Transient ischemic attack (TIA) is the most important risk factor for complete cerebral infarction, which was once called intermittent claudication of the brain and has been likened to angina attack in cardiology. Although the recovery of clinical symptoms and signs is very fast, it can cause pathological damage to brain tissue and form cerebral infarction due to repeated cerebral ischemic attacks. Therefore, attention should be paid to the regression of transient ischemic attack.
I. Changes in the definition of TIA
Traditionally, TIA is defined as a rapid onset of focal or whole-brain cerebral dysfunction with clinical signs lasting less than 24 h, with the exception of obvious non-vascular causes. However, with the accumulation of clinical data, it has been found that common TIA episodes last only 1 min on average, usually less than 5 min, so this definition has recently been suggested to be modified to transient episodes of neurological dysfunction caused by focal cerebral or retinal ischemia, with clinical signs usually lasting less than 1 h and without evidence of acute cerebral infarction.
II. The relationship between TIA and cerebral infarction
More than 50% of cerebral infarcts had different degrees of TIA episodes before the onset. Stroke occurs in 5.3% of patients within 2 d after a TIA episode and develops in 1/9 of patients within 3 months. about 1/3 of patients develop a large infarct in brain tissue within 5 years. Therefore, some people call it mini-stroke, transient stroke or unstable cerebral infarction. Some studies have shown that 31%-39% of patients with TIA are found to have infarct foci by conventional MRI and 2%-48% by CT, suggesting a proportional coexistence of TIA and cerebral infarction.
III. Pathogenesis
Causes of TIA include microthrombosis, vasospasm, hemodynamic changes, and vascular stenosis, with atherosclerosis being the most important cause [4]. Atherosclerosis and thrombosis are a multifactorial process and mutually causal, in which platelet activation and bridging action of fibrinogen play an important role in thrombus formation and expansion.
IV. Predictive indicators for the development of TIA into cerebral infarction
(I) Laboratory indicators
1. Increased CRP and D-dimer may be one of the pathological bases of ischemic changes associated with TIA in the elderly, which can independently predict the morbidity and mortality of stroke.
2. Determination of fibrinogen (Fg) and thrombospondin (TpP) levels in TIA patients is convenient for timely prevention and intervention of TIA occurrence and development, and can also be used to evaluate the effect of treatment.
(ii) Imaging indicators The frequency of vascular stenosis is quite high in patients with TIA, and patients with stenosis have a significantly higher probability of stroke than those without stenosis, especially younger patients are more likely to have cerebral infarction. DWI abnormalities are present in 44%-50% of patients with conventionally defined TIA, suggesting a significantly increased risk of recent stroke once imaging changes are present. Some authors believe that functional imaging will potentially be a beneficial tool for objective clinical determination of TIA regression.
(iii) Duration and frequency of TIA episodes Studies have shown that the longer the duration of TIA episodes and the more frequent the episodes, the greater the risk of stroke; patients with hypertension, hyperglycemia, hypercholesterolemia; patients who are seen and receive anticoagulation and antiplatelet therapy later are more likely to have cerebral infarction [11].
V. Predictive models for the development of TIA into cerebral infarction
(a) If TIA attacks are allowed to develop naturally without appropriate treatment, about 1/3 of patients have the possibility of developing complete cerebral infarction within a few years; about 1/3 experience long-term recurrent attacks that impair brain function; and 1/3 may experience spontaneous remission.
(II) ABCD model
Criteria Score (points)
Age (A) ≥60 years 1
Blood pressure(B) ≥140/90mmHg 1
Clinical symptoms (C) Unilateral weakness 2
Speech impairment without weakness 1
Duration(D) ≥60min 2
10-59min 1
The incidence of stroke within 7 days in patients with post-TIA scores of 0-4, 5 and 6 was 5%, 40% and 50%, respectively
(C) ABCD2: a modified model for predicting stroke risk after TIA
ABCD2 stroke risk prediction model (high risk: 6-7 points; medium risk: 4-5 points; low risk: 0-3 points)
Criteria Score (points)
Age(A) ≥60 years 1
Blood pressure(B) ≥140/90mmHg 1
Clinical symptoms(C) Unilateral weakness 2
Speech impairment without weakness 1
Duration(D) ≥60 min 2
10-59 min 1
Diabetes mellitus(D) 1
The rates of stroke in high-risk, intermediate-risk and low-risk patients within 2 days after TIA were 8.1%, 4.1% and 1.0%, respectively
VI. Management of TIA
Opinions differ as to when patients with TIA require emergency management or hospitalization, but many recent guidelines point to the need for formal inpatient care.
(i) Evaluation of patients with TIA Laboratory tests, cardiac examinations, brain imaging (CT/CTA, MRI/MRA, TCD, DSA), carotid imaging (color Doppler, CTA, 3D CE-MRA, DSA)
(ii) Control of risk factors in patients with TIA including cardiovascular risk, hypertension, high cholesterol, hyperglycemia, obesity and lifestyle changes.
(iii) Internal medicine treatment
1. Antiplatelet Including aspirin, clopidogrel, dipyridamole, etc.
2. Anticoagulation including heparin, low molecular heparin and warfarin, etc.
3. Lipid regulation, plaque stabilization, including statin, etc.
4. Vasodilatation, volume expansion, lowering blood viscosity, improving blood circulation, such as salvia, pethidine, low molecular dextrose, etc.
5. Fibrin-lowering and thrombolytic treatment such as fibrin-lowering enzyme, urokinase and r-tPA, etc.
(iv) Surgical treatment
The current AHA guidelines recommend CEA for symptomatic patients with stenosis of 50%-99% if the risk of perioperative stroke or death is <6%; CEA is also recommended for asymptomatic patients with stenosis of 60%-99% if the risk of perioperative stroke or death is <3%.
2. Stenting (CAS) CAS is superior to CEA for high-risk patients, skull base lesions, and carotid initiation, and has a tendency to gradually replace CEA.
3. Revascularization and intracranial-extracranial bypass surgery have high surgical risk and difficult clinical application.
4. Mechanical embolization In 2005, the Cerebral Ischemia Mechanical Embolization Trial Group published the results of its study, which concluded that Merci’s embolization apparatus had better results, but its reliability and effectiveness were debated.