Seven geriatric patients presented with displaced Type II odontoid fractures. All patients underwent a posterior C1-C2 transarticular fixation between November 1994 and December 1996. Ages ranged between 63 and 88 years.
METHODS
Fractures were treated with placement of bilateral transarticular screws, allowing immediate fixation, except in one patient, for whom only a unilateral screw was used. An autograft interspinous strut was also placed, allowing three-point fixation. Mean follow-up was 10.6 months.
RESULTS
Six patients received rigid fixation and developed a stable union. One patient died before any follow-up could be obtained. Two other patients died within 1 year of unrelated causes. The remaining four patients remain active and independent. One intraoperative vertebral artery injury was identified. No clinical sequalae were noted.
CONCLUSION
Posterior transarticular screw fixation is a reasonable option in treating these controversial fractures. Seven geriatric patients tolerated this surgery well, and were mobilized early, avoiding complications related to external immobilization. 相似文献
Calcium (Ca2+) dysregulation has been linked to neuronal cell death, including in hereditary retinal degeneration. Ca2+ dysregulation is thought to cause rod and cone photoreceptor cell death. Spatial and temporal heterogeneities in retinal disease models have hampered validation of this hypothesis. We examined the role of Ca2+ in photoreceptor degeneration, assessing the activation pattern of Ca2+-dependent calpain proteases, generating spatiotemporal maps of the entire retina in the cpfl1 mouse model for primary cone degeneration, and in the rd1 and rd10 models for primary rod degeneration. We used Gaussian process models to distinguish the temporal sequences of degenerative molecular processes from other variability sources.In the rd1 and rd10 models, spatiotemporal pattern of increased calpain activity matched the progression of primary rod degeneration. High calpain activity coincided with activation of the calpain-2 isoform but not with calpain-1, suggesting differential roles for both calpain isoforms. Primary rod loss was linked to upregulation of apoptosis-inducing factor, although only a minute fraction of cells showed activity of the apoptotic marker caspase-3. After primary rod degeneration concluded, caspase-3 activation appeared in cones, suggesting apoptosis as the dominant mechanism for secondary cone loss. Gaussian process models highlighted calpain activity as a key event during primary rod photoreceptor cell death. Our data suggest a causal link between Ca2+ dysregulation and primary, nonapoptotic degeneration of photoreceptors and a role for apoptosis in secondary degeneration of cones, highlighting the importance of the spatial and temporal location of key molecular events, which may guide the evaluation of new therapies. 相似文献