Cerebral infarction

From Wikipedia, the free encyclopedia
Jump to: navigation, search
Cerebral infarct
Classification and external resources
ICD-10 I63
ICD-9 434.01, 434.11, 434.91
eMedicine stroke.htm neuro/ischemic stroke http://emedicine.medscape.com/article/1916852-overview
MeSH D002544



There are various classification systems for a cerebral infarction.





Whether a cerebral infarction is thrombotic or embolic is based its pathophysiology, or the observed conditions and underlying mechanisms of the disease. In thrombotic ischemic stroke, a thrombus forms and blocks blood flow.[5] A thrombus forms when theendothelium is activated by a variety of signals to result in platelet aggregation in the artery. This clump of platelets interacts with fibrin to form a platelet plug.[6] This platelet plug grows into a thrombus, resulting in a stenotic artery. Thrombotic ischemia can occur in large or small blood vessels. The most common cause of thrombi in large vessels is artherosclerosis or vasoconstriction. In small vessels, the most common cause is lipohyalinosis.[7] Lipohyalinosis is when high BP and aging causes a a build-up of fatty hyaline matter in blood vessels. Atheroma formation can also cause small vessel thrombotic ischemic stroke.[8]

An embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). The embolus may be of cardiac origin due to Atrial fibrillation, Patent foramen ovale or from atherosclerotic plaque of another (or the same) large artery. Cerebral artery gas embolism (e.g. during ascent from a SCUBA dive) is also a possible cause of infarction (Levvett & Millar, 2008)

Risk factors[edit]

Major risk factors for cerebral infarction are generally the same as for atherosclerosis: high blood pressure, Diabetes mellitus, tobacco smoking, obesity, and dyslipidemia.[9][10][11][12][13] The American Heart Association/American Stroke Association (AHA/ASA) recommends controlling these risk factors in order to prevent stroke.[14] The AHA/ASA guidelines also provide information on how to prevent stroke if someone has a more specific concerns, such as Sickle-cell disease or pregnancy. It is also possible to calculate the risk of stroke in the next decade based on information gathered through the Framingham Heart Study.[15]





Cut-away view of the Merci L5 retrieval system, used for clot removal in ischemic stroke patients

If cerebral infarction is caused by a thrombus occluding blood flow to an artery supplying the brain, definitive therapy is aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The more rapidly blood flow is restored to the brain, the fewer brain cells die.[16] In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery. Another intervention for acute cerebral ischaemia is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[17][18][19][20] though no differences have been found between newer and older versions of the devices.[21] The devices have only been tested on patients treated with mechanical clot embolectomy within eight hours of the onset of symptoms.





  1. ^ Ropper, Allan H.; Adams, Raymond Delacy; Brown, Robert F.; Victor, Maurice (2005). Adams and Victor's principles of neurology. New York: McGraw-Hill Medical Pub. Division. pp. 686–704. ISBN 0-07-141620-X. 
  3. ^ Bamford JM (2000). "The role of the clinical examination in the subclassification of stroke". Cerebrovasc. Dis. 10 Suppl 4: 2–4. doi:10.1159/000047582. PMID 11070389. 
  4. ^ Adams HP, Bendixen BH, Kappelle LJ, et al. (January 1993). "Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment" (PDF). Stroke 24 (1): 35–41. doi:10.1161/01.STR.24.1.35. PMID 7678184. 
  5. ^ Louis R. Caplan (2009). Caplan's Stroke: A Clinical Approach. Elsevier Health Sciences. ISBN 1-4160-4721-2. 
  6. ^ Samad F, Ruf W (November 2013). "Inflammation, obesity, and thrombosis". Blood 122 (20): 3415–22. doi:10.1182/blood-2013-05-427708. PMID 24092932. 
  7. ^ Lastilla M (2006). "Lacunar infarct". Clin. Exp. Hypertens. 28 (3-4): 205–15. PMID 16833026. 
  8. ^ Caplan LR (September 1989). "Intracranial branch atheromatous disease: a neglected, understudied, and underused concept". Neurology 39 (9): 1246–50. PMID 2671793. 
  9. ^ Bogousslavsky J, Regli F, Van Melle G (September 1985). "Risk factors and concomitants of internal carotid artery occlusion or stenosis. A controlled study of 159 cases". Arch. Neurol. 42 (9): 864–7. PMID 4026630. 
  10. ^ Candelise L, Bianchi F, Galligoni F, et al. (1984). "Italian multicenter study on reversible cerebral ischemic attacks: III--Influence of age and risk factors on cerebrovascular atherosclerosis". Stroke 15 (2): 379–82. PMID 6701947. 
  11. ^ Crouse JR, Toole JF, McKinney WM, et al. (1987). "Risk factors for extracranial carotid artery atherosclerosis". Stroke 18 (6): 990–6. PMID 3686596. 
  12. ^ Harmsen P, Lappas G, Rosengren A, Wilhelmsen L (July 2006). "Long-term risk factors for stroke: twenty-eight years of follow-up of 7457 middle-aged men in Göteborg, Sweden". Stroke 37 (7): 1663–7. doi:10.1161/01.STR.0000226604.10877.fc. PMID 16728686. 
  13. ^ Hankey GJ (August 2006). "Potential new risk factors for ischemic stroke: what is their potential?". Stroke 37 (8): 2181–8. doi:10.1161/01.STR.0000229883.72010.e4. PMID 16809576. 
  14. ^ Furie KL, Kasner SE, Adams RJ, et al. (January 2011). "Guidelines for the prevention of stroke in patients with stroke or transient ischemic attack: a guideline for healthcare professionals from the american heart association/american stroke association". Stroke 42 (1): 227–76. doi:10.1161/STR.0b013e3181f7d043. PMID 20966421. 
  15. ^ D'Agostino RB, Wolf PA, Belanger AJ, Kannel WB (January 1994). "Stroke risk profile: adjustment for antihypertensive medication. The Framingham Study". Stroke 25 (1): 40–3. PMID 8266381. 
  23. ^ Ropper, A.H.; Brown, R.H. (2005). Adams and Victor's Principles of Neurology. p. 698. ISBN 0-07-141620-X