Transient ischemic attack is a temporary acute disorder of cerebral circulation, accompanied by the appearance of neurological symptoms, which completely regresses no later than 24 hours later. The clinic varies depending on the vascular basin in which there was a decrease in blood flow. Diagnosis is carried out taking into account anamnesis, neurological examination, laboratory data, results of ultrasound, duplex scanning, CT, MRI, PET of the brain. Treatment includes disaggregant, vascular, neurometabolic, symptomatic therapy. Operations aimed at preventing repeated attacks and stroke are carried out.
General information
Transient ischemic attack (TIA) is a separate type of ACVA, occupying about 15% in its structure. Along with hypertensive cerebral crisis, it is included in the concept of TVCC — a transient violation of cerebral circulation. It is most common in the elderly. In the age group from 65 to 70 years, men dominate among the patients, and in the group from 75 to 80 years — women.
The main difference between TIA and ischemic stroke is the short-term nature of cerebral blood flow disorders and the complete reversibility of the symptoms that have arisen. However, a transient ischemic attack significantly increases the likelihood of a cerebral stroke. The latter is noted in about a third of patients who have undergone TIA, and 20% of such cases occur in the 1st month after TIA, 42% – in the 1st year. The risk of cerebral stroke is directly correlated with age and the frequency of TIA.
Causes
In half of the cases, transient ischemic attack is caused by atherosclerosis. Systemic atherosclerosis covers, including cerebral vessels, both intracerebral and extracerebral (carotid and vertebral arteries). The resulting atherosclerotic plaques are often the cause of occlusion of the carotid arteries, blood flow disorders in the vertebral and intracerebral arteries. On the other hand, they act as a source of blood clots and emboli, which spread further through the bloodstream and cause occlusion of smaller cerebral vessels. The cause of about a quarter of TIA is arterial hypertension. With a prolonged course, it leads to the formation of hypertensive microangiopathy. In some cases, TIA develops as a complication of a cerebral hypertensive crisis. Atherosclerosis of the cerebral vessels and hypertension play the role of mutually reinforcing factors.
In about 20% of cases, a transient ischemic attack is a consequence of cardiogenic thromboembolism. The causes of the latter may be various cardiac pathology: arrhythmias (atrial fibrillation, atrial fibrillation), myocardial infarction, cardiomyopathy, infectious endocarditis, rheumatism, acquired heart defects (calcifying mitral stenosis, aortic stenosis). Congenital heart defects (aortic coarctation, etc.) are the cause of TIA in children.
Other etiofactors cause the remaining 5% of TIA cases. As a rule, they act in young people. Such factors include: inflammatory angiopathies (Takayasu’s disease, Behcet’s disease, antiphospholipid syndrome, Horton’s disease), congenital vascular anomalies, arterial wall dissection (traumatic and spontaneous), Moya-Moya syndrome, hematological disorders, diabetes mellitus, migraine, oral contraceptives. Smoking, alcoholism, obesity, and physical inactivity can contribute to the formation of conditions for the occurrence of TIA.
Pathogenesis
There are 4 stages in the development of cerebral tissue ischemia. At the first stage, autoregulation occurs — compensatory expansion of cerebral vessels in response to a decrease in perfusion pressure of cerebral blood flow, accompanied by an increase in the volume of blood filling the vessels of the brain. The second stage is oligemia — a further drop in perfusion pressure cannot be compensated by an autoregulatory mechanism and leads to a decrease in cerebral blood flow, but the level of oxygen metabolism does not suffer yet. The third stage — ischemic penumbra — occurs with a continued decrease in perfusion pressure and is characterized by a decrease in oxygen metabolism, leading to hypoxia and impaired function of cerebral neurons. This is reversible ischemia.
If at the stage of ischemic penumbra there is no improvement in blood supply to ischemic tissues, which is most often realized due to collateral circulation, then hypoxia worsens, dysmetabolic changes in neurons increase and ischemia passes into the fourth irreversible stage — an ischemic stroke develops. Transient ischemic attack is characterized by the first three stages and subsequent restoration of blood supply to the ischemic area. Therefore, the accompanying neurological manifestations have a short-term transient character.
Classification
According to ICD-10, transient ischemic attack is classified as follows:
- TIA in the vertebrobasilar basin (VBB)
- TIA in the carotid basin
- Multiple and bilateral TIA
- Transient blindness syndrome
- TGA – transient global amnesia
- other TIA, unspecified TIA.
It should be noted that some specialists in the field of neurology attribute TGA to migraine paroxysms, and others to manifestations of epilepsy.
In frequency, transient ischemic attack is rare (no more than 2 times a year), of medium frequency (ranging from 3 to 6 times a year) and frequent (monthly and more often). Depending on the clinical severity, there are mild TIA lasting up to 10 minutes, moderate TIA lasting up to several hours and severe TIA lasting 12-24 hours.
Transient ischemic attack symptoms
Since the basis of the TIA clinic is temporarily emerging neurological symptoms, often at the time of the patient’s consultation with a neurologist, all the manifestations that have occurred are already absent. Manifestations of TIA are established retrospectively by interviewing the patient. Transient ischemic attack can manifest itself in various, both cerebral and focal symptoms. The clinical picture depends on the localization of cerebral blood flow disorders.
TIA in the vertebrobasilar basin is accompanied by transient vestibular ataxia and cerebellar syndrome. Patients report unsteadiness of walking, instability, dizziness, blurred speech (dysarthria), diplopia and other visual disturbances, symmetrical or unilateral motor and sensory disorders.
TIA in the carotid basin is characterized by a sudden decrease in vision or complete blindness of one eye, impaired motor and sensory function of one or both extremities of the opposite side. Convulsions may occur in these extremities.
Transient blindness syndrome occurs with TIA in the blood supply area of the retinal artery, ciliary or orbital artery. A typical short-term (usually for a few seconds) loss of vision is more often in one eye. Patients themselves describe such a TIA as the spontaneous appearance of a “flap” or “curtain” pulled over the eye from below or above. Sometimes the loss of vision affects only the upper or lower half of the visual field. As a rule, this type of TIA tends to be stereotypically repeated. However, there may be a variation in the area of visual disorders. In some cases, transient blindness is combined with hemiparesis and hemihypesthesia of the collateral limbs, which indicates TIA in the carotid basin.
Transient global amnesia is a sudden loss of short—term memory while retaining memories of the past. It is accompanied by confusion, a tendency to repeat already asked questions, incomplete orientation in the situation. Often, TGA occurs when exposed to factors such as pain and psychoemotional overstrain. The duration of an episode of amnesia varies from 20-30 minutes to several hours, after which 100% memory recovery is noted. Paroxysms of TGA are repeated no more than 1 time in several years.
Diagnostics
Transient ischemic attack is diagnosed after a thorough study of anamnestic data (including family and gynecological anamnesis), neurological examination and additional examinations. The latter include: blood test with mandatory determination of glucose and cholesterol levels, coagulogram, ECG, duplex scanning or ultrasound of blood vessels, CT or MRI.
An ECG is supplemented, if necessary, by an echocardiogram followed by consultation with a cardiologist. Duplex scanning and ultrasound of extracranial vessels are more informative in the diagnosis of pronounced occlusions of vertebral and carotid arteries. If it is necessary to diagnose moderate occlusions and determine the degree of stenosis, cerebral angiography is performed, or better, an MRI of the cerebral vessels.
CT of the brain at the first diagnostic stage makes it possible to exclude other cerebral pathology (subdural hematoma, intracerebral tumor, AVM or cerebral vascular aneurysm); to carry out early detection of ischemic stroke, which is diagnosed in about 20% of the initially suspected TIA in the carotid basin. MRI of the brain has the greatest sensitivity in the visualization of foci of ischemic lesions of brain structures. Ischemic zones are determined in a quarter of TIA cases, most often after repeated ischemic attacks.
PET of the brain allows you to simultaneously obtain data on both metabolism and cerebral hemodynamics, which makes it possible to determine the stage of ischemia, to identify signs of restoration of blood flow. In some cases, a study of evoked potentials (EP) is additionally prescribed. Thus, visual EP is examined for transient blindness syndrome, somatosensory EP — for transient paresis.
Transient ischemic attack treatment
TIA therapy aims to stop the ischemic process and restore normal blood supply and metabolism of the ischemic cerebral area as soon as possible. It is often performed on an outpatient basis, although given the risk of stroke in the first month after TIA, a number of specialists consider hospitalization of patients justified.
The primary task of pharmacological therapy is to restore blood flow. The expediency of using direct anticoagulants for this purpose (calcium nadroparin, heparin) is debated in view of the risk of hemorrhagic complications. Preference is given to antiplatelet therapy with ticlopidine, acetylsalicylic acid, dipyridamole or clopidogrel. Transient ischemic attack of embolic genesis is an indication for indirect anticoagulants: acenocumarol, ethylbiscumacetate, fenindione. To improve blood rheology, hemodilution is used — drip administration of 10% glucose, dextran, salt combined solutions. The most important point is the normalization of blood pressure in the presence of hypertension. For this purpose, various antihypertensive agents are prescribed (nifedipine, enalapril, atenolol, captopril, diuretics). The treatment regimen for TIA also includes pharmaceuticals that improve cerebral blood flow: nicergoline, vinpocetine, cinnarizine.
The second task of TIA therapy is to prevent the death of neurons due to metabolic disorders. It is solved with the help of neurometabolic therapy. Various neuroprotectors and metabolites are used: diavitol, pyritinol, piracetam, methylethylpyridinol, ethylmethylhydroxypyridine, carnitine, semax. The third component of TIA treatment is symptomatic therapy. When vomiting, thiethylperazine or metoclopramide is prescribed, with intense headache — metamizole sodium, diclofenac, with the threat of brain edema — glycerin, mannitol, furosemide.
Physiotherapeutic effects in TIA include oxygenobarotherapy, electroson, electrophoresis, DDT, SMT, microwave therapy, circular shower, massage, therapeutic baths (coniferous, radon, pearl).
Prevention
The measures are aimed at both preventing repeated TIA and reducing the risk of stroke. These include correction of the patient’s existing risk factors for TIA: quitting smoking and alcohol abuse, normalization and control of blood pressure figures, adherence to a low-fat diet, refusal of oral contraceptives, therapy of heart diseases (arrhythmias, valvular defects, coronary artery disease). Preventive treatment provides for a long (more than a year) intake of antiplatelet agents, according to indications — taking a hypolipidemic drug (lovastatin, simvastatin, pravastatin).
Prevention also includes surgical interventions aimed at eliminating the pathology of cerebral vessels. If indicated, carotid endarterectomy, extra-intracranial microshunt, stenting or prosthetics of carotid and vertebral arteries are performed.