Large cerebral infarcts mostly lead to cerebellar curtain herniation, which has a high mortality rate with conservative treatment, and timely decompression with debridement can often save the patient’s life. Large-scale cerebral infarction is mostly a large hemispheric infarction caused by complete occlusion of the internal carotid artery or middle cerebral artery, often accompanied by infarction of the posterior cerebral artery. Hypertensive atherosclerosis leads to thrombosis of the internal carotid artery or middle cerebral artery, complete occlusion of the internal carotid artery or middle cerebral artery after aneurysm surgery, complete occlusion of the internal carotid artery complicated by saddle area tumor resection, complete occlusion of the common carotid artery or internal carotid artery due to local hematoma compression from cervical trauma, or complete occlusion of the internal carotid artery or middle cerebral artery due to dislodged emboli. Occlusion of the middle cerebral artery or internal carotid artery can produce cerebral edema with obvious occupying effect. Although dehydration treatment has certain effect, some patients die from cerebellar curtain notch herniation, and surgery can significantly reduce the mortality rate. If patients with brain herniation can receive timely and appropriate surgical treatment, most patients’ lives can still be saved. Therefore, in case of large cerebral infarction with ipsilateral pupillary dilatation, immediate surgical treatment should be performed to relieve the life-threatening effects of cerebral herniation. CT is often the first choice for large cerebral infarction, and MRI diffusion examination can be done when available, which can detect cerebral ischemic changes at an early stage. After the formation of cerebral herniation in cerebral infarction, decompression surgery should be performed immediately to rapidly relieve intracranial hypertension and relieve the threat of cerebral herniation to life. After surgery, the pupil can be narrowed quickly, and the patient can be responsive to light, and the patient can recover consciousness completely in a short period of time. If intraoperative cerebral bulge occurs, a wide range of resection of relatively non-functional areas such as frontal pole and temporal base can be effectively performed without affecting the circulation in the infarcted area and without pulling the brain tissue, which provides conditions for the patient to recover neurological function. The removal of the large bone flap effectively reduces the intracranial pressure, relieves the brainstem from pressure, restores the blood circulation of the brain tissue in the normal blood supply area, and facilitates the establishment of collateral circulation, which promotes the recovery of neurological function. Surgical methods: 1. Frontotemporal parietal infarction The operation is performed under general anesthesia, with the patient’s side facing upward, and the operation is performed with large bone flap craniotomy. The frontotemporal parietal horseshoe-shaped or inverted question mark-shaped incision is located in the hairline near the midline, posteriorly reaching the parietal nodes and extending downward to the middle cranial fossa, the scalp is cut along the posterior edge of the superficial temporal artery, preserving the main trunk and anterior and posterior branches of the superficial temporal artery, cutting the temporal muscle, separating the temporal muscle retrograde, protecting the periosteum under the temporal muscle as much as possible, together with the flap-temporal muscle is turned downward, the bone flap is removed and the temporal bone is occluded to reach the middle cranial fossa, forming a bone flap of 12-15 cm The dura was suspended at the edge of the bone window to prevent epidural hematoma, and the dura was cut radially to see the outwardly expanded ischemic edema of the brain tissue, and the arachnoid was torn several times along the edge of the cerebral sulcus or blood vessels on the brain surface. After surgery, the pupil generally returned to normal soon, and CT showed that the cricoid pool and tetraspanic pool were clear, and the brainstem pressure was normalized, and the midline was not displaced. It has been well established that in cases where simple decompression by debridement can save life, the removal of the patient’s brain tissue should be avoided, besides, intraoperative removal of brain tissue may result in different degrees of functional deficits after surgery. When cranial closure is not possible after brain expansion or when brain tissue rises and spills, internal decompression is feasible. The temporalis muscle is attached to the ischemic brain tissue, and the scalp is sutured in full layers. 2.Temporoparietal-occipital infarction The operation is performed under general anesthesia in lateral position with the diseased side facing upward, and a large bone flap craniotomy is used. The temporoparietal-occipital craniotomy was performed, the anterior lower part was located at the upper edge of the zygomatic arch within the temporal hairline, upward along the frontoparietal junction 3cm from the sagittal suture, curved to the parieto-occipital, downward to 2cm from each of the transverse and sagittal sinuses, forming a bone flap of 12-15cm. the rest was the same as the frontotemporoparietal infarction craniotomy. For postoperative treatment, 125 ml of mannitol was alternated with 40 mg of tachyphylaxis or 250 ml of glycerol fructose, which can effectively lower the intracranial pressure and avoid the damage of renal function by large doses of mannitol. Glycerol fructose has a good dehydration effect on the edema of brainstem. Close attention to the observation of vital signs, early tracheotomy for patients in deep coma within 3 days after surgery, and early rehabilitation treatment such as hyperbaric oxygen and functional training during the postoperative recovery period can effectively improve the prognosis and enhance the quality of life. Patients with cerebral herniation in cerebral infarction lose blood due to surgery as well as high-dose application of dehydrating agents to reduce the degree of cerebral herniation and reset the cerebral herniation, meanwhile, they are prone to hypovolemia and electrolyte balance disorder, appearing symptoms of hypovolemia such as fine and rapid pulse, wet and cold extremities, unstable or decreasing blood pressure, which are often mistakenly thought to be caused by brainstem failure in the late stage of cerebral herniation, and considering the above factors, correct diagnosis and treatment can reduce mortality.