The data presented here demonstrate that sympathetic neurons have the potential to activate two alternative caspasedependent pathways either of which is capable of mediating death induced by NGF deprivation and that these neurons have the potential to switch from one pathway to the other. The presence of these two alternative pathways to trophic factor deprivation-induced death may have implications for ensuring the correct development of the nervous system. In wild-type neurons, a caspase-2-dependent pathway is required for death, and a caspase-9-dependent pathway appears to be suppressed by endogenous inhibitors of apoptosis proteins (IAPs). In contrast, for caspase-2-null neurons, death is dependent on the caspase-9 pathway. The mechanism underlying the shift is the result of a threefold compensatory elevation of caspase-9 expression and a doubling of levels of direct IAP binding protein with low pI (DIABLO)/second mitochondriaderived activator of caspase (Smac), an IAP inhibitor, both at the mRNA and protein levels. These findings resolve seemingly discrepant findings regarding the roles of various caspases after NGF deprivation and raise a cautionary note regarding the interpretation of findings with caspase-null animals. The choice of the death-mediating caspase pathway in the sympathetic neurons is thus dependent on the regulated relative expression of components of the pathways including those of caspases, IAPs, and IAP inhibitors.

Level IV, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.

No abstract

There was no significant difference between 1- and 5-year mortality in patients treated operatively or nonoperatively. Regardless of treatment Charlson score had a significant impact on mortality. Age significantly affected mortality in patients treated surgically.

This case-control study of 5766 patients who underwent elective thoracolumbar degenerative spine surgery revealed a prevalence of VTE of 1.5%, with a prevalence of PE of 0.88% and DVT of 0.66%. Patients with increasingly extensive surgery had a higher risk of PE, specifically those undergoing fusion of ≥5 segments.

Patients undergoing AC surgery had a significant increase in the degree of dysphagia 3 weeks after surgery compared with patients undergoing PL surgery. By final follow-up, swallowing in the AC group recovered to a level similar to preoperative and comparable to that in patients undergoing lumbar surgery at 1.5 years. Smoking, chronic obstructive pulmonary disease, and female sex are possible factors in the development of postoperative dysphagia.

No abstract

Symptomatic adjacent segment disease (ASD) after anterior cervical fusion (ACF) is reported in 25% of patients at 10 years postoperatively. Debate continues as to whether this degeneration is due to the natural history of the disk or the changed biomechanics after ACF. This study explored whether congenital stenosis predisposes patients to an increased incidence of ASD after ACF. A retrospective review of 635 patients with myelopathy or radiculopathy was performed; 364 patients had complete records for review. Patients underwent 1- to 5-level ACF (94 one-level, 145 two-level, 79 three-level, 45 four-level, and 1 five-level). Radiographs were evaluated for bony congenital stenosis using validated parameters, and ASD was measured according to Hilibrand's criteria and correlated with symptomatic ASD. Congenital stenosis was found in 21.7% of patients and radiographic ASD in 33.5%, with a significant association between these parameters. However, symptomatic ASD occurred in 11.8% of patients; no association between congenital stenosis and symptomatic ASD or myelopathy and ASD was found. Clinical results demonstrated excellent or good Robinson scores in 86.2% of patients and Odom scores in 87% of patients. Despite mostly excellent to good outcomes, symptomatic ASD is common after ACF. Although congenital stenosis appears to increase the incidence of radiographic ASD, it does not appear to predict symptomatic ASD.