Hypertensive cerebral hemorrhage (HICH) is a disease with high morbidity, mortality (40%-50%), and disability (50%-85% of survivors). The causes of disability and death are mainly intracranial occupancy of the acute hematoma and a series of pathological changes caused by brain and vascular damage by the hemorrhage itself. The current direction of surgical treatment is to remove the hematoma as much as possible, minimize the damage to normal brain tissue, and improve the surgical outcome. Cerebral hemorrhage in the basal ganglia accounts for 70% of hypertensive cerebral hemorrhage and is usually thought to be related to the vascular pathway of the blood supplying the basal ganglia. The medial and lateral ductus arteriosus supplying the basal ganglia emanates at right angles from within 10 mm proximal to the horizontal segment of the middle cerebral artery. This anatomical relationship is thought to predispose the small arteries in this region to rupture due to pressure changes. Alternatively, microaneurysm formation in the basal ganglia region is elevated with hypertension and age. A straight incision at the midpoint of the zygomatic bone in line with the parietal node or a temporal horseshoe incision with a bone window size of approximately 5 cm × 5 cm is used, and the lateral fissure is revealed after the dura is cut intraoperatively. The following operations were performed under a microscope. The arachnoid was incised at the superior edge of the lateral fissure, and the vein was drawn toward the temporal lobe. The branches of the middle cerebral artery were visible in the lateral fissure, and they were divided toward the frontal lobe, and the insula was seen about 1.5 cm into the frontal lobe. The insula cortex was selected as an avascular area for electrocoagulation, and the hematoma in this area was exposed by retraction with an automatic cerebral pressure plate. The angle of the cerebral pressure plate and microscope was adjusted to fully remove the hematoma under direct vision, and the active bleeding point was hemostatically treated with low output power electrocoagulation. The wall of the hematoma cavity was covered with cotton sheets from superficial to deep, and after the hematoma was cleared, the cotton sheets were then removed from the inside out and electrocoagulated to completely stop the hemorrhage, and rinsed repeatedly with saline until it was clear. All patients underwent subtemporal muscle reduction suture, and drainage tubes were left in the hematoma cavity and removed after 24h. It saved surgical time and reduced surgical trauma compared with temporal flap craniotomy. In some cases of shell-nucleus-external capsule hemorrhage, the edges of the hematoma can be accessed even during dissection of the lateral fissure, and hematoma removal is performed. This approach is shorter than the transmedial temporal gyrus approach and does not damage the temporal cortex, and does not cause additional damage to the speech center and the visual tract, which is in line with the principle of minimal invasion. In addition, this approach is closer to the perforating vessels in the shell nucleus, which makes it easier to reveal and control the bleeding point. After the surgery, the temporal muscle was closed with subtotal suture, which has a good effect on reducing postoperative cerebral edema, and the patient does not need to undergo skull repair after recovery, which improves the patient’s quality of life and reduces the cost of treatment. The advantages of microsurgery for hypertensive cerebral hemorrhage are complete and thorough removal of the hematoma, precise electrocoagulation of the bleeding point, minimization of damage to the surrounding brain tissue, timely reduction of intracranial pressure, improvement of cerebral microcirculation, and release or termination of the pathological changes of brain herniation.