Diagnosis of TIA
The diagnosis of TIA relies on the medical history and physical examination. Since most of the episodes have already ended by the time the patient is seen, it is more important to ask detailed questions about the episode. The diagnosis of TIA depends on the history and physical examination.
Clinical manifestations
(1) TIA of the internal carotid artery system with sudden onset of transient lateral motor or sensory deficits, transient darkness in one eye; transient aphasia (dominant hemisphere ischemia).
(2) TIA of the vertebrobasilar system mainly presents with vertigo, nausea, vomiting, diplopia, transient blackness; crossed motor and sensory impairment; transient loss of consciousness or sudden collapse attack.
Auxiliary examination
CT scan of the head, ECG and TCD examination should be done at the first consultation, especially the first two special examinations. CT scan is particularly important in patients with TIA who have hemiparesis. Clinically, 1% of patients with TIA are found to have non-ischemic vascular lesions on CT, including cerebral swelling and subdural hematoma, and a small number of patients with cerebral hemorrhage may have similar clinical manifestations. Therefore, an early CT scan can also help in the differential diagnosis of TIA.
Differential diagnosis
Sudden onset of consciousness without neurological localization signs; sudden onset of consciousness with convulsive seizures only (epilepsy); simple dysphagia seizures (A-Syndrome). Differentiation from cerebral hemorrhage (CT, CSF, etc.) (b) Treatment of TIA.
Etiology-based treatment
1, hypertensive cerebral vasospasm theory: If the patient’s TIA attack is closely related to the elevated blood pressure and TCD suggests partial vasospasm, then the patient can use antihypertensive and calcium antagonists, including nimodipine or lorazepam, when the vascular spasm is released and the blood pressure is controlled in a relatively normal range, the patient will not have another attack.
2, high blood viscosity, hypercoagulable state theory: If the patient is found to have too many platelets in the blood components or higher than normal fibrous white yuan, platelet aggregation is too high, the use of targeted drugs, including anti-platelet aggregation function with aspirin 100mg once a day orally, female patients should be added with Pansentin 25mg once a day orally, patients who can not use aspirin can be used to resist kleider. Fibrinogen is higher than 400mg% patients can use intravenous fibrinogen 5-10BL to add saline 250ml in a slow sedation once and closely observe the change of fibrinogen index after medication, keep the index between 200-300mg%.
3.Microembolism theory: Microembolism refers to the microembolism dropped by the heart and the microembolism dropped by the sclerotic plaque of large blood vessels, which temporarily embolizes the small blood vessels at the end. In this case, in addition to reducing blood viscosity, anticoagulants such as oral warfarin or injection of low-molecular heparin can be used.
4.Surgical treatment of carotid artery stenosis (carotid A endarterectomy). In addition, patients with coronary artery disease, arrhythmia, cardiac insufficiency and valvular disease should be treated for heart disease.
Patients with TIA have a much higher chance of developing a stroke than the general population. The incidence of TIA is significantly lower in the vertebrobasilar supply area than in the internal carotid artery supply area; however, the prognosis for VBTIA is better than that for CA supply area.
Acute cerebral infarction
Cerebral infarction is the name of the pathology, which refers to the softening and necrosis of local brain tissue due to ischemia and hypoxia caused by the obstruction of cerebral blood supply. The acute phase of cerebral infarction mostly refers to the period from the onset to one week after the disease.
Pathophysiology of acute cerebral infarction
The purpose of understanding the pathophysiology of cerebral infarction is to guide clinical treatment. The occurrence of cerebral infarction depends on the paradox of the vessel wall and blood composition. The most common cause of cerebral infarction is atherosclerosis. Atherosclerosis causes narrowing of the lumen, and when the narrowing is greater than 80%, a decrease in cerebral blood flow occurs. Experiments have shown that when the local cerebral blood flow decreases to 15 ml/100 mg/min, the somatosensory evoked potentials disappear, but the extracellular K activity is not changed;
The neuronal damage at this point was reversible. When the local cerebral blood flow decreased to 6 ml/100 mg/min, the extracellular K activity suddenly increased, and the structural damage was irreversible at this time. This suggests the necessity and importance of early clinical treatment of ischemic infarction. The mechanism leading to cerebral infarction is currently considered to be the most likely to be arterial-arterial embolism, with emboli mostly originating from sclerotic plaques or broken microemboli in the wall of large arteries, in addition to intracardiac flab and, to a lesser extent, thrombosis.
The causes of acute cerebral infarction
1.Vascular lesion factors: hypertension, atherosclerosis, diabetes and inflammation, etc.
2.Blood component factors: hypercoagulable state – increased platelets, increased fibrinogen, increased blood viscosity, etc.
3, mechanical factors: emboli, from the heart, large vessels or trauma-induced fat embolism; traumatic vascular occlusion.
4, blood perfusion factors: chronic hypotension caused by the watershed cerebral infarction, white matter ischemia, etc. Different patients with cerebral infarction have different causes of the disease, and different treatment methods should be chosen for different causes, so we must actively search for the causes after making the diagnosis.
(1) Based on medical history, vascular examination and cardiac and cerebral examination, determine the possibility of cardiac emboli source and evidence of carotid artery stenosis.
(2) Look for risk factors, mainly hypertension, diabetes mellitus, increased erythrocyte pressure, hypercoagulable state, smoking and hyperlipidemia.
Diagnosis of acute cerebral infarction
Clinical manifestations
The focal symptoms of cerebral infarction are divided into symptoms of the internal carotid artery system and symptoms of the vertebral basilar artery system, and the onset of cerebral infarction is usually in relative silence, and there may be no headache, vomiting, or impaired consciousness in the early stage.
Paramedical examination
The first choice in the diagnosis of cerebral infarction is cranial CT, which can distinguish cerebral hemorrhage on the one hand and non-stroke diseases such as brain tumor on the other. In general, the diagnosis of cerebral infarction is made by CT scan only, without the injection of intensifier. The typical presentation of cerebral infarction on CT is a hypointense lesion, but it takes more than 24 hours from the onset of symptoms to the appearance of a hypointense lesion. The earlier the appearance of hypointense lesions, the more severe the disease, the worse the prognosis, and the more likely to have post-infarction hemorrhage.
Regardless of positive CT findings, as long as there are no signs of bleeding, the lesion should be treated as an infarct. If the lesion is too small or if posterior cranial sulcus infarction is suspected, CT is difficult to show, and MRI can be considered at this time.
In addition, auxiliary tests should be done
(1) Electrocardiogram and X-ray examination to exclude heart disease;
(2) Blood cell and platelet counts, prothrombin time, etc;
(3) Blood electrolytes, blood glucose, liver and kidney function tests, and blood gas test if hypoxemia is suspected;
(4) Generally, lumbar puncture is not done, but cerebrospinal fluid examination is done when subarachnoid hemorrhage is suspected and CT is negative or when intracranial infection is suspected;
(5) EEG can be done when epilepsy is suspected.
Differential diagnosis.
The difference between cerebral infarction and cerebral hemorrhage is that cerebral hemorrhage mostly develops under dynamic and is accompanied by headache, vomiting, impaired consciousness, and bloody cerebrospinal fluid. Before diagnosis, non-stroke neutral diseases such as brain tumor should be excluded. Syncope. Epilepsy, etc.