[Definition] Post-traumatic hydrocephalus is a common secondary lesion after craniocerebral trauma, especially severe craniocerebral trauma, and it is one of the important factors affecting the prognosis of patients with traumatic brain injury. Subarachnoid hemorrhage is more common after cerebral contusion, and the large amount of bloody cerebrospinal fluid produces strong irritation to the meninges, causing a sterile inflammatory response, and therefore, adhesions between the soft membranes and arachnoid and even blockage of the arachnoid villi, thus causing impaired circulation and absorption of cerebrospinal fluid. As a result, patients often show symptoms of increased intracranial pressure, and the ventricular system is enlarged, and if they do not receive timely and reasonable treatment, the condition will deteriorate day by day old. Etiology and pathophysiology】 Traumatic hydrocephalus is divided into two types: acute hydrocephalus and chronic hydrocephalus. Once hydrocephalus occurs, it means that there is an obstruction in the cerebrospinal fluid circulation pathway, which can be divided into obstructive hydrocephalus and traffic hydrocephalus according to the different obstruction sites. 1, acute hydrocephalus often occurs within 2 weeks after traumatic brain injury, the main reasons for its formation are: ① hematoma compression of cerebrospinal fluid circulation pathway; ② intracranial hematoma or cerebral edema compression of intracranial venous sinus, making its return obstruction; ③ intracranial hematoma breaking into the ventricular system causing obstructive hydrocephalus; ④ arachnoid villi covered by red blood cells to prevent cerebrospinal fluid absorption; ⑤ due to inappropriate decompression of large bone flap, brain tissue is severely expanded and displaced, resulting in obstruction of cerebrospinal fluid circulation. resulting in obstruction of cerebrospinal fluid circulation and associated hydrocephalus. 2, chronic hydrocephalus occurs more than 3 weeks after traumatic brain injury, mostly traffic hydrocephalus. After subarachnoid hemorrhage, the red blood cells contained in the cerebrospinal fluid generally rupture and decompose within 2 weeks, and the red blood cell fragments or fibrin products easily block the subarachnoid cavity with the cerebrospinal fluid circulation, resulting in reduced absorption and cessation of cerebrospinal fluid due to adhesion of arachnoid granules, and finally the formation of hydrocephalus. In addition, some data show that the lower the GCS score, the higher the chance of hydrocephalus. It is possible that severe traumatic brain injury can directly cause damage to the choroid plexus and ventricular canal, which interferes with the blood-brain barrier and blood. Cerebrospinal fluid barrier, which promotes the occurrence and development of hydrocephalus. The pathological changes of traumatic hydrocephalus are enlargement of the ventricular system, adhesions and occlusion of the subarachnoid space of the cerebral convexity or the base of the brain ∞ one. The pathogenesis of traumatic hydrocephalus is generally believed to be due to blockage of the midbrain aqueduct by traumatic blood clots, obstruction of the subarachnoid space by red blood cells or fibrin, which impairs the absorption of cerebrospinal fluid, and late arachnoid fibrosis, which impairs the absorption of cerebrospinal fluid by arachnoid granules. Due to the formation of fibrin adhesions and mechanization in the arachnoid granules on the cerebral base and brain surface, the cerebral sulcus and cerebral pools and arachnoid granules are blocked, preventing cerebrospinal fluid circulation. If the ventricular pressure rises again beyond the elastic tension of the ventricular wall, the ventricle enlarges again. According to the mechanical principle, the enlargement of the lateral ventricles is greater than that of the third and fourth ventricles, and the frontal horn is the most prone to expansion. The anterior cerebral artery and its branches are strained above the corpus callosum, causing impaired blood supply to the frontal and paracentral lobules innervated by this vessel, which are the higher centers for managing intelligence, lower limb movement and urinary and bowel functions. As the disease progresses, urinary and bowel disorders appear, with urinary incontinence being the most common. The above symptoms tend to become apparent within weeks or months. Clinical examination shows no optic papilledema in the fundus and intracranial pressure in the normal range or lumbar puncture with cerebrospinal fluid pressure below 180 mm water column. Brain CT or magnetic resonance imaging is characterized by a marked enlargement of the ventricular system, including the four ventricles, with no significant changes in the cerebral sulci or brain pools. Cerebrospinal fluid uptake is related to the pressure difference between the subarachnoid space and the superior sagittal sinus and the resistance of the arachnoid villi granules. When the intracranial pressure increases after traumatic brain injury, the pressure in the superior sagittal sinus increases, making the pressure difference between the subarachnoid space and the superior sagittal sinus smaller, thus compressing or even closing the tiny tubular system of the arachnoid villi, which directly affects the absorption of cerebrospinal fluid. The accumulation of cerebrospinal fluid causes an increase in intracerebroventricular hydrostatic pressure and progressive enlargement of the ventricles. Therefore, in the initial stage of chronic hydrocephalus, the intracranial pressure of patients is higher than normal. After the ventricles expand to a certain degree, the absorption surface is increased, and the intracranial pressure gradually decreases to the normal range, so it is clinically called normal pressure hydrocephalus. However, because the water pressure of cerebrospinal fluid has exceeded the pressure that the ventricular wall can withstand, the ventricles continue to expand and brain atrophy worsens, resulting in progressive dementia.