Navigated Simultaneous Lateral Minimally Invasive Tubular and Posterior Mini-Open Access for Removal and Revision of Triangular Sacroiliac Joint Implants: A Technical Note.

BACKGROUND: Sacroiliac joint (SIJ) fusion, to treat back pain caused by SIJ dysfunction, can employ open or minimally invasive surgery (MIS) techniques and either cylindrical (screw-shaped) or triangular (wedge-shaped) implants. Fusion nonunion sometimes explains recurrent SIJ pain following fusion and occasionally requires hardware revision. MIS revision minimizes patient pain, infection, and disability, but due to the triangular implant size and form factor, implant removal can present challenges for MIS access during the explantation and achieving good bony purchase for reinstrumentation. Here, we report a prone single-position lateral MIS/posterior mini-open procedure for triangular-implant SIJ fusion revision. METHODS: The patient is a 72-year-old female who underwent right SIJ fusion for lower back and leg pain sustained after a fall 2 years prior but experienced recurrent pain over the subsequent 2 years, with imaging findings of right SIJ peri-hardware lucencies and diagnostic injections confirming persistent right-sided sacroiliitis. RESULTS: The patient underwent hardware removal using the lateral MIS incision with table-mounted tubular access and image-guided navigation to maintain exposure, plus simultaneous reinstrumentation using a navigated S2-alar-iliac screw and iliac bolt construct with connecting rod through the posterior mini-open incision made for the navigation reference frame spinous process clamp. CONCLUSIONS: The use of navigation and MIS access can significantly decrease the complexity of lateral hardware removal, and mini-open navigated screw-and-rod constructs offer reinstrumentation options accessible to surgeons unfamiliar with specialized posterior SIJ systems.

Adult Prg4+ progenitors repair long-term articular cartilage wounds in vivo.

The identity and origin of the stem/progenitor cells for adult joint cartilage repair remain unknown, impeding therapeutic development. Simulating the common therapeutic modality for cartilage repair in humans, i.e., full-thickness microfracture joint surgery, we combined the mouse full-thickness injury model with lineage tracing and identified a distinct skeletal progenitor cell type enabling long-term (beyond 7 days after injury) articular cartilage repair in vivo. Deriving from a population with active Prg4 expression in adulthood while lacking aggrecan expression, these progenitors proliferate, differentiate to express aggrecan and type II collagen, and predominate in long-term articular cartilage wounds, where they represent the principal repair progenitors in situ under native repair conditions without cellular transplantation. They originate outside the adult bone marrow or superficial zone articular cartilage. These findings have implications for skeletal biology and regenerative medicine for joint injury repair.

Surgical anatomy, radiological features, and molecular biology of the lumbar intervertebral discs.

The intervertebral disc (IVD) is a joint unique in structure and functions. Lying between adjacent vertebrae, it provides both the primary support and the elasticity required for the spine to move stably. Various aspects of the IVD have long been studied by researchers seeking a better understanding of its dynamics, aging, and subsequent disorders. In this article, we review the surgical anatomy, imaging modalities, and molecular biology of the lumbar IVD. Clin. Anat. 30:251-266, 2017. © 2017 Wiley Periodicals, Inc.

Reversal of preoperative catatonic state by surgical resection of an adult-onset craniopharyngioma: case report and review of the literature.

OBJECTIVE: To describe a case of a rare adult-onset craniopharyngioma presenting as rapidly progressive catatonia that was reversed after surgical resection of the tumor. BACKGROUND: Profoundly depressed states of awareness classified as either catatonia or akinetic mutism have been reported in patients with hypothalamic neoplasms, but reports of improvement in consciousness level after surgical resection are rare and limited to very large tumors. METHOD: Medical, neurologic, and psychiatric histories, physical examination findings, laboratory workup results, pathologic and imaging studies, and response to surgical treatment were documented. RESULT: The patient showed progressive improvement in mental status and overall neurologic function after surgical treatment. CONCLUSIONS: The search for an etiology of a profound catatonic state should include the probability of a suprasellar/hypothalamic lesion, which in this case was owing to the rare finding of an imaging-documented adult-onset craniopharyngioma.

VEGF Stimulates the ERK 1/2 signaling pathway and apoptosis in cerebral endothelial cells after ischemic conditions.

BACKGROUND AND PURPOSE: Cerebral endothelial cells that line microvessels play an important role in maintaining blood flow homeostasis within the brain-forming part of the blood-brain barrier. These cells are injured by hypoxia-induced reperfusion, leading to blood-brain barrier breakdown and exacerbation of ischemic injury. We investigated the roles of vascular endothelial growth factor (VEGF) and the downstream extracellular signal-regulated kinase (ERK) protein after oxygen-glucose deprivation (OGD) in primary endothelial cells. METHODS: Primary mouse endothelial cells were isolated and subjected to OGD. Western analysis of VEGF and ERK 1/2 protein levels was performed. Cells were transfected with VEGF small interference RNA. A terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) assay and DNA fragmentation assay were used on mouse endothelial cells that overexpress copper/zinc-superoxide dismutase (SOD1). RESULTS: VEGF protein expression was induced and its receptor, Flk-1, was stimulated by OGD. Phosphorylation of ERK 1/2 protein levels was upregulated. Inhibition of phosphorylated ERK (pERK) expression by U0126 reduced endothelial cell death by OGD. Transfection of small interfering RNA for VEGF also inhibited an increase in pERK, suggesting that VEGF acts via ERK. The TUNEL and DNA fragmentation assays showed a significant decrease in TUNEL-positivity in the SOD1-overexpressing endothelial cells compared with wild-type cells after OGD. CONCLUSIONS: Our data suggest that OGD induces VEGF signaling via its receptor, Flk-1, and activates ERK via oxidative-stress-dependent mechanisms. Our study shows that in cerebral endothelial cells the ERK 1/2 signaling pathway plays a significant role in cell injury after OGD.

Outcomes of surgery for resection of regions of symptomatic radiation injury after stereotactic radiosurgery for arteriovenous malformations.

OBJECTIVE: Although radiation injury after stereotactic radiosurgery (SRS), including radiation necrosis (RN), is often treated with surgical resection, detailed outcome data are lacking after resection of symptomatic radiation-injured regions with imaging characteristics suspicious for RN after SRS for arteriovenous malformations (AVM). We present outcomes in seven such patients. METHODS: We conducted a retrospective chart review of seven patients with AVMs of Spetzler-Martin Grades II (n = 1), III (n = 2), and IV (n = 4) who underwent helium ion, proton beam, or gamma knife SRS and required resection of RN-suspicious tissue 1 to 24 months after post-SRS symptom onset. Postoperative outcomes included Karnofsky Performance Scale (KPS) score and time to symptomatic improvement. RESULTS: Symptomatic improvement required at least 9 months in the three patients with large regions suspicious for RN (>or=4 cm), whereas of four patients with smaller regions (<4 cm), three showed improvement within 2 months (P < 0.05). The remaining patient, who showed no benefit, underwent resection 2 years after the onset of RN symptoms (compared with

Carbohydrate source influences gelatinase production by mouse astrocytes in vitro.

Molecular mediators of ischemic brain injury include intercellular adhesion molecule-1 (ICAM-1) and matrix metalloproteinase-9 (MMP-9), involved in the alteration of blood-brain barrier permeability and induced in astroglial cultures by tumor necrosis factor-alpha (TNF-alpha). Hyperglycemia is known to aggravate in vivo ischemic brain damage, while treatment with sorbitol shows benefit in reducing vasogenic brain edema. This study investigated whether a culture medium carbohydrate source could alter the astrocyte production of MMP-9 and ICAM-1 in vitro. The growth of astrocytes in 12.5 mM glucose, 25 mM glucose, or 25 mM sorbitol for 14 days did not alter cellular release of lactate dehydrogenase, uptake of Trypan blue, or surface expression of glial fibrillary acidic protein (GFAP). ICAM-1 levels were similar in astrocytes grown in glucose or sorbitol both under basal conditions and after TNF-alpha stimulation for 48 h. In contrast, levels of proMMP-9 released from astrocytes cultured for 14 days in 25 mM sorbitol reached only 55-28% of those obtained from cultures in 25 mM glucose after stimulation with 1,000 U/ml (P = 0.05) or 5,000 U/ml (P < 0.025) TNF-alpha, respectively. Limiting the duration of pre-stimulation sorbitol exposure to 48 h resulted in lower proMMP-9 levels than in glucose cultures after 5,000, but not 1,000, U/ml TNF-alpha, and differences were not significant when sorbitol exposure was further reduced to 24 h. Incubation in mixed glucose/sorbitol media did not affect the release of proMMP-9. These findings suggest that MMP-9 production may be increased in astrocytes as a consequence of glucose metabolism, which can be avoided by growth in sorbitol alone.