Posterior dynamic stabilization in the treatment of degenerative lumbar stenosis: validity of its rationale.

OBJECT: The authors undertook this study to investigate the validity of the rationale for posterior dynamic stabilization using the Device for Intervertebral Assisted Motion (DIAM) in the treatment of degenerative lumbar stenosis. METHODS: A cohort of 31 patients who underwent single-level decompression and DIAM placement for degenerative lumbar stenosis were followed up for at least 2 years and data pertaining to their cases were analyzed prospectively. Of these patients, 7 had retrolisthesis. Preoperative and postoperative plain lumbar radiographs obtained in all patients and CT images obtained in 14 patients were analyzed. Posterior disc heights; range of motion (ROM) of proximal, distal, and implant segments; lordotic angles of implant segments; percentage of retrolisthesis; and cross-sectional area and heights of intervertebral foramina on CT sagittal images were analyzed. Clinical outcomes were evaluated using visual analog scale scores and Oswestry Disability Index scores. RESULTS: The mean values for posterior disc height before surgery, at 1 week after surgery, and at the final follow-up visits were 6.4 ± 2.0 mm, 9.7 ± 2.8 mm, and 6.8 ± 2.5 mm, respectively. The mean lordotic angles at the implant levels before surgery, at 1 week after surgery, and at the final follow-up visits were 7.1° ± 3.3°, 4.1° ± 2.7°, and 7.0° ± 3.7°, respectively. No statistically significant difference was found between the preoperative values and values from final follow-up visits for posterior disc height and lordotic angles at implant levels (p = 0.17 and p = 0.10, respectively). There was no statistically significant difference between the preoperative and final follow-up visit values for intervertebral foramen cross-sectional area and heights on CT images. The ROMs of proximal and distal segments also showed no significant decrease (p = 0.98 and p = 0.92, respectively). However, the ROMs of implant segments decreased significantly (p = 0.02). The average 31.4-month improvement for all clinical outcome measures was significant (p < 0.001). CONCLUSIONS: Based on radiological findings, the DIAM failed to show validity in terms of the rationale of indirect decompression, but it did restrict motion at the instrumented level without significant change in adjacent-segment ROM. The clinical condition of the patients, however, was improved, and improvement was maintained despite progressive loss of posterior disc height after surgery.

Pregabalin as a neuroprotector after spinal cord injury in rats: biochemical analysis and effect on glial cells.

As one of trials on neuroprotection after spinal cord injury, we used pregabalin. After spinal cord injury (SCI) in rats using contusion model, we observed the effect of pregabalin compared to that of the control and the methylprednisolone treated rats. We observed locomotor improvement of paralyzed hindlimb and body weight changes for clinical evaluation and caspase-3, bcl-2, and p38 MAPK expressions using western blotting. On histopathological analysis, we also evaluated reactive proliferation of glial cells. We were able to observe pregabalin's effectiveness as a neuroprotector after SCI in terms of the clinical indicators and the laboratory findings. The caspase-3 and phosphorylated p38 MAPK expressions of the pregabalin group were lower than those of the control group (statistically significant with caspase-3). Bcl-2 showed no significant difference between the control group and the treated groups. On the histopathological analysis, pregabalin treatment demonstrated less proliferation of the microglia and astrocytes. With this animal study, we were able to demonstrate reproducible results of pregabalin's neuroprotection effect. Diminished production of caspase-3 and phosphorylated p38 MAPK and as well as decreased proliferation of astrocytes were seen with the administration of pregabalin. This influence on spinal cord injury might be a possible approach for achieving neuroprotection following central nervous system trauma including spinal cord injury.

Vertebral compression fracture in the middle of fused segments without a history of injury: a case report.

STUDY DESIGN: A case report and review of the literature. OBJECTIVES: To report a rare case of a vertebral compression fracture in the middle of fused segments in the absence of a history of trauma, and to investigate the contributory factors. SUMMARY OF BACKGROUND DATA: Few articles have been published on vertebral fractures among fused segments. However, several articles have addressed fractures at juxtafused segments after implant removal. To the best of the authors' knowledge, only one case of compression fracture within fused segments has been previously reported. METHODS: This study involved the case of a 62-year-old woman with vertebral compression fracture of L4 within a solid fused segment region after implant removal. An investigation was conducted to identify the factors that contributed to this compression fracture. RESULTS: Plain radiographs and bone scanning showed a compression fracture of L4 within a region of fused segments (L3-S1) after implant removal without the history of injury. BMD revealed osteopenia of -2.3 SD on the neck of the femur. The patient's symptoms were relieved by conservative treatment. The contributory factors may have been persistent anterior motion, osteopenia and/or osteoporosis, and a subcortical substance defect associated with screw tracks after implant removal. CONCLUSION: Vertebral compression fractures in solid fused segments may occur as a complication of implant removal. Accordingly, if spinal implant removal is needed for revision surgery, surgeons should be aware of this significant complication.

Kyphotic angle progression of thoracic and thoracolumbar tuberculous spondylitis after surgical treatment: comparison with predicted kyphosis outcome after conservative treatment.

STUDY DESIGN: Retrospective comparative study. PURPOSE: To compare the progression of the kyphotic angle (KA) in a surgically treated group with the predicted outcome of a conservatively treated group. OVERVIEW OF LITERATURE: Late onset kyphosis is a complication of tuberculous spondylitis making its prevention a major goal of surgery. METHODS: Twenty six consecutive patients underwent an anterior reconstruction and posterior instrumented fusion in conjunction with antituberculous chemotherapy. The mean follow up was 56 months (range, 28 to 112 months). The patients were divided into subgroups based on the involved region of the thoracic and the thoracolumbar spine, initial KA, and the initial vertebral body loss (VBL(x)). The predicted KA (KA(Pd)) was calculated using the formula, KA(Pd)=5.5+30.5 VBL(x), to predict the final gibbus deformity. Kyphotic angle progression (DeltaKA) based on the radiographic measurements after surgery (DeltaKA(R)), and the predicted outcome of conservative treatment (DeltaKA(P)) with chemotherapy were compared. RESULTS: Among the subgroups of the regions involved and initial KA, the DeltaKA was radiographically superior with a reduced amount of kyphogenesis in the surgery group than the predicted outcome of the conservatively treated patients (p<0.05). The radiographic DeltaKA was similar (p>0.05) with VBL(x)

Pregabalin as a neuroprotector after spinal cord injury in rats.

The over-expression of excitotoxic neurotransmitter, such as glutamate, is an important mechanism of secondary injury after spinal cord injury. The authors examined the neuroprotective effect of pregabalin (GP) which is known as to reduce glutamate secretion, in a rat model of spinal cord injury. Thirty-two male Sprague-Dawley rats were randomly allocated to four groups; the control group (contusion injury only), the methylprednisolone treated group, the minocycline treated group and the GP treated group. Spinal cord injury was produced by contusion using the New York University impactor (25 g-cm, at the 9th-10th thoracic). Functional evaluations were done using the inclined plane test and a motor rating scale. Anti-apoptotic and anti-inflammatory effects were evaluated by in situ nick-end labeling staining technique (TUNEL) and immunofluorescence staining of cord tissues obtained at 7 days post-injury. Pregabalin treated animals showed significantly better functional recovery, and anti-apoptotic and anti-inflammatory effects. Mean numbers of TUNEL positive cells in the respective groups were 63.5 +/- 7.4, 53.6 +/- 4.0, 44.2 +/- 3.9 and 36.5 +/- 3.6. Double staining (TUNEL and anti-CC1) for oligodendrocyte apoptosis, was used to calculate oligodendrocyte apoptotic indexes (AI), using the following formula AI = (No. of doubly stained cells/No. of anti-CC1 positive cells) x 100. Mean group AIs were 88.6, 46.7, 82.1 and 70.3%, respectively. Mean numbers of activated microglia (anti-OX-42 positive cells) in high power fields were 29.8 +/- 3.9, 22.7 +/- 4.1, 21.0 +/- 3.9 and 17.8 +/- 4.3, respectively. This experiment demonstrates that GP can act as a neuroprotector after SCI in rats, and its anti-apoptotic and anti-inflammatory effects are related to its neuroprotective effect. Further studies are needed to unveil the specific mechanism involved at the receptor level.