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Tae Seok Jeong, Seong Son, Sang Gu Lee, Yong Ahn, Jong Myung Jung, and Byung Rhae Yoo


The object of this study was to compare, after a long-term follow-up, the incidence and features of adjacent segment disease (ASDis) following lumbar fusion surgery performed via an open technique using conventional interbody fusion plus transpedicular screw fixation or a minimally invasive surgery (MIS) using a tubular retractor together with percutaneous pedicle screw fixation.


The authors conducted a retrospective chart review of patients with a follow-up period > 10 years who had undergone instrumented lumbar fusion at the L4–5 level between January 2004 and December 2010. The patients were divided into an open surgery group and MIS group based on the surgical method performed. Baseline characteristics and radiological findings, including factors related to ASDis, were compared between the two groups. Additionally, the incidence of ASDis and related details, including diagnosis, time to diagnosis, and treatment, were analyzed.


Among 119 patients who had undergone lumbar fusion at the L4–5 level in the study period, 32 were excluded according to the exclusion criteria. The remaining 87 patients were included as the final study cohort and were divided into an open group (n = 44) and MIS group (n = 43). The mean follow-up period was 10.50 (range 10.0–14.0) years in the open group and 10.16 (range 10.0–13.0) years in the MIS group. The overall facet joint violation rate was significantly higher in the open group than in the MIS group (54.5% vs 30.2%, p = 0.022). However, in terms of adjacent segment degeneration, there were no significant differences in corrected disc height, segmental angle, range of motion, or degree of listhesis of the adjacent segments between the two groups during follow-up. The overall incidence of ASDis was 33.3%, with incidences of 31.8% in the open group and 34.9% in the MIS group, showing no significant difference between the two groups (p = 0.822). Additionally, detailed diagnosis and treatment factors were not different between the two groups.


After a minimum 10-year follow-up, the incidence of ASDis did not differ significantly between patients who had undergone open fusion and those who had undergone MIS fusion at the L4–5 level.

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Ik-Seong Park, Joseph R. Meno, Cordelie E. Witt, Abhineet Chowdhary, Thien-Son Nguyen, H. Richard Winn, Al C. Ngai, and Gavin W. Britz


Cerebrovascular dysfunction after subarachnoid hemorrhage (SAH) may contribute to ischemia, but little is known about the contribution of intracerebral arterioles. In this study, the authors tested the hypothesis that SAH inhibits the vascular reactivity of intracerebral arterioles and documented the time course of this dysfunction.


Subarachnoid hemorrhage was induced using an endovascular filament model in halothane-anesthetized male Sprague-Dawley rats. Penetrating intracerebral arterioles were harvested 2, 4, 7, or 14 days postinsult, cannulated using a micropipette system that allowed luminal perfusion and control of luminal pressure, and evaluated for reactivity to vasodilator agents.


Spontaneous tone developed in all pressurized (60 mm Hg) intracerebral arterioles harvested in this study (from 66 rats), with similar results in the sham and SAH groups. Subarachnoid hemorrhage did not affect dilation responses to acidic pH (6.8) but led to a persistent impairment of endothelium-dependent dilation responses to adenosine triphosphate (p < 0.01), as well as a transient attenuation (p < 0.05) of vascular smooth muscle–dependent dilation responses to adenosine, sodium nitroprusside, and 8-Br-cyclic guanosine monophosphate (cGMP). Impairment of NO-mediated dilation was more sustained than adenosine- and 8-Br-cGMP–induced responses (up to 7 days postinsult compared with 2 days). All smooth muscle–dependent responses returned to sham levels by 14 days after SAH.


Subarachnoid hemorrhage led to a persistent impairment of endothelium-dependent dilation and a transient attenuation of vascular smooth muscle–dependent dilation responses to adenosine. Impairment of NOmediated dilation occurred when the response to cGMP was intact, suggesting a change in cGMP levels rather than an alteration in intracellular mechanisms downstream from cGMP.