Transient ischemic attack, or TIA, is also known as transient ischemic attack or mini-stroke. It refers to the brain dysfunction caused by the reduction of cerebral blood flow within a short period of time, and each attack lasts for a short period of time, usually seconds, minutes or hours, with the maximum duration not exceeding 24 hours. It is often overlooked because the symptoms come and go quickly and do not leave any after-effects after recovery. In fact, although the symptoms of TIA are mild, the consequences are serious. If not treated in time, according to statistics, about 25% to 40% of patients will have severe cerebral infarction within 5 years, which will threaten patients’ lives. And 1/3 to 2/3 of the patients with cerebral infarction have had transient ischemic attack. Therefore, medical doctors often see it as a precursor or danger signal of cerebrovascular disease.
(A) Risk factors triggering transient cerebral ischemia.
(1) Atherosclerosis, temporary occlusion of certain small cerebral arteries, when the collateral circulation is established and recanalized in time, the improvement of blood supply makes the symptoms disappear within 24 hours.
(2) Hypertensive disease, causing cerebral vascular spasm, poor blood flow and insufficient blood supply.
(3) Micro thromboembolism, which is eliminated by the action of the body itself and the blood circulation is recanalized, but can cause the same symptoms to recur in relapse.
(4) High blood viscosity due to thrombocytosis and insufficient blood oxygen content, as well as anemia, heart disease, and myocarditis can cause transient cerebral ischemic attacks.
(B) Etiology and pathogenesis:
The disease is mostly associated with hypertensive atherosclerosis, and its pathogenesis may be caused by a variety of factors.
(1) Microthrombosis: The attached thrombus, sclerotic plaque and the blood decomposition and platelet aggregates in them are free and dislodged from the atherosclerotic stenosis of the internal carotid artery and vertebral a basilar artery system, blocking the cerebral arteries, and the ischemic symptoms disappear when the emboli break up or move distally.
② Cerebral vasospasm: Atherosclerotic plaque in the internal carotid artery or vertebral a basilar artery system narrowed the lumen of the vessel, and the vortex flow of blood was generated there. When the vortex flow accelerated, it stimulated the vessel wall causing vasospasm and transient ischemic attack, and the symptoms disappeared when the vortex decelerated.
(3) Cerebral hemodynamic changes: When the carotid artery and vertebral a basilar artery system is occluded or narrowed, if the patient suddenly has a transient hypotension, the attack of this disease will occur due to the reduction of cerebral blood flow; after the blood pressure rises, the symptoms disappear. The disease is most often seen when the blood pressure fluctuates and is prone to episodes of this disease. In addition, cardiac arrhythmia, atrioventricular block, and myocardial damage can also cause the onset of the disease due to a sudden decrease in local cerebral blood flow.
(4) Twisting, overgrowth, knotting, narrowing of the cervical artery or compression of the vertebral artery by cervical vertebral bone spurs can cause an attack when the head is turned.
(iii) Clinical manifestations of transient cerebral ischemic attack.
1. Sudden, transient, focal neurological deficit attacks recover in 24 hours with no sequelae ;
The main symptoms of focal neurological deficits are.
(1) hemiparesis, hemianesthesia, hypesthesia, visual impairment;
(2) vertigo, headache, tinnitus, blackness in front of the eyes, facial numbness, weakness of the limbs, choking on water, and slurred speech.
Many of the above symptoms can last for a few minutes or hours and then return to normal, a few patients last to more than ten hours, but all return to normal within 24 hours.
2. Recurrent attacks The above clinical symptoms appear repeatedly.
3.Onset age Mostly above 50 years old with a history of heart disease and atherosclerosis.
(iv) Treatment.
Those with frequent seizures have a high possibility of cerebral infarction in the near future and should be treated actively to prevent the occurrence of cerebral infarction.
1.Actively treat risk factors such as hypertension, hyperlipidemia, heart disease, diabetes, cerebral atherosclerosis.
2.Drug treatment.
①Anti-platelet accumulation drugs, such as aspirin, etc.
②Anticoagulation: anticoagulation should not be used as routine treatment for patients with TIA. For patients with TIA with atrial fibrillation and coronary artery disease (except for infective endocarditis), anticoagulation is recommended; TIA treated with platelets and still frequent attacks, anticoagulation should be considered. Low-molecular heparin 4000-5000 IU can be used, subcutaneously injected into the abdominal wall twice daily for 7-10 days.
③Calcium antagonists, which can stop intracellular calcium overload, prevent vasospasm, increase blood flow and improve microcirculation. Nimodipine 20-40mg, 3 times a day; flunarizine hydrochloride 5mg, taken orally once a day before bedtime.
④Other: Chinese herbal medicine can be applied, and vasodilators are also available. If the blood fibrinogen level is significantly elevated, the application of fibrin-lowering enzyme can be considered.
Surgical treatment:
In patients with single or multiple TIAs, if antiplatelet medication is not effective and carotid stenosis exceeds 70%, carotid endarterectomy or endovascular stentoplasty is feasible.