Transient Ischaemic Attack (TIA)
Original Editor - Wendy Walker
A transient ischaemic attack (TIA) is an acute episode of temporary neurologic dysfunction that typically has the following characteristics
- lasts less than an hour (often less than 30 minutes)
- results from focal cerebral, spinal cord, or retinal ischaemia
- is not associated with acute tissue infarction
The concept of TIA emerged in the 1950s, with the observation by C Miller Fisher, and others, that ischaemic stroke often followed transient neurological symptoms in the same arterial territory.
Mechanism of Injury / Pathological Process
Like ischaemic strokes, TIAs are due to locally decreased blood flow to the brain, causing focal neurological symptoms. Decreased blood flow results from either embolism into a cerebral supply artery (from the heart, or the great proximal vessels, extracranial or intracranial arteries, usually affected by atherosclerosis), or in situ occlusion of small perforating arteries.
Resolution of symptoms probably occurs by spontaneous lysis or distal passage of the occluding thrombus or embolus, or by compensation through collateral circulation restoring perfusion into the ischaemic brain area.
The incidence of TIAs increases with age, from 1-3 cases per 100,000 in those younger than 35 years to as many as 1500 cases per 100,000 in those older than 85 years. Fewer than 3% of all major cerebral infarcts occur in children. Paediatric strokes often can have quite different etiologies from those of adult strokes and tend to occur with less frequency.
The incidence of TIAs in men (101 cases per 100,000 population) is significantly higher than that in women (70 per 100,000).
Clinical manifestations will vary, depending on the vessel involved and the cerebral territory it supplies.
The key rule here is that symptoms of TIA should mimic known stroke syndromes, and so depend on the arterial territory involved; see the Stroke page for details
A TIA may last only minutes, therefore symptoms have often resolved before the patient presents to a clinician. Thus, historical questions should be addressed not just to the patient but also to family members or friends who were present at the time of TIA. Witnesses often perceive abnormalities that the patient cannot, such as changes in behaviour, speech, gait, memory, and movement.
The main diagnostic challenge of TIA is that the symptoms and signs have usually resolved by the time of assessment.
There is no test for TIA: the gold standard remains assessment as soon as possible by a clinical expert.
The diagnosis relies heavily on the patient's account of their history and on expert interpretation of that history. Interobserver agreement for the diagnosis of TIA between different stroke-trained physicians and non-neurologists is poor.
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Recent Related Research (from Pubmed)
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- Albers GW, Caplan LR, Easton JD, Fayad PB, Mohr JP, Saver JL, et al. Transient ischemic attack--proposal for a new definition. N Engl J Med. Nov 21 2002;347(21):1713-6
- Estol CJ (March 1996). "Dr C. Miller Fisher and the history of carotid artery disease". Stroke 27 (3): 559–66.
- Truelsen T, Begg S, Mathers C. World Health Organization. The global burden of cerebrovascular disease. Global Burden of Disease 2000
- Giles MF, Rothwell PM. Risk of stroke early after transient ischaemic attack: a systematic review and meta-analysis. Lancet Neurol. Dec 2007;6(12):1063-72
- Kleindorfer D, Panagos P, Pancioli A, et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. Apr 2005;36(4):720-3
- Bots ML, van der Wilk EC, Koudstaal PJ, Hofman A, Grobbee DE. Transient neurological attacks in the general population. Prevalence, risk factors, and clinical relevance. Stroke. Apr 1997;28(4):768-73
- Sheehan OC, Merwick A, Kelly LA, et al. Diagnostic usefulness of the ABCD2 score to distinguish transient ischemic attack and minor ischemic stroke from noncerebrovascular events: the North Dublin TIA Study. Stroke 2009;40:3449–54