With the widespread use of CT and MRI, intracranial arachnoid cyst (IAC) has been increasingly reported at home and abroad, accounting for about 1%-3% of intracranial occupying lesions, with a higher proportion in children. Intracranial arachnoid cysts are cysts formed when colorless, clear fluid like cerebrospinal fluid is encapsulated in a pocket-like structure formed by the arachnoid membrane. The disease occurs in the middle cranial fossa, the lateral fissure, the convex surface of the brain, the midline of the posterior cranial fossa, and the tetrapyramidal pool, and is usually solitary, occasionally multiple.
1, etiology and pathogenesis: most authors believe that they can be divided into two main categories.
(1) primary (congenital) IAC, these cysts are cysts formed by congenital embryonic developmental malformations or tissue ectopic developmental abnormalities, mostly seen in children and young people, early asymptomatic due to small cyst volume or communication with the subarachnoid space, and later formed clinically symptomatic cysts due to intracapsular hyperosmolarity, formation of live valves between the cyst and subarachnoid space and secretion of fluid from the cyst wall, resulting in an increase in cyst volume.
(2) Secondary (acquired) IAC, mostly found in larger brain pools, is mainly due to craniocerebral injury or intracranial infection, surgery, hemorrhage, birth injury, radiation therapy and other causes of arachnoid adhesions, so that the distal outlet of the pool is occluded, and CSF can only enter the sac but not flow out, and over time the original normal subarachnoid space will compensate for the enlargement of cysts. Most cysts are formed along the axis of the main cerebral artery, and the pulsation of this artery becomes the driving force for CSF impact, causing the cystic cavity to gradually increase in size and symptoms to appear.
2.Clinical manifestation and diagnosis
The clinical manifestations of IAC are related to its occurrence site and size, and the clinical symptoms themselves are not characteristic.
(1) It occurs in adolescent male patients.
(2) It can be asymptomatic, but is only detected by CT or MRI examination due to headache or dizziness.
(3) The onset of the disease is often chronic, but can be sudden when trauma causes intracapsular hemorrhage in the IAC.
(4) Hydrocephalus is caused by the cyst blocking the CSF circulation, and may also be associated with impaired absorption of CSF, manifesting as symptoms of increased intracranial pressure.
(5) Focal neurological deficits, cyst compression may present with epilepsy, mild motor and sensory deficits.
(6) Young children may present with cranial enlargement and paralysis.
Diagnosis of IAC: mainly relies on CT or MRI. IAC appears on CT as a well-defined hypodense foci outside the cerebral cortex, in complete agreement with the density of cerebrospinal fluid, with CT values ranging from 7.2 to 15 Hu. The cyst wall has no enhancing effect, is round or oval, the surrounding subarachnoid space can be deformed and displaced, the local brain tissue is compressed and atrophied or underdeveloped, there can be lateral ventricular enlargement (hydrocephalus) and midline displacement of MRI shows extracerebral occupancy with consistent signal and clear borders within the cyst, low signal on T1-weighted images and high signal on T2-weighted images, completely consistent with cerebrospinal fluid signal, localized brain tissue compression and atrophy, and no surrounding edema.IAC often needs to be differentiated from other intracranial low-density lesions such as lipoma, cholesteatoma, dermatomal or epidermoid cysts, and other Other cystic tumors such as glioma and hemangioblastoma can usually be distinguished by nodularity and significant enhancement.
3.Surgical indications
The clinical management of primary and secondary IAC is basically the same but varies according to their size, location and clinical symptoms.
(1) Those who have obvious intracranial pressure increase.
(2) Those with intracapsular hemorrhage.
(3) frequent epileptic seizures
(4) those with focal neurological deficits
(5) Cysts combined with hydrocephalus.
In children, a positive attitude should be taken to remove the cyst to facilitate brain development and improve brain function, especially if the cyst is located in the temporal region. In addition, intracapsular hemorrhage or subdural hematoma can occur in these children with minor head trauma. For small asymptomatic cysts, most scholars advocate withholding surgery, close observation, and regular review of CT to understand the growth of the cysts. In case of pediatric patients with asymptomatic but restricted brain development on the side of the cyst or cysts located in functional areas, surgery should be considered.
4. Choice of surgical method
At present, there are many surgical methods for IAC, including craniotomy of IAC, cyst and surrounding brain pool traffic, cyst-abdominal shunt, etc. The purpose of surgery is to remove cyst fluid, excise cyst wall, release its compression on brain tissue, establish effective cerebrospinal fluid circulation and prevent recurrence. External cyst drainage has been abandoned due to many complications. Cyst-abdominal shunt is also not suitable for patients with high protein content of cystic fluid or intracapsular hemorrhage because of easy blockage of the shunt, so it is generally not preferred, but only for IAC with severe hydrocephalus and older patients who cannot tolerate craniotomy. In recent years, with the development of microsurgery, open cranial cyst microdissection plus cystic subarachnoid cerebral pool communication has the most positive effect, and the best result for cysts in the posterior cranial fossa, multiple atrial or combined intracapsular hemorrhage. The surgical principle is to select the surgical approach according to the general craniotomy principle because of the location of IAC, and perform microscopic resection of most of the cyst wall, and try to remove the cyst wall as much as possible, while opening the subarachnoid cavity on the surface of the cerebral cortex around the cyst cavity, the key is to establish the cyst cavity and subarachnoid cavity, brain pool or ventricle communication, which is the key to prevent the recurrence of IAC. If complete resection is not possible, cerebral pool subarachnoid evacuation should be performed to establish good circulatory access. In some epileptic patients, we should carefully check whether there is white shiny fiber perithelium on the surface of the blood vessels on the peripheral cortex of the cyst and whether the brain tissue supplied by this blood vessel is white, if found, we must cut off the perithelium with a hook knife and loosen the blood vessels to the peripheral 2-3 cm of the perithelium to improve the blood supply to the cortex, then we can see that the original ischemic white cerebral cortex will become red and moist. If the cystic cavity is reduced after surgery and the hydrocephalus does not resolve or the cyst recurs, ventriculoperitoneal shunts or cystoperitoneal shunts are feasible. In the surgical treatment of IAC, some authors found that the cyst recurred in a considerable number of cases. Although the cyst wall was removed and the communication between the cystic cavity and the subarachnoid cavity and the brain pool was established in these cases, the subarachnoid brain pool around the cystic cavity was occluded and narrowed due to the compression of the cyst for a long time, which was different from the normal state, in which the pathway of cerebrospinal fluid circulation was changed. Therefore, it may seem that the cystic cavity and subarachnoid cavity are communicated, but in fact it is not always effective. In the case of arachnoid cysts caused by traumatic brain injury, the surgical results are relatively poor because of extensive adhesions. In addition, inadequate and timely drainage of postoperative bloody cerebrospinal fluid may be the cause of recurrence in this subset of cases. Performing cyst-abdominal shunt for recurrent IAC is still not a bad alternative.
In conclusion, the clinical manifestations of IAC are closely related to the size of the site where it occurs, and the speed of brain tissue repositioning and the degree of IAC reduction after treatment depend on age factors. Therefore, IAC with indications for surgery in the adolescent group should be actively treated surgically, while IAC with atypical or asymptomatic symptoms and small size can be treated conservatively in patients aged 50 years or older.