Brain herniation is a late complication of increased intracranial pressure and is one of the leading causes of death in neurosurgical patients. As intracranial pressure continues to increase, its autoregulatory mechanisms fail to compensate and some brain tissue is displaced from higher to lower pressures, herniating through normal physiologic orifices and compressing the brainstem and adjacent vital vessels and nerves, resulting in unique clinical manifestations and life-threatening conditions. Once a child develops brain herniation, if not treated in a timely manner, the child will soon die due to respiratory and circulatory failure. The neurosurgery department of our hospital has successfully rescued many children with brain herniation through timely treatment. The key point of brain herniation is the timely detection of pre-herniation symptoms and effective treatment. First of all, let us understand the common clinical manifestations of various types of brain herniation patients. （Symptoms of increased intracranial pressure: severe headache and frequent vomiting, which are more intense than before brain herniation, and irritability. 2. Disorders of consciousness: The early manifestation of the child is blurred consciousness and delirium, etc. When brain herniation is formed, the child is mostly in coma, and almost all of them fall into deep coma when the condition is further aggravated. Therefore, the sudden onset of impaired consciousness should be regarded as a danger signal. The more sudden it occurs, the greater the possibility of brain herniation, and the deeper the coma, the worse the prognosis. It is also important to mention that in cases with a slower progression of the disease, it is often observed that the altered consciousness occurs earlier in the case of foramen magnum herniation and vice versa in the case of foramen occipitalis herniation, because the part of the reticular formation associated with consciousness is located in the midbrain. In individual cases of foramen occipitalis herniation, the consciousness remains normal until the child has stopped breathing. Pupillary changes: First, the pupil on the side of the herniated brain is slightly dilated (usually for a short time and easily ignored); then it is gradually dilated and the light response is diminished; finally, all the pupils are herniated and the direct and indirect light responses disappear before or after the pupil on the side of the herniated brain is completely herniated. If the condition continues to deteriorate, the contralateral pupil will also change according to a uniform pattern, but the process is generally faster than that of the brain herniated side, which is caused by the malfunction of the nucleus accumbens in the brainstem due to compression. In addition, the herniated side may also have ptosis and exophthalmos. When herniation of the foramen magnum occurs, there is no direct impact on the oculogyric nerve, so the symptoms of oculogyric nerve compression do not occur. At this time, the pupil changes: initially it is often symmetrically narrowed, then dilated, and the light reflex is also weakened and disappears. This is a consequence of acute hypoxia of the brainstem that affects the nucleus accumbens, similar to that seen in simple asphyxia. 4. Motor disorders: Most of them occur on the opposite side of the dilated pupil and are characterized by reduced or absent voluntary movement of the limbs. The continued development of brain herniation causes the symptoms to spread bilaterally, resulting in decreased muscle strength of the limbs or intermittent head and neck tilting back, straightening of the limbs and dorsal hyperextension of the trunk in the form of coracocephaly, which is called decerebrate ankylosis and is a characteristic manifestation of severe brainstem damage. 5.Disorder of vital signs: It shows the change of blood pressure, pulse, respiration and body temperature. In the early stage, the cerebral blood circulation is impaired due to the elevated intracranial pressure, causing acute hypoxia in brain tissue, and compensatory respiration deepens and increases, blood pressure rises and pulse rate accelerates. With the aggravation of brain herniation, blood pressure further increases and slow pulse (Cushing’s reaction) appears. Finally, the respiration stops, and finally the blood pressure drops and the heart stops and death occurs. (b) Herniation of the foramen magnum The herniation of the foramen magnum has no definite lateral signs, but mostly presents with clinical manifestations due to compression and pulling of the medulla oblongata and cervical nerve roots. The child often presents with severe headache, recurrent vomiting, disturbances in vital signs (slowed respiration and heart rate, increased blood pressure) and cervical tonicity, with late onset of consciousness, no pupillary changes and early onset of respiratory arrest. It is important to emphasize that in some cases where the intracranial pressure increases slowly, the tonsils have fallen deeply into the vertebral canal, but the symptoms of brain herniation do not appear, but when this is combined with a trigger, such as coughing, struggling, forcibly flexing the neck or lumbar puncture to release the cerebrospinal fluid, the tonsils can become more tightly embedded in the posterior border of the foramen magnum, leading to sudden increase in brain herniation, resulting in sudden respiratory arrest, followed by cardiac arrest and death. The brain herniation may cause sudden aggravation of brain herniation, resulting in sudden respiratory arrest, followed by cardiac arrest and death, etc. (iii) Subfalx herniation An occupying lesion of one side of the cerebral hemisphere can push the cingulate gyrus of the medial side of the cerebral hemisphere and the adjacent frontal gyrus, ventricular septum and lateral ventricle to the opposite side via the lower part of the free edge of the cerebral falx. Subfalcine herniation of the brain is not a serious injury due to direct compression or nudging of the brainstem, and children rarely have clinical signs of impaired consciousness. Brain herniation is caused by acute increase of intracranial pressure. While making the diagnosis of brain herniation, rapid sedation of dehydrating agent to reduce intracranial pressure and oxygen should be performed according to the principles of management of increased intracranial pressure to relieve the condition and buy time. Then the necessary diagnostic tests should be performed to clarify the nature and location of the lesion. When the diagnosis is confirmed, the preoperative preparation for craniotomy should be completed quickly according to the condition, and the cause of the disease should be removed by surgery as soon as possible, such as removal of intracranial hematoma or brain tumor. If it is difficult to confirm the diagnosis or if the cause cannot be removed despite the diagnosis, the following palliative surgery can be used to reduce intracranial hypertension and salvage brain herniation. 1.Lateral ventricular extracorporeal drainage: Through the tremor, orbit, occipital rapid skull drilling or cone skull, puncture the lateral ventricle and place silicone drainage tube to drain the cerebrospinal fluid extracorporeally, in order to rapidly reduce intracranial pressure and relieve the condition. It is especially suitable for patients with severe hydrocephalus, which is one of the auxiliary resuscitation measures commonly used before cranial surgery. 2, cerebrospinal fluid shunt: cases of hydrocephalus can be performed lateral ventricular – ventral shunt. Lateral ventricular-atrial shunt is now less commonly used. If the catheter is obstructed or narrowed, pool shunt or catheter sparing surgery. Lateral ventricle-occipital pool shunt or conduit sparing can be used. 3, decompression surgery: the cerebellar curtain incision herniation can be used sub-temporal muscle decompression surgery; occipital foramen magnum herniation can be used suboccipital muscle decompression surgery. Severe craniocerebral injury resulting in severe cerebral edema and increased intracranial pressure, can be used to decompress the bone flap. The above methods are called external decompression. During craniotomy, swelling and bulging of brain tissue may be encountered, and part of the non-functional brain lobes can be removed to achieve decompression, which is called internal decompression.