Stroke: diagnosis

Diagnosis of stroke includes two phases. First, it is necessary to establish the very fact of occlusion of the artery, which is usually confirmed by the features of the course of the disease and the nature of the symptomatology. Secondly, the cause of occlusion should be identified. The second step is not critical to the choice of urgent therapeutic intervention, since treatment in most cases of ischemic stroke is carried out the same way (regardless of its etiology) and includes measures to protect the brain and restore its blood supply. Nevertheless, the establishment of the cause of occlusion is important for the choice of treatment aimed at preventing subsequent ischemic episodes.

It is useful to compare cerebral and cardiac ischemia, despite the profound differences that exist between them. Against the background of rapid progress in the development of methods for treating myocardial ischemia, the advances in stroke therapy look more modest and occur more slowly. Drawing parallels between cerebral and cardiac ischemia, it may be possible to find new approaches to the treatment of cerebral ischemia, based on the successes that have been achieved with respect to myocardial ischemia.

Methods of diagnosing myocardial ischemia are well known to clinicians, and clinical manifestations of this condition are for patients and their relatives. So, compressive pain behind the sternum, shortness of breath, profuse sweat and other signs of circulatory failure usually cause patients to seek emergency medical care. With myocardial ischemia, patients immediately consult a doctor when a complex of symptoms appears, including intense pain and a sense of imminently approaching death. In those patients with ischemia of the heart who do not experience pain, the likelihood of timely diagnosis and treatment of the disease is significantly reduced, as, for example, it often occurs among patients with diabetes mellitus.

At the same time, because the stroke is not accompanied by pain, patients often do not attach importance to the initial symptoms. This entails a delay in seeking medical help, and, accordingly, treatment is often delayed until the moment when brain damage becomes irreversible. So, a patient who wakes up with a paralyzed hand may not know whether the weakness is caused by the fact that he "lain" his arm during sleep or has a stroke. Despite the suspicion that this is something more than nerve compression, patients often delay seeking medical help in the hope of spontaneous improvement.

The diagnostic methods used in cardiac ischemia are significantly more reliable than those used in cerebral ischemia. So, the diagnosis of cardiac ischemia is refined with the help of electrocardiography (ECG), which is usually quite accessible, and its data is easily interpreted. ECG provides very important information, including previous episodes of ischemia, reversibility of current ischemia, localization of old and new ischemic zones.

On the contrary, in cerebral stroke, the diagnosis is based solely on clinical data. In this case, the clinician should recognize the clinical syndrome caused by the acute occlusion of the cerebral artery. Although the occlusion of a large vessel - such as, for example, the middle cerebral artery - causes an easily recognizable syndrome, the blockage of smaller vessels may manifest symptoms that are difficult to interpret. Moreover, in the presence of a previous ischemic injury, recognition of new lesions is difficult.

To confirm the diagnosis of a stroke, there is no such simple procedure as an ECG. Although computed tomography (CT) and magnetic resonance imaging (MRI) can confirm the diagnosis of a stroke, they usually do not detect changes at the time when the symptoms have just appeared and the treatment can be most effective. In this regard, a special responsibility in the diagnosis of a stroke lies with the doctor, who must connect the neurological syndrome that emerged with the loss of function in the basin of a particular vessel. In the acute phase of ischemic stroke, the main task of neuroimaging is to exclude other causes that can cause neurological symptoms, such as hemorrhage, tumors, or multiple sclerosis. In acute development of neurological defect CT should be performed immediately, and MRI - after 1-2 days to confirm the diagnosis of a stroke if neurologic symptoms persist. To establish the etiology of stroke in combination with other methods, magnetic resonance angiography (MRA) is used.

[1], [2], [3]

Diagnosis of the affected vessel

Ischemic stroke is manifested by the acute development of a focal neurological defect, characteristic of the occlusion of one of the arteries of the brain. In most cases, the patient presents complaints that reflect the acute loss of function of one of the departments of the central nervous system, corresponding to the syndrome of involvement of a particular artery. The condition of the correct diagnosis is knowledge of both functional and vascular anatomy of the brain, because the clinical manifestations of the syndrome depend on the affected vessel. Urgent therapy, developed to date, should begin before neuroimaging methods can confirm the localization and size of the infarction. Therefore, the diagnosis should be rapid and based solely on clinical data.

Stroke is characterized by a rapid onset - a slowly increasing symptomatology is not characteristic of cerebral ischemia. A slow start is possible only in the event that a successive occlusion of many small vessels occurs. In this case, a thorough inquiry will reveal a step-like type of progression, characteristic of multiple small successive small ischemic episodes. Multiple small infarctions lead to the development of vascular dementia, which can be distinguished from Alzheimer's disease by the presence of focal neurological symptoms and multiple discrete lesions on MRI and CT.

In ischemic stroke, the caliber of the affected vessel determines the size of the brain lesion and, accordingly, the prevalence of neurological symptoms: the occlusion of a large vessel usually causes a more extensive neurologic defect, whereas small vessel occlusions - more limited neurological disorders. Deep parts of the brain are supplied with long penetrating vessels, which are predisposed to the development of occlusion with the formation of characteristic small-focal cerebral infarcts. Syndromes associated with the occlusion of small vessels are often called lacunar, since in these cases, small pores (lacunae) usually appear in autopsy in deep brain structures. Vascular lesion of the brain, leading to the appearance of the corresponding symptomatology, is called, respectively, a lacunar stroke.

Although the detection of the affected vessel is key to the diagnosis of stroke, it has only limited value in establishing the etiology of stroke, since the caliber of the affected vessel and the localization of the occlusion do not allow us to establish its cause. To solve this problem, it is necessary to examine the entire vascular tree proximal to the occlusion zone to identify a possible source of embolism. Although small penetrating vessels can be damaged primarily, they are also often blocked by arterio-arterial emboli, the source of which may be a larger vessel from which this artery flows, or small emboli from the heart. In addition, the source of embolism can be a venous channel - if there is a discharge of blood from the right to the left in the heart.

[4], [5]

Methods of neuroimaging and progression of histological changes

There is no consensus on when to perform neuroimaging in a patient with suspected ischemic stroke, because at the time of the onset of symptoms, they are only able to exclude a tumor or hemorrhage. If the symptoms are caused by ischemia, changes in the brain of MRI and CT will not appear until a few hours later. Moreover, the changes caused by ischemia can not be detected by these methods of research for several days. The situation is further complicated by the fact that a significant number of patients with stroke with CT and MRI do not detect focal changes at all.

Knowing the pathological changes that occur in stroke helps to understand why CT and MRI have limited clinical relevance in the acute phase of a stroke. Depending on the level of hemoperfusion, the affected area of the brain can continue to experience an energy deficit for many hours. With the complete cessation of perfusion, for example, with cardiac arrest, energy deficiency develops within a few minutes. With a minimum degree of ischemia, which can cause damage to the brain substance, the energy deficit may appear after 6 or more hours. This is the time it can take to make changes in the brain substance that could be identified by histological examination. Even with insufficient energy, histological changes may be minimal, as indicated by the absence of ischemic changes in autopsy. So, if ischemic damage occurs instantaneously, then during autopsy, massive changes in the brain that appear at the time of death and are not associated with primary ischemic lesions will be revealed. The characteristic changes associated with ischemia occur only when the affected area of the brain is perfused for several hours.

The degree of ischemia determines the speed and severity of pathological changes in the infarction zone. The most severe change is necrosis, characterized by complete loss of tissue structure. Less severe damage is manifested by selective loss of neurons with preservation of glia and tissue structure. In both cases, as the pathological changes in brain tissue develop, excess water accumulates causing edema. Only later, as the necrotic area of the brain is reorganized, the tissue volume decreases.

On CT and MRI, there are usually no changes in the first 6-24 hours after the onset of symptoms. Of the two methods of neuroimaging, MRI has a higher sensitivity because it better identifies the accumulation of water - this zone on the T2-weighted images looks hyperintensive. Older infarcts on MRI have the form of hypo-intensive zones on T1-weighted images.

Since changes in the brain are characteristic of ischemic stroke, time is needed, MRI and CT can not confirm the diagnosis in the first hours of the disease, but can exclude other causes that can cause neurologic symptoms. In all patients with a pronounced neurologic defect, urgent neuroimaging is necessary, primarily CT, to exclude other diseases, such as intracranial hemorrhage. MRI should be delayed at least 1 day after the onset of symptoms.

Diagnosis of the cause of ischemic stroke

Ischemic stroke occurs due to the occlusion of the artery and the violation of the blood supply of a specific area of the brain. Determining the cause of occlusion is necessary to select the most effective long-term therapy. To do this, it is necessary to examine the vascular bed proximal to the occlusion zone. For example, with occlusion of the carotid artery, the primary pathology can be localized in the heart, the aorta or the artery itself. The cause of the occlusion of a small vessel that leaves the carotid artery may be an embolus that forms at any level between the heart and the given vessel.

Although it is difficult to resist the temptation to assume that the nature of the onset and establishment of the affected vessel can help in establishing the etiology of stroke, clinical experience shows that these signs are unreliable. For example, although a stroke with acute development of symptoms, which immediately reaches a maximum, often has an embolic origin, a similar picture is possible in patients with carotid bifurcation lesions, which may require surgical intervention.

The caliber of the affected vessel also does not help in establishing the etiology of the stroke. On the one hand, small vessels can be clogged with an embolus formed in the heart or proximal part of a large artery. On the other hand, the lumen of the vessel can be closed by an atherosclerotic plaque in the place of its passage from the intracranial artery or as a result of its primary damage. There is also some uncertainty about the concept of lacunar disease, suggesting that in the small penetrating arteries there may be a particular type of pathomorphological changes. Although this process, called lipogialinosis, certainly exists, it can explain the stroke only after the more proximal pathology of the heart and arteries is excluded.

Often also mistakenly substitute for the concepts of "etiology of stroke" and "risk factors for stroke." Etiology is associated with pathomorphological changes directly responsible for the development of occlusion of the artery. These processes may include the formation of a blood clot in the left atrium, atherosclerosis of the vessel wall, the state of hypercoagulation. At the same time, risk factors are identified states that increase the likelihood of a stroke. These factors are often multiple and are able to interact with each other. So, smoking is a risk factor for stroke, but not its immediate cause. Since smoking causes various physiological and biochemical changes, there are a number of possible ways that lead to an increased risk of stroke, including smoking-induced hypercoagulation or an increased risk of developing atherosclerosis.

Given the multiplicity of these effects, the impact of risk factors is complex. For example, arterial hypertension is a risk factor for atherosclerosis at several levels, including in small penetrating arteries, larger intracranial arteries, and carotid bifurcation areas. It is also a risk factor for coronary heart disease, which, in turn, can cause atrial fibrillation and myocardial infarction, which can lead to cardiogenic embolism.

Because of this, it is impossible, by examining the patient, to decide whether a stroke is caused by hypertension, diabetes, smoking, or some other single risk factor. Instead, a basic condition should be established, which directly led to occlusion of the artery. This is not just of academic interest, since therapy aimed at preventing a subsequent stroke is chosen taking into account the etiology.

[6], [7], [8]

Methods of examination of the cardiovascular system

A number of non-invasive techniques have been developed that can reveal cardiac or arterial lesions that cause occlusion of the cerebral vessel. A common strategy is to quickly identify any possible cause that requires immediate correction in order to prevent a second stroke. The choice of medicines depends on the risk of stroke in this pathology. As a rule, conditions with a high risk of stroke require the use of warfarin, whereas at low risk, aspirin is used.

In all patients with ischemia in the anterior vascular basin, non-invasive examination of carotid arteries is indicated, mainly to establish indications for carotid endarterectomy. The effectiveness of surgical removal of atherosclerotic plaque in endarterectomy has been debated for many years due to the lack of clear clinical evidence. A North American study of carotid endarterectomy in patients who underwent TIA or stroke demonstrated the effectiveness of surgical treatment. Since a significant advantage of the method was noted only in patients with stenoses exceeding 70%, the degree of stenosis should be taken into account in determining the indications for the operation, regardless of which carotid pool damage caused cerebral ischemia.

A standard non-invasive method for examining carotid bifurcations is duplex ultrasound scanning (ultrasonography), which gives reliable results provided it is performed by a well-trained specialist. His alternative was the MRA, which has several advantages. If duplex ultrasonography provides information only on the bifurcation of the carotid artery, then with the help of MRA it is possible to examine the entire internal carotid artery, including the area of the siphon. In addition, with the help of MRA it is possible to obtain an image of the vertebral arteries and the entire Willis circle. On the other hand, duplex ultrasonography, in contrast to MRA, does not require the patient to stay in a stationary state for a long time in conditions that often provoke claustrophobia, and, therefore, is more convenient. Although the accuracy of MRA in identifying the lesion of carotid bifurcation is comparable to the accuracy of duplex ultrasonography, it has not been studied in the same thorough manner. In contrast to MRA, duplex ultrasonography also provides information on the rate of blood flow, which complements the anatomical data.

Since duplex ultrasonography can be performed more rapidly, it should be performed soon after the patient enters the anterior vascular pool. With negative results, MRA can later be performed to identify pathology at other levels of the vascular system. With delayed MRA, the probability of identifying an ischemic area with MRI is increased.

Angiography remains the gold standard in the study of cerebral vessels. However, its implementation is associated with a known risk of stroke and death, which is 0.5%. Due to the presence of non-invasive ultrasound and magnetic resonance techniques, angiography should be performed only to address specific issues, the answer to which may affect the choice of treatment.

Transcranial Doplerography (TKD) is a useful supplement that allows to identify the lesion of intracranial vessels. Although the TCD does not allow us to obtain as detailed a picture as duplex ultrasonography, measurement of blood flow velocity and pulsation rate provides important information about the atherosclerotic lesion of the vessels of the Willis circle. For example, if the MRA revealed changes in the basilar artery, the middle cerebral artery, the TCD provides additional information that may be important for the interpretation of cerebral angiograms.

While ultrasound and MRA provide information on extracranial and intracranial vessels, echocardiography is the best method for identifying a cardiac source of embolism. Echocardiography is shown in two essentially different groups of patients. The first one includes people with a heart pathology, which is detected anamnestic or according to clinical examination (for example, in the presence of auscultatory signs of damage to the heart valves or other cardiac diseases). The second group includes patients whose cause of stroke remains unclear. In approximately 50% of patients, the stroke is previously classified as "cryptogenic", but many of them subsequently reveal either a hidden cardiac pathology predisposing to embolism or a violation of the blood coagulation system. With intensive additional examination, in most cases it is possible to establish the nature of vascular lesion, especially when using MRA for noninvasive examination of large intracranial vessels.

Several studies have shown that transthoracic echocardiography usually does not reveal the cause of a stroke in those cases when there is no anamnestic indication of cardiac pathology, and in the physical examination of the cardiovascular system, there are no deviations, which makes it unsuitable for patients with cryptogenic stroke. This is also true for obese patients and patients with emphysema, in which a more informative method is transesophageal echocardioscopy (ECT). TEK - a method of choice in those cases when it was not possible to identify the pathology of cerebral vessels. In the ECT, an ultrasound sensor is inserted into the esophagus to better examine the heart, which in this case is not obstructed by the ribs and lungs. In this way, the condition of the aorta can be assessed, which makes it possible to identify large or protruding atherosclerotic plaques on the aorta that can serve as a source of embolism. In the absence of pathology of the heart and blood vessels, the occlusion of the artery may be the result of a hereditary or acquired blood clotting disorder. Some conditions, such as the Tissot syndrome, characterized by an increase in blood coagulability against a malignant neoplasm, may be the only cause of stroke in patients with a healthy heart and uninjured cerebral vessels. Other conditions can only be a risk factor for stroke. These include, for example, the presence of antiphospholipid antibodies, which are often detected in the elderly and increase the risk of stroke. As in the case of cardioembolic stroke, long-term treatment with warfarin is indicated for hypercoagulability with a high risk of stroke.