No abstract

Introduction. Spinal mobile tumors are very rare. We herein report a case of paraplegia caused by migration and incarceration of thoracic mobile schwannoma after myelography. Case Presentation. A 25-year-old man who had weakness and numbness in both his legs also had pain radiating to the back that was induced by back flexion or extension and jumping. Magnetic resonance imaging (MRI) showed an intradural extramedullary lesion at the T10 and T11 levels. Myelography was performed but discontinued due to his back and lower limb pain. Computed tomography after myelography revealed a rostrally migrated intradural mass with a discrepancy in the exact location in comparison to the MRI findings. He underwent a second lumbar puncture and drained the cerebrospinal fluid (CSF) to aid the spinal cord, because the symptoms gradually worsened and led to paraplegia. After the drainage of the CSF, his symptoms were immediately resolved. The day after myelography, he underwent complete resection of the tumor with the diagnosis of schwannoma. One year after the surgery, he had been working despite having hyperreflexia in his lower limbs with no weakness or sensory disturbance. Conclusion. Severe neurological deficits associated with spinal cord damage can occur due to migration of mobile tumors.

Background. Spinal sarcoidosis is a rare subgroup of neurosarcoidosis. Although most sarcoid lesions develop in the intramedullary compartment, intradural extramedullary (IDEM) spinal sarcoidosis is an extremely rare entity. Case Presentation. We herein report a case of IDEM spinal sarcoidosis mimicking a meningioma. A 32-year-old man presented to the hospital with clumsy hands and was unable to walk without assistance. Magnetic resonance imaging (MRI) of the cervical spine revealed a dural tail sign that is common in meningiomas. The patient underwent gross total resection. The pathological findings consisted with a sarcoid leision of the spinal cord. The patient’s myelopathy recovered after surgery. Conclusions. Physicians should be alert for the possibility of IDEM sarcoidosis mimicking a meningioma in the differential diagnosis of IDEM spinal cord tumors.

This case report was approved by the institutional review boards at Gunma University and the institutional review board overseeing the central data management center.

Although congenital scoliosis is defined as a genetic disease characterized by a congenital and abnormal curvature of the spinal vertebrae, our knowledge of the genetic underpinnings of the disease is insufficient. We herein show that the downregulation of the retinol‐retinoic acid metabolism pathway is involved in the pathogenesis of congenital scoliosis. By analyzing DNA microarray data, we found that the expression levels of genes associated with the retinol metabolism pathway were decreased in the lumbar spine of Ishibashi rats (IS), a rat model of congenital kyphoscoliosis. The expression of Adh1 and Aldh1a2 (alcohol dehydrogenase), two enzymes that convert retinol to retinoic acid in this pathway, were decreased at both the gene and protein levels. Rarα, a receptor of retinoic acid and bone morphogenetic protein 2, which play a central role in bone formation and are located downstream of this pathway, were also downregulated. Interestingly, the serum retinol levels of IS rats were higher than those of wild‐type control rats. These results indicate that the adequate conversion from retinol to retinoic acid is extremely important in the regulation of normal bone formation and it may also be a key factor for understanding the pathogenesis of congenital scoliosis.