Chiari I malformation (CMⅠ) is a congenital craniocervical junction malformation characterized by herniation of the cerebellar tonsils into the foramen magnum with or without spinal cavity. It is believed that the cerebellar tonsils herniate into the spinal canal due to the overcrowding of the posterior cranial fossa due to the delayed development of the occipital bone during the embryonic period and the narrow posterior cranial fossa with normal cerebellar development. It is characterized by insidious onset, progressive aggravation, and mostly associated with spinal cord cavitation, and symptoms often appear in adulthood. Guo Yongchuan, Department of Neurosurgery, China-Japan Friendship Hospital, Jilin University Main symptoms and clinical signs include head or neck and shoulder pain, loss of sensation in the limbs, sensory hypersensitivity, decreased muscle strength, muscle atrophy in the limbs, posterior group cranial nerve dysfunction (symptoms such as swallowing and choking, hoarseness, etc.), dysfunction in both bowels, Honer’s sign (excessive sweating in half of the limbs), intermittent dyspnea, combined scoliosis deformity, etc. MRI of the head and neck is the key to the diagnosis of this disease, which can accurately evaluate the level of submicrocephalic herniation, subarachnoid changes in the occipitocervical region, the presence of combined hydrocephalus, atlanto-occipital fusion, spinal cord cavity, and can exclude malformations such as dentate dislocation. We found that abnormal bone structure is only one aspect of Chiari malformation, and thickened atlanto-occipital fascia forming fasciculations and thickened arachnoid adhesions blocking the median foramen are also the pathological norm, although these changes may also be secondary to long-term bony compression. Surgery is the treatment of choice for Chiari malformation. Currently, the posterior median incision is mostly used, reaching 2 cm above the external occipital ramus and 2 cm below the level of the 6th-7th cervical vertebrae, with cranial resection up to the transverse sinus and laterally to the ethmoid sinus and 2 cm to the posterior arch of the atlantoaxial spine. some hospitals do this to the end. Some continue to cut through the thickened circumoccipital fascia or continue to cut through the dura to expand the repair. We believe that this procedure is very damaging and does not resolve the spinal cord cavity or hydrocephalus caused by the thickened arachnoid adhesions blocking the median foramen due to the abnormal bone structure and thickened atlanto-occipital fascia of Chiari malformation. We used a small 3-4 cm incision at the circumoccipital junction to occlude the posterior border of the foramen magnum and the posterior arch of the atlantoaxial spine, and occluded the occipital scales at the superior border of the foramen magnum up to the inferior collar line to form a bone window of no more than 4 cm in longitudinal direction and about 1.5 cm in transverse diameter for bony decompression. After that, the thickened circumoccipital fascia in the occipital neck was incised and the dura was cut, and the adhesions between the two tonsils were separated under the microscope, and the lower herniated cerebellar tonsils were crumpled by bipolar electrocoagulation or the lower herniated cerebellar tonsils were excised under the soft meninges to release the compression of the cerebellar tonsils on the medulla oblongata and the latch of the central canal. Afterwards, the median foramen of the fourth ventricle was explored to ensure the patency of the fourth ventricular outflow tract and to facilitate the formation of traffic between the fourth ventricle and the medulla oblongata pool. Postoperatively, the patient is usually immobilized in a cervical brace for 2 weeks. The patient’s pain symptoms improved significantly half a month after surgery, and the improvement in motor function was more pronounced than the improvement in sensory function. The surgery should achieve three goals: 1) decompression of the inferior surface of the cerebellum, 2) expansion of the volume of the posterior cranial recess, and 3) reconstruction of cerebrospinal fluid circulation. These goals are independent of each other, and posterior cranial recess volume expansion is only one aspect of the surgical goal; volume expansion does not mean adequate cerebellar decompression or cerebrospinal fluid circulation is reestablished. In our surgical approach, the posterior cranial recess decompression is generally controlled within 2 cm above the foramen magnum, while the lower herniated portion of the cerebellar tonsils is reduced by submural resection or bipolar weak electrocoagulation, and the median foramen is explored and the choroid plexus of the four ventricles is observed. This series of steps is of great importance to ensure normal cerebrospinal fluid outflow, reconstruct cerebrospinal fluid circulation, achieve good surgical results, and reduce symptoms. Completely relieving the compression factors in the greater occipital foramen area and restoring the unobstructed CSF circulation here are the only indicators of whether the decompression is complete, while blindly pursuing a wide range of decompression is undesirable.