The purpose of this retrospective clinical study was to evaluate the factors that affect recompression of operated vertebrae after percutaneous balloon kyphoplasty (PKP) for osteoporotic vertebral compression fractures (VCFs) and assess their clinical importance. PKP has been used for VCFs with satisfactory results. Several studies about subsequent VCFs adjacent to cemented vertebrae have been reported after PKP. However, the presence and significance of recompression of operated vertebrae have not been adequately described. In total, 80 patients treated with PKP for single thoracolumbar VCFs were reviewed. The follow-up period was at least 1 year. Patients were divided into those without recompression (maintained group, n = 70) and those with recompression (recompressed group, n = 10). Plain roentgenography (preoperative, operative, and last), preoperative BMD, and preoperative MRI were checked. Age, gender, T-score in BMD, duration of symptom, compression rate (CR) of VCF, reduction rate, kyphotic angle (KA), reduction angle, intervertebral cleft (IVC), and non-PMMA-endplate-contact (NPEC) were evaluated. To evaluate the clinical results, we checked the VAS score at each follow-up period. All data were analyzed statistically. The CR for the recompressed group increased significantly after surgery and decreased at the last follow-up (p \ 0.05). The last CR was not significantly different from the preoperative CR. The KA showed the same pattern. The preoperative, postoperative, and last VAS scores were significantly different from one another in both groups (p \ 0.05). Between the groups, preoperative KA, postoperative KA, last KA, IVC, and NPEC were significantly different (p \ 0.05). In particular, last KA, IVC, and NPEC showed highly significant differences (p \ 0.001). In a correlation test for the evaluated factors, IVC (r = 0.557) and NPEC (r = 0.496) were the most significant. The presence of IVC and NPEC may play an important role in inducing recompression of treated vertebrae after PKP. Careful observation of patients with these conditions is necessary to prevent deterioration of their clinical course.

No abstract

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 SpragueDawley 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 gcm, 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 antiapoptotic 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) 9 100.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.

Oxidative stress caused apoptosis of rat notochordal cells via both intrinsic and extrinsic (Type I and Type II) pathways. Because caspase inhibitors are being used in clinical trials, inhibition of both pathways using caspase inhibitors might be of future therapeutic importance in oxidative stress-induced apoptosis of notochordal cells. Our results suggest that inhibition of inappropriate or premature oxidative stress-induced apoptosis of notochordal cells may delay the starting point of disc degeneration.

Lumbar interbody fusion (LIF) is an effective and popular surgical procedure for the management of various spinal pathologies, especially degenerative diseases. Currently, LIF can be performed with posterior, transforaminal, anterior, and lateral approaches by open surgery or minimally invasive surgery (MIS). Each technique has its own advantages and disadvantages. In general, posterior LIF is a well-established procedure with good fusion rates and low complication rates but is limited by the possibility of iatrogenic injury to the neural structures and paraspinal muscles. Transforaminal LIF is frequently performed using an MIS technique and has an advantage of reducing these iatrogenic injuries. Anterior LIF (ALIF) can restore the disk height and sagittal alignment but has inherent approach-related challenges such as visceral and vascular complications. Lateral LIF and oblique LIF are performed using an MIS technique and have shown postoperative outcomes similar to ALIF; however, these approaches carry a risk of injury to psoas, lumbar plexus, and vascular structures. Herein, we provide a detailed description of the surgical procedures of each LIF technique. We shall then consider the pearls and pitfalls, as well as propose surgical indications and contraindications based on the available evidence in the literatures.