Main causes of ischemic injury
Impaired local blood flow in the brain develops according to several main scenarios, depending on the etiology and vessel size:
- Cardiogenic embolism (about 20% of cases). Emboli reach the brain from the heart. Contributing factors include atrial fibrillation (thrombi in the left atrium), infective endocarditis, transmural myocardial infarction, myocardial aneurysm, and prosthetic heart valves. Paradoxical embolism stands apart: a thrombus migrates from veins or the right atrium through congenital defects (patent foramen ovale, septal defects).
- Small vessel disease (15–30%). Damage to perforating branches 40–80 µm in diameter against the background of hypertension, diabetes, or age-related changes (lipohyalinosis, arteriolosclerosis). Microinfarcts up to 15 mm in diameter develop, leaving behind cavities — lacunae. Typical localization: white matter, brainstem, subcortical nuclei.
- Rare causes (5–10%). Include carotid and vertebral artery dissection, fibromuscular dysplasia, arteritis, and hematologic disorders (polycythemia, leukemia, sickle cell anemia).
- In young patients, hypercoagulopathies (antiphospholipid syndrome) and migraine with aura come to the forefront.
Pathogenesis of local ischemia: core and penumbra
Any etiological factor causing blood deficiency triggers a pathobiochemical cascade. The outcome is cell death via necrosis or apoptosis. However, the lesion zone is heterogeneous:
- Infarct core. The central area where blood flow has dropped to critical values, and changes are completely irreversible.
- Ischemic penumbra. The zone surrounding the core. Blood flow here is reduced, cells cannot function normally, but perfusion remains above the threshold of 10–15 ml/100 g/min. Neurons in the penumbra remain viable for several hours (the "therapeutic window"). If blood flow is restored in time, the tissue survives; if not, the infarct core expands due to the death of the penumbra.
Development of brain edema and risks
The scale of brain edema is directly proportional to the size of the infarct: it is massive in atherothrombotic and cardioembolic variants, but almost absent in lacunar stroke. The process proceeds in two stages:
- Cytotoxic edema. Starts a few minutes after the vascular catastrophe. Due to cell membrane failure, water accumulates inside neurons.
- Vasogenic edema. Develops a few days later. The blood-brain barrier (BBB) is damaged, and plasma leaks into the extracellular space.
Dynamics and complications: Edema reaches its maximum severity on days 2–4. During this time, intracranial pressure rises sharply. The most formidable complication is the displacement (herniation) of diencephalic and midbrain structures with tentorial herniation. This is the main cause of patient mortality in the first week. If the patient survives, the edema regresses within 1–2 weeks, and a cyst or gliomesodermal scar forms at the site of the dead tissue.
Clinical presentation
Ischemic vascular events are characterized by hyperacute onset: neurological deficit (motor, speech, sensory) develops in a matter of seconds or minutes, rarely stretching over hours. In clinical practice, stroke-in-evolution is also distinguished — a form in which symptoms and the depth of focal deficit increase gradually and stepwise.
Briefly: answers to topical questions
What stages are distinguished in the clinical course of chronic cerebral ischemia (circulatory encephalopathy)?
The clinical course of circulatory encephalopathy distinguishes three stages depending on the severity of cognitive impairment.
- Stage I — mild decrease in concentration, memory impairment, slowed thinking, decreased speed of motor reactions and regulatory functions.
- Stage II — more significant decline in memory and cognitive functions, appearance of difficulties when performing complex intellectual activities.
- Stage III — severe decline in memory and cognitive functions, impaired adaptation in professional, social, and/or daily activities with the development of dementia.
What exact cerebral blood flow values are characteristic of the infarct core and the penumbra zone?
The infarct core and the ischemic penumbra zone are characterized by different cerebral blood flow velocity values.
- Infarct core — cerebral blood flow velocity is less than 10 ml per 100 g per minute, leading to irreversible tissue damage (necrosis).
- Penumbra zone (penumbra) — cerebral blood flow velocity is within the range of 10–20 ml per 100 g per minute, while the tissue remains potentially viable.
What are the main causes of ischemic stroke identified in young patients?
In young and middle-aged patients, hypercoagulopathies, such as antiphospholipid syndrome, and migraine with aura are significantly more common.
What classic clinical syndromes are characteristic of lacunar strokes?
Lacunar strokes are characterized by the development of five main clinical syndromes.
- Pure motor stroke — isolated motor deficit.
- Pure sensory stroke — isolated sensory deficit (isolated hemihypesthesia).
- Sensory-motor deficit — a combination of hemihypesthesia and hemiparesis.
- Dysarthria-clumsy hand syndrome — a specific speech and motor impairment.
- Ataxic hemiparesis — a combination of paresis and ataxia.
The clinical picture of lacunar stroke is generally nonspecific.
What cognitive and psychoemotional disorders are characteristic of chronic cerebral ischemia.
Chronic cerebral ischemia is characterized by intellectual-mnestic disorders of varying severity, up to the development of vascular dementia.
- Stage I: mild decrease in concentration, memory impairment, slowed thinking, decreased speed of motor reactions and other regulatory mental functions.
- Stage II: more significant decline in memory and other cognitive functions, difficulties in performing complex mental activities.
- Stage III: severe decline in memory and cognitive functions, impaired adaptation in professional, social, and/or daily activities with the development of dementia.
How are lacunar strokes visualized on MRI in various modes (T1, T2, FLAIR)?
On MRI, lacunar strokes are visualized as small lesions whose characteristics depend on the mode used.
- T1-weighted imaging — single or multiple infarcts in the white matter and basal ganglia are visualized.
- T2-weighted imaging — the infarct is identified as a hyperintense lesion.
- FLAIR mode — the lesion appears as a hyperintense zone, while high resolution allows establishing its exact anatomical localization.
Also in DWI mode, a fresh lacunar stroke appears as a zone of marked hyperintensity.
To remember the two stages of edema, focus on anatomy: first the CELL itself suffers (cytotoxic — minutes), and then the VESSELS and barriers (vasogenic — days).
Class and exam questions
What is paradoxical embolism?
This is a condition in which an embolus from the veins or the right atrium enters the cerebral arteries. This is only possible if there are congenital pathological communications in the heart, such as a patent foramen ovale.
Where are lacunar infarcts most commonly localized?
They usually occur in the white matter of the hemispheres, subcortical ganglia, and brainstem, much less frequently affecting the cerebellum.
What do lacunar infarcts look like on MRI?
On T1-weighted MRI, they are visualized as single (for example, with enlargement of the head of the caudate nucleus) or multiple small lesions in the basal ganglia and white matter.
What else to study on this topic
- Diagnostic criteria and patient management within the "therapeutic window".
- Mechanisms of necrosis and apoptosis in cerebral ischemia at the biochemical level.
- Herniation syndromes and brainstem displacement.
- Antiphospholipid syndrome as a cause of stroke in young people.
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