It refers to cerebral artery thrombosis, which leads to cerebral circulatory disorders, cerebral ischemia, or infarction. It is more common in middle-aged and elderly people, with atherosclerosis being a frequent cause.

bubble_chart Auxiliary Examination

A few patients may experience increased intracranial pressure and grade I elevation of cerebrospinal fluid protein levels. Cranial CT can reveal low-density softening lesions 24 to 48 hours after onset. Magnetic resonance angiography (MRA) of the brain is more advantageous, as it can also display occlusions in secondary or higher cerebral arteries. Peripheral blood rheology may show abnormalities. Carotid and transcranial Doppler ultrasound can detect the affected sites and degree of stenosis in cervical and skull base arteries, as well as abnormalities in blood flow.

bubble_chart Diagnosis

1. Medical history and symptoms: Patients may have a history of long-term cerebral arteriosclerosis or transient ischemic attacks. Some patients experience prodromal symptoms such as dizziness, limb numbness, and lack of strength. The onset often occurs during quiet sleep, with most patients remaining conscious and typically without headache, nausea, or vomiting. Blood pressure at onset is usually normal or slightly elevated. Focal neurological signs are related to factors such as the location and degree of vascular occlusion and the status of collateral circulation. When taking the medical history, attention should be paid to the presence of these characteristics.
2. Physical examination findings: Common findings include hemiplegia, hemisensory impairment, homonymous hemianopia, aphasia, psychiatric symptoms, urinary dysfunction, and unconsciousness. Other possible manifestations include cortical blindness, thalamic sensory impairment, ataxia, dysarthria, ocular muscle paralysis, dysphagia, crossed paralysis or quadriplegia, and locked-in syndrome.

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bubble_chart Treatment Measures

1. Bed rest should be emphasized, with strengthened care for skin, oral cavity, respiratory tract, and urine/stool to prevent various complications. For those unable to eat within 24–48 hours, nasogastric tube feeding with liquid diet should be administered.
2. During the acute phase, antihypertensive drugs are generally not used to avoid worsening the condition. Instead, 706 plasma substitute or low-molecular-weight dextran can be administered, along with invigorating blood and resolving stasis Chinese medicinals (compound formulas such as Salvia, Sichuan Lovage Rhizome, and Dengzhanhua Su, etc.) to improve cerebral blood circulation. For cerebral edema, 20% mannitol or 10% glycerol should be used. Patients within 6 hours of onset may receive high-dose urokinase (1–2 million units) for thrombolytic therapy. Alternatively, t-PA activators with defibrinogenating, anticoagulant, and thrombolytic effects (e.g., Dongshui Kelp Base Peel, Defibrase 10 units via IV drip) can be administered. Cerebral cell activators such as citicoline, coenzyme Q10, cytochrome C, piracetam, coenzyme A, and flunarizine may be used. Vasodilators like papaverine hydrochloride, pentoxifylline, betahistine hydrochloride, kallidinogenase, and cyclandelate should be used with caution.
3. Other treatments include free radical scavengers like vitamins C and E, as well as hyperbaric oxygen therapy, external counterpulsation, and ultraviolet blood irradiation and oxygenation.
4. For patients with acute cerebellar infarction leading to cerebral swelling and hydrocephalus, emergency lateral ventricle drainage or removal of necrotic brain tissue may be performed. For cases of large-area cerebral infarction unresponsive to dehydration therapy, subtemporal decompressive craniectomy may be considered.
5. During the convalescence stage, patients should focus on functional rehabilitation, physical therapy, and acupuncture, along with prophylactic use of antiplatelet aggregation agents.

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bubble_chart Differentiation

It should be differentiated from cerebral hemorrhage, cerebral embolism, and intracranial space-occupying lesions.