Transient ischemic attack

Transient ischemic attack
Classification and external resources
Specialty Neurology
ICD-10 G45.9
ICD-9-CM 435.9
DiseasesDB 13253
MedlinePlus 000730
eMedicine emerg/604
MeSH D002546

A transient ischemic attack (TIA) is a transient episode of neurologic dysfunction caused by ischemia (loss of blood flow) – either focal brain, spinal cord, or retinal – without acute infarction (tissue death). TIAs have the same underlying cause as strokes: a disruption of cerebral blood flow (CBF), and are often referred to as mini-strokes. Symptoms caused by a TIA resolve in 24 hours or less.[1][2] TIA was originally defined clinically by the temporary nature of less than 24 hours of the associated neurologic symptoms. Recently, the American Heart Association and American Stroke Association (AHA/ASA) defined TIA as transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.[1] TIAs cause the same symptoms associated with stroke, 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 (amaurosis fugax), aphasia, slurred speech (dysarthria) and mental confusion. But unlike a stroke, the symptoms of a TIA can resolve within a few minutes or within 24 hours. 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 or a silent stroke.[3][1]

A silent stroke, also known as silent cerebral infarct (SCI), differs from a TIA in that there are no immediately observable symptoms. An SCI may still cause long lasting neurological dysfunction affecting such areas as mood, personality and cognition. An SCI often occurs before or after a TIA or major stroke.[4]

A cerebral infarct that lasts longer than 24 hours but fewer than 72 hours is called a reversible ischemic neurologic deficit or RIND.

Signs and symptoms

Symptoms can vary widely across people, and across brain regions. The most frequent symptoms include temporary loss of vision (typically amaurosis fugax); difficulty speaking (aphasia); weakness on one side of the body (hemiparesis); and numbness or tingling (paresthesia), usually on one side of the body. Impairment of consciousness is very uncommon. There have been cases of temporary and partial paralysis affecting the face and tongue of the afflicted. The symptoms of a TIA are short-lived and usually last a few seconds to a few minutes and most symptoms disappear within 60 minutes. Some individuals may have a lingering feeling that something odd happened to the body. Dizziness, lack of coordination or poor balance are also symptoms related to TIA. Symptoms vary in severity.


The most common cause of a TIA is an embolus that occludes an artery in the brain. This usually arises from a dislodged atherosclerotic plaque in one of the carotid arteries (i.e. two of the four major arteries supplying the brain) or from the vertebral-basilar arteries. Another common cause is from a thrombus (i.e. a blood clot) that has originated from the (usually left) atrium of the heart due to atrial fibrillation. In a TIA, the blockage period is very short-lived and hence there is no permanent damage.[5] The cholesterol build-up is gradual and eventually narrows the lumen. With time, blood flow to that side of the brain is reduced and a stroke may occur as a result. In other cases, cholesterol particles from the atherosclerotic plaque may suddenly break off and enter the brain. In some people, these fragments come off from the heart and go to the brain. This often happens during a heart attack or an infection of the valves.[6]

Other reasons include excessive narrowing of large vessels resulting from an atherosclerotic plaque and increased blood viscosity caused by some blood diseases. TIA is related to other medical conditions such as hypertension, heart disease (especially atrial fibrillation), migraine, hypercholesterolemia, and diabetes mellitus.

Risk factors


TIA will usually be diagnosed after a doctor performs a history and a physical exam. There are several radiological tests that are done to evaluate patients who have had a TIA. These include a CT scan or an MRI of the brain, ultrasound of the neck, or an echocardiogram of the heart. In most cases, the source of atherosclerosis is usually identified with an ultrasound.[7]

Differential diagnoses

Other diagnoses may have symptoms similar to those of a TIA:

  1. Atypical migraine if visual symptoms occur such as the perception of wavy or jagged lines or tiny specks of light and if a headache occurs. Typically a history of prior migraines is present.
  2. Partial seizure in the parietal area of the brain
  3. Glucose abnormalities; these could be distinguished by a history of diabetes mellitus and a loss of consciousness
  4. Electrolyte abnormalities
  5. Hypertensive encephalopathy (headache, delirium, hypertension, cerebral edema)
  6. Subdural hematoma (history of trauma, headache, loss of consciousness)
  7. Brain tumor (mode of onset, progressive headaches, increased intracranial pressure)
  8. Demyelinating disease
  9. Conversion disorder


A TIA may be prevented by changes in lifestyle; although most of these recommendations have no solid empirical data, most medical professionals believe them to be so.[8] These include:


The mainstay of the treatment following acute recovery from a TIA depends on the underlying cause. It is not always immediately possible to tell the difference between a CVA (stroke) and a TIA. Most patients who are diagnosed at a hospital's emergency department as having suffered from a TIA will be admitted to the hospital if it is their first TIA, for telemetry, blood pressure monitoring and other specific tests. If it is a second or subsequent TIA, most patients will be discharged home and advised to contact their primary physician to organize further investigations. A TIA is often the last warning before a CVA occurs. The cause of TIA should be immediately investigated by imaging of the brain. Occasionally, none of these tests will determine the cause, but the symptoms show that the stroke did occur. Actually TIA is a form of stroke in nature.

To reduce risk of recurrence, patients are recommended to undergo lifestyle changes including quitting smoking, losing weight, eating more fruits and vegetables and exercising regularly.[9][10]


Anti-platelet medications such as aspirin are generally recommended. They reduce the overall risk of recurrence by 13% with greater benefit early on.[11] The initial treatment is aspirin, second line is clopidogrel (Plavix), third line is ticlopidine. If TIA is recurrent after aspirin treatment, the combination of aspirin and dipyridamole maybe recommended. Some people may also be given modified-release dipyridamole or clopidogrel.

An electrocardiogram (ECG) may show atrial fibrillation, a common cause of TIAs, or other arrhythmias that may cause embolisation to the brain. An echocardiogram is useful in detecting thrombus within the heart chambers. Such people may benefit from anticoagulation such as heparin and warfarin.


If the TIA affects an area that is supplied by the carotid arteries, an ultrasound (TCD) scan may demonstrate carotid stenosis. For people with a greater than 70% stenosis within the carotid artery, removal of atherosclerotic plaque by surgery, specifically a carotid endarterectomy, may be recommended. The blood vessel is opened up and the plaque is removed. The carotid may be replaced with a vessel retrieved from the lower leg or foot. The procedure is not technically difficult but carries the potential complication of inducing a stroke. A stroke can occur during surgery or after the procedure. The chance of a stroke ranges from 1–4 percent.[12]


People diagnosed with TIA are sometimes said to have had a warning for an approaching stroke. If the time period of blood supply impairment lasts more than a few minutes, the nerve cells of that area of the brain die and cause permanent neurologic damage. One third of the people with TIA later have recurrent TIAs and one third have a stroke because of permanent nerve cell loss. Other sources cite that 10% of TIAs will develop stroke within 90 days, half of which will occur in the first two days following the TIA.[13] The risk of a stroke occurring after a TIA can be predicted using the ABCD² score. However the ABCD² score ironically does not reliably predict the level of carotid artery stenosis (thought to be a major cause of stroke)in TIA patients. Instead, a person's age is more reliable in predicting any level of carotid stenosis in either symptomatic or asymptomatic side in transient ischaemic attack. [14] Response to aspirin treatment and prognosis in people with TIA could be predicted using emerging new blood tests. [15]


  1. 1 2 3 Easton, JD; Saver, JL; Albers, GW; Alberts, MJ; Chaturvedi, S; Feldmann, E; Hatsukami, TS; Higashida, RT; Johnston, SC; Kidwell, CS; Lutsep, HL; Miller, E; Sacco, RL; American Heart Association; American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; Interdisciplinary Council on Peripheral Vascular Disease (June 2009). "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; a journal of cerebral circulation. 40 (6): 2276–93. doi:10.1161/strokeaha.108.192218. PMID 19423857.
  2. "TIA (Transient Ischemic Attack)". American Heart Association & American Stroke Association. 28 March 2016.
  3. Ferro, J. M.; Falcão, I.; Rodrigues, G.; Canhao, P.; Melo, T.P.; Oliveira, V.; Pinto, A.N.; Crespo, M.; Salgado, A.V.; et al. (1996). "Diagnosis of transient ischemic attack by the nonneurologist. A validation study". Stroke. 27 (12): 2225–9. doi:10.1161/01.STR.27.12.2225. PMID 8969785.
  4. Coutts, S. B.; Hill, M. D.; Simon, J. E.; Sohn, C. -H.; Scott, J. N.; Demchuk, A. M.; Vision Study Group; et al. (2005). "Silent ischemia in minor stroke and TIA patients identified on MR imaging". Neurology. 65 (4): 513–7. doi:10.1212/01.WNL.0000169031.39264.ff. PMID 16116107.
  5. Archived April 8, 2011, at the Wayback Machine.
  6. MedlinePlus Overview transientischemicattack
  7. Transient Ischemic Attack at eMedicine
  8. "Transient ischaemic attack (TIA) - Prevention - NHS Choices". 2014-10-15. Retrieved 2015-08-19.
  9. Lifestyle changes after transient ischaemic attack (TIA) Retrieved on 2013-04-09
  10. Reducing risk for a Second Stroke or TIA Retrieved on 2013-04-09
  11. Rothwell, Peter M; Algra, Ale; Chen, Zhengming; Diener, Hans-Christoph; Norrving, Bo; Mehta, Ziyah (May 2016). "Effects of aspirin on risk and severity of early recurrent stroke after transient ischaemic attack and ischaemic stroke: time-course analysis of randomised trials". Lancet. doi:10.1016/S0140-6736(16)30468-8. PMID 27209146.
  12. Gonzalez, Hector A. "Myoclonus - Brain Spinal Cord and Nerve Disorders - Merck Manuals Consumer Version". Retrieved 2015-08-19.
  13. "What is TIA?". Retrieved 2015-08-19.
  14. Mannu, G. S., Kyu, M. M., Bettencourt-Silva, J. H., Loke, Y. K., Clark, A. B., Metcalf, A. K., Potter, J. F. and Myint, P. K. (2015), Age but not ABCD2 score predicts any level of carotid stenosis in either symptomatic or asymptomatic side in transient ischaemic attack. Int J Clin Pract, 69: 948–956. doi:10.1111/ijcp.12637
  15. Mannu, G. S., Macartney, A., Lambert, J. R. A., Bettencourt-Silva, J. H., Lawn, M., Lyall, H., Metcalf, A. K., Potter, J. F., Wood, J., Clark, A., Baglin, T., Myint, P. K. and Bowles, K. M. (2015), The clinical utility of Multiplate analyser measurement in platelet function testing following stroke and transient ischaemic attack. Eur J Haematol, 94: 138–144. doi:10.1111/ejh.12406
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