Main pathogenetic types of ischemia
Clinical syndromes and the dynamics of symptom development depend on the type of cerebral infarction. Three main variants are distinguished:
- Hemodynamic infarction. Develops against the background of severe stenosis of large vessels (e.g., 90–95% narrowing of the internal carotid artery, ICA, by an atherosclerotic plaque). The clinical debut often coincides with physical activity, when the brain experiences an increased demand for blood flow. A typical presentation is the development of hemiparesis with decreased muscle tone. On MRI, such an infarction appears as multiple lesions in the deep white matter, resembling a chain (end-artery zones).
- Lacunar infarction. Characteristic of patients with prolonged, poorly controlled arterial hypertension. Small penetrating arteries are affected. Typical localization is the internal capsule. Symptoms may be limited to purely motor impairments (e.g., right-sided brachiofacial hemiparesis and dysarthria) with a complete absence of sensory disturbances.
- Embolic (territorial) infarction. Occurs when a vessel is occluded by an embolus originating from the heart chambers or from an ulcerated plaque in the carotid artery. The lesion strictly corresponds to the territory of the occluded vessel (e.g., the middle cerebral artery, MCA).
The role of neuroimaging in diagnosis
The main goal of examination is the precise establishment of the etiology of the lesion to select adequate therapy. Imaging methods solve different tasks:
- Computed tomography (CT): The primary method of choice in an emergency situation. The main task is to exclude intracranial hemorrhage as quickly as possible. The disadvantage is the "blind spot"—the inability to see ischemia in the first hours, as well as artifacts in the posterior cranial fossa area.
- Magnetic resonance imaging (MRI): Diffusion-weighted imaging (DWI) can detect cytotoxic edema (slowing of water molecule movement due to swelling of energy-deprived cells) within the first minutes after a vascular event. The FLAIR sequence is excellent for showing anatomy, but a high-intensity signal persists in it for a long time, so only a combination with DWI makes it possible to establish the age of the lesion.
- Ultrasonic Dopplerography (USDG) and MR angiography: Safe imaging methods for evaluating the vessels themselves. They allow assessment of the degree of neck stenosis and detection of signs of plaque ulceration (blood pooling into crater-like depressions).
Paradoxical clinical presentation and vascular anomalies
Sometimes the clinical picture contradicts classical concepts of topical diagnosis. Understanding individual arterial anatomy helps resolve these contradictions.
Consider the situation: a patient with stenosis of the left ICA develops right-sided hemiparesis (which is logically explained by an infarction in the left parietal lobe). However, sensory disturbances in the left leg appear simultaneously, which is characteristic of a right anterior cerebral artery (ACA) lesion.
Such paradoxical symptoms are possible if the patient has an anatomical variant—both ACAs receive blood supply from a single left internal carotid artery (against the background of hypoplasia of the precommunicating segment on the other side). In this case, a single stenosis causes transient ischemia in the territories of both hemispheres.
Acute-phase treatment tactics
Accurate and rapid syndrome diagnosis makes it possible to apply radical blood flow restoration methods.
- Intra-arterial thrombolysis: Used for embolic occlusion of a large vessel (e.g., the MCA trunk) and the development of acute hemiplegia. If less than 3 hours have passed since the onset, and the MRI does not yet show massive irreversible brain tissue damage, a microcatheter is advanced to the thrombus and a thrombolytic agent (urokinase) is administered. This can lead to complete recanalization and regression of the deficit.
- Surgical treatment: For hemodynamically significant stenosis with signs of plaque ulceration, emergency carotid endarterectomy is indicated.
Briefly: answers to topical questions
What clinical symptoms are included in the full-blown middle cerebral artery (MCA) syndrome?
The full-blown syndrome of total middle cerebral artery infarction includes motor, sensory, and cognitive impairments.
The symptom complex consists of the following manifestations:
- Motor and sensory impairments — contralateral hemiplegia (or brachiofacial hemiparesis), hemianesthesia (hemihypesthesia), as well as central-type facial and tongue muscle paresis.
- Vision and oculomotor functions — contralateral homonymous hemianopsia and cortical gaze palsy.
- Higher cortical function disturbances — in dominant hemisphere lesions, total (motor and/or sensory) aphasia, acalculia, agraphia, alexia, and apraxia occur; in non-dominant hemisphere lesions, anosognosia, body schema disorders, and neglect syndrome occur.
What neurological symptoms are characteristic of an isolated anterior cerebral artery (ACA) lesion?
An isolated anterior cerebral artery lesion manifests predominantly as motor disorders and, in cases of bilateral involvement, mental status changes.
Characteristic neurological symptoms:
- Motor impairments — contralateral hemiparesis with predominance in the leg and proximal arm, isolated leg monoparesis, or paraparesis.
- Sensory impairments — mild hypesthesia in the paretic limbs is possible.
- Sphincter disorders — urinary retention or incontinence.
- Mental and cognitive impairments (with bilateral lesions) — severe motivation impairment (apathy), neuropsychological deficit (apraxia).
- Pathological reflexes (with bilateral lesions) — appearance of primitive reflexes (grasp, sucking, palmomental).
What branches does the internal carotid artery (ICA) give off in the cranial cavity before dividing into its terminal branches?
Before dividing into its terminal branches (the anterior and middle cerebral arteries), the internal carotid artery gives off a series of intradural and extradural branches.
In the cranial cavity, it gives off:
- Fine extradural branches — supply the floor of the tympanic cavity, the dura mater of the clivus, the trigeminal ganglion, and the hypophysis.
- Ophthalmic artery (a. ophthalmica) — arises intradurally medial to the anterior clinoid process.
- Posterior communicating artery (a. communicans posterior) — participates in the formation of the circle of Willis.
- Anterior choroidal artery (a. choroidea anterior) — supplies deep brain structures.
For differential diagnosis of causes: Territorial infarction — look for an embolic source (heart, carotid bifurcation). Hemodynamic — look for stenosis and relation to exertion. Lacunar — look for arterial hypertension and motor deficit without sensory impairment.
Class and exam questions
Why is CT always performed first when ischemic stroke is suspected?
In an emergency situation, it is critically important to exclude hemorrhagic stroke (hemorrhage), which requires completely different management tactics. CT allows blood to be visualized immediately and is performed faster than MRI.
Can contrast be used in CT during the first days of a stroke?
This is not recommended without strict necessity. By days 4–6, the infarction core begins to accumulate contrast due to blood-brain barrier breakdown, which can become a diagnostic trap and mimic a brain tumor.
Why is a functional heart study necessary in cerebral infarction?
ECG and echocardiography are necessary to search for cardiac causes of ischemia: intracardiac thrombi (source of embolism), arrhythmia, or heart failure, which reduce cardiac output and provoke hypoperfusion.
What else to study on this topic
- Cytotoxic edema in ischemia and its MRI appearance
- Ultrasonic signs of atherosclerotic plaque ulceration
- Collateral blood flow via the posterior communicating artery system
- Indications for brain positron emission tomography (PET)
- Indications and risks of digital subtraction angiography (DSA)
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