Cerebral thrombosis is an acute ischemic cerebrovascular disease characterized by localized neurological dysfunction. It is caused by vascular thromboembolism leading to focal cerebral ischemia, hypoxia, and subsequent ischemic necrosis of brain tissue. As the most common type of ischemic stroke, cerebral thrombosis has a high incidence in middle-aged and elderly populations with cardiovascular risk factors.
Etiology & Pathogenesis
Atherosclerosis and hypertension are the two predominant causes of cerebral thrombosis. Predilection sites include the middle cerebral artery, carotid siphon, vertebral artery, and middle and distal segments of the basilar artery. Approximately 20%–30% of thrombotic lesions occur in large cervical arteries. Cerebral atherosclerosis primarily affects medium and large-caliber intracranial arteries, causing intimal hyperplasia, cholesterol deposition, and vascular calcification, which gradually lead to arterial stenosis.
Due to sufficient collateral circulation in the distal vascular territory, mild arterial stenosis often remains asymptomatic under normal conditions. Thrombosis is triggered when blood pressure drops, blood flow slows, blood viscosity increases, and coagulation function becomes abnormal. These hemodynamic changes commonly occur during sleep, extreme fatigue, or in patients with heart failure, myocardial damage, arrhythmia, shock, and acute blood loss.
Secondary pathogenic factors include cerebral arteritis, craniocervical trauma, polycythemia vera, and sickle cell anemia. In young patients, cerebral thrombosis is mostly associated with connective tissue diseases, congenital vascular malformations, and inflammatory cerebral vasculitis, while atherosclerosis is a rare cause in younger populations.
Modern clinical research confirms that artery-to-artery embolism (thrombus-infarction phenomenon) is a critical trigger for cerebral infarction. Shed atherosclerotic plaque fragments and adherent substances, composed of cholesterol crystals, fibrin clots, and platelet aggregates, occlude distal arteries. These emboli not only induce transient ischemic attacks (TIA) but also cause permanent cerebral infarction.
Pathological Changes of Cerebral Infarction
Brain tissue is extremely sensitive to ischemia and hypoxia. Complete arterial occlusion rapidly leads to ischemic necrosis (cerebral softening) in the corresponding perfused area. No obvious pathological changes are observed within the first 6 hours after occlusion, and neuronal damage is reversible during this window.
From 8 to 48 hours post-occlusion, significant cerebral edema develops, characterized by narrowed cerebral sulci, flattened cerebral gyri, and blurred boundaries between gray and white matter. Cerebral softening and necrosis peak at 7–14 days, accompanied by progressive tissue liquefaction. Occlusion of major arteries such as the middle cerebral artery causes extensive cerebral edema, midline shift, and even fatal cerebral herniation.
Three to four weeks after onset, necrotic tissue is gradually liquefied, phagocytosed, and absorbed. Glial hyperplasia occurs as a reparative response. Small lesions form glial scars, while large infarcts evolve into stroke cysts. The entire repair process may last several months to 1–2 years.
Clinical Diagnostic Criteria
Cerebral thrombosis predominantly affects patients aged 50–60 years with atherosclerosis, with a slight male predominance. Onset typically occurs during resting or sleeping states. Individual cases exhibit stepwise neurological deterioration over 1–2 weeks. Statistically, about 40% of patients have a prior history of transient ischemic attacks (TIA). Clinical manifestations vary significantly according to the occluded vascular territory.
1. Internal Carotid Artery Thrombosis
Symptoms are similar to middle cerebral artery occlusion, classified into four types:
Acute apoplectic type: Sudden onset of hemiplegia, hemisensory disturbance, and aphasia. Severe cases present with varying degrees of disturbance of consciousness and coma, accompanied by psychiatric symptoms and epileptic seizures.
Subacute recurrent type: Transient amaurosis fugax and crossed hemiplegia (ipsilateral visual impairment, contralateral limb weakness and numbness) with complete symptomatic remission within minutes to hours. No disturbance of consciousness, but progressive cognitive decline and agnosia may occur.
Chronic progressive type: Gradually worsening hemiplegia, hemisensory dysfunction, personality and cognitive changes, and papilledema, mimicking intracranial tumor manifestations.
Asymptomatic type: No clinical symptoms, incidentally detected via cerebral angiography or routine physical examination.
2. Middle Cerebral Artery Thrombosis
Main trunk infarction: Central facial and lingual paralysis, hemianopia, severe hemiplegia (upper limb involvement more severe than lower limb), and hemisensory disturbance. Dominant hemisphere lesions cause aphasia, accompanied by variable consciousness disorders.
Deep branch infarction: Classic triad of hemiplegia, hemianopia, and hemisensory disturbance; aphasia in dominant hemisphere injury.
Superficial branch infarction: Contralateral limb weakness and sensory deficits. Dominant hemisphere lesions induce diverse aphasias, including motor, sensory, anomic, alexic, and acalculic aphasia.
3. Anterior Cerebral Artery Thrombosis
Initial transient contralateral lower limb weakness and numbness progress to severe lower-limb-dominant hemiplegia, central facial and lingual paralysis, and cortical sensory dysfunction of the lower limbs. Pathological primitive reflexes (grasping, groping, sucking reflexes), urinary incontinence, dementia, personality changes, transient hemianopia, and dominant hemisphere aphasia may occur. Paracentral artery occlusion causes monoplegia of the lower limb; callosomarginal artery occlusion leads to lower limb monoplegia plus apraxia.
4. Posterior Cerebral Artery Thrombosis
Thalamogeniculate artery occlusion is most common, resulting in thalamic syndrome, including contralateral hemiparesis, superficial sensory disturbance, ataxia, hemianopia, spontaneous cephalalgia, and athetosis.
5. Vertebral Artery Thrombosis
Proximal unilateral vertebral artery occlusion with intact contralateral perfusion presents no obvious signs. Occlusion near the origin of the posterior inferior cerebellar artery manifests identical to posterior inferior cerebellar artery infarction. Anterior spinal artery occlusion leads to tetraplegia.
6. Basilar Artery Thrombosis
Rapid complete occlusion of the basilar artery causes acute coma, bilateral miosis, areflexia, hyperthermia, and often rapid mortality.
7. Posterior Inferior Cerebellar Artery Thrombosis
Ipsilateral facial and contralateral trunk and limb pain-temperature sensory disturbance, ipsilateral bulbar paralysis (dysphagia, soft palate palsy, hoarseness), ipsilateral cerebellar ataxia, nystagmus, and ipsilateral Horner’s syndrome (mild miosis, ptosis, enophthalmos, conjunctival congestion, and ipsilateral forehead anhidrosis).
Auxiliary Examinations
Cerebrospinal fluid (CSF) test: Generally normal. Large-area infarction may cause elevated intracranial pressure and mild increase in CSF cell count and protein levels several days after onset.
Cerebral angiography: Abrupt arterial cutoff with distal vascular non-filling, visible intravascular thrombotic defects.
Cranial ultrasound: No midline shift in the early stage; significant midline shift occurs 1–2 days post-infarction due to severe cerebral edema (accounting for 17% of cases).
Electroencephalography (EEG): Diffuse abnormal waves in the acute phase, more prominent in the lesional hemisphere.
CT scan: Low-density infarct lesions become visible 24–48 hours after onset.
MRI scan: Detects infarct lesions within the first 24 hours, showing characteristic long T1 and long T2 signals undetectable by early CT.
Scalp Acupuncture Treatment for Cerebral Thrombosis
Standardized scalp acupuncture is the core TCM rehabilitation therapy for cerebral thrombosis and ischemic stroke sequelae. Targeted cranial zone stimulation improves intracranial microcirculation, activates residual nerve function, promotes neural remodeling, and effectively repairs motor, sensory, cognitive, and language dysfunction caused by cerebral infarction.
Standard Scalp Acupuncture Zones (Unaffected Side)
1. Motor Area
Location: The upper reference point is 0.5 cm posterior to the midpoint of the anteroposterior midline (glabella to external occipital protuberance). The lower reference point is the intersection of the eyebrow-occipital line and the anterior temporal hairline. The connecting line forms the motor area: upper 1/5 for lower limb function, middle 2/5 for upper limb function, lower 2/5 for facial function.
2. Sensory Area
Location: A parallel line 1.5 cm posterior to the motor area, with identical functional zoning as the motor area.
3. Foot Motor-Sensory Area
Location: On the vertex, 1 cm posterior to the upper sensory area endpoint and 1 cm lateral to the anteroposterior midline, forming a 3 cm forward parallel line.
4. Speech Area 2
Location: Draw a line parallel to the anteroposterior midline from the parietal tubercle; extend a 3 cm vertical line downward from 2 cm posterior to the parietal tubercle along the parallel line.
5. Vasomotor Area
Location: A 3 cm parallel line anterior to the motor area.
Clinical Operation Protocol
Patients adopt a seated position. Acupuncture zones are selected based on individual symptoms:
Upper and lower limb hemiplegia and hemisensory abnormalities: Select the upper 1/5 and middle 2/5 of the motor and sensory areas.
Lingual paralysis, motor aphasia, and salivation: Add the lower 2/5 of the motor area.
Sensory aphasia: Add Speech Area 3.
Anomic aphasia: Add Speech Area 2.
Lateral limb edema: Add the vasomotor area.
After routine local disinfection, apply 30-gauge 1.5-inch filiform needles for relay needling or single-point needling in the selected zones. Perform initial twirling manipulation at 200 rotations per minute, or adopt air-injection and air-extraction manipulation. Retain needles for 60 minutes, with repeated twirling every 20 minutes. Apply gentle compression on pinholes after needle withdrawal to prevent bleeding.
Treatment is administered once daily. Ten sessions constitute one therapeutic course, with a 5-day rest interval between courses.
Clinical Comments & Prognosis
Scalp acupuncture achieves the best therapeutic efficacy for middle cerebral artery thrombosis, followed by anterior and posterior communicating artery infarction. Thalamic and cerebellar infarction yield relatively mild but definite improvement. For large-area cerebral infarction with coma, patients must first stabilize vital signs in the acute stage before receiving acupuncture rehabilitation.
Early intervention is critical. Scalp acupuncture initiated within 5 days post-onset delivers the most significant recovery outcomes. Therapeutic effect gradually declines with prolonged disease course. Sequelae lasting more than 3.5 months are treatable but require longer rehabilitation cycles. Patients with tendon stiffness on the hemiplegic side present a more refractory recovery state.
In summary, standardized scalp acupuncture is a safe and effective core rehabilitation method for cerebral thrombosis. Timely early intervention can significantly improve neurological function and reduce long-term stroke disability.