リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

リケラボ 全国の大学リポジトリにある学位論文・教授論文を一括検索するならリケラボ論文検索大学・研究所にある論文を検索できる

リケラボ 全国の大学リポジトリにある学位論文・教授論文を一括検索するならリケラボ論文検索大学・研究所にある論文を検索できる

大学・研究所にある論文を検索できる 「上肢反復運動の新規評価法開発 : パーキンソン病での検討と補足運動野神経修飾の影響の検討」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

コピーが完了しました

URLをコピーしました

論文の公開元へ論文の公開元へ
書き出し

上肢反復運動の新規評価法開発 : パーキンソン病での検討と補足運動野神経修飾の影響の検討

佐藤, 和也 東京大学 DOI:10.15083/0002006964

2023.03.24

概要

[課程-2]
審査の結果の要旨
氏名 佐藤 和也
本研究はパーキンソン病(PD)に対する反復経頭蓋磁気刺激(rTMS)による新規治療
法の開発を目指すにあたり、適切な評価手法の開発と rTMS の刺激方法の検討を行ったも
のであり、下記の結果を得ている。
1. 補足運動野(SMA)に対する rTMS 治療では PD の動作緩慢に効果があったと報告
されており、動作緩慢で評価される上肢反復運動のうち指タッピング(FT)と手の
回内回外運動(P-S)の 2 つをモーションキャプチャーシステムで評価した。27 名
の PD 患者と 25 名の健常コントロール(HC)を比較し、PD では薬物内服後の on
時と薬効が切れた off 時の 2 条件で評価を行った。先行研究が多く微細な運動である
FT と、報告が少なくより粗大な運動である P-S は、いずれも PD の off 時に運動の
振幅と速度の低下を示し、FT での既報告と合致する動作緩慢の特徴を示した。しか
し PD の off と on の比較において、FT では各項目に有意な改善がなかった一方、PS では複数の項目が有意に改善し、P-S は FT と比較して症状の改善を反映しやすい
可能性が示唆された。また、HC と比較して PD では運動の各要素の不規則さが大き
く、特徴的な結果が示された。
2. 17 名の健常者を対象とし、PD の病態において重要である SMA に対して従来の
rTMS と比較してより安定して高い効果が得られる単相性 4 連発磁気刺激法
(QPS)による刺激を行い、生理学的な影響を検討した。一次運動野(M1)を刺激
した際に M1 興奮性を促通する QPS5、M1 興奮性を抑制する QPS50 と Sham 刺激
の 3 条件で SMA に対する QPS(SMA-QPS)を行い、M1 興奮性の変化を MEP
(motor evoked potential)で評価した。SMA に対する QPS5 で MEP は増大し、
QPS50 では MEP は低下する傾向にあり、QPS5 と QPS50 間で MEP 振幅に統計学
的に有意な差を認めた。その一方で、QPS5、QPS50 と Sham の間では統計学的な
有意差が示されなかった。また、M1 での大脳皮質内における抑制性機構を反映する
短潜時皮質内抑制(SICI)
、皮質内促通(ICF)はいずれの刺激条件においても変化
しなかった。この結果により、SMA-QPS は M1 の皮質興奮性を変化させることが示
され、かつその変化は M1 の皮質内の抑制性・促通性機構とは別個の機序によりも
たらされることが示唆された。QPS と Sham 間で差が有意でなかった一因は今回の
刺激強度が比較的弱かったことと考察された。
3. PD 患者に対して SMA-QPS を行う前段階として 6 名の健常成人を対象に SMA-QPS
を行い、上肢の反復運動として FT、P-S の変化を評価した。QPS50 を刺激条件とし

た SMA-QPS50、M1-QPS50、SMA-Sham の 3 条件間で、FT、P-S のいずれの測定
項目にも変化を認めなかった。参加者が 6 名と非常に少ないことに加え、比較的若
年な健常成人を対象としたため FT、P-S のパフォーマンスが高く、天井効果により
効果が表れにくかったことなどを原因に挙げ、実際にこれらの運動が障害されてい
る PD でより多数例の検討が必要であることを考察した。
以上、本論文は PD の動作緩慢の評価として上肢反復運動では FT 以外に P-S の客観的
計測が有用である可能性を新規に報告した。また、SMA に対する QPS が M1 の興奮性を
修飾可能であることを初めて示した。SMA-QPS は PD の rTMS 治療に応用できる可能性
があり、本研究での上肢反復運動の評価手法はその効果判定に有効であると考えられる。
これまでに定量的な運動評価により rTMS の治療効果の判定を試みた報告はなく、本研究
は今後の rTMS による新規治療法開発において重要な貢献をなすと考えられる。
よって本論文は博士( 医学 )の学位請求論文として合格と認められる。

この論文で使われている画像

参考文献

[1]

日本神経学会、「パーキンソン病診療ガイドライン」作成委員会(編), “パーキ

ンソン病診療ガイドライン2018,” 2018.

[2]

M. Yamawaki, M. Kusumi, H. Kowa, and K. Nakashima, “Changes in prevalence and

incidence of Parkinson’s disease in Japan during a quarter of a century,”

Neuroepidemiology, vol. 32, no. 4, pp. 263–269, 2009.

[3]

S. Lesage and A. Brice, “Parkinson’s disease: From monogenic forms to genetic

susceptibility factors,” Hum. Mol. Genet., vol. 18, no. R1, pp. 48–59, 2009.

[4]

H. Deng, P. Wang, and J. Jankovic, “The genetics of Parkinson disease,” Ageing Res.

Rev., vol. 42, no. September 2017, pp. 72–85, 2018.

[5]

D. Chang et al., “HHS Public Access,” vol. 49, no. 10, pp. 1511–1516, 2018.

[6]

A. J. Hughes et al., “A Clinicopathologic Study of 100 Cases of Parkinson’s Disease

Mini-Mental State examination6 and Diagnostic and Sta¬ tistical Manual of Mental

Disorders, Third Edition criteria. Dementia was defined as a Mini-Mental State

examination score of less than 20,” 2015.

[7]

J. Jankovic, “Parkinson’s disease: Clinical features and diagnosis,” J. Neurol.

Neurosurg. Psychiatry, vol. 79, no. 4, pp. 368–376, 2008.

[8]

R. B. Postuma et al., “MDS clinical diagnostic criteria for Parkinson’s disease,” Mov.

144

Disord., vol. 30, no. 12, pp. 1591–1601, 2015.

[9]

R. Djaldetti, I. Ziv, and E. Melamed, “The mystery of motor asymmetry in Parkinson’s

disease,” Lancet Neurol., vol. 5, no. 9, pp. 796–802, 2006.

[10]

S. Y. Lim and A. E. Lang, “The nonmotor symptoms of Parkinson’s disease-An

overview,” Mov. Disord., vol. 25, no. SUPPL. 1, 2010.

[11]

M. Coelho and J. J. Ferreira, “Late-stage Parkinson disease,” Nat. Rev. Neurol., vol. 8,

no. 8, pp. 435–442, 2012.

[12]

G. E. Alexander, M. R. DeLong, and P. L. Strick, “Parallel organization of

functionally segregated circuits linking basal ganglia and cortex.,” Annu. Rev.

Neurosci., vol. 9, no. 1, pp. 357–81, 1986.

[13]

G. E. Alexander and M. D. Crutcher, “Functional architecture of basal ganglia circuits:

neural substrates of parallel processing.,” Trends Neurosci., vol. 13, no. 7, pp. 266–71,

Jul. 1990.

[14]

M. R. DeLong and T. Wichmann, “Circuits and circuit disorders of the basal ganglia,”

Arch. Neurol., vol. 64, no. 1, pp. 20–24, 2007.

[15]

M. R. DeLong, “Primate models of movement disorders of basal ganglia origin,”

Trends Neurosci., vol. 13, no. 7, pp. 281–285, 1990.

[16]

C. Buhmann, V. Glauche, H. J. Stürenburg, M. Oechsner, C. Weiller, and C. Büchel,

“Pharmacologically modulated fMRI - Cortical responsiveness to levodopa in drug145

naive hemiparkinsonian patients,” Brain, vol. 126, no. 2, pp. 451–461, 2003.

[17]

C. Tessa et al., “Decreased and increased cortical activation coexist in de novo

Parkinson’s disease,” Exp. Neurol., vol. 224, no. 1, pp. 299–306, 2010.

[18]

H. Yu, D. Sternad, D. M. Corcos, and D. E. Vaillancourt, “Role of hyperactive

cerebellum and motor cortex in Parkinson’s disease.,” Neuroimage, vol. 35, no. 1, pp.

222–33, Mar. 2007.

[19]

G. Deuschl et al., “A Randomized Trial of Deep-Brain Stimulation for Parkinson’s

Disease,” N. Engl. J. Med., vol. 355, no. 9, pp. 896–908, 2006.

[20]

J. M. Bronstein et al., “Deep brain stimulation for Parkinson disease an expert

consensus and review of key issues,” Arch. Neurol., vol. 68, no. 2, pp. 165–171, 2011.

[21]

A. Horn et al., “Deep brain stimulation induced normalization of the human functional

connectome in Parkinson’s disease,” Brain, vol. 142, no. 10, pp. 3129–3143, 2019.

[22]

H. Mure et al., “Improved sequence learning with subthalamic nucleus deep brain

stimulation: Evidence for treatment-specific network modulation,” J. Neurosci., vol.

32, no. 8, pp. 2804–2813, 2012.

[23]

G. Goldberg, “Supplementary motor area structure and function: Review and

hypotheses,” Behav. Brain Sci., vol. 8, no. 4, pp. 567–588, 1985.

[24]

J. Tanji, “New concepts of the supplementary motor area,” Curr. Opin. Neurobiol.,

vol. 6, no. 6, pp. 782–787, 1996.

146

[25]

P. Nachev, C. Kennard, and M. Husain, “Functional role of the supplementary and presupplementary motor areas,” Nat. Rev. Neurosci., vol. 9, no. 11, pp. 856–869, 2008.

[26]

D. Athauda and T. Foltynie, “The ongoing pursuit of neuroprotective therapies in

Parkinson disease,” Nat. Rev. Neurol., vol. 11, no. 1, pp. 25–40, 2015.

[27]

J. G. Nutt, “Pharmacokinetics and pharmacodynamics of levodopa,” Mov. Disord., vol.

23, no. SUPPL. 3, pp. 580–584, 2008.

[28]

A. Antonini, E. Tolosa, Y. Mizuno, M. Yamamoto, and W. H. Poewe, “A reassessment

of risks and benefits of dopamine agonists in Parkinson’s disease,” Lancet Neurol.,

vol. 8, no. 10, pp. 929–937, 2009.

[29]

S. P. Bratsos, D. Karponis, and S. N. Saleh, “Efficacy and Safety of Deep Brain

Stimulation in the Treatment of Parkinson’s Disease: A Systematic Review and Metaanalysis of Randomized Controlled Trials,” Cureus, vol. 10, no. 10, 2018.

[30]

K. A. Follett et al., “Pallidal versus Subthalamic Deep-Brain Stimulation for

Parkinson’s Disease,” N. Engl. J. Med., vol. 362, no. 22, pp. 2077–2091, 2010.

[31]

F. M. Weaver et al., “Randomized trial of deep brain stimulation for Parkinson

disease: Thirty-six-month outcomes,” Neurology, vol. 79, no. 1, pp. 55–65, 2012.

[32]

A. A. Othman et al., “Jejunal Infusion of Levodopa–Carbidopa Intestinal Gel Versus

Oral Administration of Levodopa–Carbidopa Tablets in Japanese Subjects with

Advanced Parkinson’s Disease: Pharmacokinetics and Pilot Efficacy and Safety,” Clin.

147

Pharmacokinet., vol. 54, no. 9, pp. 975–984, 2015.

[33]

D. Nyholm et al., “Pharmacokinetics of levodopa, carbidopa, and 3-O-methyldopa

following 16-hour jejunal infusion of levodopa-carbidopa intestinal gel in advanced

parkinson’s disease patients,” AAPS J., vol. 15, no. 2, pp. 316–323, 2013.

[34]

K. Wirdefeldt, P. Odin, and D. Nyholm, “Levodopa–Carbidopa Intestinal Gel in

Patients with Parkinson’s Disease: A Systematic Review,” CNS Drugs, vol. 30, no. 5,

pp. 381–404, 2016.

[35]

U. Ziemann et al., “Consensus: Motor cortex plasticity protocols,” Brain Stimul., vol.

1, no. 3, pp. 164–182, 2008.

[36]

S. Rossi et al., “Safety, ethical considerations, and application guidelines for the use of

transcranial magnetic stimulation in clinical practice and research,” Clin.

Neurophysiol., vol. 120, no. 12, pp. 2008–2039, 2009.

[37]

A. Zanjani, K. K. Zakzanis, Z. J. Daskalakis, and R. Chen, “Repetitive transcranial

magnetic stimulation of the primary motor cortex in the treatment of motor signs in

Parkinson’s disease: A quantitative review of the literature,” Mov. Disord., vol. 30, no.

6, pp. 750–758, 2015.

[38]

Y. H. Chou, P. T. Hickey, M. Sundman, A. W. Song, and N. K. Chen, “Effects of

repetitive transcranial magnetic stimulation on motor symptoms in parkinson disease:

A systematic review and meta-analysis,” JAMA Neurol., vol. 72, no. 4, pp. 432–440,

148

2015.

[39]

C. L. Chung and M. K. Y. Mak, “Effect of Repetitive Transcranial Magnetic

Stimulation on Physical Function and Motor Signs in Parkinson’s Disease: A

Systematic Review and Meta-Analysis,” Brain Stimul., vol. 9, no. 4, pp. 475–487,

2016.

[40]

J. P. Lefaucheur et al., “Evidence-based guidelines on the therapeutic use of repetitive

transcranial magnetic stimulation (rTMS),” Clin. Neurophysiol., vol. 125, no. 11, pp.

2150–2206, 2014.

[41]

J. P. Lefaucheur et al., “Evidence-based guidelines on the therapeutic use of repetitive

transcranial magnetic stimulation (rTMS): An update (2014–2018),” Clin.

Neurophysiol., vol. 131, no. 2, pp. 474–528, 2020.

[42]

M. Hamada et al., “High-frequency rTMS over the supplementary motor area for

treatment of Parkinson’s disease,” Mov. Disord., vol. 23, no. 11, pp. 1524–1531, 2008.

[43]

Y. Shirota, H. Ohtsu, M. Hamada, H. Enomoto, and Y. Ugawa, “Supplementary motor

area stimulation for Parkinson disease: A randomized controlled study,” Neurology,

vol. 80, no. 15, pp. 1400–1405, 2013.

[44]

濱田雅, “パーキンソン病に対する 磁気刺激治療,” Jpn J Rehabil Med, vol. 56, no.

1, pp. 44–47, 2019.

[45]

C. Ramaker, J. Marinus, A. M. Stiggelbout, and B. J. van Hilten, “Systematic

149

evaluation of rating scales for impairment and disability in Parkinson’s disease,” Mov.

Disord., vol. 17, no. 5, pp. 867–876, 2002.

[46]

C. G. Goetz et al., “Movement Disorder Society-Sponsored Revision of the Unified

Parkinson’s Disease Rating Scale (MDS-UPDRS): Scale presentation and clinimetric

testing results,” Mov. Disord., vol. 23, no. 15, pp. 2129–2170, 2008.

[47]

C. G. Goetz, G. T. Stebbins, T. A. Chmura, S. Fahn, W. Poewe, and C. M. Tanner,

“Teaching program for the Movement Disorder Society-sponsored revision of the

Unified Parkinson’s Disease Rating Scale: (MDS-UPDRS),” Mov. Disord., vol. 25, no.

9, pp. 1190–1194, 2010.

[48]

Movement Disorder Society Task Force on Rating Scales for Parkinson’s Disease,

“The Unified Parkinson’s Disease Rating Scale (UPDRS): status and

recommendations.,” Mov. Disord., vol. 18, no. 7, pp. 738–50, Jul. 2003.

[49]

M. Bologna et al., “Bradykinesia in early and advanced Parkinson’s disease,” J.

Neurol. Sci., vol. 369, pp. 286–291, 2016.

[50]

A. J. Espay, D. E. Beaton, F. Morgante, C. A. Gunraj, A. E. Lang, and R. Chen,

“Impairments of speed and amplitude of movement in Parkinson’s disease: A pilot

study,” Mov. Disord., vol. 24, no. 7, pp. 1001–1008, 2009.

[51]

A. J. Espay et al., “Differential response of speed, amplitude, and rhythm to

dopaminergic medications in Parkinson’s disease.,” Mov. Disord., vol. 26, no. 14, pp.

150

2504–8, Dec. 2011.

[52]

H. Ling, L. A. Massey, A. J. Lees, P. Brown, and B. L. Day, “Hypokinesia without

decrement distinguishes progressive supranuclear palsy from Parkinson’s disease,”

Brain, vol. 135, no. 4, pp. 1141–1153, 2012.

[53]

M. Bologna et al., “Neurophysiological correlates of bradykinesia in Parkinson’s

disease,” Brain, vol. 141, no. 8, pp. 2432–2444, 2018.

[54]

M. Hamada, Y. Ugawa, and S. Tsuji, “High-frequency rTMS over the supplementary

motor area improves bradykinesia in Parkinson’s disease: Subanalysis of double-blind

sham-controlled study,” J. Neurol. Sci., vol. 287, no. 1–2, pp. 143–146, 2009.

[55]

M. M. Hoehn and M. D. Yahr, “Parkinsonism: onset, progression and mortality.,”

Neurology, vol. 17, no. 5, pp. 427–42, May 1967.

[56]

K. Kashihara et al., “Official Japanese Version of the International Parkinson and

Movement Disorder Society–Unified Parkinson’s Disease Rating Scale: Validation

Against the Original English Version,” Mov. Disord. Clin. Pract., vol. 1, no. 3, pp.

200–212, 2014.

[57]

D. A. Heldman et al., “The modified bradykinesia rating scale for Parkinson’s disease:

reliability and comparison with kinematic measures.,” Mov. Disord., vol. 26, no. 10,

pp. 1859–63, Aug. 2011.

[58]

T. Endo, M. Yokoe, H. Fujimura, and S. Sako, “Novel Methods to Evaluate Symptoms

151

in Parkinson’s Disease – Rigidity and Finger Tappin,” Diagnostics Rehabil. Park. Dis.,

2011.

[59]

W. P. Teo, J. P. Rodrigues, F. L. Mastaglia, and G. W. Thickbroom, “Comparing

kinematic changes between a finger-tapping task and unconstrained finger flexionextension task in patients with Parkinson’s disease,” Exp. Brain Res., vol. 227, no. 3,

pp. 323–331, 2013.

[60]

E. Růžička, R. Krupička, K. Zárubová, J. Rusz, R. Jech, and Z. Szabó, “Tests of

manual dexterity and speed in Parkinson’s disease: Not all measure the same,” Park.

Relat. Disord., vol. 28, pp. 118–123, 2016.

[61]

W. R. Gibb and A. J. Lees, “The relevance of the Lewy body to the pathogenesis of

idiopathic Parkinson’s disease.,” J. Neurol. Neurosurg. Psychiatry, vol. 51, no. 6, pp.

745–52, Jun. 1988.

[62]

R. Agostino, A. Berardelli, A. Currà, N. Accornero, and M. Manfredi, “Clinical

impairment of sequential finger movements in Parkinson’s disease,” Mov. Disord., vol.

13, no. 3, pp. 418–421, 1998.

[63]

R. Agostino, A. Currà, M. Giovannelli, N. Modugno, M. Manfredi, and A. Berardelli,

“Impairment of individual finger movements in Parkinson’s disease,” Mov. Disord.,

vol. 18, no. 5, pp. 560–565, 2003.

[64]

R. C. Oldfield, “The assessment and analysis of handedness: the Edinburgh

152

inventory,” Neuropsychologia, vol. 9, no. 1, pp. 97–113, 1971.

[65]

G. T. Stebbins, C. G. Goetz, D. J. Burn, J. Jankovic, T. K. Khoo, and B. C. Tilley,

“How to identify tremor dominant and postural instability/gait difficulty groups with

the movement disorder society unified Parkinson’s disease rating scale: Comparison

with the unified Parkinson’s disease rating scale,” Mov. Disord., vol. 28, no. 5, pp.

668–670, 2013.

[66]

J. C. van den Noort et al., “Quantification of Hand Motor Symptoms in Parkinson’s

Disease: A Proof-of-Principle Study Using Inertial and Force Sensors,” Ann. Biomed.

Eng., vol. 45, no. 10, pp. 2423–2436, 2017.

[67]

J. Rusz et al., “Comparative analysis of speech impairment and upper limb motor

dysfunction in Parkinson’s disease,” J. Neural Transm., vol. 124, no. 4, pp. 463–470,

2017.

[68]

J. Jankovic et al., “Variable expression of Parkinson’s disease: a base-line analysis of

the DATATOP cohort. The Parkinson Study Group.,” Neurology, vol. 40, no. 10, pp.

1529–34, Oct. 1990.

[69]

A. T. Barker, R. Jalinous, and I. L. Freeston, “Wireless light-weight IEC 61850 based

loss of mains protection for smart grid,” Lancet, vol. 325, no. 8437, pp. 1106–1107,

1985.

[70]

R. Chen et al., “Depression of motor cortex excitability by low-frequency transcranial

153

magnetic stimulation,” Neurology, vol. 48, no. 5, pp. 1398–1403, 1997.

[71]

A. Pascual-Leone, J. Valls-Solé, J. P. Brasil-Neto, A. Cammarota, J. Grafman, and M.

Hallett, “Akinesia in Parkinson’s disease. II. Effects of subthreshold repetitive

transcranial motor cortex stimulation.,” Neurology, vol. 44, no. 5, pp. 892–8, May

1994.

[72]

A. Berardelli et al., “Facilitation of muscle evoked responses after repetitive cortical

stimulation in man,” Exp. Brain Res., vol. 122, no. 1, pp. 79–84, 1998.

[73]

F. Maeda, J. P. Keenan, J. M. Tormos, H. Topka, and A. Pascual-Leone,

“Interindividual variability of the modulatory effects of repetitive transcranial

magnetic stimulation on cortical excitability,” Exp. Brain Res., vol. 133, no. 4, pp.

425–430, 2000.

[74]

P. B. Fitzgerald, S. Fountain, and Z. J. Daskalakis, “A comprehensive review of the

effects of rTMS on motor cortical excitability and inhibition,” Clin. Neurophysiol., vol.

117, no. 12, pp. 2584–2596, 2006.

[75]

Y. Z. Huang, M. J. Edwards, E. Rounis, K. P. Bhatia, and J. C. Rothwell, “Theta burst

stimulation of the human motor cortex,” Neuron, vol. 45, no. 2, pp. 201–206, 2005.

[76]

G. W. Thickbroom, M. L. Byrnes, D. J. Edwards, and F. L. Mastaglia, “Repetitive

paired-pulse TMS at I-wave periodicity markedly increases corticospinal excitability:

A new technique for modulating synaptic plasticity,” Clin. Neurophysiol., vol. 117, no.

154

1, pp. 61–66, 2006.

[77]

M. Hamada et al., “Bidirectional long-term motor cortical plasticity and metaplasticity

induced by quadripulse transcranial magnetic stimulation,” J. Physiol., vol. 586, no.

16, pp. 3927–3947, 2008.

[78]

M. Hamada and Y. Ugawa, “Quadripulse stimulation - A new patterned rTMS,”

Restor. Neurol. Neurosci., vol. 28, no. 4, pp. 419–424, 2010.

[79]

M. Hamada, N. Murase, A. Hasan, M. Balaratnam, and J. C. Rothwell, “The role of

interneuron networks in driving human motor cortical plasticity,” Cereb. Cortex, vol.

23, no. 7, pp. 1593–1605, 2013.

[80]

K. Nakamura et al., “Variability in Response to Quadripulse Stimulation of the Motor

Cortex,” Brain Stimul., vol. 9, no. 6, pp. 859–866, 2016.

[81]

R. Hanajima et al., “The effect of age on the homotopic motor cortical long-term

potentiation-like effect induced by quadripulse stimulation,” Exp. Brain Res., vol. 235,

no. 7, pp. 2103–2108, 2017.

[82]

A. Tiksnadi, T. Murakami, W. Wiratman, H. Matsumoto, and Y. Ugawa, “Direct

Comparison of Efficacy of the Motor Cortical Plasticity Induction and the

Interindividual Variability between TBS and QPS,” Brain Stimul., vol. 13, no. 6, pp.

1824–1833, 2020.

[83]

F. Fregni, D. K. Simon, A. Wu, and A. Pascual-Leone, “Non-invasive brain

155

stimulation for Parkinson’s disease: A systematic review and meta-analysis of the

literature,” J. Neurol. Neurosurg. Psychiatry, vol. 76, no. 12, pp. 1614–1623, 2005.

[84]

M. Yokoe et al., “The optimal stimulation site for high-frequency repetitive

transcranial magnetic stimulation in Parkinson’s disease: A double-blind crossover

pilot study,” J. Clin. Neurosci., vol. 47, pp. 72–78, 2018.

[85]

A. R. Mitz and S. P. Wise, “The somatotopic organization of the supplementary motor

area: Intracortical microstimulation mapping,” J. Neurosci., vol. 7, no. 4, pp. 1010–

1021, 1987.

[86]

M. Matelli, G. Luppino, and G. Rizzolatti, “Architecture of superior and mesial area 6

and the adjacent cingulate cortex in the macaque monkey,” J. Comp. Neurol., vol. 311,

no. 4, pp. 445–462, 1991.

[87]

I. Fried et al., “Functional organization of human supplementary motor cortex studies

by electrical stimulation,” J. Neurosci., vol. 11, no. 11, pp. 3656–3666, 1991.

[88]

G. Luppino, M. Matelli, R. Camarda, and G. Rizzolatti, “Corticocortical connections

of area F3 (SMA‐proper) and area F6 (pre‐SMA) in the macaque monkey,” J. Comp.

Neurol., vol. 338, no. 1, pp. 114–140, 1993.

[89]

R. P. Dum and P. L. Strick, “Frontal lobe inputs to the digit representations of the

motor areas on the lateral surface of the hemisphere,” J. Neurosci., vol. 25, no. 6, pp.

1375–1386, 2005.

156

[90]

N. Arai, M. K. Lu, Y. Ugawa, and U. Ziemann, “Effective connectivity between

human supplementary motor area and primary motor cortex: A paired-coil TMS

study,” Exp. Brain Res., vol. 220, no. 1, pp. 79–87, 2012.

[91]

P. E. Green, M. C. Ridding, K. D. Hill, J. G. Semmler, P. D. Drummond, and A. M.

Vallence, “Supplementary motor area—primary motor cortex facilitation in younger

but not older adults,” Neurobiol. Aging, vol. 64, pp. 85–91, 2018.

[92]

G. Koch et al., “rTMS of supplementary motor area modulates therapy-induced

dyskinesias in Parkinson disease,” Neurology, vol. 65, no. 4, pp. 623–625, 2005.

[93]

L. Brusa et al., “Low frequency rTMS of the SMA transiently ameliorates peak-dose

LID in Parkinson’s disease,” Clin. Neurophysiol., vol. 117, no. 9, pp. 1917–1921,

2006.

[94]

Y. H. Kim et al., “Repetitive transcranial magnetic stimulation-induced corticomotor

excitability and associated motor skill acquisition in chronic stroke,” Stroke, vol. 37,

no. 6, pp. 1471–1476, 2006.

[95]

V. López-Alonso, B. Cheeran, D. Río-Rodríguez, and M. Fernández-Del-Olmo, “Interindividual variability in response to non-invasive brain stimulation paradigms,” Brain

Stimul., vol. 7, no. 3, pp. 372–380, 2014.

[96]

J. F. M. Müller-Dahlhaus, Y. Orekhov, Y. Liu, and U. Ziemann, “Interindividual

variability and age-dependency of motor cortical plasticity induced by paired

157

associative stimulation,” Exp. Brain Res., vol. 187, no. 3, pp. 467–475, 2008.

[97]

M. C. Ridding and U. Ziemann, “Determinants of the induction of cortical plasticity by

non-invasive brain stimulation in healthy subjects,” J. Physiol., vol. 588, no. 13, pp.

2291–2304, 2010.

[98]

S. Kadowaki, H. Enomoto, T. Murakami, S. Nakatani-Enomoto, S. Kobayashi, and Y.

Ugawa, “Influence of phasic muscle contraction upon the quadripulse stimulation

(QPS) aftereffects,” Clin. Neurophysiol., vol. 127, no. 2, pp. 1568–1573, 2016.

[99]

S. Simeoni et al., “Effects of Quadripulse Stimulation on Human Motor Cortex

Excitability: A Replication Study.,” Brain Stimul., vol. 9, no. 1, pp. 148–50, 2016.

[100] S. Rossi et al., “Safety and recommendations for TMS use in healthy subjects and

patient populations, with updates on training, ethical and regulatory issues: Expert

Guidelines,” Clin. Neurophysiol., no. xxxx, 2020.

[101] P. M. Rossini et al., “Non-invasive electrical and magnetic stimulation of the brain,

spinal cord, roots and peripheral nerves: Basic principles and procedures for routine

clinical and research application: An updated report from an I.F.C.N. Committee,”

Clin. Neurophysiol., vol. 91, no. 2, pp. 79–92, 1994.

[102] K. Matsunaga, A. Maruyama, T. Fujiwara, R. Nakanishi, S. Tsuji, and J. C. Rothwell,

“Increased corticospinal excitability after 5 Hz rTMS over the human supplementary

motor area,” J. Physiol., vol. 562, no. 1, pp. 295–306, 2005.

158

[103] Y. Terao et al., “Interhemispheric transmission of visuomotor information for motor

implementation,” Cereb. Cortex, vol. 15, no. 7, pp. 1025–1036, 2005.

[104] Y. Terao et al., “Modifying the cortical processing for motor preparation by repetitive

transcranial magnetic stimulation,” J. Cogn. Neurosci., vol. 19, no. 9, pp. 1556–1573,

2007.

[105] M. C. Kujirai T, Caramia MD, Rothwell JC, Day BL, Thompson PD, Fervert A, Wroe

S, Asselman P, “Corticocortical inhibition in human motor cortex.,” J. Physiol., vol.

471, pp. 501–519, 1993.

[106] V. Di Lazzaro et al., “Direct demonstration of the effect of lorazepam on the

excitability of the human motor cortex,” Clin. Neurophysiol., vol. 111, no. 5, pp. 794–

799, 2000.

[107] T. V. Ilić, F. Meintzschel, U. Cleff, D. Ruge, K. R. Kessler, and U. Ziemann, “Shortinterval paired-pulse inhibition and facilitation of human motor cortex: The dimension

of stimulus intensity,” J. Physiol., vol. 545, no. 1, pp. 153–167, 2002.

[108] U. Ziemann, R. Chen, L. G. Cohen, and M. Hallett, “Dextromethorphan decreases the

excitability of the human motor cortex,” Neurology, vol. 51, no. 5, pp. 1320–1324,

1998.

[109] R. Chen et al., “The clinical diagnostic utility of transcranial magnetic stimulation:

Report of an IFCN committee,” Clin. Neurophysiol., vol. 119, no. 3, pp. 504–532,

159

2008.

[110] V. Rizzo et al., “Shaping the excitability of human motor cortex with premotor

rTMS,” J. Physiol., vol. 554, no. 2, pp. 483–495, 2004.

[111] F. Gilio, V. Rizzo, H. R. Siebner, and J. C. Rothwell, “Effects on the right motor handarea excitability produced by low-frequency rTMS over human contralateral

homologous cortex,” J. Physiol., vol. 551, no. 2, pp. 563–573, 2003.

[112] N. Arai et al., “State-dependent and timing-dependent bidirectional associative

plasticity in the human SMA-M1 network,” J. Neurosci., vol. 31, no. 43, pp. 15376–

15383, 2011.

[113] M. Hamada et al., “Primary motor cortical metaplasticity induced by priming over the

supplementary motor area,” J. Physiol., vol. 587, no. 20, pp. 4845–4862, 2009.

[114] Y. Shirota, R. Hanajima, S. Ohminami, R. Tsutsumi, Y. Ugawa, and Y. Terao,

“Supplementary motor area plays a causal role in automatic inhibition of motor

responses,” Brain Stimul., vol. 12, no. 4, pp. 1020–1026, 2019.

[115] T. Shimizu et al., “Plasticity induction in the pre-supplementary motor area (pre-SMA)

and SMA-proper differentially affects visuomotor sequence learning,” Brain Stimul.,

vol. 13, no. 1, pp. 229–238, 2020.

[116] O. Rascol et al., “Supplementary and Primary Sensory Motor Area Activity in

Parkinson’s Disease: Regional Cerebral Blood Flow Changes During Finger

160

Movements and Effects of Apomorphine,” Arch. Neurol., vol. 49, no. 2, pp. 144–148,

1992.

[117] B. Haslinger et al., “Event-related functional magnetic resonance imaging in

Parkinson’s disease before and after levodopa,” Brain, vol. 124, no. 3, pp. 558–570,

2001.

[118] T. Eckert, T. Peschel, H. J. Heinze, and M. Rotte, “Increased pre-SMA activation in

early PD patients during simple self-initiated hand movements,” J. Neurol., vol. 253,

no. 2, pp. 199–207, 2006.

[119] E. D. Playford, I. H. Jenkins, R. E. Passingham, J. Nutt, R. S. J. Frackowiak, and D. J.

Brooks, “Impaired mesial frontal and putamen activation in Parkinson’s disease: A

positron emission tomography study,” Ann. Neurol., vol. 32, no. 2, pp. 151–161, 1992.

[120] W. Strube, T. Bunse, B. Malchow, and A. Hasan, “Efficacy and interindividual

variability in motor-cortex plasticity following anodal tDCS and paired-associative

stimulation,” Neural Plast., vol. 2015, 2015.

[121] B. Cheeran et al., “A common polymorphism in the brain-derived neurotrophic factor

gene ( BDNF) modulates human cortical plasticity and the response to rTMS,” J.

Physiol., vol. 586, no. 23, pp. 5717–5725, 2008.

[122] N. Arai et al., “Differences in after-effect between monophasic and biphasic highfrequency rTMS of the human motor cortex,” Clin. Neurophysiol., vol. 118, no. 10, pp.

161

2227–2233, 2007.

[123] K. Nakamura et al., “Variability in Response to Quadripulse Stimulation of the Motor

Cortex,” Brain Stimul., vol. 9, no. 6, pp. 859–866, 2016.

[124] T. D. Sanger, R. R. Garg, and R. Chen, “Interactions between two different inhibitory

systems in the human motor cortex,” J. Physiol., vol. 530, no. 2, pp. 307–317, 2001.

[125] L. Roshan, G. O. Paradiso, and R. Chen, “Two phases of short-interval intracortical

inhibition,” Exp. Brain Res., vol. 151, no. 3, pp. 330–337, 2003.

[126] Z. J. Daskalakis, G. O. Paradiso, B. K. Christensen, P. B. Fitzgerald, C. Gunraj, and R.

Chen, “Exploring the connectivity between the cerebellum and motor cortex in

humans,” J. Physiol., vol. 557, no. 2, pp. 689–700, 2004.

[127] M. I. Garry and R. H. S. Thomson, “The effect of test TMS intensity on short-interval

intracortical inhibition in different excitability states,” Exp. Brain Res., vol. 193, no. 2,

pp. 267–274, 2009.

[128] C. Gerloff, B. Corwell, R. Chen, M. Hallett, and L. G. Cohen, “Stimulation over the

human supplementary motor area interferes with the organization of future elements in

complex motor sequences,” Brain, vol. 120, no. 9, pp. 1587–1602, 1997.

[129] M. Dafotakis, C. Grefkes, L. Wang, G. R. Fink, and D. A. Nowak, “The effects of 1

Hz rTMS over the hand area of M1 on movement kinematics of the ipsilateral hand,”

J. Neural Transm., vol. 115, no. 9, pp. 1269–1274, 2008.

162

[130] L. Jäncke, H. Steinmetz, S. Benilow, and U. Ziemann, “Slowing fastest finger

movements of the dominant hand with low-frequency rTMS of the hand area of the

primary motor cortex,” Exp. Brain Res., vol. 155, no. 2, pp. 196–203, 2004.

163

...

参考文献をもっと見る

全国の大学の
卒論・修論・学位論文

一発検索!

この論文の関連論文を見る