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われわれは2002～2009年までの7年間に144例のエピドラスコピーを行った．前半の58症例の有効率は56.9%，後半の86症例のそれは60.5%で，症例を重ねても有効率が思うように良くなっていない．この理由は慢性難治性疼痛患者の持つさまざまな要因に起因すると考えられる．したがって，術前には患者に過度の期待を抱かせないよう，慎重な術前の説明が必要である．それぞれのケースでうまくいかない可能性の予測や適応決定の参考のため，エピドラスコピーが無効であった3症例を提示した．

われわれは2002年から2008年までの間に, 慢性の腰痛, 下肢痛患者137例のエピドラスコピーを行った. これらの症例を効果と合併症についてレトロスペクティブに調べた. エピドラスコピーを受けた患者の62%で有意な痛みの軽減がみられた. 術後合併症として, 4例の大腿前面の知覚障害, 2例の下肢筋力低下, 2例の遷延性の頭痛を経験したが, これらはすべて3週間以内に消失した. 網膜出血やくも膜下出血などの重篤な合併症は経験していない. これらの結果に加え, これまでの経験で培ったエピドラスコピーのコツと要点として, 適応, 硬膜外腔造影, 手術時の体位, 麻酔法, 手術手技について述べたい.

Purpose. We compared the interadductor approach of obturator nerve block with the traditional approach in terms of the insertion-adductor contraction interval (ICI), success rate, completion of the block, and plasma lidocaine concentration. Methods. An obturator nerve block by the interadductor approach was performed by needle insertion 1 cm behind the adductor longus tendon and 2 cm lateral to the pubic arch in 12 patients, and by the traditional approach in 12 patients. Results. The ICI with the interadductor approach was significantly shorter than that with the traditional approach. The success rate, completion of the block, and plasma lidocaine concentrations were similar with both approaches. Conclusion. The interadductor approach can provide faster identification of the obturator nerve than the traditional approach.

This article introduces the equipment used for epiduroscopy and describes its indications, procedures for use, treatment outcomes, the potential complications and future developments. Epiduroscopy is used in the treatment and diagnosis of intractable low back and leg pain in patients in whom nerve block is not efficacious and when pain recurs after operation. The characteristics of epiduroscopy are that it is: 1) safe and less invasive; 2) used for endoscopic washing of the epidural space and fluoroscopic X-ray; 3) it allows injection of an agent into the lesion; and 4) it results in no change in the normal lumbar structure after operation. Epiduroscopy is expected to provide successful outcomes for many patients with intractable low back and leg pain through further improvements in equipment related to epiduroscopy, advances in technology, the accumulation of data regarding its efficacy and safety, and the coverage of treatment by insurance.

ディスポーザブル持続注入器シリンジェクター®には,従来にない注入速度可変設定機能がついている.この機能により,同一注入器で三速の注入速度が選択できるようになった.シリンジェクター®の1機種では,注入速度を1,2,及び3ml・h-1で選択でき,他の機種では注入速度を2,3,及び5ml・h-1で選択できる.3ml・h-1の注入速度を,前者は二つの制御管で,後者は一つの制御管でつくりだしている.今回,シリンジェクター®の注入速度可変設定機能の有用性を検討するため,先述の2機種の持続注入器の注入速度を3ml・h-1に設定し,両者を比較した.結果は,時間毎注入速度に有意な差は認めなかったが,可変注入速度1,2,及び3ml・h-1の持続注入器の各注入器ごとの注入速度のばらつきは,可変注入速度2,3,及び5ml・h-1の持続注入器より有意に大きかった.この理由は,制御管の誤差が,前者では後者より大きくなるためと考えられた.結論として,注入速度可変設定機能は,各機種ごとの注入速度のばらつきを大きくするといえる.

The distribution of somatic, fibre-like and punctate, non-somatic reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity was examined in dog spinal cord using horizontal, sagittal and transverse sections. The morphological features of NADPH diaphorase exhibiting neurons divided into six different neuronal types (N1–N6) were described and their laminar distribution specified. Major cell groups were identified in the superficial dorsal horn and around the central canal at all spinal levels, and in the intermediolateral cell column at thoracic level. NADPH diaphorase exhibiting neurons of the pericentral region were distributed in a thin subependymal cell column containing longitudinally-arranged small bipolar neurons with processes penetrating deeply into the intermediolateral cell column and/or running rostrocaudally in the subependymal layer. The second pericentral cell column located more laterally in lamina X contains large, intensely-stained NADPH diaphorase exhibiting neurons with long dendrites radiating in the transverse plane. Neurons of the sacral parasympathetic nucleus seen in segments S1–S3 exhibited prominent NADPH diaphorase activity accompanied by heavily-stained fibres extending from Lissauer's tract through lamina I along the lateral edge of the dorsal horn to lamina V. A massive dorsal gray commissure, with high NADPH diaphorase activity, was found in segments S1–S3. At the same segmental level a prominent group of moderately-stained motoneurons was detected in the dorsolateral portion of the anterior horn. Fibre-like NADPH diaphorase activity was found in the superficial dorsal horn and pericentral region in all segments studied. Punctate, non-somatic NADPH diaphorase activity was detected in the superficial dorsal horn, in the pericentral region all along the rostrocaudal axis and in the nucleus phrenicus (segments C4–C5), nucleus dorsalis (segments Th2–L2), nucleus Y (segments S1–S3), and the dorsal part of the dorsal gray commissure (S1–S3). A schematic diagram documenting the segmental and laminar distribution of NADPH diaphorase activity is given.

末梢組織に損傷が起こると,一次求心性神経の感受性の亢進が起こる(末梢性感作).これが脊髄への入力をいっそう増加させる.連続性のC線維の発火により脊髄後角では,C線維末端からグルタミン酸が放出され脊髄後角細胞のNMDA-receptorが活性化され,細胞内にCa++が流入する.これによりサイクロオキシゲナーゼ,一酸化窒素合成酵素が活性化されプロスタグランディンE2,一酸化窒素が産生される.これらの物質は細胞外に拡散し,近隣のC線維に作用し,神経伝達物質の放出を促す.その結果,末梢からの侵害刺激に対する後角細胞の応答は増幅される(中枢性感作).鎮痛を行なう際には求心性入力,末梢および中枢性感作の制御を考慮することが重要である.

Background and Purpose Cross-clamping of the thoracic aorta results in spinal cord ischemia and prominent systemic hypertension. Using a rat model of transient spinal cord ischemia, we examined the effects of manipulation of proximal aortic blood pressure on spinal cord blood flow (SCBF), neurological dysfunction, and changes in spinal histopathology after increasing intervals of aortic occlusion. Methods Aortic occlusion was induced by the inflation of a 2F Fogarty catheter placed into the thoracic aorta in rats anesthetized with halothane (1.5%). A tail artery was cannulated to monitor distal arterial pressure (DAP). To measure SCBF, a laser probe was implanted into the epidural space of the L-2 vertebra. To manipulate proximal arterial pressure (PAP), the left carotid artery was cannulated with a 20-gauge polytetrafluoroethylene catheter to permit blood withdrawal and infusion from a peripheral reservoir during aortic occlusion. In a survey study, spinal cord ischemia was induced in single animals at intervals of 6, 10, 15, 30, or 40 minutes with PAP controlled at 40, 60, 80, and 110 to 120 mm Hg. In a second series, ischemia was induced in groups of animals for 0, 6, 8, 10, and 12 minutes with PAP controlled at 40 mm Hg. After ischemia the animals survived for 2 to 3 days. During this recovery period, neurological functions were evaluated, followed by quantitative histopathology of the spinal cord. Results Under normal conditions, cross-clamping yields an acute proximal hypertension (125 to 135 mm Hg), a fall of DAP to 15 to 22 mm Hg, and a decrease in SCBF to 7% to 11% of baseline values. With the use of the external reservoir, proximal hypertension could be abolished and the PAP maintained at target pressures. In these studies a typical syndrome of tactile allodynia, spastic paraplegia, and necrotic changes affecting the central part of the gray matter after 24 to 48 hours of reperfusion was observed at the following combinations of ischemic intervals and PAP values: >10 minutes/40 mm Hg; >12 minutes/60 mm Hg; >16 minutes/80 mm Hg; and >30 minutes/uncontrolled. Lowering PAP resulted in a corresponding decrease in residual SCBF. Systematic studies at a PAP of 40 mm Hg at occlusion intervals of 6, 8, 10, and 12 minutes revealed that 100% of rats were paraplegic after 10- and 12-minute ischemia, and these rats showed corresponding signs of spinal histopathology. Conclusions The present study shows that systemic intraischemic hypotension (40 mm Hg) significantly potentiates neurological dysfunction after transient aortic occlusion. The mechanism of the observed effect may include elimination of collateral flow during aortic occlusion and/or consequent potentiation of hypoperfusion during reperfusion. These data indicate that PAP during occlusion should be monitored and/or controlled because it is a critical variable in the determination of outcome in this model of spinal cord ischemia.

UNLABELLED We have previously demonstrated that intrathecal morphine given after a noninjurious interval of spinal cord ischemia induced transient spastic paraparesis in a rodent model. However, the mechanism of this paraparesis is unknown. We hypothesized that morphine inhibits gamma-aminobutyric acid (GABA)ergic interneurons that control the tonus of spinal cord alpha-motoneurons and that inhibition of spinal cord interneurons may cause spastic paraparesis. In this study, we investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarified the mechanism of the spastic paraparesis induced by intrathecal morphine. Spinal cord ischemia was induced by aortic occlusion lasting 6 min. We first determined whether intrathecally administered GABA agonists (muscimol or baclofen) improve the spastic paraparesis in this model. GABA agonists did not improve the paraparesis. Next, we examined the effect of GABA antagonists (bicuculline or 5-aminovaleric acid) and determined the interaction between morphine and GABA antagonists. In an isobolographic analysis, the 50% effective dose decreased below the theoretical additive line, indicating a synergistic interaction between morphine and GABA antagonists. These results indicate that the spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors. IMPLICATIONS The purpose of this study was to investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarify the mechanism of the spastic paraparesis induced by intrathecal morphine. The spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors.

Segmental and laminar distribution of Fos-like immunoreactive, reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-exhibiting and double-labeled (Fos-like immunoreactive and NADPHd-exhibiting) neurons was examined in lower lumbar and sacral segments of the dog spinal cord using the model of multiple cauda equina constrictions. NADPHd histochemistry was used as marker of nitric oxide synthase-containing neurons. The appearance and the time-course of Fos-like immunoreactive, NADPHd and double-labeled neurons was studied at 2 h and 8 h postconstriction characterized as the incipient phase of cauda equina syndrome. The occurrence of Fos-like immunoreactive and NADPHd-exhibiting neurons in fully developed cauda equina syndrome was studied at five days postconstriction. An increase in Fos-like immunoreactivity in superficial laminae (I-II) and an enhanced NADPHd staining of lamina VIII neurons were found. A statistically significant increase in Fos-like immunoreactive neurons was found in laminae I-II and VIII-X 8 h postconstriction, and in contrast, a prominent decrease in Fos-like immunoreactive neurons was found in laminae I-II, accompanied by a statistically significant increase in Fos-like immunoreactive neurons in more ventrally located laminae VII-X at five days postconstriction. Quantitative analysis of laminar distribution of constriction-induced NADPHd-exhibiting neurons revealed a considerable increase in these neurons in laminae VIII-IX 8 h postconstriction and a statistically highly significant increase in NADPHd-exhibiting neurons in laminae VII-X five days postconstriction. Concurrently, the number of NADPHd-exhibiting neurons in laminae I-II was greatly reduced. While a low number of double-labeled neurons was found throughout the gray matter of lower lumbar and sacral segments at 2 h postconstriction, a statistically significant number of double-labeled neurons was found in lamina X 8 h and in laminae VII-X five days postconstriction. The course and distribution of anterograde degeneration resulting five days after multiple cauda equina constrictions are compared with segmental and laminar distribution of Fos-like immunoreactive and NADPHd-exhibiting neurons. Prominent involvement of the spinal cord neurons appearing in the lumbosacral segments at the early beginning and in fully developed cauda equina syndrome results in a Fos-like immunoreactivity and strongly enhanced NADPHd staining of some neuronal pools. Under such circumstances, an early cauda equina decompression surgery is advisable aimed at decreasing or preventing the derangement of the neural circuits in the lumbosacral segments.

Segmental and laminar distributions of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-exhibiting neurons were examined in the rabbit spinal cord by using horizontal, sagittal, and transverse sections. A large number of NADPHd-positive neurons in the spinal cord of rabbit appeared to fall into six categories (N1–N6), but others could not be classified. Major cell groups of NADPHd-exhibiting neurons were identified in the superficial dorsal horn and around the central canal at all spinal levels and in the intermediolateral cell column at thoracic and upper lumbar levels. NADPHd-exhibiting neurons of the pericentral region were divided into a thin subependymal cell column containing longitudinally arranged, small bipolar neurons with processes penetrating deeply into the intermediolateral cell column and/or running rostrocaudally in the subependymal layer. The second pericentral cell column located more laterally in lamina X contains large, intensely stained NADPHd-exhibiting neurons with long dendrites radiating in the transverse plane. In the pericentral region (lamina X), close association of NADPHd-exhibiting somata and fibers and mostly longitudinally oriented blood vessels were detected. Neurons of the sacral parasympathetic nucleus, seen in segments S1–S3, exhibited prominent NADPHd cellular staining accompanied by heavily stained fibers extending from Lissauer's tract through lamina I along the lateral edge of the dorsal horn to lamina V. A massive dorsal gray commissure, highly positive in NADPHd staining, was found in segments S1–S3. Scattered positive cells were also found in the deeper dorsal horn, ventral horn, and white matter. Fiberlike NADPHd staining was found in the superficial dorsal horn and pericentral region in all the segments studied. Dense, punctate, nonsomatic NADPHd staining was detected in the superficial dorsal horn, in the pericentral region all along the rostrocaudal axis, and in the nucleus phrenicus (segments C4–C5), nucleus dorsalis (segments Th2–L2), Onuf's nucleus (segments S1–S3), and the dorsal part of the dorsal gray commissure (S1–S3). J. Comp. Neurol. 406:263–284, 1999. © 1999 Wiley-Liss, Inc.

Background Previous data have shown that postischemic brain hypothermia is protective. The authors evaluated the effect of postischemic spinal hypothermia on neurologic function and spinal histopathologic indices after aortic occlusion in the rat. Methods Spinal ischemia was induced by aortic occlusion lasting 10 min. After ischemia, spinal hypothermia was induced using a subcutaneous heat exchanger. Three studies were conducted. In the first study, the intrathecal temperature was decreased to 34, 30, or 27 degrees C for 2 h beginning with initial reperfusion. In the second study, hypothermia (target intrathecal temperature 27 degrees C) was initiated with reflow and maintained for 15 or 120 min. In the third study, the intrathecal temperature was decreased to 27 degrees C for 2 h starting 5, 60, or 120 min after normothermic reperfusion. Animals survived for 2 or 3 days, at which time they were examined and perfusion fixed with 4% paraformaldehyde. Results Normothermic ischemia followed by normothermic reflow resulted in spastic paraplegia and spinal neuronal degeneration. Immediate postischemic hypothermia (27 degrees C for 2 h) resulted in decreasing motor dysfunction. Incomplete protection was noted at 34 degrees C. Fifteen minutes of immediate cooling (27 degrees C) also provided significant protection. Delay of onset of post-reflow hypothermia (27 degrees C) by 5 min or more failed to provide protection. Histopathologic analysis revealed temperature-dependent suppression of spinal neurodegeneration, with no effect of delayed cooling. Conclusions These findings indicate that the immediate period of reperfusion (0-15 min) represents a critical period that ultimately defines the degree of spinal neuronal degeneration. Hypothermia, when initiated during this period, showed significant protection, with the highest efficacy observed at 27 degrees C.