Diagnosis of ischemic stroke

When collecting an anamnesis of the disease, it is necessary to find out when the cerebral circulatory disorder has started, as well as the speed and sequence of occurrence of various symptoms. Particular importance is attached to the dynamics of cerebral palsy (impaired consciousness, vomiting, generalized convulsions) and focal (motor, speech, sensory disorders) of symptoms. The stroke is characterized, as a rule, by the sudden occurrence of neurologic symptoms; Focal symptomatology is crucial for the diagnosis of acute impairment of cerebral circulation.

When collecting a history of life, it is necessary to identify possible risk factors for stroke - arterial hypertension, diabetes mellitus, atrial fibrillation and other cardiac arrhythmias, atherosclerosis, vascular diseases (eg, myocardial infarction, acute cerebrovascular accident), hypercholesterolemia, smoking, etc. To clarify the hereditary history of vascular pathology in the relatives of the patient.

[1], [2], [3], [4], [5], [6], [7], [8],

Physical examination

Physical examination of a patient with acute impairment of cerebral circulation is carried out according to generally accepted rules for organ systems (respiratory, cardiovascular, digestive, urinary, etc.). When assessing the neurological status, the presence and severity of cerebral symptoms (impaired consciousness, headache, nausea, vomiting, generalized convulsions), meningeal symptoms and focal neurologic symptoms are noted. To identify the latter, a consistent evaluation of the functions of the cranial nerves, the motor system, the sensitive and coordinating spheres, the vegetative system, and higher mental functions is necessary.

Quantitative assessment of the severity of neurological deficit in patients with stroke is possible with the use of specialized scoring scales such as the stroke scale of the National Institutes of Health (NIH Stroke Scale), the Scandinavian scale, etc. The degree of functional recovery of patients with stroke is assessed by the Barthel index, the modified Rankine scale, the scale outcomes of Glasgow.

Laboratory Diagnosis of Ischemic Stroke

Patients with stroke should perform a clinical blood test (including platelet count), biochemical analysis (glucose, creatinine, urea, bilirubin, total protein, electrolytes, CK), coagulogram (fibrinogen content, activated partial thromboplastin time, international normalized ratio), total Analysis of urine.

Instrumental diagnostics

The basis of instrumental diagnostics in stroke is the methods of neuroimaging, in particular CT and MRI. These methods are used for differential diagnosis between stroke and other forms of intracranial pathology, clarifying the nature of the stroke (ischemic or hemorrhagic) and controlling the nature of tissue changes in the affected area in the treatment of stroke.

In the acute period of cerebral infarction, the dominant type of tissue changes in the area of ischemic damage is cytotoxic edema, and vasogenic edema is usually associated with it in the lesion of the microcirculatory bed. On CT images, the cerebral infarction zone during the first week of the disease looks like a uniformly hypodensitive site, which usually has a moderate volumetric effect on the surrounding brain structures. In most cases, this site corresponds to a certain vascular pool and has a wedge shape with a base outward. The zone of cerebral infarction begins to be visualized on CT images usually 10-14 hours after the onset of the disease.

The earliest CT-sign of ischemic damage in the system of the middle cerebral artery is the lack of visualization of the lenticular nucleus or cortex of the island in connection with the development of the cytotoxic edema of the brain in the affected area. With large hemispheric cerebral infarctions during the first hours of the stroke, even before the appearance of hypodensitive changes in the brain material, it is possible to detect a local volumetric effect in the form of a narrowing of the cortical furrows in the affected area and the absence of a contrast between the gray and white matter.

In some cases, in cases of ischemic stroke, as early changes, hyperdensity of the areas of the middle, less often - posterior cerebral artery on the side of the lesion is revealed, which indicates the presence of thrombosis or embolism of these vessels. In CT, it is also possible to identify various vascular changes potentially capable of causing ischemic brain damage: calcifications in atherosclerotic plaques in artery walls, tortuosity and vasodilatation, in particular vascular deregoectasis of the vertebrobasilar system, cerebral vascular malformations.

Since the end of the first week in the gray matter in the ischemic lesion zone, an increase in density has been observed before the isodensic and, sometimes, to a slightly hyper-sensitive state, which is associated with the development of neovagesis and the restoration of blood flow. This phenomenon gives the "fogging effect", which makes it difficult to identify the true boundaries of the zone of ischemic damage in the subacute period of the cerebral infarction. But in connection with the development of neovaginosis in this period, the accumulation of a contrast agent in the gray matter of the affected area (the so-called gyral type of contrast enhancement) is noted, which makes it possible to accurately determine the boundaries of the cerebral infarction. During the 2 nd week of a cerebral infarction, the positive effect of volumetric exposure usually regresses, and later the effect of loss of brain substance begins to appear. After 1,5-2 months on the CT images, hypodensitive changes, corresponding to the emerging postinfarction cyst, are revealed.

At CT, hemorrhagic transformation in the zone of acute ischemic damage by type of blood impregnation of brain substance or in the form of hematoma formation is well revealed. Correspondingly, moderately pronounced or pronounced hyperdense changes are observed in the zones of hemorrhagic transformation.

MRI changes with a cerebral infarction occur before CT changes. On T2-weighted images, the increase in the signal for cerebral infarction is generally observed a few hours earlier than the hypotensive changes in CT images, which is associated with the high sensitivity of T2-weighted images to an increase in the water content in the brain substance. On T1-weighted images, the decrease in the signal in the cerebral infarction zone is moderate and for diagnosis is poorly informative. But for hemorrhagic transformation, an increase in the signal on T1-weighted images, associated with the appearance of methemoglobin in the extracellular space, is the main diagnostic criterion. This symptom begins to appear 5-7 days after the development of hemorrhagic transformation and persists for several weeks, when CT-signs of this complication of cerebral infarction already regress.

Along with the change in the intensity of the signal on MP images, a bulk effect appears in cerebral infarction, which is manifested by the smoothness of the pattern of furrows and gyri of the brain, compression of the outer and inner liquor spaces. These changes in MRI reveal more accurately compared with CT in connection with the possibility of obtaining images in different projections.

In the process of organizing a cerebral infarction, two main types of tissue changes in the affected area are observed: the formation of cystic cavities filled with liquor-like fluid (cystic transformation), and the proliferation of glia (gliosis transformation). Differentiation of these types of tissue changes is difficult both for CT images and for conventional T2 and Tl-weighted images, since in the areas of glial transformation the total water content is also increased, although to a lesser extent than in postinfarction cysts.

On the images obtained using the mode with the suppression of the free water signal (FLAIR), the areas of gliose transformation have a high signal, since the water in glial cells is bound; in contrast, postinfarction cysts will be hypointense, since they contain mostly free water. The use of this regimen makes it possible to determine the ratio of the two types of tissue changes in the area of a chronic cerebral infarction and, accordingly, to study the effect on them of various factors, including therapeutic effects.

The use of CT or MP angiography makes it possible to detect occlusions and stenoses of cerebral and extraocerebral vessels in ischemic stroke, and also to evaluate the variants of the structure of the Willis circle and other vascular structures.

In recent years, methods of assessing cerebral blood flow based on not only CT, but also MP technologies have been introduced into clinical practice. Both methods are based on the bolus injection of an appropriate contrast preparation and allow to obtain CT perfusion and MRI images weighted by various parameters of cerebral perfusion (relative regional cerebral blood flow, transit time, blood volume in the brain substance). These methods allow to identify areas of brain hypoperfusion, which is very important for acute violations of the cerebral circulation.

New and effective in vascular lesions of the brain is the mode of MRI-study, which allows to obtain diffusion-weighted images. The development of cytotoxic edema in acute ischemic brain damage is accompanied by a transition of water molecules from the extracellular to the intracellular space, which leads to a decrease in the rate of their diffusion. This is manifested in diffusion-weighted MRI images in the form of signal enhancement. Such hyperintensive changes usually indicate the development of irreversible structural damage to brain matter and are manifested in the zone of the infarction already in the first minutes of the latter's development.

The use of diffusion-weighted and perfusion MR-images allows solving diagnostic problems that can not be solved using other methods of CT and MRI. Perfusion MR images reveal areas of brain hypoperfusion. Comparison of the prevalence of these changes with the magnitude of hyperintensive sites on diffusion-weighted images makes it possible to differentiate the zone of irreversible ischemic damage to brain matter from the penumbra-the zone of hypoperfusion with potentially reversible tissue changes.

The current level of development of CT and MRI diagnostic methods makes it possible to successfully solve most diagnostic problems in acute disorders of cerebral circulation. The use of some of them in dynamics allows to control the course of tissue changes in the area of ischemic damage, which opens up new possibilities for choosing the most appropriate methods of therapeutic influence and monitoring the effectiveness of new methods of treating acute disorders of cerebral circulation.

MRI is the most informative method of intravital diagnosis of cerebral infarction, visualization of acute focal cerebral ischemia is possible within a few minutes after its onset (using diffusion and perfusion-weighted sequences). The limitations of MRI are longer time and higher cost of research, inability to study patients with metallic bodies in the cranial cavity and pacemakers. Currently, the standard for the study of patients with acute vascular neurological pathology is the preferred use of CT in the first day of the disease for differential diagnosis between ischemic injury and hemorrhagic stroke, since at this time the detection of hemorrhages at CT is higher than with MRI, except for cases of use Special research modes on high-field MR scanners.

Differential diagnosis of ischemic stroke

Ischemic stroke must be differentiated first of all from intracerebral hemorrhages. A crucial role is played by neurovisualizing studies - CT or MRI. Also, sometimes there is a need for differential diagnosis with the following conditions and diseases:

• traumatic brain injury;
• metabolic or toxic encephalopathy (hypo- or hyperglycemia, hepatic encephalopathy, alcohol poisoning);
• epileptic seizures (Todd's paralysis or an uncontrolled seizure);
• acute hypertensive encephalopathy;
• a brain tumor;
• infectious brain lesions (encephalitis, abscess);
• multiple sclerosis, etc.

[9], [10], [11], [12], [13]