Cerebral infarction caused by head trauma is called traumatic cerebral infarction. The disease is mostly seen in adolescents, all of whom have a history of head trauma, and the neurological localization signs mostly appear within 24 hours after the injury. Cerebral angiography, CT or MRI can help to confirm the diagnosis. I. Pathogenesis: It is related to arterial intima injury and vasospasm. During head trauma, the sudden extension and flexion of the head and neck causes the pulling of the blood vessels in the neck, resulting in contusion of the vessel wall or damage to the intima, which directly forms traumatic thrombosis on the one hand; on the other hand, it can reflexively cause vasospasm. Vascular spasm itself provides the possibility for thrombosis. Because of vascular injury, spasm, or thrombosis producing ischemic changes, the injured vessel wall can be the site of delayed thrombus formation. The thrombus enlarges or the thrombus dislodges and embolizes the basilar artery or the posterior cerebral artery, thus causing cerebral infarction. Alternatively, traumatic cerebral infarction may be associated with the formation of a coarctation aneurysm. Between the inner and middle layers of the cerebral vessels, the blood flow impingement effect after traumatic damage leads to progressive separation of the inner membrane from the middle layer, and the formation of intercalated aneurysm, progressive narrowing of the lumen of the vessel, which eventually leads to occlusion of the vessel. As for pediatric patients, due to the incomplete development of brain and vegetative nerves, coupled with the physiological anatomical characteristics of blood vessels such as slender, and poor self-regulation ability, a slight traumatic blow can cause cerebral infarction due to occlusion of deep penetrating intracranial branches and branches. CT and MRI are of definite value for definite diagnosis, estimation of lesion degree and prognosis. Magnetic resonance spectroscopy analysis found that the brain tissue in the injured area is ischemic at 3h after cranial injury, and reaches a peak at 24h after injury. Treatment should emphasize early and effective measures, and the treatment of this disease is basically the same as that of ischemic cerebrovascular disease, improving cerebral microcirculation, correcting cerebral ischemia, and reducing secondary brain damage. Cerebral protective drugs should be used in combination to target ischemia-induced cell damage, including anti-free radical therapy; application of neurotrophic drugs, such as neurotrophic factor and cerebrofacial; prevention of intracellular calcium ion overload and early application of calcium ion antagonists.