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Kimiaki Sato, Kensei Nagata, and Yasuo Sugita

Object

Spinal extradural meningeal cysts are uncommon and rarely cause neural compression. The clinical, radiological, and histopathological characteristics of the lesions are discussed and previous reports reviewed.

Methods

The authors describe five cases of a spinal extradural meningeal cyst (three female and two male patients, with a mean age of 47 years (range 14–75 years). Four of the cysts were located at the thoracolumbar level, the fifth at the sacral level. Radiological and neuroimaging-based diagnosis was made using a combination of magnetic resonance imaging, myelography, and/or computerized tomography (CT) myelography.

A connection between the spinal subarachnoid space and the cyst cavity was demonstrated on myelography and/or CT myelography in all cases, and dural defects were confirmed visually intraoperatively. In all cases histopathological examination confirmed that the cyst wall was formed by nonspecific fibrous connective tissue without a single-cell layer of inner arachnoid lining.

Conclusions

A diagnosis of spinal extradural meningeal cyst is difficult to make based solely on histopathological examination. It is essential that the final characterization and diagnosis be based on intraoperative inspection combined with radiological and histopathological findings.

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Hisato Tanaka, Kensei Nagata, Akio Inoue, and Mitsuaki Yoshizuka

The authors conducted a study in which they applied the spinal cord compression-decompression model in rabbits to investigate the morphological changes and histopathological findings in the deformed spinal cord over a long-term period after performing decompressive surgery.

Throughout the experimental period, mangnetic resonance (MR) images were obtained frequently; after obtaining a final MR image, the spinal cord was dissected and underwent histological examination.

Immediately after decompressive surgery, axial T1-wieighted MR imaging revealed an increase in the cross-sectional area of the spinal cord during the 1st and 2nd weeks. The spinal cord area achieved a peak at an average of 5.9 weeks after decompressive surgery, when it displayed isointensity on T1- and high-intensity on T2-weighted images. The main histological findings were spongy changes in the white matter, which persisted for 4 months postsurgery. There was a significant correlation between the presurgical spinal cord area and the postsurgical decreased number of motor neuron cells.

Based on the MR imaging and histopathological studies, although the deformed spinal cord that underwent compression for 3 months was immediately restored morphologically after decompressive surgery, the change in quality in the spinal cord persisted at least 4 months.

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Jin Soo Park, Isao Shirachi, Kimiaki Sato, Noriyuki Ando, and Kensei Nagata

✓ The authors present the case of a 60-year-old woman with a neck lipoma that developed dumb-bell extradural extension, causing radiculopathy. To the best of the authors' knowledge, this is the first report of a lipoma originating in the neck with dumb-bell extradural extension through the intervertebral foramen and into the spinal canal. The lipoma was first excised from the foramen via a posterior approach to allow decompression of the nerve roots. The remaining lipomatous tissue was then resected via an anterior approach to avoid the region around the vertebral artery.

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Kotaro Jimbo, Jin Soo Park, Kimiaki Yokosuka, Kimiaki Sato, and Kensei Nagata

Object. Interleukin-1β (IL-1β) induces neurological symptoms in intervertebral disc herniation (IDH). Recently, the existence of a positive feedback loop of IL-1β, which encourages an inflammatory reaction or degeneration in the cells of tendon, has been reported. The authors hypothesized that there is a positive feedback loop of IL-1β in the cells of IDH.

Methods. Eight human intervertebral disc specimens were harvested during spinal surgery for lumbar disc herniation. The cells were stimulated in serum-free medium with or without exogenous IL-1β. The messenger RNA (mRNA) was extracted for reverse-transcription polymerase chain reaction (PCR) and real-time PCR to quantify the mRNA of endogenous IL-1β, IL-6, cyclooxygenase-2 (COX-2), and matrix metalloproteinases (MMPs). The cells were then stimulated in serum-free medium with or without exogenous IL-1β, and then exogenous IL-1β was removed. After 2, 4, and 6 days, the medium was collected, and enzyme-linked immunosorbent assay was used to measure the protein concentration of endogenous IL-1β. The mRNA expressions of endogenous IL-1β, IL-6, COX-2, and MMPs were increased significantly depending on the concentration of exogenous IL-1β. The protein concentration of endogenous IL-1β was increased over time.

Conclusions. There was a positive feedback loop of IL-1β in the cells of IDH. Furthermore, the productions of IL-6, COX-2, MMP-1, and MMP-3 were upregulated as a result of the increasing concentration of IL-1β in a positive feedback loop of IL-1β. The authors concluded that this positive feedback loop of IL-1β upregulated the production of mediators and thus can cause cessation of symptoms in IDH.

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Tatsuhiro Yoshida, Jin Soo Park, Kimiaki Yokosuka, Kotaro Jimbo, Kei Yamada, Kimiaki Sato, and Kensei Nagata

Object

Neurotropin is a nonprotein extract from the inflamed skin of rabbits inoculated with vaccinia virus. In the present study the authors sought to clarify the focal antiinflammatory effects of Neurotropin in intervertebral disc cells, and these effects were compared with those induced by the selective cyclooxygenase (COX)–2 inhibitor 6-methoxy-2-naphthylacetic acid (nabumetone).

Methods

Six human intervertebral disc specimens were harvested during spinal surgery for lumbar disc herniation. Cells were stimulated with 500 pg/ml of interleukin (IL)–1β in the presence of various concentrations of Neurotropin (0, 10−5, 10−4, and 10−3 Neurotropin Units/ml) or 50 μg/ml of nabumetone for 3 hours. The mRNA was extracted for polymerase chain reaction (PCR), and real-time PCR was used to quantify the mRNA levels of COX- 2, tumor necrosis factor (TNF)–α, and phospholipase A2. Cyclooxygenase-2, TNFα, and prostaglandin E2 (PGE2) protein concentrations were each determined by enzyme-linked immunosorbent assay.

Results

Neurotropin was found to significantly suppress the expression of COX-2 and TNFα at mRNA levels as well as the concentration of COX-2 at protein levels in a dose-dependent manner. Nabumetone was found to significantly increase COX-2 at mRNA levels but directly suppress the concentration of PGE2 in culture medium.

Conclusions

Results in this study suggest that Neurotropin has an analgesic effect through the suppression of COX-2 and TNFα in a focal area, and nabumetone shows this same effect through the suppression of PGE2 production. Thus, Neurotropin could decrease pain by blocking the central pain pathway or increasing focal antiinflammatory effects.

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Kimiaki Yokosuka, Jin Soo Park, Kotaro Jimbo, Kei Yamada, Kimiaki Sato, Michiyo Tsuru, Masayoshi Takeuchi, Sho-Ichi Yamagishi, and Kensei Nagata

Object

The authors sought to clarify the role, if any, of advanced glycation end-products (AGEs) in disc degeneration.

Methods

Intervertebral discs were analyzed for the presence of AGEs and of their receptor (RAGE) by immunohistochemical analysis. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to detect any RAGE gene expression, and real-time PCR was used to quantify messenger RNA (mRNA) levels of aggrecan and collagen types I and II in nucleus pulposus cells treated with AGEs. Aggrecan protein concentration was determined by enzyme-linked immunosorbent assay.

Immunohistochemical analysis revealed that AGEs and RAGE were localized in the nucleus pulposus of the intervertebral disc. Advanced glycation end-products were found to significantly suppress the expression of aggrecan at both mRNA and protein levels in a dose- and time-dependent manner. The levels of collagen types I and II remained unchanged after treatments with AGEs.

Conclusions

These results suggest that the accumulation of AGEs and their interaction with their receptor in the nucleus pulposus might result in the downregulation of aggrecan production responsible for disc degeneration.