先端医療シリーズ14 神経・筋疾患 神経・筋疾患の最新医療

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21世紀の冒頭に当たって、これまで難病中の難病といわれてきた数多くの神経疾患に、多少とも根本的な治療法の開発に対する曙がやっと少し見えてきた。この画期的な時期に当たって、神経・筋疾患の最前線の知見を集めて1冊の成書にしようという試みがなされたことは、まさに時宜を得た重要な企画であると考えられる。(序文より）

目次

  • 表紙
  • カラーグラビア
  • 著者一覧
  • 本書を推薦する
  • 序文
  • 目次
  • 第1章 神経・筋疾患診療の課題と展望
  • 1. 遺伝子治療
  • 1.1 はじめに
  • 1.2 遺伝子治療の対象疾患
  • 1.3 代表的な遺伝子導入用ウイルスベクター
  • 1.4 アデノ随伴ウイルス(AAV)ベクター
  • 1.4.1 AAVベクターの特徴
  • 1.4.2 AAVベクターの神経系疾患遺伝子治療への応用
  • 1.4.3 AAVベクター研究の最近の動向
  • 1.5 レトロウイルスベクター
  • 1.6 レンチウイルスベクター
  • 1.7 アデノウイルスベクター
  • 1.8 おわりに
  • 2. 神経幹細胞
  • 2.1 はじめに
  • 2.2 神経幹細胞の特徴
  • 2.3 局在
  • 2.4 培養法
  • 2.4.1 Neurosphere法
  • 2.4.2 低密度培養法
  • 2.5 マーカー
  • 2.6 選別
  • 2.7 神経再生への応用
  • 2.7.1 内在性神経幹細胞の賦活化
  • 2.7.2 神経幹細胞の移植
  • 2.7.2.1 パーキンソン病
  • 2.7.2.2 脊髄損傷
  • 2.7.3 移植の問題点
  • 2.8 おわりに
  • 3. 薬物依存
  • 3.1 はじめに
  • 3.2 依存性薬物の型とその特徴
  • 3.2.1 依存性薬物の薬理作用
  • 3.2.2 薬物依存に関与する神経回路
  • 3.3 依存性薬物による遺伝子発現
  • 3.3.1 モルヒネによる遺伝子発現
  • 3.3.2 メタンフェタミンによる遺伝子発現
  • 3.4 展望
  • 4. アルツハイマー病における神経細胞死
  • 4.1 はじめに
  • 4.2 アルツハイマー病の病理変化
  • 4.3 老人斑、神経原線維変化と神経脱落
  • 4.4 老人斑と神経原線維変化の経時変化
  • 4.5 神経原線維変化形成機構
  • 4.6 タウ蛋白異常による神経細胞死
  • 4.7 アルツハイマー病における神経原線維変化と神経細胞死
  • 5. 遺伝性パーキンソン病の発症機構
  • 5.1 はじめに
  • 5.2 常染色体劣性パーキンソン病(AR-JP)の臨床学的特徴
  • 5.3 parkin遺伝子の単離そしてその変異
  • 5.4 parkinの機能解析
  • 5.5 parkinの細胞内局在
  • 5.6 parkinの基質
  • 5.7 孤発型PDと家族性PD
  • 第2章 神経・筋疾患の分子生物学の進歩
  • 1. 酵素異常による神経疾患
  • 1.1 概説
  • 1.2 酵素異常における代謝障害
  • 1.2.1 中間代謝産物による代謝異常
  • 1.2.2 物質の生成障害を来す代謝障害
  • 1.2.3 ビタミン、その他の補酵素あるいは活性化物質の欠損症
  • 1.2.4 酵素の成熟障害による二次的な酵素異常症
  • 1.2.5 物質の転送蛋白欠損症
  • 1.2.6 各種リセプター異常症
  • 1.3 酵素異常による神経障害の病因に関して
  • 1.3.1 代謝産物の蓄積による神経細胞障害
  • 1.3.2 細胞膜の機能障害による神経細胞障害
  • 1.3.3 生成物の合成異常に伴う神経細胞の機能障害
  • 1.3.4 その他 : 脳内リセプター異常による酵素の細胞内への転送
  • 1.4 酵素異常に基づく神経疾患の治療法の開発
  • 1.4.1 食事療法
  • 1.4.2 臓器移植
  • 1.4.3 骨髄幹細胞移植
  • 1.4.4 酵素補充療法
  • 1.4.5 酵素活性化物質の投与あるいは合成酵素阻害剤の投与
  • 1.4.6 細胞治療/遺伝子治療による神経疾患への諸療法の開発
  • 2. 細胞内シグナル伝達
  • 2.1 細胞内シグナル伝達-特にセカンドメッセンジャーについて
  • 2.2 活性化アデニル酸シクラーゼの変化
  • 2.3 PKA(Protein kinase A)のcyclic AMP結合能の変化
  • 2.4 CREBリン酸化
  • 2.5 小胞体Ca2+動態と神経系
  • 2.6 成長因子(growth factors)
  • 3. チャネル遺伝子異常による神経・筋疾患
  • 3.1 はじめに
  • 3.2 P/Q型CaチャネルαIAサブユニット(CACNAIA)遺伝子異常症
  • 3.3 L型Caチャネルα1Sサブユニット(CACNAIS)遺伝子異常症
  • 3.4 Caチャネルβ4サブユニット(CACNB4)遺伝子異常症
  • 3.5 Naチャネルαサブユニット(SCN4A)遺伝子異常症
  • 3.6 Naチャネルβ1サブユニット(SCNIB)遺伝子異常症
  • 3.7 Naチャネルα1サブユニット(SCNIA)遺伝子異常症
  • 3.8 Kチャネル(KCNA1)遺伝子異常症
  • 3.9 Kチャネル(KCNQ2, KCNQ3)遺伝子異常症
  • 3.10 Clチャネル(CLCN1)遺伝子異常症
  • 3.11 おわりに
  • 4. トリプレットリピート病
  • 4.1 はじめに
  • 4.2 トリプレットリピート病
  • 4.2.1 リピート数
  • 4.2.2 表現促進現象(anticipation)
  • 4.2.3 存在領域
  • 4.3 疾患各論
  • 4.3.1 球脊髄性筋萎縮症(spinal artd bulbar muscular atrophy;SBMA/Kennedy-Alter-Sung disease;KAS)
  • 4.3.2 ハンチントン病(Huntington disease;HD)
  • 4.3.3 歯状核赤核淡蒼球ルイ体萎縮症(dentatorubral-pallidoluysian atrophy; DRPLA)
  • 4.3.4 脊髄小脳失調症1型(spinocerebellar ataxial; SCA1)
  • 4.3.5 脊髄小脳失調症2型(SCA2)
  • 4.3.6 Machado-Joseph disease; MJD/脊髄小脳失調症3型(SCA3)
  • 4.3.7 脊髄小脳失調症6型(SCA6)
  • 4.3.8 脊髄小脳失調症7型(SCA7)
  • 4.3.9 脊髄小脳失調症8型(SCA8)
  • 4.3.10 脊髄小脳失調症12型(SCA12)
  • 4.3.11 脊髄小脳失調症17型(SCA17)
  • 4.3.12 フリードライヒ失調症(Friedreich ataxia; FRDA)
  • 4.3.13 脆弱X症候群(Fragile X syndrome)
  • 4.3.14 筋緊張性ジストロフィー(myotonic dystrophy; DM)
  • 4.3.15 眼咽頭型筋ジストロフィー(oculopharyngeal muscular dystrophy; OPMD)
  • 4.3.16 鎖骨頭蓋異形成症(cleidocranial dysplasia; CCD)
  • 4.3.17 合多指症/多合指症(synpolydactyly/poly-syndactyly)
  • 4.3.18 仮性軟骨発育不全症/多発性骨端形成不全症(pseudoachondroplasia; PSACH/multiple epiphyseal dysplasia; MED)
  • 4.3.19 ジェイコブセン症候群(Jacobsen syndrome)
  • 4.3.20 脊髄小脳失調症10型(SCA10)
  • 4.3.21 進行性ミオクローヌスてんかん(progressive myoclonic epilepsy type1; EPM1)
  • 4.4 おわりに
  • 第3章 脳血管障害とその治療
  • 1. 脳保護療法
  • 1.1 はじめに
  • 1.2 脳保護という考え方
  • 1.3 脳虚血に伴う傷害の進展機構
  • 1.4 虚血傷害を軽減させる薬剤-Neuroprotectant-
  • 1.4.1 グルタミン酸受容体拮抗薬
  • 1.4.2 GABA受容体作動薬
  • 1.4.3 Ca2+チャンネル遮断薬
  • 1.4.4 NO合成経路阻害薬およびフリーラジカル消去薬
  • 1.4.5 細胞膜に作用する薬剤
  • 1.4.6 微小循環障害の改善と脳保護
  • 1.5 低体温療法(脳低温療法)
  • 1.6 脳保護薬の臨床試験は何故成功しないか
  • 1.6.1 ヒト脳梗塞の多様性
  • 1.6.2 実験モデルの均一性
  • 1.6.3 最適用量と副作用の問題
  • 1.6.4 有効な治療開始時間(therapeutic time window)の設定ミス
  • 1.7 今後の課題と展望
  • 1.8 おわりに
  • 2. 脳梗塞の血栓溶解療法
  • 2.1 はじめに
  • 2.2 血栓溶解薬の種類
  • 2.2.1 第1世代の血栓溶解薬
  • 2.2.2 第2世代の血栓溶解薬(第1世代t-PA)
  • 2.2.3 第3世代の血栓溶解薬(第2世代t-PA)
  • 2.3 超急性期脳梗塞における血栓溶解療法の理論と歴史
  • 2.3.1 理論
  • 2.3.2 血栓溶解療法の歴史(1980年代まで)
  • 2.3.3 静注法に関する大規模臨床試験
  • 2.4 治療成績を左右する要因
  • 2.4.1 病型
  • 2.4.2 治療可能時間(therapeutic time window)
  • 2.4.3 臨床的重症度、血管閉塞部位など
  • 2.4.4 その他
  • 2.5 問題点と今後の課題
  • 2.5.1 t-PA静注法に関するガイドライン
  • 2.5.2 適応症例の選択
  • 2.5.3 脳保護療法との併用
  • 2.6 日本の現状と今後の課題
  • 3. 脳梗塞の抗凝固療法・抗血小板療法
  • 3.1 はじめに
  • 3.2 脳梗塞急性期における血小板・凝固活性化
  • 3.3 抗凝固療法
  • 3.3.1 ヘパリン
  • 3.3.2 低分子ヘパリン
  • 3.3.3 ヘパリノイド
  • 3.3.4 アルガトロバン
  • 3.4 抗血小板療法
  • 3.4.1 選択的トロンボキサンA2合成阻害薬(オザグレルナトリウム)
  • 3.4.2 アスピリン
  • 3.5 おわりに
  • 4. 新しい抗血小板療法-GPIIb/IIIa阻害薬-
  • 4.1 はじめに
  • 4.2 薬理作用機序
  • 4.3 臨床試験成績
  • 4.4 問題点と今後の展望
  • 5. 低体温療法
  • 5.1 はじめに
  • 5.2 脳梗塞治療の考え方
  • 5.3 脳卒中後の高体温と脳損傷
  • 5.4 低体温の脳保護効果
  • 5.5 低体温療法の実際
  • 5.5.1 適応
  • 5.5.2 導入、維持、復温
  • 5.5.3 治療効果
  • 5.6 線溶療法併用の有無
  • 5.7 低体温療法の大規模試験
  • 5.7.1 脳梗塞の大規模試験
  • 5.7.2 頭部外傷の大規模試験
  • 5.8 平温療法
  • 6. 脳動脈狭窄症に対するPTAおよびステント留置術
  • 6.1 はじめに
  • 6.2 適応
  • 6.3 方法
  • 6.4 結果
  • 第4章 アルツハイマー病の発症機序
  • 1. プレセニリン変異とアルツハイマー病
  • 1.1 はじめに
  • 1.2 プレセニリン変異と種類
  • 1.3 プレセニリン変異と頻度
  • 1.4 プレセニリン蛋白複合体
  • 1.5 プレセニリン変異とAβ
  • 1.6 プレセニリンとNotch
  • 1.7 プレセニリントランスジェニックマウス、ノックインマウス
  • 1.8 プレセニリンと細胞死
  • 1.9 プレセニリンとERストレス
  • 1.10 おわりに
  • 2. 異常リン酸化タウとアルツハイマー病
  • 2.1 はじめに
  • 2.2 神経原線維変化とPHF
  • 2.3 PHFタウの異常リン酸化
  • 2.3.1 免疫化学的方法
  • 2.3.2 蛋白化学的手法
  • 2.4 リン酸化部位とキナーゼ
  • 2.5 タウのリン酸化と機能
  • 2.6 タウのリン酸化と線維化
  • 2.7 FTDP-17の変異とリン酸化
  • 2.8 リン酸化タウの蓄積と神経変性
  • 2.9 まとめ
  • 3. コレステロール代謝からみたアルツハイマー病
  • 3.1 はじめに
  • 3.2 アルツハイマー病の遺伝要因とコレステロール代謝
  • 3.3 アミロイド・カスケードとコレステロール代謝系との接点
  • 3.3.1 Aβ産生とコレステロール
  • 3.3.2 Aβ凝集・沈着とコレステロール
  • 3.3.3 Aβ凝集体(オリゴマー、アミロイド)によるコレステロール代謝変動
  • 3.3.4 コレステロール代謝変動とタウ蛋白のリン酸化異常
  • 3.4 おわりに
  • 4. アポリポ蛋白Jからみたアルツハイマー病
  • 4.1 はじめに
  • 4.2 アポリポ蛋白Jの生理機能
  • 4.3 アポリポ蛋白Jと可溶性Aβ
  • 4.3.1 "In Vitro"
  • 4.3.2 "In Vivo"
  • 4.3.3 アポリポ蛋白J結合型AβのBBBを介した血液から脳内輸送
  • 4.3.4 リボ蛋白フリーAβのBBBを介した血液から脳内輸送
  • 4.4 今後の課題
  • 第5章 パーキンソン病
  • 1. α-synucleinからみたパーキンソン病
  • 1.1 はじめに
  • 1.2 α-synuclein A53T変異-Contursi家系
  • 1.3 A30P変異-ドイツ家系
  • 1.4 α-synucleinとLewy小体
  • 1.5 α-synucleinの凝集・蓄積と神経変性
  • 1.6 おわりに
  • 2. 酸化ストレスから見たドパミン神経細胞死の機序
  • 2.1 はじめに
  • 2.2 パーキンソン病における細胞死と酸化ストレス
  • 2.3 パーキンソン病とアポトーシスシグナル
  • 2.4 細胞内分子の酸化修飾とアポトーシスシグナルの活性化
  • 2.5 パーキンソン病の真の病因は何なのか
  • 2.6 ミトコンドリア : 神経細胞の生と死を制御する細胞内小器官
  • 2.7 おわりに
  • 3. DA作動薬の適応と選択
  • 3.1 はじめに
  • 3.2 DA作動薬の種類と特徴
  • 3.3 DA作動薬使用の適応
  • 3.4 DA作動薬の使い分けは可能か?
  • 3.5 DA作動薬に神経保護作用があるか?
  • 3.6 おわりに
  • 4. 手術療法の適応-深部脳刺激療法(DBS)を含めて
  • 4.1 はじめに
  • 4.2 外科治療
  • 4.2.1 大脳基底核と標的部位
  • 4.2.2 手術方法
  • 4.2.3 破壊術と刺激療法の違い
  • 4.2.4 標的神経核の選択と適応症状
  • 4.3 視床下核
  • 4.3.1 視床下核の同定
  • 4.3.2 刺激の臨床効果
  • 4.4 淡蒼球内節
  • 4.4.1 破壊または刺激の臨床効果
  • 4.5 視床VL核・Vim核
  • 4.5.1 破壊または刺激の臨床効果
  • 4.6 おわりに
  • 5. 細胞移植療法の現況と展望
  • 5.1 はじめに
  • 5.2 これまでの細胞移植の研究の概説
  • 5.3 胎児黒質細胞移植
  • 5.4 パラニューロンの移植
  • 5.5 カプセル化細胞移植
  • 5.6 神経幹細胞、胚性幹細胞の移植
  • 5.7 おわりに
  • 第6章 感染症と脱髄疾患
  • 1. プリオン病
  • 1.1 はじめに
  • 1.2 WHOの審議会によるプリオン病の感染対策に関するガイドライン
  • 1.2.1 一般的事項
  • 1.2.1.1 プリオン病の感染媒体の性質、感染性の評価
  • 1.2.1.2 対象者の同定
  • 1.2.1.3 組織の感染性
  • 1.2.1.4 暴露の経路
  • 1.2.2 患者のケア
  • 1.2.2.1 一般的事項
  • 1.2.2.2 診断的処置
  • 1.2.2.3 外科的処置
  • 1.2.2.4 外科器具の取り扱い
  • 1.2.2.5 麻酔
  • 1.2.2.6 妊娠と出産
  • 1.2.3 職業上の事故
  • 1.2.3.1 職業上での暴露
  • 1.2.3.2 暴露後の処置
  • 1.2.4 検査室における諸検査
  • 1.2.4.1 臨床検査室での安全性
  • 1.2.4.2 臨床診断における検査
  • 1.2.5 汚染除去の手順
  • 1.2.5.1 一般的事項
  • 1.2.5.2 器具の汚染除去
  • 1.2.5.3 作業場の表面の汚染除去
  • 1.2.5.4 廃棄物関連の汚染除去
  • 1.2.5.5 汚染除去のリスクのカテゴリー
  • 1.2.6 廃棄物処理
  • 1.2.7 死亡後
  • 1.2.7.1 患者死亡後の処置に関する注意
  • 1.2.7.2 剖検
  • 1.2.7.3 病理組織検査
  • 1.2.7.4 葬儀に関する事項
  • 1.2.8 Annex III. プリオン病に関する汚染除去法
  • 1.2.9 Annex IV. 発症の危険を有する健常者への対応
  • 1.2.9.1 移植、その他の治療を受けた患者
  • 1.2.9.2 家族性プリオン病
  • 1.2.10 Annex V. 変異型CJD患者、疑い患者への対応
  • 1.3 結語
  • 2. AIDS痴呆症候群
  • 2.1 AIDS痴呆症候群の概念
  • 2.2 AIDS痴呆症候群の臨床像
  • 2.3 AIDS痴呆症候群の病理組織像
  • 2.4 AIDS痴呆症候群の発症病態
  • 2.5 AIDS痴呆症候群の研究の新しい展開
  • 2.5.1 HIV-1のコレセプター発見とAIDS痴呆症候群
  • 2.5.2 HAARTとAIDS痴呆症候群
  • 2.6 おわりに
  • 3. 多発性硬化症の免疫病態と新しい治療戦略-NK細胞とNKT細胞をめぐって
  • 3.1 はじめに
  • 3.2 MSの発症機構
  • 3.2.1 脳炎惹起性T細胞
  • 3.2.2 MSの標的自己抗原
  • 3.3 MS病態の抑止機構iと免疫調節細胞
  • 3.3.1 NK細胞を介した免疫調節機構
  • 3.3.2 MSにおけるNKT細胞を介した免疫調節とその変化
  • 3.3.3 そのほかの調節細胞
  • 3.4 新しいMSの予防・治療戦略
  • 3.4.1 NK細胞を標的とした予防と治療
  • 3.4.2 NKT細胞を標的とした治療法
  • 3.5 おわりに
  • 4. 急性散在性脳脊髄炎
  • 4.1 はじめに
  • 4.2 疾患概念と病理
  • 4.3 病型
  • 4.4 臨床症候
  • 4.5 検査所見
  • 4.6 診断
  • 4.7 治療方針
  • 4.7.1 副腎皮質ステロイド薬の投与
  • 4.7.2 血漿交換療法
  • 4.7.3 免疫グロブリン大量静注療法(IVIG)
  • 4.8 予後
  • 4.9 アトピー素因を伴う脊髄炎
  • 第7章 脊髄小脳変性症と運動ニューロン疾患
  • 1. 多系統萎縮症
  • 1.1 はじめに
  • 1.2 歴史的背景
  • 1.3 臨床診断基準
  • 1.4 疫学
  • 1.5 臨床所見の特徴
  • 1.6 画像所見(MRI, Mrspectroscopy, PET)
  • 1.7 鑑別診断
  • 1.8 病理
  • 1.9 予後
  • 1.10 原因
  • 1.11 治療
  • 2. 遺伝性脊髄小脳変性症
  • 2.1 はじめに
  • 2.2 脊髄小脳変性症の分類と遺伝性脊髄小脳変性症
  • 2.3 遺伝性脊髄小脳変性症の全体的な特徴
  • 2.4 主要な遺伝性脊髄小脳変性症と診断のポイント
  • 3. 筋萎縮性側索硬化症(ALS)
  • 3.1 はじめに
  • 3.2 ALSにおける運動ニューロン死のメカニズム
  • 3.2.1 SOD1変異とALS
  • 3.2.2 グルタミン酸とALS
  • 3.3 ALSの治療
  • 3.4 まとめ
  • 4. 球脊髄性筋萎縮症
  • 4.1 はじめに
  • 4.2 病態
  • 4.3 病理
  • 4.4 診断
  • 4.4.1 遺伝
  • 4.4.2 初発症状と発症年齢
  • 4.4.3 神経学的所見
  • 4.4.4 検査所見
  • 4.4.5 その他の症候
  • 4.4.6 経過
  • 4.4.7 DNA診断
  • 4.4.8 鑑別診断
  • 4.5 治療
  • 第8章 Tauopathy
  • 1. タウの構造と生理機能
  • 1.1 はじめに
  • 1.2 タウの分子構造と発現
  • 1.2.1 タウの遺伝子
  • 1.2.2 タウ蛋白とその構造
  • 1.2.3 タウの局在
  • 1.2.4 タウの発育変化
  • 1.3 タウの機能
  • 1.3.1 微小管への結合
  • 1.3.2 タウ結合蛋白質
  • 1.3.3 タウの遺伝子導入
  • 1.3.4 タウのノックアウトマウス
  • 1.3.5 タウと細胞死
  • 2. タウ蛋白の異常リン酸化機構
  • 2.1 はじめに
  • 2.2 サイクリン依存性キナーゼ
  • 2.3 グリコーゲンシンターゼキナーゼ3(GSK-3)
  • 2.4 MAPキナーゼ
  • 2.5 その他のキナーゼ
  • 2.6 タウ蛋白を脱リン酸化するフォスファターゼ
  • 2.7 まとめ
  • 3. タウのアイソフォームとグリアの異常
  • 3.1 はじめに
  • 3.2 タウ蛋白質とそのアイソフォームに関する基礎的事項
  • 3.3 タウのアイソフォームと疾患
  • 3.4 グリアに出現するタウ凝集物
  • 3.4.1 アストロサイトのGTA
  • 3.4.2 オリゴテンドログリアのGTA
  • 3.5 GTAとNTAの異同とアイソフォームについて
  • 3.6 おわりに
  • 4. 進行性核上性麻痺と皮質基底核変性症 Corticobasal degeneration(CBD)
  • 4.1 歴史
  • 4.2 タウパチーにおける位置づけ
  • 4.3 神経病理学的特徴
  • 4.3.1 概論
  • 4.3.2 進行性核上性麻痺
  • 4.3.3 皮質基底核変性症
  • 4.4 臨床的特徴
  • 4.4.1 概論
  • 4.4.2 進行性核上性麻痺
  • 4.4.3 皮質基底核変性症
  • 4.5 考察並びにまとめ-自験例を含めた今後の展望
  • 5. Tauopathyの立場からみた前頭側頭型痴呆
  • 5.1 はじめに
  • 5.2 前頭側頭型痴呆の疾患概念の変遷
  • 5.3 家族性前頭側頭型痴呆とFTDP-17
  • 5.4 前頭側頭型痴呆とTauopathy
  • 5.5 Tauopathyをもつ(タウ陽性の病理像をもつ) 前頭側頭型痴呆
  • 5.5.1 タウ遺伝子変異により引き起こされる前頭側頭型痴呆
  • 5.5.1.1 Exon10以外のexonに起こったmutation
  • 5.5.1.2 Exon10に起こったmutation
  • 5.5.1.3 Exon10に引き続くintronに起こったmutation
  • 5.5.2 Tauopathyをもつがタウ遺伝子に変異がみつからない前頭側頭型痴呆
  • 5.5.2.1 Alnyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS/PDC) of Guam
  • 5.5.2.2 Amyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS/PDC) of Kii
  • 5.6 Tauopathyをもたない(病理像がタウ陰性の) 前頭側頭型痴呆
  • 5.6.1 Hereditary dysphasic disinhibit,ion dementia 2 (HDDD2)
  • 5.6.2 Seattle B family
  • 5.6.3 Dementia lacking distinctive histopathology (DLDH)
  • 5.6.4 タウ陰性の封人体が脳内に認められる前頭側頭型痴呆
  • 5.6.5 染色体17番以外に連鎖する前頭側頭型痴呆
  • 5.7 おわりに
  • 第9章 末梢神経疾患
  • 1. 糖尿病性ニューロパチーの成因と治療
  • 1.1 はじめに
  • 1.2 ポリニューロパチーの成因と治療
  • 1.2.1 危険因子
  • 1.2.2 成因仮説と治療法
  • 1.2.2.1 血糖管理
  • 1.2.2.2 ポリオール代謝異常
  • 1.2.2.3 血管性因子の異常
  • 1.2.2.4 蛋白糖化
  • 1.2.2.5 酸化ストレス
  • 1.2.2.6 PKC活性異常
  • 1.2.2.7 神経再生異常
  • 1.2.2.8 MAPK (mitogen-activated protein kinase)活性異常
  • 1.2.2.9 糖尿病とアポトーシス
  • 2. 慢性炎症性脱髄性ポリニューロパチー
  • 2.1 はじめに
  • 2.2 疫学的事項
  • 2.3 臨床徴候
  • 2.4 臨床検査
  • 2.5 共存疾患
  • 2.6 電気生理学的所見
  • 2.7 生検腓腹神経組織所見
  • 2.8 診断基準
  • 2.9 CIDPの亜型
  • 2.10 治療
  • 2.10.1 副腎皮質ステロイド療法
  • 2.10.2 血漿浄化療法
  • 2.10.3 ヒト免疫グロブリン大量静注療法(IVIG)
  • 2.10.4 難治例について
  • 3. Guillain-Barre症候群
  • 3.1 はじめに
  • 3.2 Guillain-Barre症候群の病態
  • 3.2.1 GBSと抗糖脂質抗体
  • 3.2.2 抗糖脂質抗体と先行感染
  • 3.2.3 抗糖脂質抗体の病態との関わり
  • 3.2.4 細胞性免疫
  • 3.3 Guillain-Barre症候群の治療
  • 3.4 おわりに
  • 4. 遺伝性運動感覚性ニューロパチー
  • 4.1 はじめに
  • 4.2 CMTの疫学的側面
  • 4.3 CMTの病型分類
  • 4.3.1 CMT1型
  • 4.3.2 CMTX型
  • 4.3.3 CMT2型
  • 4.3.4 CMT3型 (Dejerine-Sottas病 : DSD)
  • 4.3.5 CMT4型
  • 4.3.6 遺伝性圧脆弱性ニューロパチー (HNPP)
  • 4.3.7 Refsum病
  • 4.3.8 HMSN5型、6型、7型
  • 4.4 その他の新たなCMT
  • 4.5 遺伝性感覚性ニューロパチー(hereditary sensory neuropathy : HSN)
  • 4.5.1 HSN1型
  • 4.5.2 HSN2型
  • 4.5.3 HSN3型
  • 4.5.4 HSN4型(無痛無汗症)
  • 4.5.5 HSN5型
  • 4.6 治療・予後
  • 4.7 おわりに
  • 5. 家族性アミロイドポリニューロパチー(FAP)
  • 5.1 はじめに
  • 5.2 分類及び臨床症状
  • 5.3 FAPの新たな診断法
  • 5.4 FAPの肝移植
  • 5.5 FAPの遺伝子治療
  • 5.6 むすび
  • 第10章 筋疾患
  • 1. 筋疾患の遺伝子・再生治療
  • 1.1 はじめに
  • 1.2 筋ジストロフィーの原因遺伝子と分子病態
  • 1.3 筋ジストロフィーに対する治療
  • 1.3.1 遺伝子治療
  • 1.3.2 細胞移植治療
  • 1.3.3 薬物治療
  • 1.4 まとめ
  • 2. 筋ジストロフィーのステロイド療法
  • 2.1 はじめに
  • 2.2 筋ジストロフィーの薬物治療
  • 2.3 筋ジストロフィーに対するステロイド治療
  • 2.4 他の筋ジストロフィー病型に対するステロイド治療
  • 2.5 ステロイド効果の発現機序
  • 2.6 ステロイド治療の実際
  • 2.7 おわりに
  • 3. ミトコンドリア脳筋症
  • 3.1 はじめに
  • 3.2 ミトコンドリア脳筋症の分類
  • 3.2.1 生化学的異常による分類
  • 3.2.2 臨床症状による分類
  • 3.2.2.1 CPEO
  • 3.2.2.2 MERRF
  • 3.2.2.3 MELAS
  • 3.2.2.4 レーベル遺伝性視神経萎縮症(レーベル病)
  • 3.2.2.5 リー脳症
  • 3.2.2.6 糖尿病/難聴
  • 3.2.2.7 ピアソン病
  • 3.2.2.8 NARP
  • 3.2.2.9 MNGIE
  • 3.3 ミトコンドリア脳筋症の分子遺伝学的特徴
  • 3.3.1 mtDNA異常
  • 3.3.2 核DNA変異
  • 3.4 ミトコンドリア脳筋症の治療
  • 3.4.1 エネルギー代謝改善薬
  • 3.4.2 適切な対症療法
  • 3.4.3 薬物選択の注意事項
  • 3.5 おわりに
  • 4. 筋疾患における呼吸不全の治療法
  • 4.1 はじめに
  • 4.2 心肺不全の診断
  • 4.3 呼吸不全の特徴
  • 4.4 呼吸筋病理
  • 4.5 呼吸不全治療
  • 4.5.1 原理
  • 4.5.2 方法
  • 4.5.3 実際的手技
  • 4.5.4 患者・家族の指導のポイント
  • 4.6 在宅治療の必要性
  • 4.7 人工呼吸器治療の対象疾患
  • 4.8 適応
  • 4.9 合併症
  • 4.10 在宅での留意点
  • 5. DMD/BMD
  • 5.1 はじめに
  • 5.2 DMD/BMD
  • 5.3 DMD/BMDにおけるジストロフィン遺伝子変異
  • 5.4 遺伝子異常と臨床症状
  • 5.5 遺伝子診断
  • 5.6 DMD/BMDの保因者診断
  • 5.6.1 保因者診断の重要
  • 5.6.2 発端者にジストロフィン遺伝子に欠失、重複を認める場合
  • 5.6.3 発端者にジストロフィン遺伝子に微小変異を認める場合
  • 5.6.4 発端者に遺伝子の欠失、重複を認めない場合
  • 5.6.5 保因者診断の問題点
  • 5.7 出生前診断、着床前診断
  • 5.8 おわりに
  • 第11章 診断法の進歩
  • 1.脳磁図
  • 1.1 脳磁図の概要
  • 1.1.1 脳磁図検査の原理
  • 1.1.2 等価電流双極子推定-ダイポール推定
  • 1.2 脳磁図の特徴
  • 1.2.1 検出する細胞群の違い
  • 1.2.2 信号源推定の精度
  • 1.3 脳磁図測定の具体的方法
  • 1.3.1 データ記録時の留意点
  • 1.3.2 データ処理
  • 1.3.3 てんかん棘波の処理
  • 1.4 脳磁図の臨床応用
  • 1.4.1 誘発磁場
  • 1.4.2 自発脳活動
  • 1.5 臨床的にみた脳磁図と脳波の違い
  • 1.5.1 波形
  • 1.5.2 空間分解能
  • 1.6 てんかん診療での脳磁図でのトピックス
  • 1.6.1 内側側頭葉てんかん
  • 1.6.2 焦点性皮質形成異常(Focal cortical dysplasia、FCD)
  • 1.6.3 弁蓋部の検索
  • 1.7 まとめ
  • 2. 神経領域におけるマルチスライスCTの応用
  • 2.1 はじめに
  • 2.2 MDCT装置の機構と特徴
  • 2.3 頭部のルーチン検査
  • 2.4 高分解能MPR画像診断
  • 2.5 頭部・頭頸部領域でのCTA
  • 2.5.1 閉塞性動脈病変
  • 2.5.2 脳動脈瘤
  • 2.5.3 その他の応用
  • 2.6 おわりに
  • 3. ファンクショナルMRI
  • 3.1 はじめに
  • 3.2 計測原理
  • 3.3 計測の実際
  • 3.3.1 ブロックデザイン
  • 3.3.2 事象関連デザイン
  • 3.4 fMRIの臨床応用
  • 3.4.1 優位半球の決定
  • 3.4.2 脳損傷後の機能回復
  • 3.4.2.1 運動障害
  • 3.4.2.2 言語障害
  • 3.4.2.3 記憶障害
  • 3.4.3 運動性疾患
  • 3.4.4 てんかん
  • 3.4.5 その他
  • 3.4.6 最後に
  • 4. 高磁場MRI
  • 4.1 はじめに
  • 4.2 高磁場装置の実践において特記すべきMR特性
  • 4.2.1 S/N
  • 4.2.2 磁場の均一性
  • 4.2.3 緩和特性の変化
  • 4.2.4 画像特性
  • 4.3 臨床における実践
  • 4.3.1 臨床装置としての位置付け
  • 4.3.2 T2R画像
  • 4.3.3 機能画像
  • 4.4 安全性
  • 4.5 おわりに
  • 5. PET/SPECT
  • 5.1 はじめに
  • 5.2 PET/SPECT装置の発展
  • 5.3 統計的な画像再構成法の発展
  • 5.4 放射性薬剤の開発
  • 5.5 統計学的画像診断法、画像の重ね合わせ
  • 5.6 主な神経疾患におけるPET/SPECT
  • 5.6.1 脳血管障害
  • 5.6.2 痴呆の診断
  • 5.6.3 てんかん
  • 5.7 おわりに
  • 6. Cold Xe-CT
  • 6.1 はじめに
  • 6.2 Xenon-CT法の原理と測定法
  • 6.3 代表的な疾患への応用
  • 6.3.1 STA-MCA吻合術が著効を示した症例(もやもや病の男児)
  • 6.3.2 Hyperpefusionを来たした症例(CEAを施行した頸部頸動脈高度狭窄病変)
  • 6.3.3 AVMの集学的治療(Staged Embolization後に全摘出したlargeAVM症例)
  • 6.3.4 High flow bypassを用いた症例(海綿静脈洞部巨大動脈瘤)
  • 6.3.5 バイパス術を用いた脳腫瘍(脳主幹動脈をinvolveした腫瘍)
  • 6.3.6 電気刺激療法の症例1(中枢性疾痛の大脳皮質刺激療法)
  • 6.3.7 電気刺激療法の症例2(中枢性疾痛のDeep Brain Stimulation)
  • 6.4 まとめ
  • 7. 心・血管の超音波診断
  • 7.1 はじめに
  • 7.2 超音波検査の対象部位
  • 7.3 心臓と大動脈
  • 7.3.1 心疾患の評価
  • 7.3.1.1 左心耳内血栓
  • 7.3.1.2 右左シャント(Right-to-left shunt)
  • 7.3.1.3 Strands
  • 7.3.2 大動脈弓部複合粥腫病変
  • 7.4 頸部の動脈
  • 7.4.1 頸部血管超音波検査、Bモード断層法
  • 7.4.2 頸部血管超音波検査、パルスドプラ法と血流情報
  • 7.4.2.1 頸部内頸動脈の狭窄性病変
  • 7.4.2.2 頭蓋内の内頸動脈、中大脳動脈の狭窄性病変
  • 7.4.2.3 椎骨動脈の狭窄性病変
  • 7.4.3 経口腔頸部血管超音波法
  • 7.5 頭蓋内主幹動脈
  • 7.5.1 経頭蓋超音波ドプラ検査(transcranial Doppler, TCD)と経頭蓋カラードプラ検査(transcranial color duplex sonography, TCDS)
  • 7.5.2 超音波造影剤による右左シャントの診断
  • 7.5.3 経肺性左心系超音波造影剤と経頭蓋超音波検査
  • 7.5.4 Microembolic signals(MES)
  • 7.6 下肢静脈
  • 第12章 治療技術・装置の進歩
  • 1. ガンマナイフによる神経疾患の治療
  • 1.1 はじめに
  • 1.2 ガンマナイフ治療の実際
  • 1.3 転移性脳腫瘍
  • 1.4 三叉神経痛
  • 1.5 定位放射線治療の今後の展開
  • 2. 電気刺激による神経疾患の治療
  • 2.1 はじめに
  • 2.2 脳電気刺激療法
  • 2.2.1 脳電気刺激システム
  • 2.2.1.1 刺激装置
  • 2.2.1.2 刺激電極
  • 2.2.2 脳深部電気刺激の手術手技
  • 2.2.2.1 電極挿入位置の決定
  • 2.2.2.2 試験刺激
  • 2.2.2.3 刺激システムの埋込
  • 2.2.2.4 慢性刺激
  • 2.2.3 難治性疾痛に対する治療
  • 2.2.3.1 視床知覚中継核(VPL, VPM)刺激
  • 2.2.3.2 中心灰白質刺激
  • 2.2.3.3 第1次運動野刺激
  • 2.2.4 パーキンソン病に対する治療
  • 2.2.4.1 適応となる症例の選択
  • 2.2.4.2 刺激部位の選択
  • 2.2.4.3 視床Vim核刺激効果
  • 2.2.4.4 淡蒼球内節腹側(GPi)と視床下核(STN)の刺激効果
  • 2.3 脊髄電気刺激療法
  • 2.3.1 除痛術としての歴史的背景
  • 2.3.2 脊髄後索電気刺激における除痛機序
  • 2.3.3 適応となる疾患の選択
  • 2.3.4 手術手技
  • 2.3.4.1 電極の設置
  • 2.3.4.2 刺激装置のトラブルと合併症
  • 2.4 迷走神経刺激療法
  • 2.4.1 はじめに
  • 2.4.2 迷走神経刺激治療装置
  • 2.4.3 電極および刺激発生装置の埋め込み
  • 2.4.4 治療対象と治療方法
  • 2.4.4.1 日本における適応基準
  • 2.4.4.2 除外基準
  • 2.4.4.3 治療方法
  • 2.4.5 治療効果
  • 2.4.6 抗てんかん作用機序
  • 2.4.6.1 てんかんモデルにおけるてんかん抑制効果
  • 2.4.6.2 ヒトにおける抗てんかん作用
  • 2.4.7 結語
  • 3. 磁気刺激による神経疾患の治療
  • 3.1 はじめに
  • 3.2 磁気刺激法の原理と生理学的効果
  • 3.3 副作用
  • 3.4 うつ病に対するfast rTMSの治療手順
  • 3.5 抗うつ作用の機序と効果
  • 3.6 パーキンソン病に対するTMS治療
  • 3.7 脊髄小脳変性症に対するTMS療法
  • 3.8 抗てんかん作用
  • 3.9 局所性ジストニーに対する治療
  • 3.10 尿失禁に対する治療
  • 3.11 呼吸筋、腸管機能の改善
  • 3.12 慢性疾痛の軽減効果
  • 3.13 おわりに
  • 第13章 神経・筋疾患治療薬開発に関する情報
  • 1. 筋疾患治療薬
  • 1.1 はじめに
  • 1.2 遺伝子産物の異常をターゲットとした薬物療法
  • 1.2.1 遺伝子産物の異常に対する薬物療法の戦略
  • 1.2.2 デュシェンヌ/ベッカー型筋ジストロフィーに対するゲンタマイシン投与
  • 1.2.3 糖原病II型における欠損酵素の補充療法
  • 1.3 薬物療法につながる可能性を持つ筋ジストロフィーの病態生理に関する知見
  • 2. パーキンソン病治療薬
  • 2.1 はじめに
  • 2.2 新しいドパミンアゴニスト(ropiniroleとpramipexole)
  • 2.2.1 Ropinirole
  • 2.2.2 Pramipexole
  • 2.3 COMT阻害薬
  • 2.3.1 Entacapone
  • 2.4 Zonisamide
  • 2.5 神経保護薬
  • 2.5.1 CGP3466
  • 2.5.2 GDNF
  • 2.6 おわりに
  • 3. アルツハイマー病治療薬
  • 3.1 はじめに
  • 3.2 AChE阻害薬
  • 3.2.1 AChEとは
  • 3.2.2 donepezilの臨床効果
  • 3.2.3 年齢・遺伝子型からみたdonepezilの効果
  • 3.2.4 donepczilの副作用
  • 3.2.5 AChE活性とdonepezilの薬効評価
  • 3.2.6 donepezil以外のAChE阻害薬
  • 3.3 AChE阻害薬以外のADの治療薬
  • 3.3.1 ADの陽性症状に対する治療薬
  • 3.3.2 ADの陰性症状に対する治療薬
  • 3.3.3 ADの睡眠障害に対する治療薬
  • 3.3.4 ADに対するその他の治療薬
  • 3.4 AD予防の可能性
  • 3.5 HMGCoA還元酵素阻害薬と痴呆
  • 3.6 まとめ
  • 第14章 各種製品の臨床評価
  • 1. ガンマナイフの不随意運動への適用
  • 1.1 INTRODUCTION
  • 1.2 手術適応、計画
  • 1.3 結果
  • 1.4 再照射を要した症例
  • 1.5 まとめと結論
  • 技術資料編
  • ノルエピネフリン作動性神経機能改善剤ドプス(L-threo-DOPS)
  • 1 はじめに
  • 2 開発の経緯
  • 3 作用機序
  • 4 臨床成績
  • 4.1 家族性アミロイドポリニューロパチー
  • 4.2 パーキンソン病
  • 4.3 シャイドレーガー症候群
  • 4.4 起立性低血圧症状を伴う血液透析患者
  • 5 おわりに
  • サアミオン(ニセルゴリン) の概要
  • 1 はじめに
  • 2 脳血管障害に対するサアミオンの臨床効果
  • 3 脳循環代謝改善薬の再評価
  • 4 おわりに
  • パーキンソン病治療剤ドミン(R)錠(塩酸タリペキソール)
  • 1 はじめに
  • 2 開発の経緯
  • 3 ドミン錠の用法・用量
  • 4 臨床成績
  • 4.1 パーキンソン病に対する効果
  • 4.2 副作用
  • 5 薬物動態
  • 5.1 吸収
  • 5.2 代謝
  • 5.3 排泄
  • 5.4 分布
  • 6 薬理作用
  • 6.1 受容体に対する作用
  • 6.2 パーキンソン病モデル動物における有効性
  • 6.3 黒質線条体シナプス後膜のD2受容体刺激作用
  • 6.4 催吐作用が軽度である特長とそのメカニズム
  • 6.5 鎮静作用に関する検討
  • 6.6 プロラクチン分泌抑制
  • 7 新しい話題
  • 7.1 パーキンソン病の睡眠障害やRestless legs syndrome(RLS)に対する有効性
  • 7.2 ドパミンアゴニスト併用療法の試み
  • 7.3 セレギリン併用によるドミン錠の眠気軽減
  • 7.4 タリペキソールの神経保護作用を示す成績
  • パーキンソン病治療剤 エフピー(R)錠2.5
  • 1 はじめに
  • 2 薬理作用
  • 3 臨床試験
  • 3.1 早期患者でのレボドパ併用療法における有用性
  • 3.2 進行した患者での有用性
  • 3.2.1 レボドパ減量効果
  • 3.2.2 運動変動改善効果
  • 3.3 すくみ足に対する有用性
  • 3.4 抑うつ症状に対する有用性
  • 4 パーキンソン病の治療指針
  • 5 神経保護作用
  • 6 今後の方向
  • 超音波診断装置SONOS5500
  • 1 はじめに
  • 2 頭蓋内及び末梢血管検査について
  • 3 今後の展望
  • GE社製研究用高磁場MRI装置
  • 1 はじめに
  • 2 マグネット、装置の小型化
  • 3 SNRの向上
  • 4 ハードウェア
  • 5 3.0Tの用途
  • 光トポグラフィ(R)装置ETG-100
  • 1 はじめに
  • 2 光トポグラフィ装置の概要
  • 3 臨床への応用
  • 4 まとめ
  • 最新のデジタルビデオ脳波計
  • 1 はじめに
  • 2 デジタルビデオ脳波システム
  • 3 スパイク・発作検出プログラム
  • 4 収録データの再生および編集
  • 5 ネットワークでの運用
  • 術中・ICU脳神経モニタリングシステム(誘発電位、脳波、TCD、バイタルサインモニタ)
  • 1 はじめに
  • 2 ブラボーエンデバー
  • 2.1 マルチデータタイプ増幅器
  • 2.2 マルチユーザインターフェース
  • 2.3 術中、ICUモニタリング
  • 2.4 TCD(超音波ドプラー脳血流モニター)
  • 2.5 デジタルビデオEEG
  • 3 ネットワーク
  • 4 まとめ
  • 最新のダイポール推定ソフトウエアの紹介
  • 1 はじめに
  • 2 双極子推定法の原理
  • 3 ダイポール推定ソフトウエアSynaPointPro
  • 3.1 SynaPointProの特長
  • 3.2 SynaPointProの製品構成
  • 3.3 SynaPointProの評価指標(Risk, PCA)
  • 3.4 SynaPointProのてんかん焦点推定への応用例
  • 4 まとめ
  • ニコレー社製誘発・筋電計バイキングIV
  • 1 はじめに
  • 2 誘発筋電検査(NCS)
  • 2.1 運動神経伝導速度検査(MNC)、知覚神経伝導速度検査(SNC)
  • 2.2 F波検査(F-Waves)
  • 2.3 反復刺激検査(repetitive stimulation test)
  • 3 筋電図検査(EMG)
  • 3.1 自発筋電図検査(SPA)
  • 3.2 最大収縮電位検査(MVA)
  • 3.3 MUPの自動解析(AMUP)
  • 3.4 単一筋繊維筋電図(Single Fiber EMG)
  • 3.5 ターン&アンプリチュード検査(IPA)
  • 3.6 その他の筋電図検査
  • 4 誘発電位測定(EP)
  • 4.1 聴覚刺激誘発電位(AEP)
  • 4.2 体性感覚誘発電位(SEP)
  • 4.3 視覚刺激誘発電位(VEP)
  • 5 まとめ
  • 企業一覧(技術資料編)
  • 索引
  • 奥付

この書籍の参考文献

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本参考文献は電子書籍掲載内容を元にしております。

第1章 神経・筋疾患診療の課題と展望

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第2章 神経・筋疾患の分子生物学の進歩

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第3章 脳血管障害とその治療

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第4章 アルツハイマー病の発症機序

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第5章 パーキンソン病

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第6章 感染症と脱髄疾患

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第7章 脊髄小脳変性症と運動ニューロン疾患

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第8章 Tauopathy

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第9章 末梢神経疾患

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第10章 筋疾患

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第11章 診断法の進歩

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第12章 治療技術・装置の進歩

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第13章 神経・筋疾患治療薬開発に関する情報

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第14章 各種製品の臨床評価

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技術資料編

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