• 早期公開 J-Stage
• 地方会後抄録の検索方法について
• 転載許諾に関する規程

Vol.64

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.63

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.62

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.61

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.60

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.59

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.58

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.57

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.56

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.55

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.54

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12
• Supplement

Vol.53

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.52

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.51

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.50

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.49

• No.1
• No.2/3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

Vol.48

• No.1
• No.2
• No.3
• No.4
• No.5
• No.6
• No.7
• No.8
• No.9
• No.10
• No.11
• No.12

• Vol.47から1まではこちら
  会員専用

• ホーム
• 52巻11号
• 臨床神経, 52：1198−1200, 2012
• 52巻11号目次

＜シンポジウム（2）―14―1＞パーキンソン病の病態生理

大脳基底核疾患の病態生理

南部　篤

自然科学研究機構生理学研究所，生体システム研究部門〔〒444―8585 岡崎市明大寺町字西郷中38〕

Malfunctions of the basal ganglia cause movement disorders, such as Parkinson's disease and dystonia. Several models have been proposed to explain the pathophysiology of these disorders: (1) Firing rate model: activity imbalance between the direct and indirect pathways changes the mean firing rate of output nuclei of the basal ganglia and induces hypokinetic or hyperkinetic movement disorders; (2) Firing pattern model: oscillatory and/or synchronized activity observed in the basal ganglia disturbs information processing in the basal ganglia, resulting in motor symptoms; (3) Dynamic activity model: movement-related activity changes through the direct and indirect pathways disrupt balance between movement-related inhibition and surrounding excitation in the output nuclei, and induce motor symptoms. Each model will be critically discussed in this review.
Full Text of this Article in Japanese PDF (194K)

(臨床神経, 52：1198−1200, 2012)
key words：大脳基底核，大脳基底核疾患，パーキンソン病，病態生理

（受付日：2012年5月24日）