Overview
1. Definitions
The original concept of transient ischemic attacks (TIA) originated from the "time-symptom" theory in the 50s and 60s of the 20th century. Based on this doctrine, the duration of TA is constantly evolving. In 200, the American Stroke Association (ASA) proposed a new definition of TIA: "transient neurologic deficit without acute infarction due to focal ischemia of the brain, spinal cord, or retina."
"With the development of neuroimaging, 30%-50% of TA patients can find a new cerebral infarction in the MRI-DW sequence of the head. Therefore, in 2009, the ASA updated the definition of TIA to use the presence or absence of infarct lesions as the sole basis for distinguishing TIA from cerebral infarction, regardless of the duration of symptoms. This definition downplays the concept of "time-symptom" and emphasizes "histological damage". In addition, the new definition includes acute transient neurological deficits due to spinal cord ischemia in the scope of TIAs. (1) Time-based definition: TIA is a sudden focal neurological function (brain, spinal cord or retina) disorder caused by vascular reasons, lasting < 24 hours. (2) Histologically-based definition: TIA is transient neurological deficit caused by cerebral or spinal cord or retinal ischemia without acute infarction.
2. Epidemiology
The 2010 epidemiological study of TIA in Chinese adults showed that the prevalence of TIA in the Chinese population was 2.27%, but before the study, only 16% of patients were clinically diagnosed; the prevalence in women was higher than that in men, and the risk factors for TIA were older than men, old age, low education level, smoking/smoking history, living in rural or underdeveloped areas, hypertension, myocardial infarction, lipid metabolism disorder or diabetes mellitus. The awareness rate of non-disabling TIA was only 3.08%, and among those with TIA, only 5.02% received treatment and 4.07% received treatment recommended by the guidelines. Meta-analyses showed that the risk of stroke recurrence within the 2nd, 7th, 30th, and 90th days after the onset of TIA was 35%, 2%, 80%, and 92%, respectively. Epidemiological studies of Chinese adults based on community populations show that the prevalence of standardized TIA in the Chinese population is as high as 2.4%, and the TIA reaches 10 million to 12 million, which is much higher than the 5 million people with current stroke.
3. Clinical manifestations
The main clinical manifestations of T1A are sudden onset, rapid onset of focal nervous system or retinal dysfunction, generally recovered within 1~2 hours, and no signs of neurological deficit remained. There is often a history of recurrent seizures, and the clinical manifestations of each seizure are similar. T1A has episodic, transient, reversible and other clinical characteristics, and the diversity of clinical symptoms depends on the degree of narrowing, time and collateral compensation of the affected vessels. According to the subject
Depending on the damaged blood vessels, TIA can usually be divided into the internal carotid artery system and the vertebral artery system.
1. Internal carotid artery system TIA
(1) Common symptoms: episodic limb monoplegia, hemiplegia and facial paralysis on the opposite side of the lesion, numbness of a single limb or hemibody on the opposite side of the lesion.
(2) Characteristic symptoms: transient amaurosis or blindness of one eye on the affected side, contralateral hemiplegia and sensory impairment (ophthalmic artery paralysis): ipsilateral Homer's sign, contralateral hemiplegia (Horer's sign cross), aphasia may occur when the dominant hemisphere is involved, and body image impairment may occur in the non-dominant hemisphere.
(3) Possible symptoms: contralateral isotropy of the lesion (ischemia in the area of the cortical branch of the middle posterior cerebral artery, and involvement of the temporooccipital junction area). Limb shaking TIA is a rare form of TA in the internal carotid artery system. Its specific manifestations are unilateral limb weakness and shaking, similar to focal motor seizures, so it is easy to misdiagnose, but there is no epileptic wave release during EEG monitoring and video EEG monitoring in such patients, so EEG can be used to distinguish them. Episodic double weakness with urinary incontinence is also a rare symptom, and these patients are considered to have intermittent travel or spinal cord disease at the initial diagnosis, and MRI examination shows no abnormalities in the spinal cord and spine, and atheroma can be seen on ipsilateral internal carotid artery ultrasound.
The reason is a physiological variation of the anterior cerebral artery, one anterior cerebral artery separates from the other anterior cerebral artery, and the bilateral anterior cerebral artery is supplied by the internal carotid artery on one side, which is normally asymptomatic. If transient ischemia of the anterior cerebral artery is caused by sclerosis of the internal carotid artery and/or anterior cerebral artery on the donor side, atheroma formation, and lumen stenosis, it can manifest as episodic bilateral lower limb weakness with urinary incontinence due to damage to the work of the two frontal lobes. The diagnosis is confirmed by the combination of imaging studies. However, these patients should rule out spinal cord disorders of various causes, particularly transient spinal cord ischemia.
2. Vertebro-basilar artery system TA
(1) Common symptoms: the most common symptoms are dizziness, nausea and vomiting, most of which are not accompanied by tinnitus, which is a manifestation of brainstem vestibular system ischemia, and a few are accompanied by tinnitus, which is a symptom of labyrinthine artery ischemia.
(2) Characteristic symptoms: ischemia of brainstem reticular structure can cause fall attacks, which is manifested as the sudden appearance of both lower limbs without ground, but can immediately stand up on their own, and the whole process is conscious. Transient global amnesia (TGA): ischemia of the temporal branch of the posterior cerebral artery leading to limbic system involvement, manifested by memory loss lasting a few minutes to tens of minutes, may be accompanied by temporal and spatial disorientation, unconscious disorders, the presence of the patient's self-awareness, and more complex cortical higher activities such as writing, Calculations and conversations are intact, there are no other neurological abnormalities, symptoms persist for a few minutes or hours and then resolve, most of them do not exceed 24 hours, leaving complete or partial amnesia of episodic events (caused by ischemia in the temporal lobe, hippocampus, etc.). Occipital optic cortex involvement due to posterior cerebral artery ischemia may present with visual disturbance or visual field defects on one or both sides
(3) Possible symptoms: Brainstem and cerebellar ischemia can also cause the following symptoms, including diplopia (extraocular muscle palsy), crossover sensory impairment (dorsolateral bulbar syndrome), nystagmus, cranial nerve crossover paralysis (Weber Millard Foville and Dejerine syndrome), dysphagia and dysarthriaa (true or pseudobulbar palsy), ataxia (damage to cerebellar or cerebellar brainstem contact fibers), impaired consciousness (damage to the brainstem reticular structure), etc
In addition to the above common symptoms, TIA of the internal carotid artery system and vertebrobasilar artery system TIA may also present with impaired consciousness, hemichorea, or hemi-throwing.
4. Basis for diagnosis
Most patients present with clinical symptoms that are gone, so diagnosis is based on history. Middle-aged and elderly people with arterial hard factors, sudden onset of focal neurologic impairment, consistent with the internal carotid artery system and vertebrobasilar artery system after ischemia, lasting a few minutes or hours, can be completely recovered, should be highly suspected of the diagnosis of TA.
Because the time interval between TIA and stroke can be short, the ability to identify patients who are at high risk of developing an early stroke at an early stage will directly affect the effectiveness of TIA management. Several studies have shown that some of the risk factors that are highly predictive of prognosis are early detection of high-risk TIA patients and early treatment. These risk factors include severe carotid artery stenosis (>70%), microemboli on ipsilateral carotid atheroplaque ulcer (imaging/TCD), markedly elevated serum hypersensitive C-reactive protein and matrix metalloproteinase 9, high suspicion of emboli origin, hemispheric TIA, age > 65 years, and interval between TIAs< 24 hours, there were abnormal CT findings and other risk factors. The high-risk period in the brain is within 2~7 days after the onset of TIA, and the current guidelines in many countries recommend the use of ABCD2 score stratification and imaging-based emergency medical care mode to start TIA and secondary prevention as soon as possible. A comprehensive examination and evaluation of patients with new-onset TIA (ancillary tests) includes the following.
(1) General examination: evaluation includes electrocardiogram, complete blood count, blood electrolytes, renal function and rapid blood glucose and lipid measurement.
（2）血管检查：应用CT血管造影（CT angiography，CTA）、MRA、血管超声可发现重要的颅内外血管病变。 全脑数字减影血管造影（ digital subtraction angiography，DSA）是颈动脉内膜剥脱术和颈动脉支架治疗术前评估的金标准。
(3) Collateral circulatory compensation and cerebral blood flow reserve assessment: The evaluation of collateral circulatory compensation and cerebral blood flow reserve by DSA, cerebral perfusion imaging and/or TCD examination is necessary to identify hemodynamic TIA and guide treatment.
(4) Examination of vulnerable plaques: Vulnerable plaques are an important source of arterial emboli. Cervical vascular ultrasound, intravascular ultrasound, MRI, and TCD microemboli monitoring are helpful in the evaluation of atherosclerotic vulnerable plaques.
(5) Cardiac assessment: When cardioembolism is suspected, or the cause of cervical and cerebrovascular examination and hematology screening cannot be determined under the age of 45, transthoracic echocardiography and/or transesophageal echocardiography is recommended, which may find multiple emboli sources such as cardiac wall thrombosis, atrial septal abnormalities (atrioventricular aneurysm, patent foramen ovale, atrial septal defect), mitral valve vegetation and aortic arch atherosclerosis.
5. Differential diagnosis
(1) Temperament
Partial seizures of epilepsy generally manifest as local limb twitching, which usually originates from the corner of one side of the mouth and then extends to the face or one limb, or manifests as numbness and pinprick sensation in the limbs, and generally lasts for a shorter time. Some seizures are mostly caused by focal lesions in the brain, which may be found on CT and MRI of the head. Non-convulsive epilepsy in the elderly can be manifested as numbness of the limbs, weakness, inability to speak, misrepresentation, dizziness, blurred vision, confusion, memory loss, inability to write and other clinical symptoms, with the characteristics of transient recurrent seizures, lasting a few seconds or minutes, can be completely relieved, leaving no sequelae, very similar to TIA seizures, but the EEG of the patient can find focal epileptiform pathological waves during seizures, and TCD and MRI can find different degrees of intracranial vascular stenosis, which also shows that the etiology of senile epilepsy mostly originates from cerebrovascular diseases.
In addition, limb shaking TIA is often misdiagnosed as epilepsy. Clinically, it can manifest as one or one limb shaking, which can be combined with limb weakness, and both upper and lower limbs can be involved. These patients are often admitted to the hospital with epilepsy, where antiepileptic drugs do not respond to treatment, and imaging studies may reveal varying degrees of narrowing of the intracranial arteries or the formation of smoky blood vessels. Therefore, it is necessary to attach great importance to the symptom of episodic limb tremor, timely cerebrovascular assessment, early intervention, and prevention of stroke.
(2) Migraine
Migraine first occurs in young adults or early adulthood, and there is often a family history. According to the classification of the International Classification of Headache Disorders, third edition (beta), migraine with aura is characterized by recurrent episodes lasting several minutes with gradual onset of unilateral, fully recoverable visual, sensory, or other central nervous system symptoms, usually followed by headache and migraine-related symptoms. Fully recoverable auras include visual, sensory, phonical, and/or language, motor, brainstem, and retinal dysfunction that last 5 to 60 minutes. Migraine with brainstem aura, also known as basal migraine, can include dysarthria, vertigo, tinnitus, hearing loss, diplopia, and ataxia, most often confused with TIA. Anti-migraine treatment is effective in these patients.
(3) Meniere's disease
MD is episodic vertigo disease, which is more common in middle-aged people, and is manifested as recurrent episodes of vertigo with nausea and vomiting, which lasts for more than 20 minutes to 12 hours each time 3) Meniere's disease for several hours. The vertigo manifested during the onset of MD usually lasts for 20min-12 hours, and is often accompanied by nausea, vomiting and other autonomic dysfunction, and may also be accompanied by hearing loss, tinnitus, ear fullness, unsteady walking and other balance dysfunction, and no loss of consciousness. As the number of seizures increases, significant hearing loss develops. In addition to spontaneous nystagmus, pure-tone hearing threshold testing often reveals low-frequency hearing loss, central nervous system examination is normal, and cold and hot tests may reveal vestibular hypofunction or loss. Vertigo episodes can be confused with posterior circulation TIA. Audiological examination, vestibular function examination, balance function examination, and cranial imaging examination can be distinguished from TIA.
Medical treatment
1. Principles of treatment
TIA is one of the important cerebrovascular emergencies and should be paid great attention to. In view of the high risk of early recurrence of TIA, secondary prevention of cerebrovascular disease should be initiated as soon as possible. Because TIAs are very similar to ischemic stroke in terms of pathogenesis and clinical manifestations, TIAs and ischemic strokes are often included in the same prevention and treatment guidelines internationally. Treatment of TIAs should be individualized and holistic. The treatment principles refer to the updated version of the Chinese Expert Consensus for Transient Ischemic Attack (2011), the Chinese Guidelines for the Secondary Prevention of Ischemic Stroke and Transient Ischemic Attack 2014, the Chinese Expert Consensus on Antiplatelet Therapy for Transient Ischemic Attack and Minor Stroke (2014) and the Guidelines for the Early Diagnosis and Treatment of Transient Ischemic Attack in China (2016).
According to the consensus and guideline recommendations, the treatment of TIA is mainly divided into risk factor control, antiplatelet drugs, antithrombotic therapy for cardiac embolism, and non-pharmacological therapy. Medical treatment for TIA includes treatment modalities other than surgery, and control of this risk factor is particularly important in medical therapy. Traditional risk factors include hypertension, dyslipidemia, glucose metabolism, diabetes mellitus, smoking, sleep apnea, and hyperhomocysteinemia. For the pharmacological treatment of the above risk factors, see the Chinese Guidelines for the Secondary Prevention of Ischemic Stroke and Transient Ischemic Attack (2014) and the Guidelines for the Early Diagnosis and Treatment of Transient Ischemic Attack in China (2016). Based on recommendations, risk stratification tools such as ABCD2 are recommended to identify patients at high risk of TIA or minor stroke as soon as possible, and to initiate comprehensive interventions such as vascular assessment, antithrombosis, plaque stabilization, and blood pressure management as early as possible (category 1, level C evidence).
2. Antithrombotic therapy for secondary prevention of non-cardioembolic TIA
For antithrombotic therapy for the secondary prevention of noncardioembolic TIA, the following recommendations are made.
(1) For patients with non-cardioembolic TIA, oral antiplatelet drugs are recommended instead of anticoagulants to prevent stroke recurrence and other cardiovascular events (level 1 recommendation, level A evidence).
(2) Aspirin (50 to 325 mg/day) or clopidogrel 75 mg/day as monotherapy can be used as the preferred antiplatelet agent (level 1 recommendation, level A evidence). The optimal dose of aspirin monotherapy is 75 to 150 mg/day. Aspirin (25 mg) + extended-release didamole (200 mg) twice daily or silotamol (100 mg) twice daily can be used as an alternative to spirin and lorlogrel (A recommendation, B evidence). The choice of antiplatelet agent should be individualized based on patient risk factors, cost affordability, tolerability, and other clinical characteristics (level 1 recommendation, level C evidence)
(3) Patients with acute non-cardiac TIA who have a high risk of stroke recurrence (ABCD2 score > 4) within 24 hours of onset should be treated with aspirin combined with logrerel for 21 days as soon as possible (level 1 recommendation, level A evidence), but the risk should be closely observed. Thereafter, aspirin or clopidogrel alone can be used as first-line long-term secondary prevention of ischemic stroke (level 1 recommendation, level A evidence).
(4) Patients with TIA with symptomatic severe internal artery stenosis (stenosis rate of 70%-99%) within 30 days of onset should be given aspirin combined with clopidogrel for 90 days as soon as possible (level II recommendation, level B evidence). Thereafter, either aspirin or clopidogrel alone can be used as long-term first-line use for secondary prevention (level recommendation, level A evidence).
(S) Antiplatelet and other drug therapy is recommended for TIA patients with evidence of atherosclerotic plaque in the aortic arch (level II. recommendation, level B evidence). There is no conclusive comparison of the effects of oral anticoagulants with aspirin plus clogrerel (level II. recommendation, level B evidence).
(6) Routine long-term use of aspirin combined with clopidogrel antiplatelet therapy is not recommended for patients with non-cardioembolic TIA (level 1 recommendation, level A evidence).
3. Antithrombotic therapy for the secondary prevention of cardioembolic TIA
For antithrombotic therapy for the secondary prevention of cardioembolic TIA, the following recommendations are made.
(1) For patients with TIA with atrial facial movement (including paroxysmal), it is recommended to use appropriate doses of oral anticoagulation with warfarin to prevent further thromboembolic events. The target dose of warfarin is to maintain the prothrombin INR (International Normalized Ratio) at 2.0 to 3.0 (level 1 recommendation, level A evidence).
(2) Novel oral anticoagulants can be used as alternatives to warfarin, including dabigatran, rivaroxaban, apixaban, and duxaban (level recommendation, level A evidence), and the choice of drug should consider individualized factors.
(3) For patients with TIA with atrial movement, if they cannot receive oral anticoagulant therapy, it is recommended to use aspirin monotherapy (level 1 recommendation, level A evidence), or aspirin combined with clopidogrel antiplatelet therapy (level recommendation, level B evidence).
(4) Patients with TIA with atrial movement should choose anticoagulants according to the severity of ischemia and the risk of hemorrhagic transformation. Anticoagulation is recommended within 14 days of neurological symptoms to prevent recurrence of stroke, and the duration of anticoagulation should be appropriately extended in patients at high risk of bleeding (level II. recommendation, level B evidence).
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