Transient Ischaemic Attack (TIA)
A transient ischemic attack (spelled ischaemic in British English) (abbreviated as TIA, often colloquially referred to as “mini stroke”) is caused by the changes in the blood supply to a particular area of the brain, resulting in brief neurologic dysfunction that persists, by definition, for less than 24 hours; if symptoms persist then it is categorized as a stroke.
A cerebral infarct that lasts longer than 24 hours, but less than 72 hours is termed a reversible ischemic neurologic deficit or RIND.
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. There have been cases where there have been a temporary paralysis of a part of the face and the tongue.
Effects of a TIA
Patients diagnosed with a 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 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 ABCD2 score can predict likelihood of subsequent stroke, and is calculated as:
Age at or above 60 years = 1 point
Blood pressure at presentation at or above 140/90 mm Hg = 1 point
unilateral weakness = 2 points
speech disturbance without weakness = 1 point
Duration of attack
at or above 60 minutes = 2 points
10 to 59 minutes = 1 point
Diabetes = 1 point
Interpretation of score, the risk for stroke:
Score 1-3 (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 that occludes an artery in the brain. This most frequently arises from a dislodged 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.
If visual symptoms occur such as perception of wavy or jagged lines or tiny specks of light and if a headache occurs, this can be an atypical migraine presentation. Typically a history of prior migraines is present. Also, a partial seizure in the parietal area of the brain can mimic TIA symptoms.
The use of anti-coagulant medications, heparin and warfarin; or anti-platelet medications such as aspirin.
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 emergency department as having suffered from a TIA will be discharged home and advised to contact their primary physician to organize further investigations. TIA can be considered as the last warning. The reason for the condition should be immediately examined by imaging of the brain.
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 dipyridamole 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.
To reduce recurrence of an attack ACE Inhibitors are used. The aim is not to lower blood pressure in a hurry as too low too fast may increase ischaemic injury due to low perfusion pressure.
^ Transient Ischemic Attacks: Stroke (CVA): Merck Manual Home Edition
^ Transient ischemic attack Mount Sinai Hospital, New York
^ Johnston SC, Rothwell PM, Nguyen-Huynh MN, et alii (2007). “Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack”. Lancet 369 (9558): 283–92. doi:10.1016/S0140-6736(07)60150-0. PMID 17258668.
^ Rothwell PM, Giles MF, Flossmann E, et alii (2005). “A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack”. Lancet 366 (9479): 29–36. doi:10.1016/S0140-6736(05)66702-5. PMID 15993230.
 External links
TIAs at discovery.com
Transient Ischemic Attack at MedlinePlus