In recent years, the incidence of persistent vegetative state (PVS) after severe craniocerebral injury has been on the rise. Numerous studies have concluded that it has become an indisputable fact that patients with PVS are capable of awakening. To this day, people still lack a comprehensive understanding of the nature of PVS and its pathogenesis, this article only on the current domestic and international research on PVS is summarized as follows. Clinical research In the past 20 years, PVS after craniocerebral injury has received more and more attention in the international arena, and there are more and more reports about PVS. According to statistics, the incidence rate of PVS in some western countries is between 0.01%-0.03%, and about 0.168% in the U.S. PVS is different from brain death and coma, and it is a special kind of consciousness disorder. For the diagnosis of PVS, the diagnostic criteria vary in different countries. The criteria of the American Multidisciplinary PVS Study Group (1994) are as follows: ① Lack of awareness of oneself and surroundings and inability to talk to others; ② Lack of sustained, repeatable, purposeful or random behavioral responses to visual, auditory, tactile or noxious stimuli; ③ Lack of verbal comprehension and expressiveness; ④ Sleep-wake cycle; ⑤ Autonomic function of the hypothalamus and the brainstem is well maintained, and survival can be maintained through treatment and care; ⑥ Urinary and fecal defecation are not a part of PVS; and ⑥ PVS is not a part of the brain. (5) Autonomic function of the hypothalamus and brainstem is well maintained and can be maintained with treatment and care; (6) Urinary and fecal incontinence; (7) Cranial nerve reflexes (pupil, eye-head), corneal, vestibulo-ocular, and gag reflexes are preserved to varying degrees. American Congress of Rehabilitation Medicine criteria (1995): ① Automatic or stimulated eye opening; ② Inability to carry out commands; ③ Inability to speak or produce intelligible words; ④ Inability to carry out commands (activities such as shifting postures, avoidance of pain, or involuntary smiles are possible); ⑤ Lack of sustained eye-tracking activity when the eyes are propped up with the hands, with eye movements of no more than 45° in all directions. Criteria of the Emergency Medicine Society of the Chinese Medical Association (2001 Nanjing Criteria): ① Loss of cognitive function, no conscious activity, inability to carry out commands; ② Automatic opening of the eyes or eye opening under stimulation; ⑨ Sleep-wake cycle; ④ Purposeless eye-tracking activity; ⑤ Inability to understand and express language; ⑥ Maintenance of voluntary respiration and blood pressure; ⑦ Basic preservation of hypothalamus and brainstem function. At present, there is no consensus on the time standard of PVS[6],Japan believes that PVS(VS) must be more than 3 months to diagnose PVS, while the British and American countries advocate more than 1 month. Now our scholars also define the time of PVS as 1 month. According to the trauma coma database statistics, PVS within 3 months of consciousness recovery of about 33%, 3-6 months of 9%, 6-12 months only 10% of patients recovered consciousness. The causes of PVS include craniocerebral injury, acute cerebral hypoxia, cerebrovascular disease, various kinds of poisoning, encephalitis and so on. The damage can be extensive damage to the cerebral cortex and white matter, or incomplete damage to the mesencephalon, hypothalamus or reticular formation of the brainstem, with the structure and function of the medulla oblongata intact. Recently, it has been found that nerve cell damage caused by any reason, under certain conditions, new side branches can occur through the axon, establishing new synaptic axial connections, so that nerve function can be restored. Accordingly, many scholars have used surgery, drugs, hyperbaric oxygen, neurological rehabilitation and other comprehensive treatment has achieved better results. It is believed that damage to the dopaminergic pathway in the hypothalamus and prefrontal lobe is an important cause of PVS [8]. It may be due to the ischemia and hypoxia of brain tissue after trauma, tyrosine hydroxylase is inhibited, resulting in the reduction of DA synthesis. Now, foreign scholars use DA metabolic precursors and receptor agonists to treat PVS with good efficacy. 2.1 Electroencephalogram (EEG) Early Jennett et al. thought that isoelectric or electroencephalographic rest was the basic feature of EEG changes in PVS, but later studies found that most of the EEGs were extensive diffuse, polymorphic δ or θ activity. δ wave is a kind of common coma waveform changes in clinic, which is mainly due to the extensive involvement of cerebral cortex or the involvement of brainstem reticulum structure. As clinical symptoms improve, the δ or e waves of PVS may decrease accordingly, and alpha rhythms may reappear. Although the EEG of PVS lacks specificity, EEG monitoring of patients with PVS is of high value for the observation of its efficacy and prognostic assessment. About 10% of patients present with a normal EEG at a late stage, and typical epileptiform activity is rarely seen in PVS. 2.2 Evoked potentials mainly refer to brain-stem auditory evoked potentials (BAEP) and somatosensory evoked potentials (SEP), and BAEP is generally characterized by the disappearance or lack of clarity of waveforms above the V wave. SEP is the most sensitive and reliable electrophysiological index for diagnosis of PVS, which mainly shows prolongation of central transmission time of N13-N20 and decrease of N20 wave amplitude, and recovery of consciousness can be expected in the case of normal SEP waveform. 2.3 P300 (event-related potential, awareness-related potential) P300 is an important tool in the current study of PVS. It can be used as a reliable index to assess the efficacy and prognosis of PVS, and the existence of P300 means the preservation of cognitive function. maruta et al. found that P300 disappeared in PVS patients, and with the improvement of consciousness, P300 was restored. 2.4 Cerebral blood flow mapping with transcranial Doppler ultrasound (TCD) revealed that overall and local cerebral blood flow was reduced in patients with PVS. The blood flow in the anterior cerebral artery was obviously slowed down, while the blood flow in the vertebral basilar artery system was relatively intact, suggesting that the brainstem function of patients with PVS was relatively less impaired. 2.5 Cerebral metabolism is lower than normal in patients with PVS by about 1/2 to 1/3 as revealed by positron emission computed tomography (PET) scanning, which may be different depending on the location of the patient, and the uneven selective distribution of metabolism may be related to the difference in sensitivity to hypoxia in different parts of the brain tissues. 2.6 Main pathological changes ①Diffuse cortical laminar necrosis: this type of change is mostly seen in ischemic-hypoxic encephalopathy.Doughety et al.[15] reported that neocortical laminar necrosis, neuronal loss and gliosis can be seen at autopsy microscopy. In addition, the hippocampus, striatum, thalamus, and cerebellum may show similar changes. ② Diffuse axonal damage: common in acute craniocerebral injury, due to extensive cortical axonal damage interrupting the connection between the cerebral cortex and other parts of the brain. Selective thalamic necrosis. 2.7 Neuroimaging The etiology of PVS is complex, and its imaging (CT, MRA) changes vary greatly, with most presenting extensive and multiple soft foci in the cerebral hemispheres and brainstem, of which the cerebral hemispheres are mostly distributed in the frontal, temporal, parietal and basal ganglia regions. Brainstem lesions mainly involved the midbrain (80%) and pontine (20%), while the medulla oblongata was mostly unaffected. Andreas et al. reported 42 MRI manifestations of post-traumatic PVS, and all cases had diffuse axonal injury, with foci of damage in the white matter, corpus callosum, and dorsal side of the brainstem, and the frontal and temporal regions were the common sites of damage. Therefore, it is believed that diffuse axonal damage is the main form of primary brain damage in traumatic PVS. Clinical observation found that PVS patients also have extensive brain atrophy and cerebral white matter demyelination changes, hydrocephalus and other imaging manifestations. With the development of medical science, the treatment of acute phase of craniocerebral injury has made great progress, which is manifested in the significant reduction of acute mortality. The subsequent problem is the gradual increase in the number of people in “vegetative state of life”, and the disability rate of craniocerebral injury has not been reduced by the progress of treatment. The large number of patients with PVS has created a new medical and social problem. Although there are various means and methods of treatment for PVS, there is still a lack of very effective treatment. How to better enable patients to improve the various neurological functions of their injuries remains a worldwide therapeutic challenge. 3.1 Pharmacotherapy Research on neuroprotective drugs and strategies has been conducted for several years, however, it has not been possible to confirm the evidence of the exact efficacy of that one drug in the clinical treatment of PVS. There are two main categories of commonly used drugs, one is to promote cerebral circulation and cerebral metabolism, of which the more effective drugs are recognized as catecholaminergic agonists, cholinergic agonists, such as amphetamine, levodopa, bromocriptine, cytarabine and anticholinesterase drugs, and so on. The other category is to promote the recovery of nerve cell function drugs, such as monoamyl casein, cerebrolysin, nerve growth factor, ganglioside. Currently used in clinical practice, there are also some drugs to promote wakefulness, such as wakefulness, naloxone, Chinese medicine and so on. 3.2 Neurostimulation therapies are commonly used at present: ① Deep brain stimulation (deep brain stimulation, DBS) method: including thalamus electrical stimulation, brainstem mid-brain electrical stimulation, cerebellar electrical stimulation. The method is through stereotactic surgery DBS electrode implanted in the thalamus non-specific nuclei, cuneate nucleus of the reticular formation of the midbrain, cerebellum and other parts of the cerebellum, and then give continuous stimulation.Tsubokawa et al. applied DBS to treat 25 cases of PVS patients, of which 20% of the patients can take care of their own life, 28% of the patients can communicate with others verbally, but long-term bedridden. ② Cervical spinal epidural stimulation: the stimulator is surgically placed in the middle of the dura mater at the C2 and C4 levels and subcutaneously in the anterior thorax. According to a certain intensity and frequency of stimulation; Kanno et al [12] applied this method of treatment of 130 patients, 56 cases (43%) consciousness recovery, another 23 cases GCS score increased by 5 points; currently considered its total effectiveness rate of 20% -40%. Peripheral nerve stimulation: including median nerve, peroneal nerve, vagus nerve stimulation. ④ Other: there is controlled sensory stimulation, the method is to give patients different sensory stimulation (pleasant stimulation and unpleasant stimulation) under strict control, the literature reports that this method also has a certain effect. 3.3 Hyperbaric Oxygen Therapy Hyperbaric oxygen is a method that is more respected at home and abroad, which plays an obvious role in promoting the recovery of neurological function in the late stage of PVS. Hyperbaric oxygen can promote the repair and regeneration of diffuse axonal damage in PVS, and form new synaptic connections to promote the repair of damaged neurons. Hyperbaric oxygen can also activate the upward reticular activating system, accelerate wakefulness and promote the recovery of consciousness. Currently, it is believed that the earlier the time of hyperbaric oxygen treatment and the longer the course of treatment, the better the effect [18]. 3.4 Hydrocephalus treatment for patients after cranial debridement decompression surgery, during the treatment period, if the decompression window brain bulge is obvious, the clinical symptoms do not improve significantly, the imaging examination of the ventricular system is progressively enlarged, and the hydrocephalus is obvious, the cerebrospinal fluid shunt surgery is an important means of treatment for PVS. It is helpful to reduce and avoid the aggravation of brain damage due to hydrocephalus, and has a positive effect on promoting awakening. 3.5 Other gene therapy is a promising treatment. Experiments have confirmed that nerve growth factor obtained through genetic engineering can regulate the plasticity of adult mammalian central nervous system nerves and can promote the recovery of cortical function after injury. Therefore, people will pin their hopes on gene therapy. CNS stem cell transplantation is also a hot topic of research today, with the possible pathway of inducing differentiation of peripheral hematopoietic stem cells into the desired neural stem cells, which are then transplanted into the brain tissue to perform their function. Fetal brain transplantation is a relatively new technique, and animal experiments have transplanted fetal rat dopamine and noradrenergic neurons into the cerebral cortex, hippocampus, and caudate nucleus of adult rats. Whether this technique is effective in patients with PVS has not yet been determined. Undoubtedly, as the basic and clinical research on PVS continues to deepen, more and more effective treatments will be applied to the clinic. Prognosis PVS is a clinical syndrome in which the cortical function is lost due to severe damage to the cerebral hemispheres, while the brainstem function is relatively intact and survives in the subcortex. In its treatment, promoting awakening and cognitive function improvement are its goals. To date, there is no certainty of efficacy in PVS. Some authors have suggested that the following are helpful in the prognosis of PVS: ① MRI shows no hemorrhagic infarction in the basal ganglia region; ② Xenon-CT measures cerebral circulating blood flow in the cerebral hemisphere averaging more than 25 ml per 100 g of brain tissue per minute; ③ The rate of increase of cerebral circulating blood flow in the cerebral hemisphere in 100 g of brain tissue is more than 5 ml per minute for 20 min after acetazolamide treatment; ④ The median nerve somatosensory evoked potentials with significant N20 wave amplitude. Some authors also believe that the prognosis of PVS is also related to the following factors: the prognosis of young people is relatively better than that of the elderly; traumatic brain damage is better than that of hypoxic brain damage in terms of prognosis of neurostimulation the earlier the better the effect; EEG and SEP waveforms are normal in those who can be expected to recover their consciousness, and those whose SEPs are still missing one week after the injury have a poor prognosis; CT and MRI show that widespread atrophy of the cerebral cortex or a large area of hypodensity foci have a poor prognosis; lack of reaction to DBS Lack of response predicts that PVS is irreversible.