Vertebral hemangiomas are benign lesions and are often asymptomatic. Most vertebral hemangiomas that cause cord compression and neurological symptoms are located in the thoracic spine and involve a single vertebra. The authors report the rare case of lumbar hemangiomas in a 60-year-old woman presenting with severe back pain and rapidly progressive neurological signs attributable to 2 noncontiguous lesions. After embolization of the feeding arteries, no improvement was noted. Thus, the authors performed open surgery using a combination of posterior decompression, intraoperative kyphoplasty, and segmental fixation. The patient experienced relief from back and leg pain immediately after surgery. At 3 months postoperatively, her symptoms and neurological deficits had improved completely. To the authors' knowledge, this is the first description of 2 noncontiguous extensive lumbar hemangiomas presenting with neurological symptoms managed by such combined treatment. The combined management seems to be an effective method for treating symptomatic vertebral hemangiomas.
Bin Yu, Desheng Wu, Bin Shen, Weidong Zhao, Yufeng Huang, Jianguang Zhu and Dongduo Qi
Chih-Lung Lin, Huei-Chuan Shih, Aaron S. Dumont, Neal F. Kassell, Ann-Shung Lieu, Yu-Feng Su, Shen-Long Hwong and Chin Hsu
Sex differences in the outcome of aneurysmal subarachnoid hemorrhage (SAH) are controversial, and the potential influence of estradiol on vasodilation is unclear. In the present study the authors evaluate the effect and possible mechanism of 17β-estradiol (E2) on SAH-induced vasospasm in a two-hemorrhage rodent model of SAH.
A 30-mm Silastic tube filled with E2 in corn oil (0.3 mg/ml) was subcutaneously implanted in male rats. Serum levels of E2 were measured on Days 0, 1, 2, 3, 4, and 7 postimplantation. The degree of vasospasm was determined by averaging the cross-sectional areas of the basilar artery (BA) 7 days after the first SAH. Expressions of endothelial nitric oxide synthase (eNOS) and inducible NOS (iNOS) in the BA were also evaluated.
Serum levels of E2 in the E2-treated rats were at physiological levels (56–92 pg/ml) and were significantly higher than those in the control and vehicle-treated groups. Treatment with E2 significantly (p < 0.01) attenuated SAH-induced vasospasm. Induction of iNOS messenger (m)RNA and protein in the BA by SAH was significantly diminished by the E2 treatment but not by vehicle treatment. The SAH-induced suppression of eNOS mRNA and protein was relieved by E2 treatment.
These results suggest that continuous treatment with E2 at physiological levels prevents cerebral vasospasm following SAH. The beneficial effect of E2 may be in part related to the prevention of augmentation of iNOS expression and the preservation of normal eNOS expression after SAH. Treatment with E2 holds therapeutic promise in the treatment of cerebral vasospasm following SAH and merits further investigation.
Shiuh-Lin Hwang, Chih-Lung Lin, Ann-Shung Lieu, Kung-Shing Lee, Tai-Hung Kuo, Yan-Fen Hwang, Yu-Feng Su and Shen-Long Howng
Object. Cage-assisted anterior cervical discectomy and fusion (ACDF) has proven to be a safe and effective procedure for the treatment of one- and two-level degenerative disc disease (DDD). To the authors' knowledge, clinical results after three- and four-level interbody cage—augmented ACDF have not been reported in the literature. The authors investigated the safety and effectiveness of titanium cages used in such procedures and evaluated the results in cases with or without plate fixation.
Methods. Fifty-six patients suffering from cervical DDD were divided into two groups. Group 1 included 32 patients who underwent titanium cage—assisted ACDF; Group 2 included 24 patients who underwent the same procedure, supplemented with plate fixation. The cervical DDD was confirmed by radiography and magnetic resonance imaging. The patients underwent radiographic evaluation to assess cervical lordosis, segmental height of cervical spine, the height of the foramina, and spinal stability. Neurological outcomes were assessed using the Japanese Orthopaedic Association (JOA) scores. Neck pain was graded using a 10-point visual analog scale (VAS). The follow-up period ranged from 13 to 28 months (mean 17.2 months).
In both Groups 1 and 2 significant increase (p < 0.001) was demonstrated in the JOA scores (preoperatively 10.7 ± 2.4 and 11.1 ± 2, postoperatively 13.9 ± 2.2 and 14.1 ± 2.3, respectively) and VAS pain scores (preoperatively 8.8 ± 0.9 and 8.5 ± 1, postoperatively 3.1 ± 2.1 and 2.8 ± 1.8, respectively); however, there was no significant intergroup difference. A significant increase in the cervical lordosis, foraminal height, and segmental height was observed in both groups. Good stability of cage fusion was obtained in both groups 12 months postoperatively (90.6% in Group 1 and 91.7% in Group 2); however, there were no statistically significant intergroup differences. The complication rate in Group 2 was higher than that in Group 1. The hospital length of stay in Group 1 was significantly lower than in Group 2 (p < 0.001).
Conclusions. Analysis of these findings demonstrated that titanium cage—assisted ACDF provided long-term stabilization, increased lordosis, increased segmental height, and increased foraminal height. In both groups good neurological outcomes were achieved and donor site morbidity was avoided. The lower complication rate and shorter hospital stay, however, make the cage-assisted fusion without plate fixation better than with plate fixation.
Chih-Lung Lin, Aaron S. Dumont, Yu-Feng Su, Yee-Jean Tsai, Jih-Hui Huang, Kao-Ping Chang, Shen-Long Howng, Aij-Lie Kwan, Neal F. Kassell and Cheng-Hsing Kao
Cerebral vasospasm remains a major complication in patients who have suffered a subarachnoid hemorrhage (SAH). Previous studies have shown that 17β-estradiol (E2) attenuates experimental SAH–induced cerebral vasospasm. Moreover, E2 has been shown to reduce neuronal apoptosis and secondary injury following cerebral ischemia. Adenosine A1 receptor (AR-A1) expression is increased following ischemia and may represent an endogenous neuroprotective effect. This study was designed to evaluate the efficacy of E2 in preventing cerebral vasospasm and reducing secondary injury, as evidenced by DNA fragmentation and AR-A1 expression, following SAH.
A double-hemorrhage model of SAH in rats was used, and the degree of vasospasm was determined by averaging the cross-sectional areas of the basilar artery 7 days after the first SAH. A cell death assay was used to detect apoptosis. Changes in the protein expression of AR-A1 in the cerebral cortex, hippocampus, and dentate gyrus were compared with levels in normal controls and E2-treated groups (subcutaneous E2, 0.3 mg/ml).
The administration of E2 prevented vasospasm (p < 0.05). Seven days after the first SAH, DNA fragmentation and protein levels of AR-A1 were significantly increased in the dentate gyrus. The E2 treatment decreased DNA fragmentation and prevented the increase in AR-A1 expression in the dentate gyrus. There were no significant changes in DNA fragmentation and the expression of AR-A1 after SAH in the cerebral cortex and hippocampus in the animals in the control and E2-treated groups.
The E2 was effective in attenuating SAH-induced cerebral vasospasm, decreasing apoptosis in the dentate gyrus, and reducing the expression of AR-A1 in the dentate gyrus after SAH. Interestingly, E2 appears to effectively prevent cerebral vasospasm subsequent to SAH as well as attenuate secondary injury by reducing both apoptosis and a compensatory increase in AR-A1 expression in the dentate gyrus.