bubble_chart Overview

Transient ischemic attack refers to a group of diseases caused by transient loss of brain function due to insufficient blood supply to local brain regions.

bubble_chart Etiology

TIAs can be classified into the following three major categories based on their primary pathogenesis:

(1) **Large artery low-flow TIAs**: The common cause is severe stenosis or occlusion due to atherosclerosis at the origin or siphon segment of the internal carotid artery, leading to reduced blood flow to the brain tissue. Under normal circumstances, compensatory mechanisms such as collateral circulation can maintain effective cerebral perfusion. However, when this compensation is suddenly lost due to fluctuations in blood pressure, cardiac output, cerebral perfusion pressure, blood viscosity, vascular wall compliance, platelet aggregation, or other factors, local cerebral perfusion further decreases, triggering symptoms. These TIAs often recur in a stereotypical manner, with each episode lasting from a few minutes to several hours.

(2) **Embolic TIAs**: These may result from microemboli dislodged from atherosclerotic lesions in the walls of extracranial or skull-base large arteries, or they may be of cardioembolic origin.

(3) **Small penetrating artery TIAs**: These are caused by lipohyalinosis or atheromatous changes at the origin of deep penetrating branches arising from large cerebral arteries.

bubble_chart Clinical Manifestations

The skills of collecting and analyzing medical history are extremely important. The following single symptoms—vertigo, diplopia, dysphagia, dysarthria, drop attacks, loss of consciousness, mental confusion, amnesia, urinary incontinence, etc.—cannot diagnose TIAs. Symptoms that slowly spread to different parts of the body, rigidity, clonus, or scintillating scotoma are also not manifestations of TIAs. For patients without motor impairment, vision loss, or aphasia during an episode, a diagnosis of TIAs must be carefully considered. For patients where a conclusion is difficult to reach immediately, a diagnosis of "possible TIAs" may be made, followed by observation over a period of time.

Focal seizures often present as "positive" symptoms (limb twitching rather than paralysis, visual hallucinations rather than vision loss) and progress gradually over several minutes.

Patients diagnosed with TIAs or possible TIAs require CT or MRI to exclude transient clinical episodes of cerebral infarction or hemorrhage. A comprehensive examination should be conducted to identify potential disease causes, underlying pathological conditions, and stroke risk factors. Particular attention should be paid to abnormalities in cardiac structure/function, stenosis, thrombosis, or occlusion of large cervical arteries, and coagulation disorders. For TIAs occurring multiple times in the vertebrobasilar system within a short period, vigilance is warranted for signs of an impending catastrophic basilar artery occlusion.

bubble_chart Treatment Measures

By definition, most TIAs have already resolved by the time of medical consultation and do not require treatment. However, the occurrence of TIAs indicates the failure of primary prevention for cerebrovascular disease, with thrombotic or embolic lesions superimposed on the underlying condition of {|###|}stirred pulse{|###|} sclerosis. At this stage, the most critical task is to prevent the occurrence of {|###|}apoplexy{|###|} or new TIAs. Identify and treat risk factors for {|###|}apoplexy{|###|}. Actively control hypertension, maintaining systolic and diastolic blood pressure at levels no higher than 18.7 kPa (140 mmHg) and 12.0 kPa (90 mmHg), respectively. Absolutely prohibit smoking and alcohol consumption, reduce excessive caloric intake, lower elevated blood cholesterol and LDL levels, decrease sodium salt intake while ensuring adequate potassium intake, rigorously manage body weight and diabetes, and actively treat arrhythmias and heart diseases. For patients with significantly elevated hematocrit (>55–60%), it should be reduced and maintained at normal levels. If platelet counts exceed 600,000/mm³, the underlying {|###|}disease cause{|###|} should be identified and treated. Women using high-estrogen contraceptives should switch to alternatives. Physical exercise can reduce the risk of myocardial infarction, thereby potentially decreasing the incidence of cerebral embolism secondary to myocardial infarction.

(1) Antiplatelet Agents Platelets play a significant role in the formation of {|###|}stirred pulse{|###|} thrombi and the progression of atherosclerotic lesions in the vessel wall. For patients with TIAs (or infarctions) originating from {|###|}stirred pulse{|###|} lesions, regular oral administration of aspirin, which strongly inhibits platelet function, can prevent {|###|}apoplexy{|###|} and reduce mortality. The optimal {|###|}dose{|###|} remains under investigation. A dose of 50–300 mg taken every other day may be used. Some patients experience gastrointestinal irritation, which may improve after switching to enteric-coated tablets. Since the threat of {|###|}stirred pulse{|###|} lesions persists, treatment should be long-term. Platelet inhibitors are ineffective against red (fibrin-rich) thrombi. Therefore, they should not be used for red thrombi such as mural thrombi in the heart, venous thrombi, or large thrombi within the {|###|}stirred pulse{|###|} visible on angiography. Adding dipyridamole or other antiplatelet drugs does not enhance efficacy.

(2) Anticoagulants The efficacy of anticoagulant therapy is not well established. It may be considered for trial use in the following conditions associated with TIAs: progressing basilar {|###|}stirred pulse{|###|} thrombosis, non-valvular atrial fibrillation, recent myocardial infarction, or angiography-detected thrombi in extracranial cerebral {|###|}stirred pulse{|###|}. A CT scan should be performed to rule out intracranial hemorrhage or large cerebral infarction. Patients must have no bleeding tendencies or risks, normal liver and kidney function, and blood pressure below 2

1. 3/
2. 0 kPa (160/90 mmHg). Anticoagulant therapy should only be administered in experienced and well-equipped medical facilities. Initiate treatment with intravenous heparin and oral warfarin, closely monitoring prothrombin time (PT) and partial thromboplastin time (PTT) to adjust the drug {|###|}dose{|###|}. Once PT reaches 1

.5 times the pretreatment control value, switch to oral warfarin alone for maintenance. Adjust the daily {|###|}dose{|###|} based on PT changes. The treatment duration is typically limited to 3 months.

(3) Carotid {|###|}stirred pulse{|###|} Endarterectomy The goal of surgery is to prevent cerebral ischemia in the territory supplied by the affected {|###|}stirred pulse{|###|}. Therefore, the patient’s TIAs must be attributable to severe stenosis and ulcerative changes in the ipsilateral internal carotid {|###|}stirred pulse{|###|} on angiography, with the extracranial segment of the internal carotid {|###|}stirred pulse{|###|} being significantly more affected than the intracranial segment. Patients whose TIAs can be explained by cardiac conditions or those with complete occlusion of the {|###|}stirred pulse{|###|} are not suitable candidates for surgery. Surgery, of course, cannot prevent cerebral hemorrhage or {|###|}apoplexy{|###|} in other {|###|}stirred pulse{|###|} systems.

bubble_chart Prognosis

Approximately half of the patients may remain seizure-free for one year or longer without developing severe brain or cardiovascular diseases. However, patients with TIAs have a higher long-term risk of severe brain or cardiovascular diseases and a higher long-term mortality rate compared to the general population. One-fifth to one-quarter of patients develop cerebral infarction, cerebral hemorrhage, subarachnoid hemorrhage, or myocardial infarction within five years of the initial onset. Moreover, stroke does not necessarily occur in the same cerebral vascular system as the TIAs. Some patients experience a stroke two years or more after the resolution of TIAs. In China, the long-term mortality rate from stroke is more than three times that of heart disease, while in Western Europe and North America, heart disease accounts for more than twice the mortality rate of stroke.