2007-04-13. 
  12. ^ Ferro JM et al. Diagnosis of transient ischemic attack by the nonneurologist. A validation study. 1996 Dec;27(12):2225-9.PMID 8969785
  13. ^ Easton JD. et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists.Stroke. 2009 Jun;40(6):2276-93. Epub 2009 May 7.PMID 19423857
  14. ^ Herderscheê D et al. Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group.Stroke. 1992 Sep;23(9):1220-4.PMID 1519274
  15. ^ Leary MC, Saver JL. Annual incidence of first silent stroke in the United States: a preliminary estimate.Cerebrovasc Dis. 2003;16(3):280-5.PMID 12865617
  16. ^ Vermeer SE, et al Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study. Stroke. 2002 Jan;33(1):21-5.PMID 11779883
  17. ^ Herderscheê D, et alSilent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group. Stroke. 1992 Sep;23(9):1220-4. PMID 1519274
  18. ^ a b 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 039751820X. Freely available at NCBI Bookshelf. Retrieved on 2007-04-13.
  19. ^ "Cerebral hypoxia". MedlinePlus Medical Encyclopedia. U.S. National Library of Medicine. 2007-04-05. http://www.nlm.nih.gov/medlineplus/ency/article/001435.htm. Retrieved 2007-04-13. 
  20. ^ a b The Maryland Medical Protocols for Emergency Medical Services ProvidersPDF (1.00 MiB). Maryland Institute for Emergency Medical Services Systems (2004). Retrieved on 2007-04-13.
  21. ^ a b Richmond TS (May 1997). "Cerebral Resuscitation after Global Brain Ischemia". AACN Clinical Issues 8 (2). Retrieved on 2007-04-13. Free full text at the American Association of Critical-Care Nurses website.
  22. ^ University Of Pennsylvania Medical Center (2004-09-06). "Long-term Effects Of Carbon Monoxide Poisoning Are An Autoimmune Reaction". ScienceDaily. http://www.sciencedaily.com/releases/2004/09/040906083815.htm. Retrieved 2007-04-13. 
  23. ^ Phillips, Helen (2006-07-03). "'Rewired brain' revives patient after 19 years". New Scientist. http://www.newscientist.com/article.ns?id=dn9474&feedId=brain_rss20. Retrieved 2007-04-13. 
  24. ^ Mayo Clinic staff (2006-05-17). "Coma: Coping skills". Mayo Clinic. http://www.mayoclinic.com/health/coma/DS00724/DSECTION=10. Retrieved 2007-04-13. 
  25. ^ Wijdicks EFM, Wijdicks CA (2006). "The portrayal of coma in contemporary motion pictures". Neurology 66 (9): 1300–1303. doi:10.1212/01.wnl.0000210497.62202.e9 PMID 16682658.
  26. ^ 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.
  27. ^ Montgomery V et al. (2002). "The effect of severe traumatic brain injury on the family". J Trauma 52 (6): 1121–4. PMID 12045640.

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