Tarlov cyst with self-healing cauda equina syndrome following combined spinal-epidural anesthesia: a case report.

BACKGROUND: Cauda Equina Syndrome (CES) after Combined Spinal-Epidural Anesthesia (CSEA) is a rare disease that most of the time need surgery to relieve spinal cord compression. CASE PRESENTATION: A 34-year-old male patient underwent a procedure for prolapse and hemorrhoids (PPH) under CSEA. Anesthesia and surgery were uneventful. However, the patient gradually experienced urinary retention, lower abdomen and back pain, changes in bowel habits and neurological dysfunction of the lower limbs when the catheter was removed. It was later determined that the patient had Tarlov cyst at the left S1 level in the sacral canal. Finally, the patient completely recovered 20 days after drug conservative therapy onset. CONCLUSION: This case suggests that CES might occur even after ordinary CSEA. The risk factors are drug neurotoxicity to ropivacaine and Tarlov cyst, which helped to accumulate ropivacaine. The development of ultrasound-guided CSEA and an ultrasound atlas of the spinal canal are required.

Activin B Stimulates Mouse Vibrissae Growth and Regulates Cell Proliferation and Cell Cycle Progression of Hair Matrix Cells through ERK Signaling.

Activins and their receptors play important roles in the control of hair follicle morphogenesis, but their role in vibrissae follicle growth remains unclear. To investigate the effect of Activin B on vibrissae follicles, the anagen induction assay and an in vitro vibrissae culture system were constructed. Hematoxylin and eosin staining were performed to determine the hair cycle stages. The 5-ethynyl-2'-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays were used to examine the cell proliferation. Flow cytometry was used to detect the cell cycle phase. Inhibitors and Western blot analysis were used to investigate the signaling pathway induced by Activin B. As a result, we found that the vibrissae follicle growth was accelerated by 10 ng/mL Activin B in the anagen induction assay and in an organ culture model. 10 ng/mL Activin B promoted hair matrix cell proliferation in vivo and in vitro. Moreover, Activin B modulates hair matrix cell growth through the ERK⁻Elk1 signaling pathway, and Activin B accelerates hair matrix cell transition from the G1/G0 phase to the S phase through the ERK⁻Cyclin D1 signaling pathway. Taken together, these results demonstrated that Activin B may promote mouse vibrissae growth by stimulating hair matrix cell proliferation and cell cycle progression through ERK signaling.