In 1964, Holt and Yates  found that the cyst cavity had a clear and patent canal that communicated with reticular subarachnoid space, which was supported by myelographic investigation. Many authors subsequently reported on the existence of such valve-like communicating holes [4, 6, 7]. It is believed that a congenital defect or weakness of the dura allowed herniation of the arachnoid under the hydrostatic pressure of the CSF [12,13,14].
In the current series, communicating holes were found in all the patients. During the surgery, CSF flow through the communicating holes was found, which can be triggered by increasing the abdominal pressure using a Valsalva-like maneuver. This fact further supports following hypothesis: the CSF flows into the congenital pouch (cyst) via the communicating hole when the abdominal pressure is increased or with the pulsation of artery, but the ball-valve mechanism does not allow the CSF to flow back to the thecal sac as the communicating hole is one-way open to it, and consequently the cyst is gradually distended [2, 15].
Since not all of the sacral meningeal cysts are symptomatic, it is important to identify the cysts which are responsible for the clinical complaints, which is pivotal to successful treatment. Voyadzis  suggested that patients with neurological symptoms that are anatomically related to Tarlov cysts greater than 1.5 cm in diameter could benefit from surgical treatment. Tanaka  suggested that a positive filling defect in myelography may be an indicator of good treatment outcomes. Up to now, there have been no explicit criteria whereby to determine the indications of surgery for sacral meningeal cysts.
The clinical features and complaints caused by sacral meningeal cysts vary from simple lumbosacral pain to a spectrum of symptoms including local pain, bowel/bladder/sex dysfunction and S1 radicular symptoms. There exists controversy regarding the efficacy of surgery in the management of sciatica. Tanaka  believed that since sciatica, as with low back pain, is a nonspecific symptom of the sacral cyst, thus a patient with sciatica has little chance to be cured by surgery. However, it has been reported that sciatica and intermittent claudication were relieved following surgery in the vast majority of cases [5, 6, 17, 18]. Moreover, in our series, 13 of the 16 patients with sciatica experienced abatement of the symptom postoperatively.
It is our opinion that whether or not to have the patient treated surgically depends on whether there are neurological symptoms related to the cyst. S1 radicular symptoms, perineal/perianal pain and bowel/bladder/sex dysfunction are all caused by compression of the sacral plexus, on condition that tumor, disc herniation and the like have been ruled out and the patient fails to respond to conservative treatment, then an operation intended for sacral cyst is justified. When there were multiple cysts in one patient, although some smaller cysts were not directly related to the symptoms, we tended to treat every cyst because these smaller cysts had a large chance to expand and cause symptoms in the future due to their inherent pathophysiology (e.g. case 12).
Various strategies have been proposed to manage patients with sacral cysts, but up to now, there has not been a universally accepted one. The widely accepted strategies fall into three categories: 1. Approaches to equalize the CSF pressure between the cyst and the thecal sac [8, 19, 20]. 2. Percutaneous computed tomography-guided aspiration of the cyst with/without fibrin glue placement [9, 21, 22]. 3. Surgical removal or imbrications of the cyst wall with/without communicating hole repair [4,5,6,7, 18, 23, 24]. Each of them could achieve varying degrees of symptom relief but are inevitably associated with various complications and recurrence.
Among these popular methods, no effective blockage of the communicating hole was done [6, 7, 16]. Because the cyst cavity is not obliterated and the communicating hole is not blocked, it is reasonable to worry about a recurrence of the cyst in these methods. For blocking the communication, ligation placed at the neck portion of the cyst may cause entrapment of the nerves. Alternatively, blocking the communication using a small muscle graft is the treatment of choice because it is simple and effective. Elsawaf et al.  tried to use a local fat graft and gelatin sponge to reinforce closed cyst neck. However, this weak reinforcement was likely to fail after the degradation of the fat and gelatin sponge. Instead, a muscle graft with firm suture would provide persistent obstruction, as confirmed by case 12. The key point of the obstruction was the elasticity of the muscle graft. The nerve root was covered by the muscle graft, which was stronger than the fat but softer than the string suture, and the sutures tied the muscle graft and the surrounding tissue instead of directly ligating the nerve root. Therefore, the obstruction could be achieved without hard and direct compression on the nerve root, which was a common problem in direct ligation techniques, and the constriction of the nerve root could be avoided. Besides, the success of obstruction could be verified by the absence of intra-operative cerebrospinal fluid flow and postoperative cerebrospinal fluid leakage.
Moreover, it is unnecessary to eliminate the cyst wall altogether since it has no excretory function. To obviate the risk of damaging the nerves, during the operation we did not give any try to remove the cyst wall forcibly but left it undisturbed. The overall satisfying outcome and relatively less recurrence and complications exhibited the safety and efficacy of our strategy.
Adjuvant procedures were applied to enhance the obstruction. After the obstruction with muscle graft, the residual space was filled with gelfoam and/or fibrin glue, or a muscle flap. Such materials were not expected to fill the cavity effectively or consistently but served as temporary compression to equalize the pressure between the cavity and the dural sac. This temporary equalization might help to prevent laceration of the muscle graft and provide a stable condition for fixation of the obstruction, thus preventing recurrence. However, the confirmation of such an assumption demands histological evidence and further study. In addition, a closed non-pressure drainage was inserted into the cavity to drain the hemorrhage in the surgical site. Furthermore, if CSF leakage happened, although not seen in the current series, the leakage could be identified immediately in the drainage and managed in time. Altogether, we would like to suggest the current strategy for potential consideration by surgeons confronting a sacral meningeal cyst case.
Limitations of our study included its retrospective nature and relatively small sample size. Additionally, the subsequent changes in the muscle graft and surrounding tissues were not investigated. A prospective study with a large cohort is in need in the future, as well as histological research in the surgical site.