I. Mechanism of traumatic cerebral infarction: 1. Blood rheology and kinetic changes: post-traumatic cerebral edema, increased intracranial pressure, decreased cerebral perfusion pressure, slow blood flow and use of dehydrating drugs can all cause an increase in blood viscosity, activation of the coagulation system and intravascular thrombosis. Post-traumatic free radical reaction, post-traumatic cerebral vasospasm, and high cranial pressure can all cause peroxidation reactions in the lesion and surrounding tissues, and this malignant reaction produces a large amount of harmful substances such as lipid peroxide (LPO), which reduces superoxide dismutase (SOD) activity and causes vasoconstriction and coagulation, resulting in the formation of local infarct foci. This microcirculatory disorder and hemodynamic changes, which are already present after craniocerebral trauma, reach their peak 3-7 days after craniocerebral trauma. In addition, the cerebral cortex contains a large amount of factor III, which is released into the circulation during severe traumatic brain injury and activates exogenous coagulation pathways. 2. Cerebrovascular injury or compression: Trauma and its secondary injuries can lead to occlusion and/or rupture of blood vessels in the brain, and fracture fragments can also damage cerebrovascular vessels. (1) ICA and V-BA injury: direct injury to the anterior cervical triangle, head and neck hyperextension and rotation, resulting in damage to the ICA at the cervical transverse process, mandibular fracture, intraoral injury (tonsillar fossa), skull base fracture injury to the ICA of a bone segment, or brain displacement causing injury to the ICA at the dural ring (common in the elderly). Cervical fracture dislocation, posterior cranial fossa fracture, and posterior pharyngeal wall injury can lead to V-BA injury resulting in endothelial thrombosis, entrapment hematoma narrowing and occlusion of the injured artery, or thrombus spreading and dislodging proximally and distally to form distal infarction. (2) Penetrating artery injury: Due to the rapid rotation of the head causing inconsistency in the speed and direction of movement between deep structures in the brain, especially in the midline area, shear stress is generated and the blood vessel is injured. The penetrating arteries in the deep brain are far from the main stem, long and thin, with long and curved paths, terminal branches, few anastomosing branches, and large angles to the internal carotid artery branches in the anatomical path, plus the deep brain tissues are sensitive to hemodynamic changes and are easily affected by them. All these characteristics make basal ganglia infarction more likely to occur. (3) Direct compression of cerebral vessels In severe brain injury, hematoma or edema directly compresses blood vessels, resulting in high cranial pressure and even cerebral herniation, while prolonged cerebral herniation compresses blood vessels in the cerebral falx and cerebellar curtain notch, resulting in large infarction of tissue, such as the more common clinical herniation under the cerebellar curtain foramen that is embedded in the posterior cerebral artery, resulting in infarction of the occipital lobe on that side. (4) Inappropriate decompression surgery: postoperative cerebral bulge at the site of the bone window, which is stuck at the edge of the bone window and leads to occlusion of the drainage vein (mostly the superior cerebral vein). 3, cerebral vasospasm: cerebral vascular spasm occurs after traumatic brain injury, some people confirmed by DSA that the incidence of cerebral artery spasm in traumatic patients is up to 57%, and the increase of vasoactive substances in SAH after trauma causes vasospasm, resulting in ischemic changes and cerebral infarction. Children’s cerebral blood vessels are slender, the intima is not fully developed, the vegetative nervous system is not well developed, and the self-regulation function is poor, so a mild traumatic blow can cause spasm and occlusion of cerebral branch vessels, which is one of the reasons why traumatic cerebral infarction in childhood is more common than that in adults. 4. Medical factors: Patients with severe traumatic brain injury are accustomed to using larger doses of dehydrating drugs and hemostatic agents, and inappropriately limiting the amount of rehydration, resulting in patients often being in a state of high coagulation and low blood flow, which is prone to cerebral infarction. 5. Patients with poor cerebrovascular elasticity caused by their own factors such as atherosclerosis, hypertension and alcoholism are more likely to induce traumatic cerebral infarction after injury. In the case of insufficient cerebral blood supply such as pre-existing atheromatous plaque, cerebral artery stenosis or cervical spine osteophytes, large infarcts are likely to occur in severe craniocerebral trauma. The high incidence of cerebral infarction in patients with bilateral punctate calcification of the nucleus pulposus, with infarction occurring precisely at the adjacent calcification, is considered to be possibly related to the presence of some underlying lesion of the congenital metabolic or endocrine system. Clinical characteristics: Traumatic cerebral infarction mainly manifests as delayed progressive hemiparesis, aphasia, hemianopia, impaired consciousness and other neurological disabling symptoms that appear after trauma (1d~1w). There are two types of clinical manifestations. One is cerebral infarction mainly with microcirculatory disorders, the onset is mostly within 1 week, the infarct is small in scope, focal, often located in the white matter of the brain near the midline or in the basal nucleus area, infarction in the area of deep penetrating arterial blood supply, which is not easily detected by cerebral angiography, and the clinical diagnosis is mainly based on the symptoms of neurological deficit and CT and MRI examinations, with good results of timely treatment. However, if the injury is not controlled and the cerebral infarction appears after 1 week, the therapeutic effect is poor. Secondly, cortical infarction with thrombosis of the main blood supplying artery has a large infarct area and obvious displacement of midline structures on CT and MRI examination. Cerebral angiography can reveal the site of occlusion, mostly infarction of the internal carotid artery and its branch trunks, and the time of onset is related to the mechanism and degree of trauma, as well as to the smoothness of the treatment process. Cerebral infarction that occurs within 1 week after cranial trauma is mostly related to the mechanism and degree of trauma and can be called acute post-traumatic cerebral infarction. cerebral infarction that occurs after 1 week due to uncontrolled injury or other reasons can be called delayed post-traumatic cerebral infarction.