Definition and Overview
Cerebral infarction is the core type of ischemic stroke in which blood flow to brain tissue is blocked due to cerebral vessel occlusion or stenosis, causing irreversible neuronal damage. It accounts for approximately 80-85% of all strokes [3] and is one of the major causes of death and disability worldwide.
When cerebral infarction occurs, an ischemic core and surrounding ischemic penumbra form depending on the site of blood flow interruption. The core rapidly sustains irreversible damage, but the penumbra can potentially be salvaged through prompt reperfusion. This is the fundamental basis for acute-phase treatment.
Etiology and Pathophysiology
The TOAST classification is widely used for etiologic classification of cerebral infarction.
Large artery atherosclerosis involves plaque formation in major cerebral vessels such as the carotid and middle cerebral arteries, causing stenosis or occlusion. Cardioembolism occurs when thrombi generated in the heart due to atrial fibrillation, heart failure, or endocarditis occlude cerebral vessels. Small vessel occlusion (lacunar) results from lipohyalinosis of small cerebral vessels, producing lacunar infarcts. Other causes include coagulopathy, arterial dissection, and vasculitis, while cryptogenic cases also account for a significant proportion.
At the cellular level, cascading reactions including excitotoxicity, oxidative stress, inflammation, and apoptosis progress after ischemia, expanding neuronal damage.
Symptoms
Symptoms of cerebral infarction vary depending on the occluded vessel and the area of damage. The hallmark symptoms are summarized by FAST (Face-Arm-Speech-Time).
Key symptoms include sudden unilateral arm/leg paralysis or sensory loss, sudden speech disturbance (aphasia or dysarthria), sudden unilateral facial palsy, sudden visual field defect or diplopia, sudden severe headache (requiring differentiation from hemorrhagic stroke), and sudden gait disturbance and dizziness.
Transient ischemic attack (TIA) presents with the same symptoms as cerebral infarction but with complete recovery within 24 hours. However, it is a warning sign of impending cerebral infarction and requires immediate evaluation and treatment.
Diagnosis
When acute cerebral infarction is suspected, immediate emergency evaluation is performed.
Non-contrast CT is performed immediately for brain imaging to exclude hemorrhage. MRI (DWI, diffusion weighted imaging) can sensitively detect acute cerebral infarction even within hours of onset.
For vascular imaging, CT angiography (CTA) or MR angiography (MRA) rapidly assesses for large vessel occlusion. ECG, echocardiography, and blood tests (coagulation function, blood glucose, CBC) are also necessary for etiologic differentiation.
Treatment
The cornerstone of acute-phase treatment is rapid reperfusion.
For intravenous thrombolysis, alteplase (tPA) can be administered to eligible patients within 4.5 hours of symptom onset [1]. Tenecteplase is being studied as an alternative agent.
Mechanical thrombectomy is applicable for patients with large vessel occlusion (primarily middle cerebral artery, internal carotid artery) within 6-24 hours of last known normal, using imaging-based selection (penumbra mismatch) [2]. The DAWN trial (2018) confirmed that thrombectomy in the 6-24 hour window significantly improves functional outcomes [2].
For secondary prevention, antiplatelet agents (for large artery or small vessel infarction) or anticoagulants (for atrial fibrillation) are administered depending on the etiology. Blood pressure, blood glucose, and lipid management, smoking cessation, and carotid endarterectomy (CEA) or stenting (CAS) for carotid stenosis are also implemented [4].
Prognosis
The 1-month mortality rate for cerebral infarction is approximately 10-20%, and approximately 30-40% of survivors are left with long-term functional disability [3]. Prognosis varies greatly depending on the infarction size and location, time to treatment initiation, underlying conditions, and rehabilitation intensity.
The recurrence rate of cerebral infarction is high at approximately 10-15% within the first year, and appropriate secondary prevention treatment significantly reduces recurrence [4]. Anticoagulant therapy in atrial fibrillation patients reduces recurrent cardioembolic cerebral infarction by approximately 60-70%.
Early intensive rehabilitation improves functional recovery, and research continues on optimal timing and intensity of rehabilitation.
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