Meningiomas represent 18-20% of all intracranial tumors and have a 20-50% 10-year recurrence rate, despite aggressive surgery and irradiation. Hydroxyurea, an inhibitor of ribonucleotide reductase, is known to inhibit meningioma cells by induction of apoptosis. We report the long-term follow-up result of hydroxyurea therapy in the patients with recurrent meningiomas. Thirteen patients with recurrent WHO grade I or II meningioma were treated with hydroxyurea (1000 mg/m(2)/day orally divided twice per day) from June 1998 to February 2012. Nine female and 4 male, ranging in age from 32 to 83 years (median age 61.7 years), were included. Follow-up assessment included physical examination, computed tomography, and magnetic resonance imaging (MRI). Standard neuro-oncological response criteria (Macdonald criteria) were used to evaluate the follow-up MRI scans. The treatment was continued until there was objective disease progression or onset of unmanageable toxicity. Ten of the 13 patients (76.9%) showed stable disease after treatment, with time to progression ranging from 8 to 128 months (median 72.4 months; 6 patients still accruing time). However, there was no complete response or partial response in any patients. Three patients had progressive disease after 88, 89, 36 months, respectively. There was no severe (Grade III-IV) blood systemic disorders and no episodes of non-hematological side effects. This study showed that hydroxyurea is a modestly active agent against recurrent meningiomas and can induce long-term stabilization of disease in some patients. We think that hydroxyurea treatment is well tolerated and convenient, and could be considered as an alternative treatment option in patients with recurrent meningiomas prior to reoperation or radiotherapy.

Objective : Teriparatide is known as an effective anabolic agent not only for severe osteoporosis but also for bone healing and union. We explored the possibility of teriparatide as an alternative treatment option for osteoporotic thoracolumbar (TL) burst fracture. Methods : This retrospective study enrolled 35 female patients with mean age of 73.77±6.71 years (61-88) diagnosed as osteoporotic TL burst fracture with ≥4 of thoracolumbar injury classification and severity (TLICS) score and no neurological deficits. All patients were treated by teriparatide only (12 of group A), teriparatide plus vertebroplasty (12 of group B), or surgical fixation with fusion (11 of group C), and followed up for 12 months. Radiological outcomes were evaluated using radiological parameters including kyphotic angle (KA), segmental vertebral kyphotic angle (SVKA), compression ratio (CR), and vertebral body height (anterior [AH], middle [MH], posterior [PH]). Functional outcomes were evaluated using visual analog scale (VAS) and Macnab classification (MC). Results : There were no statistical significant differences in age, bone mineral density (-3.36±0.73), and TLICS score (4.34±0.48) among the three groups (p>0.05). Teriparatide was administered during 8.63±2.32 months in group A and B. In 12-month radiological outcomes, there were significant restoration in SVKA, CR, AH, and MH of group B and KA, SVKA, CR, AH, and MH of group C compared to group A with no radiological changes (p<0.05). All groups showed similar significant improvements in 12-month functional outcomes, although group B and C showed a better 1-month VAS, 1-month MC, 3-month MC compared to group A (p<0.05). Conclusion : Non-surgical treatment with teriparatide showed similar 12-month functional outcomes compared to surgical fixation with fusion. The additional vertebroplasty to teriparatide and surgical fixation with fusion were more helpful to improve short-term functional outcomes with structural restoration compared to teriparatide only.

Purpose: The clinical and radiological abnormal findings continue even after successful treatment in pyogenic vertebral osteomyelitis (PVO). We analyzed the clinical and radiological features of cured PVO based on ¹⁸F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (FDG-PET/MRI) and compared the radiological differences between FDG-PET and MRI for assessing therapeutic response in PVO. Methods: This study included 43 patients (28 men and 15 women) with lumbar PVO who had no recurrence after successful antimicrobial therapy. They were divided into two groups based on the location of maximum standardized FDG uptake value (SUV_max) of PVO lesion on FDG-PET/MRI when parenteral antibiotics were discontinued (31 in group A: Intervertebral structure; 12 in group B: Vertebral body and paravertebral muscle). The differences of clinical symptoms, hematological inflammatory indices, and radiological features were retrospectively analyzed. Results: The patients were treated with 42.28 ± 14.58 (21–89) days of parenteral antibiotics. There were significant differences in C-reactive protein (0.97 ± 1.10 vs. 0.51 ± 0.31 mg/dL, p = 0.041; normal range of CRP < 0.5), back pain (4.29 ± 1.13 vs. 3.50 ± 1.00, p = 0.040; visual analog scale), and SUV_max (4.34 ± 1.24 vs. 5.89 ± 1.57, p < 0.001) between the two groups. In the distribution pattern of PVO lesions, FDG-PET overall showed recovery pattern earlier than MRI did (p < 0.001). Conclusions: In cured PVO, the clinical features vary depending on the location of major structural damage of PVO lesion. The involvement of intervertebral structure is related with sustained back pain and elevation of CRP, and vertebral body/paravertebral muscle shows favorable clinical features despite advanced structural damages.

Objective: Neuropathic pain is a common secondary complication of spinal cord injury (SCI). N-methyl-D-aspartate (NMDA) receptor activation is critical for hypersensitivity in neuropathic pain. This activation requires the binding of both glutamate and the D-serine co-agonist to the NMDA glycine site. We evaluated the effects of D-serine on neuropathic pain after SCI and explored the underlying molecular mechanisms.Methods: Anesthetized rats underwent T9 spinal cord contusion (130 kdyn). D-serine (500 and 1,000 mg/kg) and MK-801 hydrogen maleate (2.0 mg/kg) were injected daily for 2 weeks, starting the day after SCI. Functional outcomes were assessed according to the Basso, Beattie, and Bresnahan scale, while histological outcomes were evaluated based on lesion volume and spared tissue area. Mechanical allodynia and thermal hyperalgesia were evaluated by measuring the withdrawal threshold of a von Frey filament and hot/cold plate latency. Western blotting was performed to determine the expression levels of Trpv1, Nav1.9, calcitonin gene-related peptide (CGRP), and β-actin in damaged tissue.Results: The withdrawal threshold values and latency of the D-serine group were significantly lower than those of the noninjection group. The MK-801 group showed higher threshold values and latencies than the other groups. Western blotting showed increased Nav1.9 and Trpv1 levels and lower CGRP levels in the D-serine group, whereas the MK-801 group showed the opposite results.Conclusion: D-serine increases neuropathic pain after traumatic SCI by mediating the NMDA receptor. NMDA receptor antagonists alleviate neuropathic pain after traumatic SCI.