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Branched-chain amino acids (BCAAs) are known to be neurorestorative after traumatic brain injury (TBI). Despite clinically significant improvements in severe TBI patients given BCAAs after TBI, the approach is largely an unrecognized option. Further, TBI continues to be the most common cause of morbidity and mortality in adolescents and adults. To date, no study has evaluated whether BCAAs can be preventive or neuroprotective if taken before a TBI. We hypothesized that if BCAAs were elevated in the circulation before TBI, the brain would readily access the BCAAs and the severity of injury would be reduced. Before TBI induction with a standard weight-drop method, 50 adult mice were randomized into groups that were shams, untreated, and pre-treated, post-treated, or pre- + post-treated with BCAAs. Pre-treated mice received BCAAs through supplemented water and were dosed by oral gavage 45 min before TBI induction. All mice underwent beam walking to assess motor recovery, and the Morris water maze assessed cognitive function post-injury. On post-injury day 14, brains were harvested to assess levels of astrocytes and microglia with glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 (IBA-1) immunohistochemistry, respectively. Pre-treated and pre- +post-treated mice exhibited significantly better motor recovery and cognitive function than the other groups. The pre- + post-treated group had the best overall memory performance, whereas the pre-treated and post-treated groups only had limited improvements in memory compared to untreated animals. Pre- + post-treated brains had levels of GFAP that were similar to the sham group, whereas the pre-only and post-only groups showed increases. Although trends existed, no meaningful changes in IBA-1 were detected. This is the first study, animal or human, to demonstrate that BCAA are neuroprotective and substantiates their neurorestorative benefits after TBI, most likely through the important roles of BCAAs to glutamate homeostasis.

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STUDY DESIGN: Retrospective analysis of patients whom underwent one-level anterior lumbar interbody fusion or posterior lumbar interbody fusion with percutaneous pedicle screws. OBJECTIVE: To determine which minimally invasive fusion technique, anterior or posterior lumbar fusions, induces the least amount of muscle damage. SUMMARY OF BACKGROUND DATA: Creatine phosphokinase is recognized as a good marker for muscle damage occurring in patients after spine surgery. Minimally invasive fusions are known to reduce the amount of muscle damage. Which surgery induces the least amount of muscle damage is yet to be determined.Minimally invasive spine surgery is becoming increasing popular due to the benefits of less muscle damage, shorter hospital length and quicker recovery. Lumbar fusions are one of the most common surgeries and is becoming less invasive with the use of percutaneous pedicle screws. METHODS: Seventy-four patients whom underwent either anterior or posterior lumbar interbody fusions with percutaneous pedicle screws had preoperative and postoperative creatine kinase levels. Statistical analysis then compared the average change between the 2 groups. RESULTS: Minimally invasive anterior lumbar interbody fusions with percutaneous pedicle screws had significantly less muscle damage (P < 0.05) than minimally invasive posterior lumbar interbody fusions with percutanoues screws. CONCLUSION: Minimally invasive anterior lumbar interbody fusions with percutaneous pedicle screws cause significantly less muscle damage than minimally invasive posterior lumbar interbody fusions with percutaneous screws. Furthermore minimally invasive anterior lumbar body interbody fusions demonstrated near the same amount of muscle damage to previously published literature on lumbar microdikectomies.

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OBJECT: The authors describe 4 cases of delayed dural laceration by hydroxyapatite (HA) spacer causing tetraparesis following double-door laminoplasty. There are few reports of iatrogenic spinal cord lesions developing after double-door laminoplasty, although some complications such as postoperative C-5 paralysis or axial symptoms have been reported. The purpose of this report is to draw attention to the possibility of delayed dural laceration and its triggering mechanism. METHODS: One hundred thirty patients treated for cervical myelopathy were followed up for an average of 2 years and 9 months after laminoplasty. RESULTS: Four patients experienced aggravation of cervical myelopathy. Anterior dislodgement of HA spacers was shown on plain lateral radiographs. Follow-up T2-weighted magnetic resonance imaging demonstrated that the dislodged HA spacers were surrounded by cerebrospinal fluid at the time of aggravation. The dislodged HA spacers were removed and the dural membrane defects were repaired by patching with the fascia of the gluteus maximus muscle. The preoperative symptoms improved after the second operation in all patients. CONCLUSIONS: It is hypothesized that the loosening of the HA spacer in split spinous processes could occur with the movement of the cervical spine and/or the breakage of the suture before bone bonding. Anterior dislodgement of the HA spacer toward the spinal canal would cause dural laceration by direct friction between the dural membrane and the dislodged HA spacer, resulting in clinical aggravation. Despite the well-documented advantages of using HA spacers for double-door laminoplasty, possible laceration due to a dislodged HA spacer should be considered as a late complication.

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