Case information The child, female, 8 years old, was found to have a right posterior occipital pigeon’s egg sized mass with no obvious cause 1 year ago, with no clear history of trauma and no other uncomfortable symptoms at that time. The mass gradually increased in size, and more than a month before admission, she developed intermittent headache with vomiting, wasting and loss of appetite. CT scan and three-dimensional reconstruction indicated that the right occipital bone was spindle-shaped enlarged, with thinning of the bone plate and localized defect of the inner plate, which protruded outward in a crater-like manner (Figure 2A-B), and the cerebrospinal fluid density shadow entered between the inner and outer plates through the defect of the inner plate. The occipital pool was enlarged and communicated with the fourth ventricle, and the cerebellar indentation was partially absent. A pulsating soft meningeal cyst in the occipital region and a Dandy-Walker variant were considered. The right occipital outer plate was found to be thin but smooth and intact, and cerebrospinal fluid gushed out after incision of the outer plate, with cystic enlargement between the inner and outer plates, and no granulation, fibrous or membranous tissue was seen. A circular defect of 1 cm in diameter was seen in the inner plate, with a dural arachnoid defect below, and no obvious cyst was seen in the occipital pool. Cerebrospinal fluid entered the plate barrier gap through the defects in the arachnoid, dura mater and inner occipital plate. The outer occipital plate was removed surgically, and part of the inner plate was removed along the perimeter of the inner plate defect, and the dura was seen to adhere closely to the wall layer of the inner plate. Postoperatively, the child had a transient cerebrospinal fluid leak, which was cured by puncture aspiration and conservative treatment, and the cyst was reduced on CT review 10 days after surgery, with the titanium plate covering the defect intact (Figure 2C-D). Discussion The main features of cerebrospinal fluid fistulae causing intralaminar cysts are an intact outer plate of the skull, a defective inner plate and dura mater, and a cystic enlargement of the lamina cribrosa and filling with cerebrospinal fluid. There is no uniform name for this condition, but the literature reports “pseudomeningeal bulge”, “soft meningeal cyst”, “arachnoid cyst” and “growth fracture” in the lamina cribrosa. The common feature of these cases is that the dura mater is torn and the intracranial plate is broken under the causative factors such as trauma, and cerebrospinal fluid enters the lamina cribrosa through the defective area, and the space between the lamina cribrosa gradually increases due to the long-term continuous pulsation of cerebrospinal fluid to form cysts. In the present case, the posterior cranial fossa was widened and an enlarged occipital pool was present, and there was no obvious arachnoid cyst present. The intraoperative findings and pathological examination mostly allowed for a clear diagnosis. If there is an obvious cyst lining within the lamina cribrosa, it can be judged by the composition of the cyst wall. Thus, some cases are pathologically diagnosed as “arachnoid cysts” [1-3], while if the wall of the cyst in the lamina propria is composed only of fibrous tissue or has no obvious wall component, it is called “pseudomeningeal bulge” or “soft meningeal cyst “[4-6]. In the present case, we found an intraoperative cystic enlargement in the right occipital lamina, the contents of which were only cerebrospinal fluid without any cystic wall or membrane-like tissue, so we believe that the diagnosis of “pseudocranial cyst in the lamina” may be more appropriate for the present child. The mechanism of cerebrospinal fluid fistula and intracranial plate defect is still unclear, and many scholars consider this condition to be a specific type of growth fracture because of the history of trauma in most cases [7]. It is now generally accepted that due to trauma resulting in a fracture of the inner plate of the skull with a normal outer plate, along with a tear in the dura mater, pulsating cerebrospinal fluid, soft meninges or arachnoid membranes enter the plate-barrier space through the fracture gap [1,3,8]. Other factors such as normal growth of brain tissue in children, combined hydrocephalus or trauma-induced cerebral edema can lead to an increase in intracranial pressure compared to that within the lamina cribrosa, which creates a live-flap effect between the intracranial and lamina cribrosa gap, with gradual expansion of the lamina cribrosa gap to form a cyst and thinning of the inner and outer plates of the skull under pressure [9]. However, there are some cases in which no cranial fracture is seen on imaging, and Menku et al [4] reported an adult case without fracture and speculated that the absence of a cranial fracture could also cause an intra-lattice cyst, thus suggesting an alternative pathogenesis in which there is an anatomical and physiological defect called “granular depression” in the inner plate of the skull, and there is no cranial fracture after trauma. There is no fracture of the skull after trauma, but the arachnoid membrane ruptures and the granular depressions, including the arachnoid granules, enter between the lamina cribrosa and form cysts. Cysts within the lamina cribrosa are more common in adults.Iplikcioglu et al [2] reviewed arachnoid cysts within the lamina cribrosa and found 13 patients between the ages of 30 and 74 years, all but one of whom were over 50 years old. In contrast, intralaminar pseudocysts associated with growth fractures tend to be traumatized in infancy and childhood and can develop in adolescents and even in middle age. Almost all cases in the literature have a clear history of trauma to the skull, which can be relatively severe or very mild or even unnoticeable [8,10]. In the present case, the child did not have a clear history of trauma, and it is possible that the trauma was relatively minor and was overlooked. Cysts can occur anywhere from a few days to several years after trauma. Although intralaminar cysts can occur in the temporal bone, parietal bone, or even in multiple cranial sites, the majority of cases are located in the occipital bone, and Martinez et al [11] suggested that the occipital bone is thicker and the outer plate of the occipital bone is protected by the stronger occipital muscle, so the inner plate is prone to dehiscence after injury while the outer plate is intact, making it easy for intralaminar cysts to form. The clinical manifestations of this disease are diverse and can be asymptomatic or associated with changes in cranial pressure or associated deformities, including localized masses, headache, vomiting, ataxia, and visual field defects. In our case, the child presented with intermittent headache and vomiting and occipital cyst, which may be related to pressure imbalance caused by cerebrospinal fluid circulation into between the plate barriers. The diagnosis of this disease relies on imaging, with cranial plain radiographs showing eggshell-like cranial changes, and CT scan and 3D reconstruction showing the skull more clearly, revealing fractures and defects in the inner plate and thinning of the inner and outer plates. Other interlaminar cystic lesions such as dermatomal or epidermoid cysts, aneurysmal bone cysts, eosinophilic granulomas, and other cranial lesions can also be distinguished by imaging. Due to the abnormal flow of cerebrospinal fluid, the child may experience intermittent headaches and vomiting. In addition, as the cyst grows, the outer plate of the skull may thin to rupture, causing leakage of cerebrospinal fluid. Moreover, the thinned affected cranial bone provides poor protection to the brain tissue. Therefore, surgical treatment should be performed in all cases with symptoms and progressively larger lesions. The surgery is relatively simple and consists of a tight repair of the dura and a cranial repair, the principle of which is to repair the dural defect without leakage, either with autologous material or artificial patches. The dura mater and venous sinus become thin and close to the inner plate wall layer due to long-term impact by cerebrospinal fluid, which sometimes leads to difficulty in tight suturing of the dura mater and rupture of the venous sinus when separating the dura mater and inner plate adhesions, so careful operation is required during surgery. Cranioplasty can be performed by reshaping the inner and outer plates of the skull with thinning, or, as in this case, by repairing with a titanium plate, which may be stronger and more protective of the child’s brain tissue. The presence of hydrocephalus or other lesions causing increased cranial pressure should also be addressed to reduce postoperative complications. The surgical risk of this condition is low and the prognosis is good.