Diagnosis of ischemic stroke

When collecting the anamnesis of the disease, it is necessary to find out when exactly the cerebrovascular accident began, as well as the speed and sequence of occurrence of certain symptoms. Particular importance is attached to the dynamics of general cerebral (impaired level of consciousness, vomiting, generalized seizures) and focal (motor, speech, sensory disorders) symptoms. As a rule, a stroke is characterized by a sudden onset of neurological symptoms; focal symptoms can be decisive for the diagnosis of acute cerebrovascular accident.

When collecting a patient's medical history, it is necessary to identify possible risk factors for stroke - arterial hypertension, diabetes mellitus, atrial fibrillation and other heart rhythm disorders, atherosclerosis, previous vascular diseases (for example, myocardial infarction, acute cerebrovascular accident), hypercholesterolemia, smoking, etc. It is also necessary to find out the hereditary medical history of vascular pathology in the patient's relatives.

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Physical examination

Physical examination of a patient with acute cerebrovascular accident 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 general cerebral symptoms (impaired level of consciousness, headache, nausea, vomiting, generalized seizures), meningeal symptoms and focal neurological symptoms are noted. To identify the latter, a consistent assessment of the functions of the cranial nerves, motor system, sensory and coordination spheres, vegetative system and higher mental functions is necessary.

Quantitative assessment of the severity of neurological deficit in patients with stroke is possible using specialized scoring scales, such as the NIH Stroke Scale, the Scandinavian scale, etc. The degree of functional recovery of patients with stroke is assessed using the Barthel index, the modified Rankin scale, and the Glasgow outcome scale.

Laboratory diagnostics of ischemic stroke

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

Instrumental diagnostics

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

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

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

In some cases of ischemic stroke, early changes reveal hyperdensity of sections of the middle, and less commonly, the posterior cerebral artery on the affected side, which indicates the presence of thrombosis or embolism of these vessels. CT can also reveal various vascular changes that can potentially cause ischemic brain damage: calcifications in atherosclerotic plaques in the walls of arteries, tortuosity and dilation of vessels, in particular dolichoectasia of the vertebrobasilar system, cerebral vascular malformations.

Beginning from the end of the first week, the gray matter in the ischemic damage zone shows an increase in density to an isodense, and sometimes to a slightly hyperdense state, which is associated with the development of neovasogenesis and restoration of blood flow. This phenomenon produces a "fogging effect," which makes it difficult to identify the true boundaries of the ischemic damage zone in the subacute period of cerebral infarction. However, due to the development of neovasogenesis during this period, an accumulation of the contrast agent is noted in the gray matter of the lesion zone (the so-called gyral type of contrast enhancement), which allows for the precise determination of the boundaries of cerebral infarction. During the 2nd week of cerebral infarction, the positive effect of volumetric exposure usually regresses, and later the effect of brain matter loss begins to appear. After 1.5-2 months, hypodense changes corresponding to the developing postinfarction cyst are detected on CT images.

CT scans clearly reveal hemorrhagic transformation in the area of acute ischemic injury, such as blood soaking of the brain tissue or hematoma formation. Accordingly, moderately expressed or expressed hyperdense changes are observed in areas of hemorrhagic transformation.

MRI changes in cerebral infarction occur earlier than CT changes. On T2-weighted images, an increase in signal in cerebral infarction is generally observed several hours earlier than hypodense changes on CT images, which is due to the high sensitivity of T2-weighted images to an increase in the water content in the brain substance. On T1-weighted images, a decrease in signal in the cerebral infarction zone is moderate and of little information for diagnosis. However, for hemorrhagic transformation, an increase in signal on T1-weighted images associated with the appearance of methemoglobin in the extracellular space is the main diagnostic criterion. This sign begins to be detected 5-7 days after the development of hemorrhagic transformation and persists for several weeks, when CT signs of this complication of cerebral infarction have already regressed.

Along with the change in signal intensity on MR images, a volumetric effect appears and increases in cerebral infarction, manifested by smoothing of the pattern of grooves and convolutions of the brain, compression of the external and internal cerebrospinal fluid spaces. These changes are detected more accurately in MRI compared to CT due to the possibility of obtaining images in various projections.

During the process of cerebral infarction, two main types of tissue changes are observed in the affected area - the formation of cystic cavities filled with cerebrospinal fluid (cystic transformation) and proliferation of glia (gliotic transformation). Differentiation of these types of tissue changes is difficult both on CT images and on conventional T2- and Tl-weighted images, since in areas of gliotic transformation the total water content is also increased, although to a lesser extent than in post-infarction cysts.

In images obtained using the Fluid Attenuated Inversion Recovery (FLAIR) mode, areas of glial transformation have a high signal, since the water in glial cells is bound; in contrast, post-infarction cysts will be hypointense, since they contain mainly free water. Using this mode allows us to determine the ratio of the 2 specified types of tissue changes in the zone of chronic cerebral infarction and, accordingly, to study the influence of various factors on them, including therapeutic effects.

The use of CT or MR angiography allows us to identify occlusions and stenoses of cerebral and extracerebral vessels in ischemic stroke, as well as to evaluate variants of the structure of the circle of Willis and other vascular structures.

In recent years, methods for assessing cerebral blood flow based on not only CT but also MR technologies have been introduced into clinical practice. Both methods are based on bolus administration of the appropriate contrast agent and allow obtaining CT perfusion and MRI images weighted by various parameters of cerebral perfusion (relative regional cerebral blood flow, blood transit time, blood volume in the brain). These methods allow identifying areas of cerebral hypoperfusion, which is very important in acute cerebrovascular accidents.

A new and effective mode for vascular brain lesions is the MRI examination mode, which allows obtaining diffusion-weighted images. The development of cytotoxic edema in acute ischemic brain damage is accompanied by the 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 as an increase in the signal. Such hyperintensive changes usually indicate the development of irreversible structural damage to the brain substance and are manifested in the infarction zone already in the first minutes of the latter's development.

The use of diffusion-weighted and perfusion MR images allows solving diagnostic problems that cannot be solved using other CT and MRI methods. Perfusion MR images reveal areas of brain hypoperfusion. Comparison of the prevalence of these changes with the size of hyperintensive areas on diffusion-weighted images allows differentiating the zone of irreversible ischemic damage to the brain substance from the penumbra - a hypoperfusion zone 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 cerebrovascular accidents. The use of some of them in dynamics allows monitoring the course of tissue changes in the ischemic injury zone, which opens up new opportunities for choosing the most adequate methods of therapeutic intervention and monitoring the effectiveness of new methods of treating acute cerebrovascular accidents.

MRI is the most informative method for intravital diagnostics of cerebral infarction; visualization of acute focal cerebral ischemia is possible within a few minutes after its onset (using diffusion- and perfusion-weighted sequences). Limitations of MRI include a longer time and higher cost of the examination, and the impossibility of examining patients with metal bodies in the cranial cavity and pacemakers. Currently, the generally accepted standard for examining patients with acute vascular neurological pathology is the preferred use of CT on the first day of the disease for the purpose of differential diagnostics between ischemic damage and hemorrhagic stroke, since at this time the detection of hemorrhages with CT is higher than with MRI, with the exception of cases of using special examination modes on high-field MRI scanners.

Differential diagnosis of ischemic stroke

Ischemic stroke must be differentiated primarily from intracerebral hemorrhages. Neuroimaging studies - CT or MRI - play a decisive role. Sometimes there is also a need for differential diagnostics with the following conditions and diseases:

• craniocerebral trauma;
• metabolic or toxic encephalopathy (hypo- or hyperglycemia, hepatic encephalopathy, alcohol poisoning);
• epileptic seizures (Todd's paralysis or non-convulsive seizure);
• acute hypertensive encephalopathy;
• brain tumor;
• infectious lesions of the brain (encephalitis, abscess);
• multiple sclerosis, etc.

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