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A transient ischemic attack (TIA, often colloquially referred to as "mini stroke") is caused by the temporary disturbance of blood supply to a restricted area of the brain, resulting in brief neurologic dysfunction that usually persists for less than 24 hours.
Symptoms vary widely from person to person, depending on the area of the brain involved. 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. If there are neurological symptoms persisting for more than 24 hours, it is classified as a cerebrovascular accident, or stroke.
Effects of a TIA
Patients diagnosed with a TIA are sometimes said to have had a warning for an approaching cerebrovascular accident. 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 deficit. One third of the people with TIA later have recurrent TIAs and one third have a stroke due to permanent nerve cell loss.
The score is calculated as:
- Age ≥ 60 years = 1 point
- Blood pressure at presentation ≥ 140/90 mm Hg = 1 point
- Clinical features
- unilateral weakness = 2 points
- speech disturbance without weakness = 1 point
- Duration of attack
- ≥ 60 minutes = 2 points
- 10–59 minutes = 1 point
- Diabetes = 1 point
Interpretation of score, the risk for stroke:
- Score 0-3 (low)
- 2 day risk = 1.0%
- 7 day risk = 1.2%
- Score 4-5 (moderate)
- 2 day risk = 4.1%
- 7 day risk = 5.9%
- Score 6–7 (high)
- 2 day risk = 8.1%
- 7 day risk = 11.7%
The most common cause of a TIA is an embolus (a small blood clot) that occludes an artery in the brain. This most frequently arises from an atherosclerotic plaque in one of the carotid arteries (i.e. a number of major arteries in the head and neck) or from a thrombus (i.e. a blood clot) in the heart due to atrial fibrillation.
Other reasons include excessive narrowing of large vessels due to an atherosclerotic plaque and increased blood viscosity due to some blood diseases. TIA is related with other medical conditions like hypertension, heart disease (especially atrial fibrillation), migraine, cigarette smoking, hypercholesterolemia, and diabetes mellitus.
The use of anti-coagulant medications, heparin and warfarin; or anti-platelet medications such as asprin.
The mainstay of treatment following acute recovery from a TIA should be to diagnose and treat 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 Accident & Emergency Department as having suffered from a TIA will be discharged home and advised to contact their primary physician to organize further investigations.
The initial treatment is Aspirin, second line is clopidogrel, third line is ticlopidine. If TIA is recurrent after Aspirin treatment, the combination of Aspirin and dipirydamole is needed (Aggrenox).
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 patients benefit from anticoagulation.
If the TIA affects an area supplied by the carotid artery, 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.
Some patients may also be given modified release dipyridamole or clopidogrel.
- Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al (2007). Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet 369 (9558): 283-92.
- Rothwell PM, Giles MF, Flossmann E, et al (2005). A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet 366 (9479): 29-36.
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