Transient ischemic attack (TIA)
Transient Ischemic Attack (TIA) is a transient or transient, focal brain or retinal dysfunction caused by an intracranial vascular lesion. Clinical symptoms usually last 10 to 15 minutes, with recovery mostly within 1 hour and no more than 24 hours. No signs and symptoms of neurological deficits remain, and there are no responsible lesions on structural imaging (CT, MRI).
TIA is a clinical syndrome caused by many factors such as atherosclerosis, arterial stenosis, cardiac disorders, blood component abnormalities and hemodynamic changes.TIA pathogenesis mainly includes.
(1) Microemboli theory;
(2) In cases of severe stenosis of intracranial arteries, fluctuations in blood pressure can cause transient ischemia in brain areas that were previously maintained by collateral circulation;
(3) Changes in blood components such as increased blood viscosity, such as increased fibrinogen content, are also associated with the development of TIA; (4) Vertebral artery-subclavian artery steal due to stenosis or occlusion of the innominate artery or subclavian artery can also trigger TIA.
Patients with TIA have a significantly higher chance of having a stroke than the general population. The incidence of stroke in patients with TIA is 13-16 times higher than that of the general population in the first year and 7 times higher in the fifth year.
The prognosis of TIA patients varies by etiology. Seventy percent of patients with TIA presenting with cerebral hemisphere symptoms and with carotid stenosis have a poor prognosis, with a 40% chance of stroke within 2 years. A smaller proportion of TIAs in the vertebrobasilar system develop cerebral infarction. In comparison, patients with isolated monocular visual symptoms have a better prognosis; younger patients with TIA have a lower risk of stroke. When evaluating patients with TIA, the etiology should be determined as soon as possible to determine the prognosis and decide on treatment.
I. Diagnosis
(a) Clinical features
1. Age and gender: TIA is more common in the elderly and more common in men than women.
2.Clinical characteristics of TIA.
(1) sudden onset;
(2) Symptoms of focal brain or retinal dysfunction;
(3) Short duration, usually 10-15 minutes, mostly within 1 hour, up to 24 hours;
(4) Complete recovery, no signs of neurological deficits remain;
(5) Most of them have a history of recurrent attacks.
3. Symptoms of TIA: are varied and depend on the distribution area of the involved vessels.
TIA of the internal carotid artery system: mostly manifests as monocular (ipsilateral) or cerebral hemispheric symptoms. Visual symptoms are manifested as transient blackness, foggy vision, black spots in the visual field, or sometimes shifting shadows and reduced light in front of the eyes. Cerebral hemisphere symptoms are mostly weakness or numbness of one side of the face or limb, and may include difficulty with speech (aphasia) and changes in cognitive and behavioral function.
TIA of the vertebrobasilar system: usually presents with vertigo, dizziness, dysarthria, drop to seizure, ataxia, abnormal eye movements, diplopia, crossed motor or sensory impairment, hemianopia or bilateral vision loss. Note, however, that clinically isolated vertigo, dizziness, or nausea are rarely caused by TIA. Patients with vertebrobasilar artery ischemia may have transient episodes of vertigo, but they need to be accompanied by other neurological symptoms or signs, and less frequently by syncope, headache, urinary and fecal incontinence, drowsiness, memory loss, or epilepsy.
(II) Auxiliary examination
The purpose of ancillary tests is to identify or exclude the causes of TIA that may require specific treatment, and to find risk factors that can be improved as well as to judge the prognosis.
1.Cranial CT and MRI
Cranial CT helps to exclude intracranial lesions with similar presentation to TIA. The positive rate of cranial MRI is higher, but MRI is not routinely used for screening in clinical practice.
2.Ultrasound examination
(1) Carotid ultrasonography: It should be used as a basic examination tool for patients with TIA and can often show atherosclerotic plaques. However, its clinical value for mild to moderate arterial stenosis is low, and it cannot discriminate between severe stenosis and complete carotid artery obstruction.
(2) Transcranial color Doppler ultrasound: It is a powerful tool to detect intracranial large vessel stenosis. It can detect severe intracranial stenosis, determine collateral circulation, perform embolic monitoring, and assess the status of cerebral blood circulation before angiography.
(3) Transesophageal echocardiography (TEE): Compared with conventional transthoracic cardiac ultrasound, it improves the visualization of the atria, atrial wall, atrial septum and ascending aorta, and can detect abnormalities of the atrial septum (aneurysm of the atrial septum, unclosed foramen ovale, atrial septal defect), atrial appendage thrombus, mitral valve redundancy and a variety of cardiogenic sources of emboli such as atherosclerosis of the aortic arch.
3.Cerebral angiography
(1) Selective arterial catheter cerebral angiography (digital subtraction angiography, DSA): It is the most accurate diagnostic tool (gold standard) for assessing intracranial and extracranial arterial vascular lesions. However, cerebral angiography is more expensive and carries certain risks, and its incidence of serious complications is about 0.5% to 1.0%.
(2) CTA (computerized imaging angiography) and MRA (magnetic resonance imaging angiography): are new non-invasive vascular imaging techniques, but they are not as detailed as the vascular situation provided by DSA and can lead to over-judgment of the degree of arterial stenosis.
4.Other tests
Special tests for pre-thrombotic status should be done in people younger than 50 years of age or in patients with TIA for which no clear cause has been found, or in patients with TIA with venous thrombosis at rare sites or with a family history of thrombosis. If abnormalities are found in routine tests such as hemoglobin, red blood cell pressure, platelet count, prothrombin time or partial thromboplastin time, other blood coagulation indicators should be further examined.
For example, an elderly male patient with hypertension who has had multiple black eye episodes should have his carotid artery checked as soon as possible, while a young female patient with a history of spontaneous abortion, venous thrombosis, and multifocal TIA should have antiphospholipid antibodies checked.
II. Treatment
TIA is a high risk factor for stroke and needs to be treated aggressively, and the whole treatment should be individualized as much as possible.
(i) Control of risk factors.
(ii) Drug therapy
1. Anti-platelet aggregation drugs
Anti-platelet therapy has been shown to be effective in preventing stroke in patients with stroke risk factors. Anti-platelet drugs should be considered first for patients with TIA, especially those with recurrent TIA.
(1) Aspirin (ASA): cyclooxygenase inhibitor. The domestic CAST trial has suggested that a therapeutic dose of 150 mg/d is effective in reducing stroke recurrence.
(2) Dipyridamole (DPA): cyclic nucleotide phosphodiesterase inhibitor, DPA extended-release agent. Combined application of small doses of ASA can enhance its pharmacological effects. Currently, the European guidelines for the treatment of acute stroke have made the combination of ASA and DPA extended-release agents the first recommended application.
(3) Ticlopidine: The antiplatelet effect is different from that of aspirin or dipyridamole. It does not affect cyclooxygenase, but inhibits adenosine diphosphate (ADP)-induced platelet aggregation, but serious complications such as neutropenia can occur and should be noted.
(4) Clopidogrel: It is an inhibitor of ADP-induced platelet aggregation with ticlopidine, but the adverse effects are less than the former, and the commonly used dose is 75 mg/d.
(5) Other: there are some intravenous anti-platelet drugs, such as Ozagrel, can also be considered, but there is a lack of large-scale clinical trials to confirm.
Recommendations.
(1) Aspirin therapy is preferred in most patients with TIA, and the recommended dose is 50-300 mg/d.
(2) A combination of low-dose aspirin (25 mg) plus pansentine extended-release (200 mg) may also be used (tablets or capsules), 2 times/d.
(3) Clopidogrel, 75 mg/d, may be used for those who have the condition, are at high risk, or are intolerant to aspirin.
(4) If ticlopidine is used, blood tests should be noted during the course of treatment.
(5) In case of frequent episodes of TIA, anti-platelet aggregation drugs by intravenous drip can be used.
2.Anticoagulant drugs
Anticoagulation has been used to treat TIA for decades. Although there is no strong evidence from clinical trials to support anticoagulation as a routine treatment for TIA, anticoagulation can be considered clinically for patients with atrial fibrillation, frequent-onset TIA or vertebrobasilar TIA.
Recommendations.
(1) Anticoagulation should not be used as routine treatment.
(2) Anticoagulation is recommended for patients with TIA associated with atrial fibrillation and coronary artery disease (except for infective endocarditis).
(3) Patients with TIA who are treated with antiplatelet therapy and still have frequent episodes of symptoms may be considered for anticoagulation therapy.
3.Fiber-lowering drugs
Patients with TIA sometimes have changes in blood composition, such as significantly increased fibrinogen content, or frequent episodes of patients can consider the use of bactrim or fibrin-lowering treatment.