In 2010, traffic injuries were ranked tenth in the global ranking of disability-adjusted life years (DALYs) and were the leading cause of death among adolescents, with traumatic brain injury (TBI) remaining the leading cause of death. Although the rapid pre-hospital emergency care and transport, the popularization of rapid imaging diagnosis, the improvement of intensive care treatment and the promotion of standardized diagnosis and treatment of TBI have created favorable conditions for the improvement of prognosis of TBI patients, the diversity of TBI patients and the complexity of secondary brain damage make us lack sufficient understanding of the pathophysiological mechanisms of secondary brain damage after TBI, and there is no breakthrough in the treatment modalities. As a result, there is no breakthrough in the therapeutic modalities, and the current clinical dominant Intracranial pressure (ICP)/Cerebral perfusion pressure (CPP)-targeted therapeutic regimen has not been confirmed by Class I evidence. Therefore, domestic and international literature reports that the overall morbidity and mortality rate of severe TBI is still above 30%, and neurosurgeons are still facing great pressure and challenges. Until new treatment protocols are proposed, one of the clinical research efforts should be on the prevention and reduction of complications associated with post-TBI. Among them, the incidence of post traumatic hydrocephalus (PTH) is gradually increasing in patients with heavy TBI, especially after decompressive craniectomy (DC), and has become one of the major factors affecting prognosis. However, the incidence of PTH (0.7% to 51.5%) reported in the literature varies widely due to differences in the era, ancillary diagnostic techniques, diagnostic criteria, and level of care for TBI. Therefore, it is necessary to discuss the progress and controversies of the hot issues related to the diagnosis and treatment of PTH in order to better standardize the research and clinical diagnosis and treatment of PTH. 1. Definition, naming and classification 1.1 Definition Due to the complexity of hydrocephalus, there exists a certain authoritative definition about its definition. The International Society for Hydrocephalus and Cerebrospinal Fluid Disorders (ISHCSF), after more than 2 years of discussion, reached a consensus in 2010 on the modern definition of hydrocephalus with 2 interpretations as follows: (1) (1) hydrocephalus is a condition characterized by an imbalance between cerebrospinal fluid production and absorption, resulting in the accumulation of cerebrospinal fluid in the ventricles and causing its enlargement; (2) hydrocephalus is a condition characterized by an imbalance between cerebrospinal fluid production and absorption, resulting in the accumulation of cerebrospinal fluid in the ventricles and causing its enlargement, which in some cases may also accumulate outside the brain tissue and may be accompanied/unaccompanied by enlargement of the ventricles. The former applies to the general reader, while the latter applies to those involved in research on the diagnosis and management of hydrocephalus. In the author’s opinion, the latter definition is more in line with the clinical reality of PTH. 1.2 Nomenclature Hydrocephalus is one of the common complications after TBI, while domestic colleagues are accustomed to the nomenclature of traumatic hydrocephalus (TTH). The literature retrieved by PubMed- Medline with the search term “post-traumatic hydrocephalus” was much more than that with the search term “traumatic hydrocephalus The search term “post-traumatic hydrocephalus” is much more than the search term “traumatic hydrocephalus”. In order to facilitate participation in international academic exchanges, the author suggests that it is more reasonable to unify the term as post-traumatic hydrocephalus (PTH). 1.3 Classification Different classification criteria have led to numerous naming of hydrocephalus in the literature.PTH occurs after TBI and falls under the category of secondary (or acquired). In contrast, according to the expert consensus of ISHCSF, all PTH are obstructive, and the site of obstruction can be anywhere in the interventricular foramen, third ventricle, aqueduct, fourth ventricle, spinal cord and cortical subarachnoid space, arachnoid granules and intracranial venous return, and the degree of obstruction can be partial or complete [13]. Common obstructive factors leading to PTH formation include intraventricular hemorrhage, compression by ventricular occupying lesions (including hemorrhage, edema, and cerebral infarction), arachnoid adhesions, and fibrosis of the arachnoid granules. And based on the perspective of clinical research, a clear conceptual definition is needed for the classification based on time, site, pressure, and progression of the disease process. 1.3.1 Classification based on time: The nomenclature of acute and chronic PTH is visible in both domestic and international literature on PTH, but none of them are defined exactly in time, causing confusion in summarizing studies and comparing between the literature. In 1997, Vale et al. in a study on the correlation between aneurysmal subarachnoid hemorrhage (SAH) and hydrocephalus shunt, proposed the following temporal classification criteria based on the findings that fibrosis occurs in the arachnoid membrane after SAH leading to arachnoid granular occlusion and absorption dysfunction, which takes at least 10 d: (1) acute ( This classification has been accepted in the literature of hydrocephalus after aneurysmal SAH, and TBI also often shares the presence of SAH with the former major pathogenesis, and the author also recommends colleagues to adopt the time definition criteria of this classification in order to better perform PTH accordingly. in order to better conduct corresponding studies of PTH and communication at home and abroad. 1.3.2 Classification according to pressure Usually, based on the measured pressure (often measured by lumbar puncture), PTH can be classified as high pressure or normal pressure, the former in the acute and subacute phase, and the latter in the chronic phase. In addition, low pressure hydrocephalus has been reported in the literature, but its definition, diagnostic criteria and the presence of this type in PTH need to be clinically summarized. 1.3.3 Classification according to the site of cerebrospinal fluid accumulation It can be classified as intraventricular (internal) PTH: simple enlargement of the ventricular system; (2) extraventricular (external) PTH: accumulation of cerebrospinal fluid in the subdural space, most commonly in the frontotemporal region, but also in the longitudinal fissure between the cerebral hemispheres; may be accompanied by/without enlargement of the ventricles. This type of PTH, because of its specificity in many aspects such as the mechanism of occurrence, clinical manifestations and diagnosis and treatment, is more often used as subdural hygroma or effusion for separate statistical studies at home and abroad, and it is recommended to still retain the nomenclature of this particular type. 1.3.4 Classification according to disease progression It can be classified as: (1) active (active): the patient has clinical and imaging manifestations of hydrocephalus with progressive exacerbation; (2) rested (rested): the accumulation of cerebrospinal fluid and the enlargement of the ventricles have stopped; (3) occult (occult): the ventricles are enlarged but the patient has no clinical manifestations of hydrocephalus. Active PTH requires active interventional treatment, while the latter two require only clinical observation and follow-up. There is a lack of consistent diagnostic criteria for PTH in the domestic and international literature, which are mainly based on clinical manifestations and imaging findings. (2) clinical manifestations: (1) patients with high-pressure PTH may have varying degrees of increased intracranial pressure, such as headache, vomiting, impaired consciousness, hypotony, and optic nerve papilledema; (2) patients with normal-pressure PTH may have one or more of the typical triad of cognitive dysfunction, gait instability, and urinary incontinence; (3) patients with TBI may have increased consciousness or worsened neurological status after early post-injury (postoperative) clinical status improvement, or/and gradual postoperative decompression window expansion, or patients with persistent low neurological status, which may be a manifestation of PTH The patient’s neurological status may be one of the manifestations of PTH, but the factors of infection, edema, infarction or other disorders need to be excluded. (3) Imaging manifestations: CT scan of the head is the most common diagnostic imaging method for the diagnosis of PTH, followed by MRI examination. (1) Enlargement of the ventricular system: manifested by enlargement of the frontal angle of the lateral ventricle (Evans index > 0.3) or/and temporal angle ≥ 2 mm and rounding of the third ventricle; (2) whether there is hypointense exudate manifestation around the ventricle depends on the duration of hydrocephalus, and the T2-weighted imaging on MRI is more favorable to confirm the presence or absence of exudate around the ventricle; (3) narrowing of the cerebral sulcus on the convex surface of the brain on CT or MRI. The history of TBI, one of the clinical manifestations and the progressive enlargement of the ventricular system on imaging are necessary for the diagnosis of PTH, while the other imaging manifestations are the reference conditions for the diagnosis. 3. Differential diagnosis Cerebral atrophy is a common phenomenon after TBI, which can have clinical manifestations similar to PTH and compensatory enlargement of the ventricular system, and needs to be differentiated from PTH. Cerebral atrophy is commonly seen after diffuse axonal injury, with the typical imaging presentation of enlargement of the ventricular system accompanied by widening of the sulcus and absence of periventricular exudative hypodensity tables. Temporally PTH occurs mostly within 3 months after injury, whereas cortical atrophic ventricular enlargement occurs mostly after 6 months or more after injury. Cerebrospinal fluid drainage testing: helps to differentiate PTH from simple compensatory ventricular enlargement and also helps to screen for normal pressure hydrocephalus as a candidate for shunt surgery. Mazzini et al. concluded that single-photon emission computed tomography (SPECT) is helpful in differentiating between cerebral atrophy and hydrocephalus. Patients with hydrocephalus showed significant temporal lobe hypoperfusion (p < 0.01) and frontal lobe hypoperfusion (p < 0.04) on SPECT, while parietal, occipital, thalamus and brainstem showed no hypoperfusion; this performance did not differ between the left and right cerebral hemispheres. However, the manifestation of hypoperfusion on SPECT in those with cortical atrophy was diffuse (p < 0.001) and not limited to the temporal lobe. Subdural effusions need to be differentiated from chronic subdural hematomas that also appear hypointense on CT, which are hyposignal on T1-weighted and high-signal on T2-weighted MRI, while the latter are high-signal on both T1- and T2-weighted. 4. Treatment strategy and some related issues 4.1 Treatment strategy Follow-up observation should be preferred for patients with unremarkable clinical manifestations, because hydrocephalus can be shown to be quiescent in some patients over time, and hydrocephalus remission has also been reported after cranial repair. In contrast, for patients with typical signs on imaging, those with clinical worsening of impaired consciousness or neurological status once improved and then worsened and those with gradual worsening of the expansion outside the decompression window, interventional treatment should be given promptly: (1) temporary: (1) pharmacotherapy: such as drugs to reduce cerebrospinal fluid secretion and diuretic dehydrating agents to lower intracranial pressure, as well as intermittent lumbar puncture and controlled lumbar pool drainage; (2) surgical treatment: commonly used are extraventricular drainage The procedure is usually a temporary treatment measure to relieve intracranial hypertension, drainage of bloody cerebrospinal fluid and control intracranial infection. Extracranial ventricular drainage is the most commonly used procedure and is usually performed by puncturing the anterior ventricular horn (preferred on the right) and, for posterior cranial fossa surgery, the occipital horn. The duration of drainage, usually about 1 week, can be changed to a different side and re-drained if the condition requires it. If a longer period of cerebrospinal fluid drainage is required, subcutaneous indwelling Ommaya capsules and subcapsular tendon shunts can be chosen; (2) permanent: (1) cerebrospinal fluid body cavity shunt: so far it is still the main modality of PTH treatment, of which ventriculo-abdominal shunt still accounts for the majority; lumbar pool-abdominal shunt has a tendency to increase in recent years but the efficacy needs more case summaries; ventriculo-atrial shunt Although gradually decreasing, it is still an irreplaceable option for those who have a history of abdominal surgery or abdominal infection after shunt and are not suitable for the first two shunts; ② Intracranial diversion of cerebrospinal fluid: endoscopic third-ventriculostomy (ETV) is the most commonly used, followed by endplate fistulostomy, midbrain catheterization and hyaline septal fistulostomy. The second most common treatment is endoscopic third-ventriculostomy (ETV). 4.2.1 Cerebrospinal fluid body cavity shunts 4.2.1.1 Ventricular puncture site and lateralization There is still a lack of consistency in deciding whether to puncture the frontal or occipital horn for ventriculo-ventricular shunts and ventriculo-atrial shunts, depending on the patient's specific condition and the physician's customary experience. In contrast, most authors believe that avoidance of the choroid plexus by the ventricular end of the shunt helps to reduce the risk of bleeding and occlusion. yamada et al. reported that for frontal horn puncture, the ventricular end of the shunt in the anterior horn of the lateral ventricle above the interventricular foramen was the optimal location with the lowest incidence of adhesions and occlusion. 4.2.1.2 Management of ventriculoperitoneal shunts Intraperitoneal shunts have been reported using laparoscopic surgery with the ventral end of the shunt fixed to the diaphragmatic surface of the liver or to the hepatic round ligament. In contrast, Liang Yumin et al. reported that in ventriculo-abdominal shunts, after the ventral end of the shunt was placed into the abdominal cavity through a small abdominal incision, the shunt could be lowered into the pelvic cavity overwhelmingly by intestinal peristalsis in 1 d postoperatively. This method, which does not require special fixation, tends to be used more and more in clinical practice. 4.2.1.3 Selection of shunts Currently, it is considered that adjustable pressure shunts are the first choice for hydrocephalus shunts, and the set pressure of the shunt pump can be adjusted according to the clinical and imaging follow-up results after surgery to reduce the complications of excessive or insufficient shunts after surgery. There is a lack of credible clinical findings on whether to choose antimicrobial shunts and anti-siphon devices. 4.2.1.4 Principles of management of subdural effusions Aaraba et al [27] reported that most subdural effusions after DC resolved spontaneously at about 17 weeks postoperatively, with only 10% of patients requiring surgical intervention. In those with extracerebral fluid with ventricular enlargement, Tzeratis et al. reported that the use of ventriculo-peritoneal shunt could resolve both intra- and extracerebral fluid. However, craniotomy is required for subdural effusions combined with pericardial formation. Borehole drainage and subdural-ventricular shunt treatment are also available; early cranial repair may help in the elimination of subdural fluid. 4.2.1.5 The gradual improvement of ETV equipment and experience has led to a new field of neuroendoscopically assisted treatment of hydrocephalus with promising results, and ETV is recognized as the treatment of choice for those with clear obstructive factors in the ventricular system, and endoscopic treatment is a reliable treatment option for those with failed shunts and intraventricular compartments, but there is uncertainty about its effectiveness in those without obstructive factors in the ventricular system. In a prospective, controlled, open-blind study comparing the efficacy of ETV and ventriculo-peritoneal shunts in the treatment of idiopathic normal pressure hydrocephalus, Pinto et al. showed that neurological recovery was significantly better in the shunt group than in the ETV group 1 year after surgery (p < 0.05). While Bonis et al. analyzed 14 cases of ETV for PTH reported in the literature between 2002 and 2011, the results showed that 93% of the patients improved and no related surgical complications occurred, and this scholar concluded that PTH is not a contraindication to ETV. It is evident that future exploratory studies are needed to obtain high-level research evidence whether PTH is suitable for ETV treatment. 5. Specifications and outlook To date, in addition to the controversies that exist in the foregoing, there are many issues that need to be clarified in the diagnosis and treatment of PTH, such as the mechanisms of occurrence, risk factors, timing and methods of efficacy assessment, and prevention and treatment of complications. SAH, which seems to be directly correlated with the occurrence of PTH, has been reported by different authors with distinctly different results of correlation and non-correlation, even in studies of hydrocephalus after aneurysmal SAH. And some studies found that the dural venous sinuses, lymphatic system, nerve root sleeves and capillaries within the brain tissue, all have cerebrospinal fluid reabsorption. And if the basis for the occurrence of hydrocephalus after infection and hemorrhage is impaired cerebrospinal fluid absorption due to adhesions to the arachnoid granules at the skull base and cerebral convexity, how can the effectiveness of this procedure be explained mechanistically after ETV in infected/hemorrhagic (those without intraventricular systemic obstruction) normal pressure hydrocephalus [37]? This illustrates the complexity and diversity of the pathophysiological mechanisms of hydrocephalus occurrence, which have so far limited our understanding. In addition to this, the literature on PTH is overwhelmingly retrospective case summaries, and there is a lack of convincing literature with high-level evidence. The domestic counterparts do not pay enough attention to this disease, considering PTH as a common disorder in TBI and lacking technical content in diagnosis and treatment, while a large number of patients are disposed of in primary care hospitals, and even in neurosurgery centers of tertiary care hospitals, most of the basic training is handled by relatively junior physicians, and there is a lack of standardized expert consensus and guidelines for diagnosis and treatment as reference, so the diagnosis and treatment are very different and fancy Even within the same unit, there is a lack of consistency in diagnostic and efficacy assessment methods, and a lack of long-term follow-up studies, making it impossible to conduct statistically valid comparative studies. Therefore, it is necessary to develop quality control standards for the diagnosis and treatment of PTH and to standardize operational procedures and objective criteria for assessing prognosis in order to conduct more rigorous basic and clinical research on PTH to reduce complications, improve outcomes, and avoid overmedication. The editorial board of the Chinese Journal of Neurosurgery has organized some domestic experts to initiate the work of expert consensus on the standardized diagnosis and treatment of hydrocephalus, which is expected to be published as soon as possible, and it is also imperative to promote and popularize the standardized diagnosis and treatment of PTH based on the summary of previous clinical studies. On the basis of this, a multicenter study to obtain a high-level diagnosis and treatment basis is also the direction of future clinical research efforts.