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5 巻 , 2 号
選択された号の論文の16件中1~16を表示しています
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  • 檀 健二郎
    5 巻 (1998) 2 号 p. 75
    公開日: 2009/12/21
    ジャーナル フリー
  • 比嘉 和夫, 森 真由美, 檀 健二郎
    5 巻 (1998) 2 号 p. 76-85
    公開日: 2009/12/21
    ジャーナル フリー
    Acute herpetic pain in the elderly and with trigeminal involvement is believed to become longer and be liable to progress into post-herpetic neuralgia. However, acute herpetic pain in the elderly even with trigeminal involvement disappears rapidly, when skin lesions of herpes zoster are mild. Analysis of 1, 431 patients for whom the treatment of acute herpetic pain was begun within 14 days after the onset revealed that the severity of skin lesions of herpes zoster at the worst phase rather than age and involved region most influenced the duration of acute herpetic pain. Elderly patients and those with trigeminal involvement showed significantly higher frequencies of severe skin lesions of herpes zoster. These findings indicate that acute herpetic pain in the elderly and involving trigeminal region becomes longer because of higher frequencies of severe herpes zoster in the elderly and trigeminal involvement and not because of “aging” or “trigeminal involvement” itself. Results of treatment of acute herpetic pain should be analyzed with respect to severity of skin lesions of herpes zoster.
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  • 村木 良一, 岩崎 琢也, 佐多 徹太郎
    5 巻 (1998) 2 号 p. 86-91
    公開日: 2009/12/21
    ジャーナル フリー
    Herpes zoster is caused by reactivation of varicella zoster virus (VZV) within the sensory ganglia and spread through the peripheral nerves into the skin of the corresponding dermatomes.
    We studied the histological changes of the skin lesions in patients with herpes zoster and examined the distributions of VZV antigens using two monoclonal antibodies detecting either nucleocapsid or glycoproteins of VZV on paraffin sections of formalin fixed biopsy material. VZV infection within the skin begins at the follicular epithelia or lower epidermis at first, then spreads to the macrophages, fibroblasts, vascular endothelia of the small vessels, and perineurium of cutaneous nerves in the dermis.
    Viral infections of the vascular endothelia around the involved follicles or vesiculated epidermis induce severe inflammation such as leukocytoclastic vasculitis and tissue destruction. In regard to the cutaneous nerves, VZV infections are observed within the perinerium, Schwann cells and vascular endothelia of neighboring vessels in the early erythematous or vesicular stages. In the full developed pustular or ulcerated stages, inflammatory cell infiltrates within the nerves and degeneration of the myelin sheath were observed. In the stage of postherpetic neuralgia, increase of thin nerve fibers without myelin sheath and intra fascicular fibrosis were observed.
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  • 山本 達郎
    5 巻 (1998) 2 号 p. 92-97
    公開日: 2009/12/21
    ジャーナル フリー
    Postherpetic neuralgia (PHN) is neuropathic pain syndrome. PHN occurred after herpes zoster which causes the peripheral nerve inflammation. PHN has been known to be relatively refractory to the standard analgesic agents, such as non-steroidal anti-inflammatory drugs and opioids. Anti-depressant drugs, anti-arrhythmic drugs and anti-convulsants are usually used for the treatment of PHN, but the results of this treatment are not always satisfactory.
    N-methyl-D-aspartate (NMDA) receptor dependent spinal sensitization has been shown to play an important role in the maintenance of neuropathic pain and NMDA receptor antagonists have been reported to alleviate the level of neuropathic pain in the animal model. Ketamine and dextromethorphan are the clinically available NMDA receptor antagonists and I tried to treat PHN with epidural ketamine and oral dextromethorphan. Both epidural ketamine and oral dextromethorphan successfully treated PHN. This suggested that PHN is maintained by the NMDA receptor dependent spinal sensitization.
    Recently, three new pharmacological approaches, such as systemic gabapentin administration, intrathecal admnistration of N-type voltage dependent Ca2+channel (VDCC) blocker and intrathecal nociceptin injection, have been tested for the treatment of neuropathic pain in the animal models. Gabapentin is a newly developed anti-convulsant drug. Oral gabapentin has already reported to treat PHN in the clinical situation. Release of neurotransmitter is regulated by the influx of Ca2+ into the nerve terminals through VDCCs, such as N-type VDCC. N-type VDCC blockers inhibit the substance P and glutamate release and intrathecal injection of N-type VDCC attenuates the level of neuropathic pain in the animal model. Nociceptin is an endogenous agonist for the opioid receptor likel receptor. Nociceptin has been reported to depress the spinal sensitization and to alleviate the level of neuropathic pain in the animal model. I believe that these three drugs will be the major approach to the treatment of PHN in near future.
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  • 南 敏明, 森 秀麿, 伊藤 誠二
    5 巻 (1998) 2 号 p. 98-103
    公開日: 2009/12/21
    ジャーナル フリー
    Prostaglandins (PGs) are ubiquitously distributed in virtually all mammalian tissues and organs, and it has been well documented that PGs are involved in various aspects of inflammation including pain. Accumulating evidence indicates that PGs are critical for the processing of pain, not only in the periphery but also at the spinal level.
    We showed that intrathecal (i.t.) administration of PGD2 and PGE2 induced hyperalgesia to noxious stimuli and that i.t. PGE2 and PGF induced allodynia, a state of discomfort and pain evoked by innocuous stimuli, in conscious mice. PGF augmented the allodynia evoked by PGE2 additively at submaximal doses. On the other hand, PGD2 blocked the allodynia induced by PGE2, but did not affect the PGF-induced one, suggesting that the mechanisms of allodynia induced by PGE2 and PGF may be different.
    Both glutamate and nitric oxide (NO) have recently been paid much attention because they are reported to be involved in long-term potentiation (LTP), a potential cellular mechanism for memory and learning. We demonstrated from pharmacological studies that PGE2-and PGF-induced allodynia are mediated by activation of glutamate receptors and following NO production, but in a defferent manner.
    We have recently secceeded in purification and characterization of a novel heptadecapeptide called nociceptin in bovine brains as an endogenous ligand for ROR-C, an opioid receptor homologue cloned from rat cerebrum. Intrathecal administration of nociceptin induced allodynia by innocuous tactile stimuli and hyperalgesia by noxious thermal stimuli in conscious mice. PGD2 blocked the allodynia induced by nociceptin, but did not affect the nociceptin-induced hyperal-gesia. Furthermore, the allodynia caused by nociceptin was dose-dependently blocked by glycine.
    These results demonstrate that there exist at least two mechanisms for induction of allodynia: disinhibition through anti-glycinergic effect and hyperexcitability through a pathway that includes the glutamate receptor-NO-cGMP system in the mouse spinal cord. These results also imply that endogenous PGD2 may play a modulatory role in the appearance of allodynia under physiological conditions. In a series of experiments, we demonstrated that PGs play central roles in pain transmission with interactions of other neurotransmitter systems, especially with the opioid system.
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  • 吉村 惠, 岡本 学, 馬場 洋, 河野 達朗, 下地 恒毅
    5 巻 (1998) 2 号 p. 104-111
    公開日: 2009/12/21
    ジャーナル フリー
    Neuropathic pain is defined as the pain that results from functional abnormalities of the nervous system: for example, deafferentiation or dysesthesia, referring to an unfamiliar unpleasant sensation, persisting for a long duration even in the absence of ongoing active tissue-damaging process to explain it. Although peripheral neural mechanisms are likely to contribute, in part, to the neuropathic pain, the persistence of pain after healing of the damaged tissue suggests that plastic changes in the CNS, including the spinal cord, may also play an important role in processing the transmission of neuropathic pain. Present study was designed to investigate the plastic change in synaptic transmission at the spinal level using whole cell patch clamp recordings from substantia gelatinosa (SG, lamina II of Rexed) neurons in spinal cord slices which retained an attached dorsal root dissected from adult rats with or without sciatic nerve transection (SNT). The normal and SNT rats showed no significant differences in passive and active membrane characteristics, including membrane potential, input resistance and configuration of action potential and spike after potentials. In the control rats, primary afferent stimuli with intensity sufficient to activate Aδ afferents elicited a monosynaptic fast excitatory postsynaptic current (EPSC) in 50% of neurons and a polysynaptic EPSC in 30%. In only 5% of neurons, the polysynaptic EPSC was elicited with intensity sufficient to activate Aβ afferents. In the SNT rats, however, a polysynaptic EPSC with a long latency was evoked in 79% of neurons by activation of Aβ afferents.
    Increasing stimulus intensity sufficient to activate Aδ afferents produced a EPSC which had a short and constant latency, suggesting that the Aδ afferents were functionally preserved after peripheral nerve transection. Aβ afferent-evoked monosynaptic EPSC was observed in only 2 of 34 neurons. The conduction velocity and minimum stimulus intensity for activation of Aβ and Aδ afferent fibers, assessed by intracellular recordings from dorsal root ganglion neurons, were not significantly altered in normal and sciatic nerve transected rats. These observations suggest that synaptic plasticity may occur in a subset of dorsal horn neurons and/or terminal arborization of primary afferent, particularly Aβ afferents, following nerve transection, consequently sensory information conveyed by Aβ afferents is transmitted to SG neurons which receive a few Aβ afferent inputs in the normal condition. This plastic changes in synaptic organization in the spinal dorsal horn may, therefore, underlie in part pathological pain such as allodynia and dysesthesia.
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  • 横田 敏勝, 檀 健二郎, 小山 なつ
    5 巻 (1998) 2 号 p. 112-118
    公開日: 2009/12/21
    ジャーナル フリー
    After chicken pox, varicella-zoster virus (VZV) establishes latent infection in satellite cells in sensory ganglia and eventually reactivates as acute herpes zoster (AHZ) or shingles. The reactivation leads to infection of other cells within the ganglion and results in inflammation of the posterior spinal cord, peripheral nerve and skin. Pain in AHZ is primarily due to inflammation of the infected structures. Epidural block soothes inflammation in the epineurium and controls the ongoing afferent barrage in the affected nerve fibers, preventing sensitization of second order neurons.
    Postherpetic neuralgia (PHN) is the commonest and perhaps most-dreaded complication of AHZ. Pain of PHN is often of three types; ongoing pain, superimposed paroxysmal pain and allodynia. An ongoing pain is described as burning, aching or tearing, and a superimposed paroxysmal pain as stabbing or electric shock-like. For many patients, sensations evoked by clothes contact or skin stretching with movement constitute the most unbearable part of PHN. There are sensory deficits affecting all modalities in the involved dermatomes, indicative of partial deafferentation. Intravenous lidocaine produces significant relief for PHN, and pain relief with topically applied lidocaine has also been reported. It is likely that ectopic impulses are generated from surviving axons and induce hypersensitivity of second-order neurons.
    The ectopic impulses are abolished by concentrations of lidocaine much lower than that required for blocking normal axonal conduction. Unfortunately lidocaine is not always effective. Thus deafferentation hyperactivity of second order neurons is another possible explanation.
    Allodynia is most often elicited by innocuous moving stimuli, and the mechanical allodynia appears to be mediated by large fibers. This implies abnormal synaptic connectivity at the spinal-cord level between large afferent fibers and the central pain signaling secondary neurons. It has been hypothesized that deafferentation of nociceptive fibers leads to vacancies at the level of second-order neurons, enabling these neurons to create new working synaptic connections with surviving large fibers. This reorganization may involve WDR neurons. Then the wind up response of WDR neurons which normally occurs in response to repetitive C fiber stimulation through activation of NMDA receptors, may be brought about by large fiber inputs. This may account for the wind up of tactile allodynia in PHN.
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  • 太田 孝一, 近藤 敦, 樽見 葉子, 前野 宏, 久原 幸, 大和田 栄治, 石谷 邦彦, 並木 昭義
    5 巻 (1998) 2 号 p. 119-124
    公開日: 2009/12/21
    ジャーナル フリー
    モルヒネ徐放錠の経口長期投与におけるモルヒネ血中濃度の推移について検討した. 症例は75歳, 女性で, 肺癌にて疼痛管理のため, モルヒネ徐放錠120mgを12時間間隔で投与していた. 症状が定常状態で安定した約7カ月間を対象として, 1週間間隔で朝のモルヒネ内服直前に採血し, 血中モルヒネ (M), モルヒネ3グルクロン酸 (M3G), モルヒネ6グルクロン酸 (M6G) 濃度を30回測定した. 血中M濃度は, 12~45ng/mlの範囲で変動し, 投与期間が長くなるにつれて低下する傾向がみられた. MとM3G, MとM6Gには, 有意な正の相関関係があった. 今回の結果より, モルヒネ徐放錠を長期内服中で, 鎮痛状態や全身状態に著変がない定常状態であっても, 血中モルヒネ濃度はかなり変動し, モルヒネ代謝物も, モルヒネと同様の変動をすることが明らかとなった.
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  • 後藤 広人, 松永 万鶴子, 檀 健二郎
    5 巻 (1998) 2 号 p. 125-133
    公開日: 2009/12/21
    ジャーナル フリー
    目的: 従来われわれは開腹術において, 術直前からの硬膜外ブロックと術後の持続硬膜外ブロックで求心性入力遮断を行なうことにより術後鎮痛を実施してきた. この方法にケタミンを術前術後に少量加えて中枢感作の抑制も考慮に入れた方法により術後痛にどのような改善効果が現われるか観察した. 対象と方法: 開腹手術を受けた患者43例を二重盲検法により第1群と第2群に分けた. 第1群は術前術後にケタミンを投与したケタミン群 (23例), 第2群は第1群のケタミンと同容量の生食を投与した生食群 (20例) とした. 硬膜外カテーテル挿入後, 両群とも気管内挿管による酸素-笑気併用の全身麻酔を行ない, 挿管直後にケタミン群はケタミン10mg, 生食群は同容量の生食を静注した. 回復室では両群ともブプレノルフィン0.2mg硬膜外投与した後, 0.25%ブピバカイン144ml+ブプレノルフィン0.6mgにケタミン群はケタミン75mgを加えたものを, 生食群はケタミンと同容量の生食を加えたものを3日間持続硬膜外投与した. 術後6, 12, 24, 36, 48, 72時間の安静および体動時の Visual Analogue Scale (VAS), 術後鎮痛剤使用回数, 副作用について観察した. 結果: 安静時および体動時のいずれにおいてもケタミン群は術後痛の程度が軽く推移した. しかも体動時にその効果が著明であった. また, 術後鎮痛剤の使用回数もケタミン群が少なく, ケタミンによると思われる副作用は特に認めなかった. 結論: 術前から術後にかけての局麻薬および局麻薬+ブプレノルフィンを用いた硬膜外ブロックによる求心性入力遮断に加え, 術前術後麻酔作用を起こさない少量ケタミンの投与により術後痛が軽減された. この鎮痛作用は投与量からケタミンの直接麻酔作用というよりNMDA受容体遮断効果による中枢感作の抑制によるものと考えられた.
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  • 志賀 麻記子, 横山 和子, 益田 律子, 雨宮 志門
    5 巻 (1998) 2 号 p. 134-137
    公開日: 2009/12/21
    ジャーナル フリー
    症例は47歳, 男性. 左脛骨高原骨折後, 左下肢反射性交感神経萎縮症となった. 治療目的で, 側腰部交感神経節 (L2, L3) アルコールブロックを1年の間隔をあけて2回施行した. 1回目のブロック後両下肢に, 2回目のブロック後は頸部以下の全身に無汗症が発症した. 無汗以外に神経学的異常所見を認めず, acetylcholine などによる局所の発汗誘発検査でも発汗が認められなかった. 交感神経節ブロックの直接的な影響は否定できないが, 特発性全身性無汗症がブロックで顕在化したことも考え, 副腎皮質ホルモンを用いた治療を開始したが, 無効であった.
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  • 清水 直子, 田代 雅文, 須加原 一博
    5 巻 (1998) 2 号 p. 138-141
    公開日: 2009/12/21
    ジャーナル フリー
    異型狭心症の治療中に, 腹痛や腹部膨満などイレウス症状を繰り返し, 腹部症状が狭心症発作を誘発する症例を経験した. 持続硬膜外ブロックによって腹痛や腹部膨満などのイレウス症状はもちろん, 狭心症症状も著明に改善した. しかし, 硬膜外注入を停止するとイレウス症状の増悪だけでなく狭心症発作が頻発するため, 2カ月以上にわたって持続硬膜外ブロックによる管理を必要とした. 入院が長期にわたるため, 外泊および外来通院による管理を余儀なくされた. 硬膜外カテーテルの長期留置による効果の減少, 注入時の背部痛などが生じ, カテーテルを抜去せざるをえなくなった. 保存的治療にて症状が改善せず, 最終的に手術が施行された.
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  • 藤本 幸弘, 菅井 直介, 鎮西 美栄子, 有田 英子, 田上 惠, 花岡 一雄
    5 巻 (1998) 2 号 p. 142-144
    公開日: 2009/12/21
    ジャーナル フリー
    両上肢に痛みと浮腫を伴う complex regional pain syndrome (CRPS, Type I) と考えられる60歳の男性患者に星状神経節ブロックとステロイド投与を行なった. その結果, 患者の両手の浮腫は次第に軽減し, 両上肢可動域は拡大し, 握力も初診時に比較して, 明らかに改善した. 本症例のようにCRPS (Type I) の急性期の患者には神経ブロックに加えてステロイド投与が有用と考える.
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  • 玉川 進, 小川 秀道, 的場 光昭
    5 巻 (1998) 2 号 p. 145-147
    公開日: 2009/12/21
    ジャーナル フリー
    胸部神経根ブロック時にフェノールにより呼吸停止を起こした1症例を報告する. 74歳, 男性.左肺癌による左胸部痛のため, 胸部神経根ブロックが行なわれた. 神経根へ10%フェノール水を注入しはじめた直後, 患者はうめき, 意識を失った. 呼吸は停止し, 血圧は190mmHgまで上昇するとともに心室性期外収縮が多発した. 人工呼吸とリドカイン静注により呼吸は2分後に, 意識は10分後に回復した. 後遺症はなかった. 本症例にみられたフェノール投与後の反応は血管内注入によるものと考えられる. 頻回の透視下確認によってフェノールの血管内誤入を避けること, 万一中毒が発生した場合には迅速に対処することが必要である.
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  • 浅野 斗志男, 太田 宗一郎, 飯田 宏樹, 竹田 智雄, 土肥 修司
    5 巻 (1998) 2 号 p. 148-152
    公開日: 2009/12/21
    ジャーナル フリー
    われわれは, 外傷性頸部症候群に伴う運動障害が交感神経ブロックによって一時的ではあったが著明に回復した2症例を経験した. 患者は65歳と34歳の男性で, それぞれ1年あるいは4カ月前に頸部に外傷を受けた後に, 握力の低下と手指の巧緻運動障害および軽度の痙痛を訴えて来院した. 他覚所見では患側上肢の触覚低下, 皮膚温の低下, 軽度の筋萎縮および膝蓋腱反射の亢進がみられた. 2症例ともCTとMRI画像上, 頸髄レベルで脊髄の圧迫がみられたが, 手術適応はないと判断された. 筋力低下や巧緻運動障害は理学療法や牽引療法では改善せず, 局所麻酔薬による星状神経節ブロックと胸部交感神経節アルコールブロックにより一時的ではあったが著明に回復した, 外傷性頸部症候群において, 機序は不明であるが, 交感神経系は骨格筋の運動機能に一部関与すると思われた.
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  • 玉川 進, 小川 秀道
    5 巻 (1998) 2 号 p. 153-155
    公開日: 2009/12/21
    ジャーナル フリー
    目的: 全身性エリテマトーデス(SLE)による多発性単一神経炎に対して腰部交感神経節ブロックを行ない, 疼痛の改善をみた1症例を経験したので報告した. 症例と結果: 42歳, 女性. 20年来のSLE. 両下肢の筋力低下, 筋萎縮, 知覚鈍麻が存在し, 3カ月前から疼痛が増強した. 非ステロイド系消炎鎮痛剤では疼痛コントロールが不良であり, 持続硬膜外ブロックを行ないながら当院に紹介された. 下肢の皮膚温上昇を目的に腰部交感神経節ブロックを行なったところ, 疼痛はほぼ消失した. しかし下肢のしびれと知覚鈍麻は改善しなかった. 結論: SLE神経炎では, 交感神経ブロックにより疼痛を軽減できる可能性がある.
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  • 5 巻 (1998) 2 号 p. 156-157
    公開日: 2009/12/21
    ジャーナル フリー
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