Salvage operation for persistent low back pain and sciatica induced by percutaneous laser disc decompression performed at outside institution: correlation of magnetic resonance imaging and intraoperative and pathological findings.

OBJECTIVE: We identified several problems associated with percutaneous lumbar disc decompression (PLDD) based on a study of patients who required salvage operations for complications after undergoing PLDD at an outside institution. BACKGROUND DATA: PLDD has been performed as a new treatment for intervertebral disc herniation in recent years, and its safety and effectiveness are in the process of being established. Because the procedure is simple to perform under local anesthesia, inappropriate irradiation and application to patients for whom it is not indicated have sometimes resulted in a poor outcome and serious complications. METHODS: The patients comprised 10 with lumbar disc herniation and three with lumbar spondylolisthesis. We analyzed the magnetic resonance (MR) imaging and operative findings as well as the pathological features of surgically obtained disc specimens and studied their relationships with the clinical outcomes of the operations. RESULTS: Initial examination of all patients at our hospital showed that PLDD had no effect on low back pain or sciatica. In patients who showed MR signal changes in the end-plate, the pathological examination revealed extensive necrosis of cartilage and bone. During salvage operations, severe adhesion of herniated masses to nerve roots was often observed, with carbonized disc tissue surrounding the nerve roots and might have their nerve root injured thermally. CONCLUSION: PLDD is associated with significant risk of disc, end-plate, and nerve root injuries, contrary to the general belief that the procedure is minimally invasive. Our findings highlight the need for careful diagnosis and sufficient technical skill when selecting PLDD as a treatment option.

Localization and changes of intraneural inflammatory cytokines and inducible-nitric oxide induced by mechanical compression.

STUDY DESIGN: Investigation of intraneural inflammation induced by mechanical compression. OBJECTIVES: In order to investigate the mechanism of neuropathy, this study used a median nerve compression model in dogs. Immunohistochemistry was used to examine the localization and changes of inflammatory cytokines and nitric oxide (NO). SUMMARY OF BACKGROUND DATA: The manifestation of pain at sites of inflammation has a close relationship with the release of mediators from macrophages such as interleulin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), as well as with NO. However, the mediators involved in inflammation of nerve due to mechanical compression remain almost unknown. METHODS: In this study, the median nerve of dogs was compressed with a clip for three weeks to observe the changes caused by compression. Immunohistochemistry was done by the avidin-biotin-peroxidase complex method to observe the changes of T cells (CD45) and macrophages (Mac-1) after compression. Antibodies against IL-1beta, TNF-alpha, and inducible nitric oxide synthesis (i-NOS) were used to examine the localization and changes of these mediators caused by nerve compression. RESULTS: In control animals, resident T cells were detected, but there were no macrophages. IL-1beta was positive in the Schwann cells and vascular endothelial cells. However, no cells showed TNF-alpha or i-NOS positively. After nerve compression, numerous T cells and macrophages appeared among the demyelinized nerve fibers. The macrophages were positive for IL-1beta, TNF-alpha and i-NOS. CONCLUSION: Inflammatory cytokines and NO may be involved in intraneural inflammatory changes arising from mechanical compression. Such mediators may be of importance in the manifestation of neuropathy.

Effect of lumbar nerve root compression on primary sensory neurons and their central branches: changes in the nociceptive neuropeptides substance P and somatostatin.

STUDY DESIGN: This study examined the effect of lumbar nerve root compression on nociceptive neuropeptides in the axonal flow using an in vivo model. OBJECTIVES: The aim was to investigate changes in axonal flow after nerve root compression by using immunohistochemical techniques to detect substance P (SP) and somatostatin (SOM), which is thought to be involved in temperature and pain sensation. SUMMARY OF BACKGROUND DATA: Disturbance of intraradicular blood flow and nerve fiber deformation caused by mechanical compression are thought to be involved in the pathophysiology of diseases characterized by radicular symptoms, such as lumbar disc herniation and lumbar canal stenosis. However, little research has been conducted into the changes of axonal flow associated with nerve root compression. METHODS: In dogs, the lumbar nerve roots were compressed using four types of clips with different pressures. Changes of SP and SOM levels in the spinal dorsal horn, dorsal root, and dorsal root ganglions were examined immunohistochemically after compression for 24 hours or 1 week. RESULTS: After compression for 24 hours, axonal flow in the dorsal root was impaired, accumulation of SP and SOM was observed distal to the site of compression, and there was a decrease in the number of dorsal root ganglion cells showing positively for these neurotransmitters. Compression for 1 week resulted in a decrease in the number of SP- and SOM-positive fibers in the spinal dorsal horn. CONCLUSION: Change of axonal flow resulting from direct nerve compression could affect the metabolism of neurotransmitters that flow inside the axons and may be a primary cause of the decline in nerve function.