臺灣博碩士論文加值系統

原發性陣發性動作型運動不良症(paroxysmal kinesigenic dyskinesia, PKD)為一不常見之神經科疾患，其臨床特徵為在一突然發生的自主動作(voluntary movement)時，患者會產生肌張力不全(dystonia)或舞蹈症(choreoathetosis)之症狀。少量的抗癲癇藥物(antiepileptic drug, AED)治療，即能改善此狀況，然而，此疾病之相關病理機轉尚不清楚。過去曾有研究指出，此疾病患者視丘以及基底核等區域之功能異常，且腦部皮質神經元有過度興奮之現象。由於此肌張力不全或舞蹈症之症狀是被患者之自主動作所誘發，探討動作相關之非同步/同步腦波律動(movement-related neuronal oscillation)將可提供關於此疾病病理基礎之資訊。其次，多數患者所產生的動作障礙，為肌張力不全，而過去研究指出，肌張力不全症患者之體感覺系統(somatosensory system)神經元過度興奮，有鑑於此，探究原發性陣發性動作型運動不良症之體感覺皮質興奮性亦為一重要之課題。
本研究透過觀察動作相關之非同步/同步腦波律動以及體感覺誘發反應(somatosensory evoked field, SEF)，探討此疾病患者腦部運動以及感覺區域的皮質興奮性(cortical excitability)。在第一個子實驗中，我們請患者自主抬動手指，記錄其動作相關非同步/同步腦波律動，將此兩種反應與健康受試者作一對照；第二個子實驗中，我們記錄正中神經電刺激(median nerve electric stimulation)所誘發之體感覺誘發反應，比較此症患者之皮質抑制能力表現，和健康受試者之間的差異，並且比較此症患者於服用藥物以及未服用藥物之狀況下，其皮質抑制能力之改變。

動作相關非同步/同步腦波律動 (Movement-Related Neuronal Oscillation)
第一個子實驗中，我們招募了16名原發性陣發性動作型運動不良症患者以及17名健康受試者，記錄自主抬動手指(finger lifting)所誘發的動作相關非同步/同步腦波律動。實驗結果中，原發性陣發性動作型運動不良症患者以及健康受試者之動作相關非同步腦波律動(alpha event-related desynchronization, alpha-ERD)並無顯著差異，但原發性陣發性動作型運動不良症患者之雙側動作相關同步腦波律動(beta event-related synchronization, beta-ERS)振幅(amplitude)較健康受試者小，且對側動作相關同步腦波律動之潛時(peak latency)較晚，其中一名患者沒有此腦磁反應。再者，16名患者中，有2名患者之動作相關同步腦波律動於腦部之分佈轉變為同側優勢，此側化分佈之改變，推測為對側動作皮質抑制功能下降所導致之代償(compensation)作用。另外，同側動作相關同步腦波律動和患者之臨床症狀嚴重度有相關性，發作頻率較低的患者，動作相關同步腦波律動振幅較大。本子實驗之結果顯示，原發性陣發性動作型運動不良症患者產生自主動作前，皮質神經活化反應正常，但動作產生後的運動皮質抑制性下降。

體感覺誘發反應 (Somatosensory Evoked Fields, SEFs)
第二個子實驗中，納入了15位病患及18位健康受試者，記錄其接受單一(single-pulse)及成對(paired-pulse)正中神經電刺激時，腦部的體感覺誘發反應。其中有12位患者於服用藥物以及停用藥物之狀況下，皆接受此試驗。計算成對刺激中兩個反應大小之比值(paired-pulse inhibition ratio, PPI ratio)，可量化感覺皮質之抑制功能。較小的比值表示較佳的抑制功能，反之，代表感覺皮質抑制性較差。停用藥物時，患者之P35m反應以及次要體感覺皮質誘發反應(secondary somatosensory cortical (SII) responses)之抑制比值較健康受試者高；服藥狀況下，此兩反應之抑制比值和健康受試者無異；比較服用藥物以及未服用藥物之狀況，P35m反應以及次要體感覺皮質誘發反應之抑制比值於停用藥物時較大。本子實驗之結果顯示，此病症之患者，體感覺皮質內抑制 (somatosensory intracortical inhibition)之能力有所缺損，服用抗癲癇藥物則可矯治此現象。

結論
本研究量測原發性陣發性動作型運動不良症患者之運動及感覺系統之皮質興奮性。相較於健康受試者，此症患者於一自主動作後，運動皮質之抑制性下降，且體感覺皮質之抑制性亦降低。整體而言，患者之運動及體感覺皮質神經抑制能力下降，體感覺皮質抑制能力的改變，對於此疾病患者之肌張力不全症狀，可能有其影響。而運動及體感覺皮質神經抑制能力改變於此病症之病理機轉所扮演的角色和生理意義，以及其對於臨床表徵之影響，仍待更多研究加以確認。

Paroxysmal kinesigenic dyskinesia (PKD) is a rare neurological disorder with dyskinetic movement triggered by sudden voluntary movements. The condition responds well to antiepileptic drugs (AEDs). However, little is known about the underlying mechanism of the disease. Previous studies have demonstrated dysfunction of thalamus or basal ganglia in patients with PKD. Corticospinal disinhibition was also reported. Since the dyskinetic movements in PKD patients are precipitated by voluntary movements, investigating changes in neural oscillatory activities related to voluntary movements may provide some information about pathophysiological basis for PKD. On the other hand, most patients with PKD experience dystonia rather than choreoathetosis. Previous studies indicated that disinhibited somatosensory system contributes to dystonic movements. Therefore, the prominent sudden dystonic movements in PKD make it important to clarify how the somatosensory cortical processing is involved in PKD. The purpose of this work is to provide new insights into the neurophysiological features of PKD by assessing excitability profile of sensorimotor system in PKD. To address a series of questions on sensorimotor cortical excitability in PKD, we have conducted a two-study plan to explore possible changes of motor and sensory excitability in PKD at cortical level. The two studies included the measurements of movement-related neuronal oscillation and somatosensory evoked fields (SEFs).

Study I. Movement-Related Neuronal Oscillation
In the first study, we examined movement-related oscillatory changes in PKD patients with a self-paced extension motor task. Neuromagnetic activity was recorded from 16 PKD patients, and movement-related alpha event-related desynchronization (alpha-ERD) and beta event-related synchronization (beta-ERS) were compared to the results obtained from 17 healthy controls. Alpha-ERD was comparable between healthy controls and PKD patients, whereas contralateral and ipsilateral beta-ERS were decreased in PKD patients, and even absent in one of the patients. Delayed peak latency of contralateral beta-ERS was also observed. Moreover, lesser degree of contralateral preponderance of beta-ERS was found in PKD. The changed lateralization of beta-ERS in PKD might possibly being a compensation of the reduced inhibitory function in contralateral hemisphere. Ipsilateral beta-ERS correlated well to clinical severity. Patients with lower attack frequency showed a larger ipsilateral beta-ERS. The data of the present study implies a relatively normal cortical activation before a voluntary movement but a decreased postmovement inhibition of motor cortex in patients with PKD.

Study II. Somatosensory Evoked Fields (SEFs)
In the second study, whole-head magnetoencephalography (MEG) was used to record somatosensory evoke fields (SEFs) elicited by paired-pulse electric stimulation of median nerve in 15 patients and 18 age-matched healthy volunteers. Twelve of the patients were studied in both drug-off and drug-on states. A paired-pulse inhibition (PPI) ratio, defined as an amplitude ratio between the responses to the second and the first stimuli, was used to reflect the intracortical inhibition. A high PPI ratio means a reduced inhibition, and low PPI ratio represents a strong inhibition. PPI ratios of either primary somatosensory cortical P35m or secondary somatosensory cortical (SII) responses were significantly larger in drug-off PKD compared to controls, but we did not find any significant difference between drug-on PKD and controls. Compared with drug-on state, PPI ratios for P35m and SII response were larger in drug-off state. The results suggested that the intracortical inhibition of the primary and secondary somatosensory cortices is impaired in patients with PKD and that the hyperexcitable phenomenon could be remediated with AEDs.

Conclusions
In conclusion, present work provides some information about excitability profile in sensorimotor system of patients with PKD. The cortical activation before and during the movement are relatively normal in PKD patients, whereas postmovement inhibition of motor cortex is altered. The reduction of inhibition in somatosensory system might partially affect sudden dyskinetic movements in the disease. Since the sensory system provides the major drive affecting the motor system, disinhibition of the somatosensory system might give rise to abnormal motor outputs. Further investigations of the role of these alterations and how these changes involved in the pathophysiologic mechanism of PKD are warranted to provide more comprehensive information about pathogenesis of PKD.

Content
Acknowledgement......................4
中文摘要...............................7
English Abstract......................11
List of Original Papers...............15
Abbreviations.........................16

Introduction
Paroxysmal Kinesigenic Dyskinesia (PKD)....18
Magnetoencephalography (MEG)...............22
Movement-related Neuronal Oscillation......24
Somatosensory Evoked Fields (SEFs).........25

Aims of the Thesis........28

Material and Methods
Study I. Movement-Related Oscillatory
Activities in Patients with PKD............30
Study II. Excitability Profile of
Primary and Secondary Somatosensory
Cortices in Patients with PKD..............34

Results
Movement-related Alpha-ERD (Study I).......40
Movement-related Beta-ERS (Study I)........41
Correlation between beta-ERS and clinical
severity (Study I).........................45
Clinical and demographic data (Study II)...47
Somatosensory evoked fields in single-pulse
paradigm (Study II)........................47
Paired-pulse inhibition (Study II).........48
Medication effect on PPI ratio (Study II)..52

Discussion
Movement-related alpha-ERD and beta-ERS
in patients with PKD (Study I)........................55
Changes of spatial pattern in beta-ERS (Study I)......56
Correlation between beta-ERS and clinical
severity (Study I)....................................57
Limitation (Study I)..................................59
Somatosensory evoked fields in single-pulse
paradigm (Study II)...................................60
Paired-pulse inhibition (Study II)....................60
Medication effect on PPI ratio (Study II).............62
Impaired intracortical inhibition of the
SI and SII cortices in patients with PKD (Study II)...65
Limitation (Study II).................................66

Conclusions............69

References.............73

List of Figures........88
List of Tables.........89
Original Papers 90




List of Figures
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Figure 15---------------------------------------------49
Figure 16---------------------------------------------51
Figure 17---------------------------------------------53
Figure 18---------------------------------------------58
Figure 19---------------------------------------------61
Figure 20---------------------------------------------63
Figure 21---------------------------------------------67


List of Tables
Table 1---------------------------------------------31
Table 2---------------------------------------------35
Table 3---------------------------------------------41
Table 4---------------------------------------------46
Table 5---------------------------------------------48

Abbruzzese G, Berardelli A (2003) Sensorimotor integration in movement disorders. Mov Disord 18:231-240.
Alexander GE, Crutcher MD (1990) Functional architecture of basal ganglia circuits: neural substrates of parallel processing. Trends in neurosciences 13:266-271.
Alexander GE, Crutcher MD, DeLong MR (1990) Basal ganglia-thalamocortical circuits: parallel substrates for motor, oculomotor, "prefrontal" and "limbic" functions. Prog Brain Res 85:119-146.
Babiloni C, Babiloni F, Carducci F, Cincotti F, Del Percio C, De Pino G, Maestrini S, Priori A, Tisei P, Zanetti O, Rossini PM (2000) Movement-related electroencephalographic reactivity in Alzheimer disease. Neuroimage 12:139-146.
Bennett LB, Roach ES, Bowcock AM (2000) A locus for paroxysmal kinesigenic dyskinesia maps to human chromosome 16. Neurology 54:125-130.
Berardelli A, Rothwell JC, Hallett M, Thompson PD, Manfredi M, Marsden CD (1998) The pathophysiology of primary dystonia. Brain 121 ( Pt 7):1195-1212.
Bhatia KP (1999) The paroxysmal dyskinesias. J Neurol 246:149-155.
Bhatia KP (2001) Familial (idiopathic) paroxysmal dyskinesias: an update. Semin Neurol 21:69-74.
Bonakis A, Papageorgiou SG, Potagas C, Karahalios G, Kalfakis N (2009) A case of refractory secondary paroxysmal kinesigenic dyskinesia with high sensitivity to phenytoin monotherapy. Parkinsonism Relat Disord 15:68-70.
Bruno MK, Hallett M, Gwinn-Hardy K, Sorensen B, Considine E, Tucker S, Lynch DR, Mathews KD, Swoboda KJ, Harris J, Soong BW, Ashizawa T, Jankovic J, Renner D, Fu YH, Ptacek LJ (2004) Clinical evaluation of idiopathic paroxysmal kinesigenic dyskinesia: new diagnostic criteria. Neurology 63:2280-2287.
Cassim F, Monaca C, Szurhaj W, Bourriez JL, Defebvre L, Derambure P, Guieu JD (2001) Does post-movement beta synchronization reflect an idling motor cortex? Neuroreport 12:3859-3863.
Chen R, Yaseen Z, Cohen LG, Hallett M (1998) Time course of corticospinal excitability in reaction time and self-paced movements. Ann Neurol 44:317-325.
Delval A, Defebvre L, Labyt E, Douay X, Bourriez JL, Waucquiez N, Derambure P, Destee A (2006) Movement-related cortical activation in familial Parkinson disease. Neurology 67:1086-1087.
Demirkiran M, Jankovic J (1995) Paroxysmal dyskinesias: clinical features and classification. Ann Neurol 38:571-579.
Derambure P, Defebvre L, Dujardin K, Bourriez JL, Jacquesson JM, Destee A, Guieu JD (1993) Effect of aging on the spatio-temporal pattern of event-related desynchronization during a voluntary movement. Electroencephalogr Clin Neurophysiol 89:197-203.
Eder CF, Sokic D, Covickovic-Sternic N, Mijajlovic M, Savic M, Sinkjaer T, Popovic DB (2006) Symmetry of post-movement beta-ERS and motor recovery from stroke: a low-resolution EEG pilot study. Eur J Neurol 13:1312-1323.
Eichelbaum M, Kothe KW, Hoffmann F, von Unruh GE (1982) Use of stable labelled carbamazepine to study its kinetics during chronic carbamazepine treatment. Eur J Clin Pharmacol 23:241-244.
Fahn S, Bressman SB, Marsden CD (1998) Classification of dystonia. Adv Neurol 78:1-10.
Franssen H, Fortgens C, Wattendorff AR, van Woerkom TC (1983) Paroxysmal kinesigenic choreoathetosis and abnormal contingent negative variation. A case report. Arch Neurol 40:381-385.
Frasson E, Priori A, Bertolasi L, Mauguiere F, Fiaschi A, Tinazzi M (2001) Somatosensory disinhibition in dystonia. Mov Disord 16:674-682.
Granger P, Biton B, Faure C, Vige X, Depoortere H, Graham D, Langer SZ, Scatton B, Avenet P (1995) Modulation of the gamma-aminobutyric acid type A receptor by the antiepileptic drugs carbamazepine and phenytoin. Mol Pharmacol 47:1189-1196.
Hallett M (1995) Is dystonia a sensory disorder? Ann Neurol 38:139-140.
Hamalainen M, Hari, R., Ilmoniemi, R. J., Knuutila, J., Lounasmaa, O. (1993) Magnetoencephalography--theory, instrumentation, and applications to noninvasive studies of the working human brain. Review of Modern Physics 65:413-497.
Hari R, Hanninen R, Makinen T, Jousmaki V, Forss N, Seppa M, Salonen O (1998) Three hands: fragmentation of human bodily awareness. Neurosci Lett 240:131-134.
Hari R, Karhu J, Hamalainen M, Knuutila J, Salonen O, Sams M, Vilkman V (1993) Functional organization of the human first and second somatosensory cortices: a neuromagnetic study. Eur J Neurosci 5:724-734.
Hari R, Reinikainen K, Kaukoranta E, Hamalainen M, Ilmoniemi R, Penttinen A, Salminen J, Teszner D (1984) Somatosensory evoked cerebral magnetic fields from SI and SII in man. Electroencephalogr Clin Neurophysiol 57:254-263.
Hoshiyama M, Kakigi R (2001) Correspondence between short-latency somatosensory evoked brain potentials and cortical magnetic fields following median nerve stimulation. Brain Res 908:140-148.
Hoshiyama M, Kakigi R (2002) New concept for the recovery function of short-latency somatosensory evoked cortical potentials following median nerve stimulation. Clin Neurophysiol 113:535-541.
Houser MK, Soland VL, Bhatia KP, Quinn NP, Marsden CD (1999) Paroxysmal kinesigenic choreoathetosis: a report of 26 patients. J Neurol 246:120-126.
Hsu FC, Smith SS (2003) Progesterone withdrawal reduces paired-pulse inhibition in rat hippocampus: dependence on GABA(A) receptor alpha4 subunit upregulation. J Neurophysiol 89:186-198.
Huang YG, Chen YC, Du F, Li R, Xu GL, Jiang W, Huang J (2005) Topiramate therapy for paroxysmal kinesigenic choreoathetosis. Mov Disord 20:75-77.
Hudgins RL, Corbin KB (1966) An uncommon seizure disorder: familial paroxysmal choreoathetosis. Brain 89:199-204.
Hurtado JM, Gray CM, Tamas LB, Sigvardt KA (1999) Dynamics of tremor-related oscillations in the human globus pallidus: a single case study. Proc Natl Acad Sci U S A 96:1674-1679.
Huttunen J, Pekkonen E, Kivisaari R, Autti T, Kahkonen S (2008) Modulation of somatosensory evoked fields from SI and SII by acute GABA A-agonism and paired-pulse stimulation. Neuroimage 40:427-434.
Jones EG (1975) Lamination and differential distribution of thalamic afferents within the sensory-motor cortex of the squirrel monkey. J Comp Neurol 160:167-203.
Joo EY, Hong SB, Tae WS, Kim JH, Han SJ, Seo DW, Lee KH, Kim MH, Kim S, Lee MH, Kim BT (2005) Perfusion abnormality of the caudate nucleus in patients with paroxysmal kinesigenic choreoathetosis. Eur J Nucl Med Mol Imaging 32:1205-1209.
Jousmaki V, Forss N (1998) Effects of stimulus intensity on signals from human somatosensory cortices. Neuroreport 9:3427-3431.
Kakigi R, Hoshiyama M, Shimojo M, Naka D, Yamasaki H, Watanabe S, Xiang J, Maeda K, Lam K, Itomi K, Nakamura A (2000) The somatosensory evoked magnetic fields. Prog Neurobiol 61:495-523.
Kanda F, Jinnai K, Takahashi K, Abe H, Yasuda M, Tada K, Fujita T (1989) Somatosensory evoked potentials in Huntington's disease--studies with paired stimulation. Electromyogr Clin Neurophysiol 29:287-291.
Kang SY, Sohn YH, Kim HS, Lyoo CH, Lee MS (2006) Corticospinal disinhibition in paroxysmal kinesigenic dyskinesia. Clin Neurophysiol 117:57-60.
Ko CH, Kong CK, Ngai WT, Ma KM (2001) Ictal (99m)Tc ECD SPECT in paroxysmal kinesigenic choreoathetosis. Pediatr Neurol 24:225-227.
Kuhn AA, Doyle L, Pogosyan A, Yarrow K, Kupsch A, Schneider GH, Hariz MI, Trottenberg T, Brown P (2006) Modulation of beta oscillations in the subthalamic area during motor imagery in Parkinson's disease. Brain 129:695-706.
Lee YC, Lee MJ, Yu HY, Chen C, Hsu CH, Lin KP, Liao KK, Chang MH, Liao YC, Soong BW (2012) PRRT2 mutations in paroxysmal kinesigenic dyskinesia with infantile convulsions in a Taiwanese cohort. PloS one 7:e38543.
Leocani L, Colombo B, Magnani G, Martinelli-Boneschi F, Cursi M, Rossi P, Martinelli V, Comi G (2001a) Fatigue in multiple sclerosis is associated with abnormal cortical activation to voluntary movement--EEG evidence. Neuroimage 13:1186-1192.
Leocani L, Toro C, Manganotti P, Zhuang P, Hallett M (1997) Event-related coherence and event-related desynchronization/synchronization in the 10 Hz and 20 Hz EEG during self-paced movements. Electroencephalogr Clin Neurophysiol 104:199-206.
Leocani L, Toro C, Zhuang P, Gerloff C, Hallett M (2001b) Event-related desynchronization in reaction time paradigms: a comparison with event-related potentials and corticospinal excitability. Clin Neurophysiol 112:923-930.
Lidsky TI, Manetto C, Schneider JS (1985) A consideration of sensory factors involved in motor functions of the basal ganglia. Brain Res 356:133-146.
Lin YY, Chen WT, Liao KK, Yeh TC, Wu ZA, Ho LT, Lee LS (2005) Differential generators for N20m and P35m responses to median nerve stimulation. Neuroimage 25:1090-1099.
Lin YY, Forss N (2002) Functional characterization of human second somatosensory cortex by magnetoencephalography. Behav Brain Res 135:141-145.
Lin YY, Kajola M (2003) Neuromagnetic somatosensory responses to natural moving tactile stimulation. Can J Neurol Sci 30:31-35.
Lin YY, Shih YH, Chang KP, Lee WT, Yu HY, Hsieh JC, Yeh TC, Wu ZA, Ho LT (2003) MEG localization of rolandic spikes with respect to SI and SII cortices in benign rolandic epilepsy. Neuroimage 20:2051-2061.
Lin YY, Simoes C, Forss N, Hari R (2000) Differential effects of muscle contraction from various body parts on neuromagnetic somatosensory responses. Neuroimage 11:334-340.
Lombroso CT (1995) Paroxysmal choreoathetosis: an epileptic or non-epileptic disorder? Ital J Neurol Sci 16:271-277.
Marelli C, Canafoglia L, Zibordi F, Ciano C, Visani E, Zorzi G, Garavaglia B, Barzaghi C, Albanese A, Soliveri P, Leone M, Panzica F, Scaioli V, Pincherle A, Nardocci N, Franceschetti S (2008) A neurophysiological study of myoclonus in patients with DYT11 myoclonus-dystonia syndrome. Mov Disord 23:2041-2048.
Margari L, Presicci A, Ventura P, Margari F, Perniola T (2005) Channelopathy: hypothesis of a common pathophysiologic mechanism in different forms of paroxysmal dyskinesia. Pediatr Neurol 32:229-235.
Marino SE, Birnbaum AK, Leppik IE, Conway JM, Musib LC, Brundage RC, Ramsay RE, Pennell PB, White JR, Gross CR, Rarick JO, Mishra U, Cloyd JC (2012) Steady-state carbamazepine pharmacokinetics following oral and stable-labeled intravenous administration in epilepsy patients: effects of race and sex. Clin Pharmacol Ther 91:483-488.
Marsden JF, Limousin-Dowsey P, Ashby P, Pollak P, Brown P (2001) Subthalamic nucleus, sensorimotor cortex and muscle interrelationships in Parkinson's disease. Brain 124:378-388.
Mauguiere F, Merlet I, Forss N, Vanni S, Jousmaki V, Adeleine P, Hari R (1997) Activation of a distributed somatosensory cortical network in the human brain. A dipole modelling study of magnetic fields evoked by median nerve stimulation. Part I: Location and activation timing of SEF sources. Electroencephalogr Clin Neurophysiol 104:281-289.
Mir P, Huang YZ, Gilio F, Edwards MJ, Berardelli A, Rothwell JC, Bhatia KP (2005) Abnormal cortical and spinal inhibition in paroxysmal kinesigenic dyskinesia. Brain 128:291-299.
Mochizuki H, Hanajima R, Kowa H, Motoyoshi Y, Ashida H, Kamakura K, Motoyoshi K, Ugawa Y (2001) Somatosensory evoked potential recovery in myotonic dystrophy. Clin Neurophysiol 112:793-799.
Naylor DE, Wasterlain CG (2005) GABA synapses and the rapid loss of inhibition to dentate gyrus granule cells after brief perforant-path stimulation. Epilepsia 46 Suppl 5:142-147.
Neuper C, Pfurtscheller G (2001) Event-related dynamics of cortical rhythms: frequency-specific features and functional correlates. Int J Psychophysiol 43:41-58.
Pfurtscheller G, Berghold A (1989) Patterns of cortical activation during planning of voluntary movement. Electroencephalogr Clin Neurophysiol 72:250-258.
Pfurtscheller G, Lopes da Silva FH (1999) Event-related EEG/MEG synchronization and desynchronization: basic principles. Clin Neurophysiol 110:1842-1857.
Pfurtscheller G, Pichler-Zalaudek K, Ortmayr B, Diez J, Reisecker F (1998) Postmovement beta synchronization in patients with Parkinson's disease. J Clin Neurophysiol 15:243-250.
Pfurtscheller G, Stancak A, Jr., Neuper C (1996a) Event-related synchronization (ERS) in the alpha band--an electrophysiological correlate of cortical idling: a review. Int J Psychophysiol 24:39-46.
Pfurtscheller G, Stancak A, Jr., Neuper C (1996b) Post-movement beta synchronization. A correlate of an idling motor area? Electroencephalogr Clin Neurophysiol 98:281-293.
Pons TP, Garraghty PE, Friedman DP, Mishkin M (1987) Physiological evidence for serial processing in somatosensory cortex. Science 237:417-420.
Porter JT, Nieves D (2004) Presynaptic GABAB receptors modulate thalamic excitation of inhibitory and excitatory neurons in the mouse barrel cortex. J Neurophysiol 92:2762-2770.
Qi HX, Jain N, Collins CE, Lyon DC, Kaas JH (2010) Functional organization of motor cortex of adult macaque monkeys is altered by sensory loss in infancy. Proc Natl Acad Sci U S A 107:3192-3197.
Reyns N, Houdayer E, Bourriez JL, Blond S, Derambure P (2008) Post-movement beta synchronization in subjects presenting with sensory deafferentation. Clin Neurophysiol 119:1335-1345.
Rossini PM, Narici L, Martino G, Pasquarelli A, Peresson M, Pizzella V, Tecchio F, Romani GL (1994) Analysis of interhemispheric asymmetries of somatosensory evoked magnetic fields to right and left median nerve stimulation. Electroencephalogr Clin Neurophysiol 91:476-482.
Salmelin R, Hamalainen M, Kajola M, Hari R (1995) Functional segregation of movement-related rhythmic activity in the human brain. Neuroimage 2:237-243.
Shin HW, Kang SY, Hallett M, Sohn YH (2010) Extended surround inhibition in idiopathic paroxysmal kinesigenic dyskinesia. Clin Neurophysiol 121:1138-1141.
Shirane S, Sasaki M, Kogure D, Matsuda H, Hashimoto T (2001) Increased ictal perfusion of the thalamus in paroxysmal kinesigenic dyskinesia. J Neurol Neurosurg Psychiatry 71:408-410.
Simoes C, Hari R (1999) Relationship between responses to contra- and ipsilateral stimuli in the human second somatosensory cortex SII. Neuroimage 10:408-416.
Singh R, Macdonell RA, Scheffer IE, Crossland KM, Berkovic SF (1999) Epilepsy and paroxysmal movement disorders in families: evidence for shared mechanisms. Epileptic Disord 1:93-99.
Stevens H (1966) Paroxysmal choreo-athetosis. A form of reflex epilepsy. Arch Neurol 14:415-420.
Tamura Y, Matsuhashi M, Lin P, Ou B, Vorbach S, Kakigi R, Hallett M (2008) Impaired intracortical inhibition in the primary somatosensory cortex in focal hand dystonia. Mov Disord 23:558-565.
Tan LC, Tan AK, Tjia H (1998) Paroxysmal kinesigenic choreoathetosis in Singapore and its relationship to epilepsy. Clin Neurol Neurosurg 100:187-192.
Tinazzi M, Priori A, Bertolasi L, Frasson E, Mauguiere F, Fiaschi A (2000) Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow. Brain 123 ( Pt 1):42-50.
Tinazzi M, Rosso T, Fiaschi A (2003) Role of the somatosensory system in primary dystonia. Mov Disord 18:605-622.
Torres-Escalante JL, Barral JA, Ibarra-Villa MD, Perez-Burgos A, Gongora-Alfaro JL, Pineda JC (2004) 5-HT1A, 5-HT2, and GABAB receptors interact to modulate neurotransmitter release probability in layer 2/3 somatosensory rat cortex as evaluated by the paired pulse protocol. J Neurosci Res 78:268-278.
Visani E, Agazzi P, Canafoglia L, Panzica F, Ciano C, Scaioli V, Avanzini G, Franceschetti S (2006) Movement-related desynchronization-synchronization (ERD/ERS) in patients with Unverricht-Lundborg disease. Neuroimage 33:161-168.
Vitek JL (2002) Pathophysiology of dystonia: a neuronal model. Mov Disord 17 Suppl 3:S49-62.
Wang JL, Cao L, Li XH, Hu ZM, Li JD, Zhang JG, Liang Y, San A, Li N, Chen SQ, Guo JF, Jiang H, Shen L, Zheng L, Mao X, Yan WQ, Zhou Y, Shi YT, Ai SX, Dai MZ, Zhang P, Xia K, Chen SD, Tang BS (2011) Identification of PRRT2 as the causative gene of paroxysmal kinesigenic dyskinesias. Brain 134:3493-3501.
Wei H, Sun Y, Chen H, Wang DQ, Li LP, Ding Y, Liu AH, Lu CF, Wang YP (2012) Somatosensory disinhibition in patients with paroxysmal kinesigenic dyskinesia. Chin Med J (Engl) 125:838-842.
Weiland BJ, Boutros NN, Moran JM, Tepley N, Bowyer SM (2008) Evidence for a frontal cortex role in both auditory and somatosensory habituation: a MEG study. Neuroimage 42:827-835.
Williams D, Tijssen M, Van Bruggen G, Bosch A, Insola A, Di Lazzaro V, Mazzone P, Oliviero A, Quartarone A, Speelman H, Brown P (2002) Dopamine-dependent changes in the functional connectivity between basal ganglia and cerebral cortex in humans. Brain 125:1558-1569.
Willow M, Gonoi T, Catterall WA (1985) Voltage clamp analysis of the inhibitory actions of diphenylhydantoin and carbamazepine on voltage-sensitive sodium channels in neuroblastoma cells. Mol Pharmacol 27:549-558.
Wilson TW, Fleischer A, Archer D, Hayasaka S, Sawaki L (2011) Oscillatory MEG motor activity reflects therapy-related plasticity in stroke patients. Neurorehabil Neural Repair 25:188-193.
Zhou B, Chen Q, Gong Q, Tang H, Zhou D (2010a) The thalamic ultrastructural abnormalities in paroxysmal kinesigenic choreoathetosis: a diffusion tensor imaging study. J Neurol 257:405-409.
Zhou B, Chen Q, Zhang Q, Chen L, Gong Q, Shang H, Tang H, Zhou D (2010b) Hyperactive putamen in patients with paroxysmal kinesigenic choreoathetosis: a resting-state functional magnetic resonance imaging study. Mov Disord 25:1226-1231.
Zoghi M, Nordstrom MA (2007) Progressive suppression of intracortical inhibition during graded isometric contraction of a hand muscle is not influenced by hand preference. Exp Brain Res 177:266-274.