Endoscopic transforaminal lumbar discectomy and reconfiguration: a postero-lateral approach into the spinal canal.

BACKGROUND: In the past, minimally invasive procedures (chemonucleolysis, laser, automated percutaneous discectomy, percutaneous manual nucleotomy, arthroscopy) have been largely confined to intradiscal work. This study represents cases of working channel, transforaminal spinal endoscopy performed using an endoscope which, because of its small size and flexibility, can bend up to 90 degrees (depending on the guiding cannula), and pass completely through the foramen into the spinal canal (truly transforaminal, as opposed to just going through part of the foramen and into the disc), to directly remove free fragments and reconfigure disc, relieving root and dural displacement at all lumbar levels. METHODS: The records of 533 patients who had outpatient, minimally invasive operations performed over a 6-year period (ending in 1995) by this author were analyzed. Of these, 110 had small scope transforaminal procedures, forming the basis of this study. RESULTS: An independent observer followed the 110 patients who had endoscopic transforaminal procedures for 2 or more years. Using MacNab's criteria, the success rate (excellent or good) was 95% in the 75 patients with disc presenting lateral to the dura-"lateral presenting,"-and 83% in the 35 patients not presenting disc for direct removal-"non-lateral presenting" (i.e., dura in the pathway)-making an overall success rate of 91%. One patient who developed discitis was the only complication. CONCLUSION: Guideable endoscopes small enough to pass completely through the foramen allow percutaneous surgery to include non-contained disc herniations and even some migrated free fragments, depending on the location. The percutaneous transforaminal endoscopic technique can be an effective, safe approach for disc removal through the foramen, especially in cases where the disc presents itself for direct removal.

How do cancer cells acquire the fuel needed to support cell growth?

In this paper we consider whether the dependency of metazoan cells on extracellular signals to maintain cell survival results in an important barrier that must be overcome during carcinogenesis. It is now generally accepted that a major barrier to cancer comes from the inability of cells to enter and progress through the cell cycle in a cell-autonomous fashion. Most of the oncogenes studied over the last two decades contribute to the ability of the cancer cell to enter and progress through the cell cycle in the absence of the instructional signals normally imparted by extracellular growth factors. Over the last two decades, it has begun to be appreciated that there is a second potential barrier to transformation. It appears that all cells in multicellular organisms need extracellular signals not only to initiate proliferation, but also to maintain cell survival. Every cell in our body expresses the proteins necessary to execute its own death by apoptosis. A cell will activate this apoptotic program by default unless it receives signals from the extracellular environment that allow the cell to suppress the apoptotic machinery it expresses. It now appears that the molecular basis of this suppression lies in the signaling pathways that regulate cellular nutrient uptake and direct the metabolic fate of those nutrients.