A type of benign brain cyst. There is an arachnoid-like cyst wall and cerebrospinal fluid-like cyst fluid. The cysts are located on the surface of the brain and are closely related to the subarachnoid space but do not invade the brain. They are mostly solitary, a few are multiple, and are often located in the cerebral fissure and brain pool. The large size may compress both brain tissue and skull, which may produce neurological symptoms and cranial changes. It is more common in children, more common in males, and more common on the left side than on the right side. It can be divided into congenital, traumatic and post-infection arachnoid cysts according to their etiology. The causes of congenital arachnoid cysts are not fully understood, but the following speculations have been made: 1. Starkman et al. (1958) suggested that the cause of the disease may be the development of a small piece of arachnoid membrane falling into the subarachnoid space during embryonic development. The cyst is located within the arachnoid membrane, and microscopically, the arachnoid membrane is seen to split into two layers around the cyst, with the outer layer forming the surface part of the cyst and the inner layer forming the base of the cyst, and there is still a subarachnoid cavity between the soft meninges and the base of the cyst. Jiang Dajie (1963) found that the surface part of the cyst wall also consisted of two layers of arachnoid membrane, that is, the cyst was all located in the subarachnoid space. 2, Many people believe that during embryonic development, due to the pulsation of the choroid plexus, which acts as a pump for cerebrospinal fluid, the perimedullary mesh, which is loose around the neural tissue, can be separated to form the subarachnoid space, and if the flow of cerebrospinal fluid is abnormal in the early stage, cysts can be formed in the perimedullary mesh. 3. Because the syndrome is often accompanied by other congenital anomalies, such as ectopic choroid plexus within the cyst, local absence of the cerebral falx, and absence of the orbital plate, temporal lobe, and internal carotid artery, all confirm that the basic cause of the syndrome is due to cerebral dysplasia (Robinson 1958). There is no unanimous opinion on the reasons for the increasing size of arachnoid cysts, but it may be that: 1. There are small holes in the wall of the cyst that are connected to the subarachnoid cavity, and cerebrospinal fluid flows into the cyst from this hole continuously. Some factors may also cause the small hole to be blocked and cause the intracranial pressure to increase. 2, There is ectopic choroid plexus inside the cyst, which secretes too much cerebrospinal fluid and cannot be absorbed. In some cases, the cyst does not communicate with the subarachnoid space, and the protein in the cystic fluid increases, causing a gradual increase in the cyst due to the difference in osmotic pressure inside and outside the cyst (Galassi et al. 1980). 4, Intracapsular or supracapsular venous hemorrhage, causing rapid enlargement of the cystic cavity (LaCour et al. 1978). Arachnoid cysts are commonly found in the lateral fissure, longitudinal fissure, surface or base of the brain, and cerebellum, and also in the saddle area, optic nerve, tegmental area, slope, and pontocerebellar horn. In young children, there is often temporal skull bulge, thin temporal scales and chronic intracranial pressure increase, but most of them are not noticed and most of them do not develop symptoms until adulthood. Symptoms are related to the size of the cyst and the site of growth. Small cysts may be asymptomatic and are occasionally found at autopsy. The common sites of the disease are described as follows: 1. Lateral fissure arachnoid cysts are the most common. The lateral fissure is enlarged and sometimes accompanied by absence of the anterior temporal lobe and inferior frontal gyrus. It is common in young men under 20 years of age, often with headache, seizures (can be limited or generalized epilepsy, psychomotor seizures), temporal bony bulge, a few with ipsilateral proptosis, and in late stages, optic papilledema and contralateral mild hemiparesis. 2.Protrusive arachnoid cysts are seen in infants or adults. Infants often have progressive cranial enlargement with asymmetry on both sides, and the cyst border is visible on transillumination test, sometimes with seizures. Adults often have headache, epilepsy, progressive contralateral mild hemiparesis, and optic papilloedema. 3, longitudinal arachnoid cysts often have no clinical symptoms, about half of them are accompanied by corpus callosum dysplasia. 4.Arachnoid cysts in the saddle area are located in the saddle or in the saddle. The suprasellar ones are rare and can occur at any age. The cyst can be connected or not connected with the optic cross pool. Small cysts can be asymptomatic, but large ones can destroy the pterygoid saddle and compress the pituitary gland, optic cross and interventricular foramen, resulting in visual impairment, pituitary hypoplasia, obstructive hydrocephalus, etc. Intrasellar cysts are mostly asymptomatic, but they can also develop in the saddle through the enlarged saddle diaphragm foramen, similar to empty butterfly saddle syndrome. 5, optic nerve arachnoid cyst There are two types: intraorbital and intracranial. The former is located in the posterior part of the eye, with symptoms such as ipsilateral vision loss, optic papilla edema, and optic ciliary nerve vein rage. The intracranial segment type can compress the optic nerve cross and produce visual impairment and visual field defects (Holt1966). 6, arachnoid cyst in the tegmental area The cyst is connected or not connected to the tegmental pool. In the early stage, it may compress the conduit and produce positive hydrocephalus and intracranial pressure increase, and about 1/4 have Parinaud syndrome. 7. Arachnoid cyst in the pontocerebellar horn has neurological deafness and hypoacusis in the early stage, and cerebellar signs and intracranial pressure increase in the late stage. Individuals may have peripheral facial palsy and trigeminal neuralgia (Bengochea et al. 1955, Sumner et al. 1975). 8. Cerebellar arachnoid cysts may be located in the cerebellar hemispheres, earthworms or occipital pool. Clinical symptoms of increased intracranial pressure are often present, and some cases have cerebellar signs. Diagnosis: In addition to clinical manifestations, the following tests can be performed: 1. Cranial X-ray: Long-term compression of the cyst can produce local changes in the skull. For example, the lateral fissure type has elevation and thinning of the pterygoid winglets, outward elevation of the large winglets and temporal scales, compression of the middle cranial recess, and destruction and absorption of the pterygoid saddle. In the cerebral eminence type, there is asymmetric enlargement of the top of the skull on both sides, local bone thinning, and separation of the bone suture. The pontocerebellar horn type shows rocky bone and rounded, smooth-edged bone resorption in the internal auditory canal area. Iodine oil pontocerebellar angiography may show cystic shadow. The other types have less cranial changes. 2. Cerebral angiography: The lateral fissure type shows the presence of vascular occupational changes in the anterior temporal and lateral fissures. The cerebral eminence type has a localized avascular area, which is difficult to distinguish from a subdural hematoma. The longitudinal fissure type shows the A2 segment encircling the avascular area, and there are adjacent vessels separated and displaced. The suprasellar type shows changes such as siphon opening and A1 elevation. Since the application of CT scan examination, cerebral angiography has been applied less often. 3.CT scan: It shows a local hypodense area (CT value approximates cerebrospinal fluid density) with clear boundary. There is no cyst wall enhancement after contrast injection. This condition should be differentiated from cerebral penetrating malformation and intracranial epithelioid or dermatomatous tumor. In the former, the brain tissue is absent and the cerebrospinal fluid fills the cavity, so the cavity is in free communication with the ventricles or subarachnoid space, which can be differentiated by CT scan. Intracranial epithelioid or dermatomatous tumors show hypodense areas on CT scan as in this case, but their margins are blurred, there is often a distance between the lateral wall and the inner plate of the skull, and the shape is irregular. It should be differentiated from chronic subdural hematoma or hydatid tumor. Although there is temporal bone augmentation in this condition, surgery is not required if there are no clinical symptoms. Those with symptoms should have surgery to remove the cystic fluid and excise the surface portion of the cystic wall, and cut the inner wall to open up to the subarachnoid space. Good results can often be obtained. For those who have hydrocephalus, if the symptoms of increased intracranial pressure are not relieved by the above surgery, or if the cyst recurs after surgery, cerebrospinal fluid shunt is feasible. If ectopic choroid plexus is found in the cyst during surgery, it should be removed by electrocoagulation. Second, post-infection arachnoid cysts are formed after meningitis due to local adhesions of the arachnoid membrane, and the cysts are filled with cerebrospinal fluid. Most of them are multiple. Mostly seen in children. They are commonly found in the optic chiasm, basal pool, cerebellar medullary pool, and cricoid pool. They may present with hydrocephalus and increased intracranial pressure due to obstruction of cerebrospinal fluid circulation. Cysts in the optic chiasm may produce visual impairment, while those in other areas may also produce limited symptoms. Children often have an enlarged skull. The diagnosis is based on a history of meningitis and signs of increased intracranial pressure. The diagnosis can be confirmed with a CT scan. However, it is sometimes difficult to differentiate from congenital arachnoid cysts. Multiple cysts should not be operated on, but the main cyst producing clinical symptoms can be removed. Cerebrospinal fluid shunts can be performed in the presence of hydrocephalus and increased intracranial pressure. Third, post-injury arachnoid cysts, also known as soft meningeal cysts. The mechanism of its occurrence is that the injury causes a linear fracture of the skull, accompanied by a tearing defect of the dura mater, with hemorrhage in the subarachnoid space below it or adhesions at the peripheral edge of the arachnoid, causing local cerebrospinal fluid circulation disorders, resulting in local arachnoid protrusion into the dural fissure and fracture line, which gradually forms a cyst under the constant impact of brain pulsation and makes the fracture edge expand continuously, called a growing fracture. The cyst may protrude under the scalp and also compress the cerebral cortex below. The cyst is filled with clear fluid and surrounded by scar tissue. If the soft meninges are broken during trauma, the brain tissue may herniate into the fracture and the ipsilateral ventricles may enlarge, even forming a cerebral penetration malformation.