Kyphoplasty increases vertebral height, decreases both pain score and opiate requirements while improving functional status.

Vertebral compression fractures can result from advanced osteoporosis, or less commonly from metastatic or traumatic insults to the vertebral column, and result in disabling pain and decreased functional capacity. Various vertebral augmentation options including kyphoplasty aim at preventing the sequelae of pain and immobility that can develop as the result of the vertebral fractures. The mechanism for pain relief following kyphoplasty is not entirely understood, and the restoration of a portion of the lost vertebral height is a subject of debate. We retrospectively reviewed radiographic imaging, pain relief, analgesic intake and functional outcomes in 67 consecutive patients who underwent single- or multilevel kyphoplasty with the primary goal of quantifying the restoration of lost vertebral height. We observed a mean of 45% of the lost vertebral height restored postprocedurally. Secondarily, kyphoplasty was associated with significant decreases in pain scores, daily morphine consumption and improvement in patient-reported functional measures.

Epidural hematoma with atypical presentation.

We present a case of massive spinal epidural hematoma with an atypical presentation characterized by unilateral, isolated motor deficit in the right lower extremity on postoperative day 2 after Collis-Nissen fundoplication and a T7-8 epidural for postoperative pain. The epidural had been placed in the preoperative theater before surgery. Subcutaneous unfractionated heparin was initiated 18 hours later on postoperative day 1 with 3 times daily dosing. The patient also received 3 doses of ketorolac starting 10 hours after epidural placement. Symptoms were first reported on postoperative day 2, 37 hours after epidural placement. Thoracic magnetic resonance imaging showed an epidural hematoma extending from T2 through T12, requiring emergent decompression and evacuation. The patient made a complete recovery without any resultant neurologic deficit.

Oncolytic HSV-1 infection of tumors induces angiogenesis and upregulates CYR61.

Oncolytic viral therapy is under evaluation for toxicity and efficacy in clinical trials relating to several different tumors. We report a significant increase in the angiogenic index of oncolytic virus (OV)-treated glioma-matrigel implants (2.83-fold, P < 0.02). In a rat intracranial glioma model, large tumors from OV-treated animals were significantly more angiogenic than the phosphate-buffered saline (PBS)-treated control tumors (OV: 101 +/- 21.6; PBS: 19.8 +/- 10; P = 0.0037). Transcript profiling of OV-treated tumors revealed dysregulation of several transcripts involved in glioma angiogenesis. OV-mediated induction of CYR61 gene expression (8.94-fold, P = 0.001) correlated significantly with the presence of OV in tumor tissue in vivo (R = 0.7, P < 0.001). Further, induction of CYR61 mRNA and protein were confirmed in multiple human cancer cell lines and primary human tumor-derived cells in vitro, and in tumor lysate and cerebrospinal fluid (CSF) in vivo. Finally, we show that treatment of glioma cells with Cilengitide, known to counter CYR61-induced integrin activation, significantly suppressed the proangiogenic effect of OV treatment of gliomas (P < 0.05).