BackgroundSurgery for symptomatic sacral perineural cysts remains an issue of discussion. Assuming micro-communications between the cyst and thecal sac resulting in a valve mechanism and trapping of CSF as a pathomechanism, microsurgical fenestration from the cyst to the thecal sac was performed to achieve free CSF communication.MethodsIn 13 consecutive patients (10 female, 3 male), MRI revealed sacral perineural cysts and excluded other pathologies. Micro-communication between the thecal sac and the cysts was shown by delayed contrast filling of the cysts on postmyelographic CT. Surgical fenestration achieved free CSF communication between the thecal sac and cysts in all patients. The patient histories, follow-up examinations and self-assessment scales were analyzed. Symptoms at initial presentation included lumbosacral pain, pseudoradicular symptoms, genital pain and urinary dysfunction. Mean follow-up was 10.7 ± 6.6 months.FindingsBesides one CSF fistula, no surgical complications were observed. Five patients did not improve after surgery; in four of these cases multiple cysts were found, but small and promptly filling cysts remained untreated. Seven patients reported lasting benefit following surgery; three of these had single cysts, and all had cysts >1 cm. One patient initially benefited from cyst fenestration but experienced recurrent pain within 2 months postoperatively. Re-myelography revealed delayed contrast filling of the recurrent cyst; however, surgical revision did not lead to an improvement despite successful fenestration and collapse of the cyst revealed by postoperative imaging.ConclusionsMicrosurgical fenestration of sacral perineural cysts to the thecal sac is a surgical approach that has shown success in the treatment of lumbosacral pain, pseudoradicular symptoms, genital pain and urinary dysfunction associated with sacral perineural cysts. Our analysis, however, shows that mainly patients with singular large cysts benefit from this treatment.

We conclude that these changes are not due to alterations of the intrinsic cross-bridge kinetics. The molecular mechanism of sarcomeric diastolic dysfunction in this FHC model is based on the impaired regulatory switch-off kinetics of cTnI, which induces incomplete inhibition of force-generating cross-bridges at low [Ca(2+)] and thereby slows down relaxation of sarcomeres. Ca(2+) sensitization and impairment of the relaxation of sarcomeres induced by this mutation may underlie the enhanced systolic function and diastolic dysfunction at the sarcomeric level.

Cerebral hypoperfusion in the first hours after subarachnoid haemorrhage (SAH) is a major determinant of poor neurological outcome. However, the underlying pathophysiology is only partly understood. Here we induced neutropenia in C57BL/6N mice by anti-Ly6G antibody injection, induced SAH by endovascular filament perforation, and analysed cerebral cortical perfusion with laser SPECKLE contrast imaging to investigate the role of neutrophils in mediating cerebral hypoperfusion during the first 24 h post-SAH. SAH induction significantly increased the intracranial pressure (ICP), and significantly reduced the cerebral perfusion pressure (CPP). At 3 h after SAH, ICP had returned to baseline and CPP was similar between SAH and sham mice. However, in SAH mice with normal neutrophil counts cortical hypoperfusion persisted. Conversely, despite similar CPP, cortical perfusion was significantly higher at 3 h after SAH in mice with neutropenia. The levels of 8-iso-prostaglandin-F2α in the subarachnoid haematoma increased significantly at 3 h after SAH in animals with normal neutrophil counts indicating oxidative stress, which was not the case in neutropenic SAH animals. These results suggest that neutrophils are important mediators of cortical hypoperfusion and oxidative stress early after SAH. Targeting neutrophil function and neutrophil-induced oxidative stress could be a promising new approach to mitigate cerebral hypoperfusion early after SAH.