They are filled with cerebrospinal fluid (CSF). The pathogenesis remains unclear: the cysts develop after congenital arachnoidal proliferations within the root sleeve or because of inflammation followed by inoculation of CSF. So the result is an obstruction of CSF flow causing cystic dilatation: CSF can enter the cyst but with restriction of its outflow. Inhibitors,research,lifescience,medical This effect has been described as a “ball valve” mechanism [5]. MRI scan is mostly currently the imaging study of choice which reveals the cysts arising from the sacral nerve root near the dorsal root ganglion [6,7]. When cysts are symptomatic and medical treatment (analgesic and physical

therapy) is unsuccessful a surgical excision is then the treatment of reference. The goal of the surgical

treatment is to relieve neural compression and to stop Inhibitors,research,lifescience,medical bone erosion. There is still no consensus on the appropriate surgical indications and techniques but percutaneous drainage or microsurgical excision combined with duraplasty or plication of the cyst wall appear to be effective and safe [8,9]. Fat embolism, now called fat embolism syndrome (FES), occurs mainly after orthopaedic injuries (lower extremity trauma and intra-medullary surgery), but it has also been seen after non-trauma conditions such as closed-chest cardiac massage and acute pancreatitis[10]. Less frequently, FES was described after spontaneous or post trauma rupture of craniopharyngioma cyst Inhibitors,research,lifescience,medical [11] or after rupture of epidermoid cyst [12]. More recently Aydin et al. described, in an experimental model, that pulmonary contusion induced more cerebral fat embolism than long bone Inhibitors,research,lifescience,medical fracture and highlighted the importance of lung pathologies in the occurrence of FES [13]. The

exact incidence and mortality rate are still unknown [10]. FES usually manifests as a multisystem disorder Inhibitors,research,lifescience,medical with a cascade of clinical signs such as petechial rash, deteriorating mental status, and progressive respiratory insufficiency, usually occurring within 24 hours of injury. The clinical diagnosis is based on the scale of Gurd and Wilson [14] who stated that at least two major signs or one major and four minor signs must be present (among a panel of 12 items). But for a decade the diagnosis has been based on MRI images Anacetrapib which typically show hyperintense dot-like lesions disseminated into the brain. In diffusion-weighted MRI imaging there are multiple microembolic infarctus mimicking “starfield” pattern [15]. The treatment is on the immobilization of the fracture with supportive care. Maintaining the oxygenation of the peripheral tissues is utmost importance. The majority of cerebral fat embolism patients recover without sequelae [10]. Conclusion Although perineurial cysts are rare, they should be considered in the diagnosis of cerebral fat embolism after lower back injury. Competing interests The authors declare that they have no competing interests.