Simple brainstem injuries are not uncommon. The brainstem includes the midbrain, pons and medulla oblongata, and when external forces act on the head, whether direct or indirect violence will cause brain tissue to impinge and move, which may cause brainstem injury. Primary brainstem injury caused by violence to the head accounts for about 2-5% of craniocerebral injury, and about 10-20% of heavy craniocerebral injury, in addition to the cranial nerve nuclei, the body’s sensory and motor conduction bundles through the brainstem, there are also nodal structures and respiratory, circulatory and other vital centers. Therefore, the disability and mortality rate is high. Generally, the violence that causes primary brainstem injury is often heavy, therefore, it is rare to see the brainstem injury alone, but it exists simultaneously with brain contusion, so the injury is also more serious than the general brain contusion. If the primary brainstem damage is accompanied by intracranial hematoma, cerebral contusion cerebral edema or diffuse brain swelling to produce cerebellar curtain incision herniation, that is, in addition to the primary brainstem injury and secondary brainstem injury, such as delayed treatment, will lead to ischemic necrosis of the stem, the consequences are extremely serious. The brainstem not only contains most of the brain nuclei (except the olfactory nerve and optic nerve), but also the whole body sensory and motor conduction bundles pass through the brainstem, and the respiratory circulation center is also located here, while the brainstem reticular formation is an important structure involved in maintaining consciousness. Therefore, after brainstem injury, in addition to the manifestation of local brain nerve damage, the manifestation of consciousness disorder, motor sensory disorder is often more serious, and there can also be respiratory and circulatory failure, which is life-threatening. 1, consciousness disorder primary brainstem injury patients, often immediately after the injury occurs coma, the lighter the pain stimulus can be responsive, the heavier the coma is deep, all reflexes disappear. Coma is persistent, more time, rarely appear in the middle of wakefulness or intermediate improvement period, if any, should be thought of combined intracranial hematoma or other causes of secondary brainstem injury. 2, the pupil and eye movement changes eye activity and pupil regulation function by the motoneuron, sliding and abduction and other brain nerve management, their nuclei are located in the brainstem, brainstem injury can have corresponding changes, clinical localization significance. In the case of midbrain injury, the pupils on both sides are not equal in size at the beginning, the pupils on the injured side are dilated, the response to light disappears, and the eyes are tilted outward; in the case of injury on both sides, the pupils on both sides are dilated and the eyes are fixed. In the case of cerebral bridge injury, signs such as extreme narrowing of the two pupils, disappearance of light reflex, inward slanting of the eyes on both sides, simultaneous obliquity or separation of the eyes on both sides may appear. 3, decortical tonicity is one of the important manifestations of midbrain injury. It is because there is a center at the level of the vestibular nucleus of the midbrain that promotes the contraction of the extensor muscle, while the red nucleus of the midbrain and its surrounding reticular structures are the center that inhibits the contraction of the extensor muscle. When the two are severed from each other, decortical tonicity occurs. This is characterized by increased extensor tone, hyperextension and internal rotation of both upper extremities, hyperextension of the lower extremities, and head tilting back in an anteverted position. The injury may be paroxysmal in milder cases, or persistent in severe cases. 4, cone bundle sign is one of the important signs of brainstem injury. Including limb paralysis, increased muscle tone, tendon reflex hyperactivity and pathological reflexes appear. In the early stage of brainstem injury, due to the influence of a variety of factors, the appearance of the cone bundle signs are often not constant. However, in the case of basal injury, the signs are often more constant. If the brainstem is injured on one side, the signs are crossed paralysis, including limb paralysis, increased muscle tone, hyperactive tendon reflexes and positive pathological reflexes. In severe injury in acute shock, all reflexes may disappear, and may appear only after the condition is stabilized. 5, changes in vital signs (1) respiratory dysfunction: brainstem injury often appears immediately after the injury respiratory dysfunction. When the lower part of the midbrain and the upper part of the brain bridge respiratory regulation center is damaged, there is a disturbance of respiratory rhythm, such as Chen-Sch respiration; when the lower part of the brain bridge long inhalation center is damaged, there can be sob-like breathing; when the medulla oblongata inhalation and expiration center is damaged, respiratory arrest occurs. In the early stage of secondary brainstem damage, such as the formation of cerebellar curtain incisional herniation, respiratory rhythm disorders appear first, Chen-Sch respiration, in the late stage of brain herniation intracranial pressure continues to rise, cerebellar tonsillar herniation appears, compressing the medulla oblongata, respiration is stopped first. (2) cardiovascular dysfunction: when the medulla oblongata injury is serious, it is manifested as rapid cessation of respiration and heartbeat, and the patient dies. Higher brainstem injury when the respiratory and circulatory disorders often first have a period of excitation, when the pulse is slow and strong, blood pressure rises, breathing deep and fast or wheezing breathing, later turning into failure, pulse frequency, blood pressure drops, breathing tidal, and finally heartbeat respiratory arrest. Generally, breathing stops first, and under the condition of artificial respiration and drugs to maintain blood pressure, the heartbeat can still be maintained for several days or months, and finally, death is often due to heart failure. (3) temperature changes: brainstem injury can sometimes appear after the hyperthermia, which is mostly due to impaired sympathetic nerve function, sweating dysfunction, affecting the body heat dissipation. When the brainstem failure, the body temperature can be reduced to below normal. 6, visceral symptoms (1) upper gastrointestinal bleeding: due to acute gastric mucosal lesions caused by brainstem injury stress. (2) Intractable erratic reflux. (3) neurogenic pulmonary edema: it is due to sympathetic excitation, which causes increased resistance of body circulation and pulmonary circulation. Correspondence between brainstem reflexes and brainstem damage planes: In severe brain injury, the degree and extent of damage in the planes below the cortex to the brainstem vary, and their clinical manifestations also vary. Therefore, the performance of certain physiological or pathological reflexes can be used to determine the location of brainstem damage, which can be used to guide clinical and prognostic purposes. The brainstem is located in the center of the brain, under which is the slope, carrying the large and small brain. When external forces act on the head, the brainstem can be directly impacted on the hard slope of the bone, but also by the brain and cerebellum pull, twist, squeeze and impact injuries, among which whiplash, twisting and posterior occipital violence to the brainstem is the most damage. Usually when the frontal injury, the brainstem can be made to impact on the slope; lateral head violence to the brainstem embedded in the ipsilateral cerebellar curtain cut, posterior occipital force to the brainstem directly impact on the slope and occipital foramen; twisting and pulling movement to cause injury can make the brainstem by the role of the large and small brain injury. In the head due to sudden supine motion whiplash injury, the medulla oblongata is more likely to be damaged; the occipital bone is fractured by depression when the feet or hips are stressed, and the medulla oblongata can be directly injured; in addition, when the head is struck causing severe deformation of the skull, the intracerebrospinal fluid shock wave through the brain can also cause injury around the midbrain aqueduct or the base of the four ventricles. The pathological changes of primary brainstem injury are often contusions with focal hemorrhage and edema, mostly in the midbrain periaqueductal region, followed by the pons and medulla periaqueductal region, and secondary lesions such as hemorrhage and softening caused by pressure displacement and deformation of the brainstem causing vascular dissection. Diffuse axonal injury (DAI) is a neural axonal injury caused by shear stress when the head is subjected to accelerated rotational violence. The pathological changes are mainly located in the medial part of the brain, i.e., corpus callosum, cerebral peduncle, brainstem and superior cerebellar peduncle, and are mostly contusions, hemorrhages and edema. Microscopically, axonal fracture and axial pulp spillage can be seen. A little longer, round retraction spheres and hemocytolysis of iron-containing hemocyanin are seen. Finally, cystic degeneration and gliosis are seen. Foreign scholars have suggested that the so-called primary brainstem injury is actually part of DAI and should not be treated as an independent sign. Usually, DAI has brainstem injury manifestations and no intracranial pressure increase, so the diagnosis needs to rely on CT or MRI examination. Secondary brainstem injuries are ischemic brainstem injuries due to temporal lobe gyrus herniation and brainstem compression. Primary brainstem injury and other craniocerebral injuries often coexist, with overlapping clinical symptoms, making differential diagnosis more difficult. For patients with immediate post-injury coma and progressive exacerbation, variable pupil size, early onset of respiratory and circulatory failure, presence of decortical tonicity and positive bilateral pathological signs, the diagnosis of primary brainstem injury is basically established. Laboratory tests: lumbar puncture, cerebrospinal fluid pressure is normal or mildly elevated, mostly hemorrhagic. Other auxiliary examinations: 1, skull X-ray plain film skull fracture incidence is high, also according to the site of the fracture, combined with the mechanism of injury to presume the brainstem injury. 2, cranial CT, MRI scan primary brainstem injury is manifested as brainstem enlargement, dotted lamellar areas of increased density, interpeduncular pool, pontine pool, tetralateral pool and fourth ventricle compression or occlusion. MRI can show small foci of hemorrhage and contusions in the brainstem, which are clearer than CT because they are not affected by bony artifacts. 3.Intracranial pressure monitoring can help to identify primary or secondary brainstem injury, and there can be a significant increase in intracranial pressure in secondary cases, but not in primary cases. 4.Brainstem auditory evoked potential (BAEP) is the electrophysiological activity in the auditory pathway of the brainstem and the far-field potential transmitted to the scalp through the cerebral cortex. It reflects the electrophysiological activity is generally not disturbed by other external lesions, and can reflect the plane and degree of brainstem injury more accurately. Primary brainstem injury is often associated with cerebral contusion or intracranial hemorrhage, and the clinical symptoms are mixed, so it is difficult to distinguish which is less severe and which is more dominant, especially in patients who present late, it is more difficult to distinguish whether the damage is primary or secondary. The difference between primary brainstem injury and secondary brainstem injury is the early and late appearance of symptoms and signs. In secondary brainstem injury, the signs and symptoms develop gradually after the injury. Continuous monitoring of intracranial pressure can also differentiate: primary intracranial pressure is not high, while secondary pressure is significantly elevated. Also, CT and MRI are effective tools for differential diagnosis. MRI is significantly better than CT in demonstrating small foci of hemorrhage or contusions in the brain parenchyma, especially for subtle damage to the corpus callosum and brainstem. brainstem auditory evoked potentials can more accurately reflect the plane and extent of brainstem injury. Waves below the focal point of the auditory pathway are usually normal, while waves at and above the level of the focal point are abnormal or absent. Continuous intracranial pressure monitoring is also useful to identify primary or secondary brainstem injury. Although the clinical manifestations are the same in both cases, the intracranial pressure is normal in the primary case and significantly elevated in the secondary case.