Hydrocephalus and arachnoid cyst are common clinical conditions, and there are controversies regarding the indications and the best surgical approach for hydrocephalus and arachnoid cysts. In recent years, although neuroendoscopic triple ventriculostomy and arachnoid cyst fistula have been widely used in clinical practice, lateral ventriculoperitoneal shunt and arachnoid cyst ventral shunt are widely used in clinical practice because of their simple operation, small trauma, and precise clinical results, but they have many complications. In this article, we will discuss the signs and symptoms of shunt dependence, which is a long-term complication of hydrocephalus and arachnoid cyst abdominal shunt. The first reports of shunt dependency (SD) appeared in the late 1980s, and so far there are few reports at home and abroad. The shunt dependency syndrome mainly presents with acute severe headache, nausea, vomiting and optic papilloedema and other cranial hypertension. The lumbar puncture pressure often exceeds 300 mmH2O, and the individual pressure even exceeds 600 mmH2O. cranial CT examination often indicates that the ventricles are normal or slightly less than normal, lacking characteristic changes, which is often ignored by the clinic and delays the diagnosis and treatment of the disease. On imaging, in the case of arachnoid cyst shunt, the cyst can be seen to shrink significantly, and in some cases, the ventricular end of the shunt can be seen to recede into the brain parenchyma. Other examinations can reveal shunt fracture, shunt obstruction, and shunt detachment. The root cause of SD is a malfunctioning drainage device that leads to poor cerebrospinal fluid shunting, and the key to treatment is to reconstruct the cerebrospinal fluid circulation pathway and relieve cranial hypertension. The key to treatment is to re-establish the cerebrospinal fluid circulation pathway and relieve cranial hypertension. Measures to re-establish the cerebrospinal fluid drainage pathway include removing the shunt obstruction, re-performing cystic ventral shunt, lateral ventricular ventral shunt, and lumbar pool ventral shunt. The choice of surgical approach should be based on the size of the patient’s lateral ventricle and cyst cavity and the operator’s experience. After surgery, all patients’ clinical symptoms can be improved, and symptoms of cranial hypertension such as headache, nausea, vomiting and optic papilloedema disappear. Mechanisms of shunt dependence There are common complications of hydrocephalus and arachnoid cyst ventral shunt such as infection, shunt obstruction and intracranial hemorrhage in the near term, and rare complications such as shunt displacement, rupture, lacunar brain syndrome and shunt dependence in the long term. Post-shunt shunt obstruction is a common complication, with an incidence of 14%-58% reported in the literature, and SD is only one of its specific types, which shows normal or shrunken ventricles on imaging and is associated with decreased compliance of the ventricular wall and brain tissue after long-term cerebrospinal fluid ventral shunts. At the same time, because of the decreased compliance of the ventricular wall, when the shunt loses its shunt function, the ventricular system can be greatly reduced, and according to the volume/pressure relationship, a small increase in cerebrospinal fluid can cause a sharp increase in intracranial pressure, which is clinically manifested as headache, nausea, vomiting and other symptoms of intracranial hypertension. The literature reports that the interval from the first shunt to the appearance of SD is 0.6-10 years. In the clinical observation that we had done in our hospital, the interval from the first shunt to the appearance of SD was 4-12 years, with an average of 6.3 years. At present, regarding the mechanism of SD, we believe that SD after cyst or ventriculoperitoneal shunt is triggered by the combined effect of disuse decreases in cerebrospinal fluid absorption and decreased compliance of the ventricular wall due to prolonged low cranial pressure after the loss of shunt function. When the shunt is obstructed or removed, the decompensated cerebrospinal fluid absorption cannot be compensated and the sudden discontinuation of drainage can lead to obstruction of cerebrospinal fluid drainage and rapid onset of cranial hypertension due to decreased compliance of the ventricular wall with prolonged hypocranial pressure. On imaging, the ventricles are normal or shrunken, and the optic papillae may not appear edematous within a short period of intracranial hypertension. SVS is due to excessive shunting, although the latter is also a complication of ventriculoperitoneal shunts or cystic ventriculoperitoneal shunts that occur several years after surgery (mean 4.5-6.5 years) and often in pediatric patients, but SVS SVS is mainly due to intermittent obstruction at the ventricular end of the shunt, so it is clinically manifested as intermittent cranial hypertension rather than progressive cranial hypertension, and the onset is relatively slow and often self-limiting. In addition, the slow filling phenomenon after shunt pump pressure and the imaging manifestation of lacunar ventricles are its characteristic manifestations. In contrast, the mechanism of SD is mainly acute onset after loss of shunt function, with a continuous progressive increase in intracranial pressure, often exceeding 300 mmH2O on lumbar puncture, or even 600 mmH2O in some cases, and imaging data showing normal size of the lateral ventricles, which are individually smaller but not reduced to a lacunar pattern, with a clear view of the cricoid pool. Therefore, SD has its own characteristics that are not completely consistent with SVS, and can be differentiated by careful history taking combined with physical signs and imaging. The strategy of management is to limit the shunt in SVS and to reconstruct the shunt in SD. How to prevent the occurrence of SD The literature reports that in the early stage of SD, the prognosis is good if treated promptly. If optic nerve impairment has already occurred, it is difficult to restore the function of the optic nerve even if the intracranial hypertension is lifted. We believe that the key is to improve the understanding of SD, because of the lack of characteristic clinical and imaging manifestations. For patients after bypass surgery, clinical symptoms of cranial hypertension such as unexplained headache, nausea, vomiting and optic papilledema, even if imaging suggests normal ventricles, it is still necessary to lumbar puncture to understand intracranial pressure, exclude SD, and play a very critical role in early diagnosis and treatment. How to take effective methods to prevent the occurrence of SD is the direction of unremitting research by neurosurgeons. It is believed that after arachnoid cyst abdominal shunt, once the cyst disappears, the shunt should be removed in time can prevent SD and the appearance of cranial hypertension symptoms. According to the mechanism of SD and summarizing the relevant literature, we believe that the following measures may be beneficial to reduce the probability of SD: first: adopt appropriate shunt pressure to avoid too rapid and excessive drainage, maintain appropriate intracranial pressure, and avoid disuse decompensation of cerebrospinal fluid absorption. The use of anti-siphon adjustable shunts may help to solve this dilemma. Second: Minimize the probability of shunt obstruction. The literature reports that most patients with SD are children at the time of their first shunt. Children are growing and the rapid growth of their bodies may lead to shunt dislocation and fracture. The main reason is still that the subcutaneous location of the shunt is too shallow, the shunt neck is aging and fixed, the ventral end of the shunt cannot be moved up, and the brain tissue and cranial developmental shunt are pulled into the brain parenchyma. In addition, the neck is highly mobile and prone to fracture at the junction when the shunt cannot be moved. Therefore, during the shunt process, the shunt is placed in the subcutaneous fat layer as much as possible to prevent the shunt from aging and fixation. In addition, using integrated shunts or placing the shunt reservoir under the frontal capillary tendon membrane can prevent the shunt connection from breaking. Of course, the design requirements of the bypass tube placement site are not consistent with different bypass tube manufacturers. In the future, the design and manufacture of shunts will have higher requirements, and intelligent pressure regulating devices, antibacterial, highly histocompatible, and self-cleaning anti-obstruction tubes will become the direction of future demand.