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  • Print publication year: 2013
  • Online publication date: June 2013

Section 1 - Background concepts

References

1. PenneyJB Jr, YoungAB. Speculations on the functional anatomy of basal ganglia disorders. Annu Rev Neurosci 1983;6:73–94.
2. AlbinRL, YoungAB, PenneyJB. The functional anatomy of basal ganglia disorders. Trends Neurosci 1989;12:366–75.
3. DeLongM, WichmannT. Update on models of basal ganglia function and dysfunction. Parkinsonism Relat Disord 2009;15 Suppl 3:S237–40.
4. ObesoJA, LanciegoJL. Past, present, and future of the pathophysiological model of the basal ganglia. Front Neuroanat 2011;5:39.
5. RommelfangerKS, WichmannT. Extrastriatal dopaminergic circuits of the basal ganglia. Front Neuroanat 2010;4:139.
6. DescarriesL, WatkinsKC, GarciaS, et al. Dual character, asynaptic and synaptic, of the dopamine innervation in adult rat neostriatum: a quantitative autoradiographic and immunocytochemical analysis. J Comp Neurol 1996;375:167–86.
7. WichmannT, DostrovskyJO. Pathological basal ganglia activity in movement disorders. Neuroscience 2011 PMID: 21723919.
8. BraakH, GhebremedhinE, RubU, et al. Stages in the development of Parkinson’s disease-related pathology. Cell Tissue Res 2004;318:121–34.
9. FearnleyJM, LeesAJ. Ageing and Parkinson’s disease: substantia nigra regional selectivity. Brain 1991;114:2283–301.
10. EusebioA, BrownP. Synchronisation in the beta frequency-band – the bad boy of parkinsonism or an innocent bystander?Exp Neurol 2009;217:1–3.
11. BrownP, WilliamsD. Basal ganglia local field potential activity: character and functional significance in the human. Clin Neurophysiol 2005;116:2510–19.
12. BrownP, OlivieroA, MazzoneP, et al. Dopamine dependency of oscillations between subthalamic nucleus and pallidum in Parkinson’s disease. J Neurosci 2001;21:1033–8.
13. PaveseN, BrooksDJ. Imaging neurodegeneration in Parkinson’s disease. Biochem Biophys Acta 2009;1792:722–9.
14. VingerhoetsFJG, SchulzerM, CalneDB, et al. Which clinical sign of Parkinson’s disease best reflects the nigrostriatal lesion?Ann Neurol 1997;41:58–64.
15. WangJ, ZuoCT, JiangYP, et al. 18F-FP-CIT PET imaging and SPM analysis of dopamine transporters in Parkinson’s disease in various Hoehn & Yahr stages. J Neurol 2007;254:185–90.
16. MooreRY, WhoneAL, BrooksDJ. Extrastriatal monoamine neuron function in Parkinson’s disease: an 18F-dopa PET study. Neurobiol Dis 2008;29:381–90.
17. RakshiJS, UemaT, ItoK, et al. Frontal, midbrain and striatal dopaminergic function in early and advanced Parkinson’s disease. A 3D [18F]Dopa-PET study. Brain 1999;122:1637–50.
18. WhoneAL, MooreRY, PicciniP, et al. Plasticity of the nigropallidal pathway in Parkinson’s disease. Ann Neurol 2003;53:206–13.
19. DoderM, RabinerEA, TurjanskiN, et al. 11C-WAY 100635 PET study. Tremor in Parkinson’s disease and serotonergic dysfunction: an 11C-WAY 100635 PET study. Neurology 2003;60:601–5.
20. PaveseN, MettaV, BoseSK, et al. Fatigue in Parkinson’s disease is linked to striatal and limbic serotonergic dysfunction. Brain 2010;133:3434–43.
21. BohnenNI, KauferDI, HendricksonR, et al. Cognitive correlates of cortical cholinergic denervation in Parkinson’s disease and parkinsonian dementia. J Neurol 2006;253:42–7.
22. BohnenNI, MüllerML, KoeppeRA, et al. History of falls in Parkinson disease is associated with reduced cholinergic activity. Neurology 2009;73:1670–6.
23. EckertT, BarnesA, DhawanV, et al. FDG PET in the differential diagnosis of parkinsonian disorders. Neuroimage 2005;26:912–21.
24. EidelbergD, MoellerJR, DhawanV, et al. The metabolic topography of parkinsonism. J Cereb Blood Flow Metab 1994;14:783–801.
25. MureH, HiranoS, TangCC, et al. Parkinson’s disease tremor-related metabolic network: characterization, progression, and treatment effects. Neuroimage 2011;54:1244–53.
26. LozzaC, BaronJC, EidelbergD, et al. Executive processes in Parkinson’s disease: FDG-PET and network analysis. Hum Brain Mapp 2004;22:236–45.
27. EidelbergD, MoellerJR, IshikawaT, et al. Regional metabolic correlates of surgical outcome following unilateral pallidotomy for Parkinson’s disease. Ann Neurol 1996;39:450–9.
28. ObesoI, RayNJ, AntonelliF, et al. Combining functional imaging with brain stimulation in Parkinson’s disease. Int Rev Psychiatry 2011;23:467–75.
29. PlayfordED, JenkinsIH, PassinghamRE, et al. Impaired mesial frontal and putamen activation in Parkinson’s disease: a PET study. Ann Neurol 1992;32:151–61.
30. JahanshahiM, JenkinsIH, BrownRG, et al. Self-initiated versus externally triggered movements. An investigation using measurement of regional cerebral blood flow with PET and movement-related potentials in normal and Parkinson’s disease subjects. Brain 1995;118:913–33.
31. SamuelM, Ceballos-BaumannAO, BoeckerH, et al. Motor imagery in normal subjects and Parkinson’s disease patients: an H215O PET study. Neuroreport 2001;12:821–8.
32. JenkinsIH, FernandezW, PlayfordED, et al. Impaired activation of the supplementary motor area in Parkinson’s disease is reversed when akinesia is treated with apomorphine. Ann Neurol 1992;32:749–57.
33. DagherA, DoyonJ, OwenAM, et al. Medial temporal lobe activation in Parkinson’s disease during fronto-striatal tasks revealed by PET: evidence for cortical reorganization?Mov Disord 1998;13 Suppl 2: 238.
34. BrooksDJ, SamuelM. The effects of surgical treatment of Parkinson’s disease on brain function: PET findings. Neurology 2000;55 Suppl 6:S52–9.
35. WuT, HallettM. A functional MRI study of automatic movements in patients with Parkinson’s disease. Brain 2005;128:2250–9.
36. MallolR, Barrós-LoscertalesA, LópezM, et al. Compensatory cortical mechanisms in Parkinson’s disease evidenced with fMRI during the performance of pre-learned sequential movements. Brain Res 2007;1147:265–71.
37. ProdoehlJ, SprakerM, CorcosD, et al. Blood oxygenation level-dependent activation in basal ganglia nuclei relates to specific symptoms in de novo Parkinson’s disease. Mov Disord 2010;25:2035–43.
38. SkidmoreFM, YangM, BaxterL, et al. Reliability analysis of the resting state can sensitively and specifically identify the presence of Parkinson disease. Neuroimage 2011; PMID: 21924367.
39. PaulsenJS. Functional imaging in Huntington’s disease. Exp Neurol 2009;216:272–7.
40. PaveseN, PolitisM, TaiYF, et al. Cortical dopamine dysfunction in symptomatic and premanifest Huntington’s disease gene carriers. Neurobiol Dis 2010;37:356–61.
41. AntoniniA, LeendersKL, EidelbergD. [11C]-raclopride-PET studies of the Huntington’s disease rate of progression: relevance of the trinucleotide repeat length. Ann Neurol 1998;43:253–5.
42. PaveseN, AndrewsTC, BrooksDJ, et al. Progressive striatal and cortical dopamine receptor dysfunction in Huntington’s disease: a PET study. Brain 2003;126:1127–35.
43. AndrewsTC, WeeksRA, TurjanskiN, et al. Huntington’s disease progression. PET and clinical observations. Brain 1999;122:2353–63.
44. HolthoffVA, KoeppeRA, FreyKA, et al. Positron emission tomography measures of benzodiazepine receptors in Huntington’s disease. Ann Neurol 1993;34:76–81.
45. WeeksRA, CunninghamVJ, PicciniP, et al. 11C-diprenorphine binding in Huntington’s disease: a comparison of region of interest analysis with statistical parametric mapping. J Cereb Blood Flow Metab 1997;17:943–9.
46. Van LaereK, CasteelsC, DhollanderI, et al. Widespread decrease of type 1 cannabinoid receptor availability in Huntington disease in vivo. J Nucl Med 2010;51:1413–17.
47. RosasHD, SalatDH, LeeSY, et al. Cerebral cortex and the clinical expression of Huntington’s disease: complexity and heterogeneity. Brain 2008;131:1057–68.
48. FeiginA, LeendersKL, MoellerJR, et al. Metabolic network abnormalities in early Huntington’s disease: an [(18)F]FDG PET study. J Nucl Med 2001;42:1591–5.
49. FeiginA, TangC, MaY, et al. Thalamic metabolism and symptom onset in preclinical Huntington’s disease. Brain 2007;130:2858–67.
50. WeeksRA, Ceballos-BaumannA, PicciniP, et al. Cortical control of movement in Huntington’s disease. A PET activation study. Brain 1997;120:1569–78.
51. BartensteinP, WeindlA, SpiegelS, et al. Central motor processing in Huntington’s disease. A PET study. Brain 1997;120:1553–67.
52. van EimerenT, SiebnerHR. An update on functional neuroimaging of parkinsonism and dystonia. Curr Opin Neurol 2006;19:412–19.
53. NeychevVK, GrossRE, LehéricyS, et al. The functional neuroanatomy of dystonia. Neurobiol Dis 2011;42:185–201.
54. TrostM, CarbonM, EdwardsC, et al. Primary dystonia: is abnormal functional brain architecture linked to genotype?Ann Neurol 2002;52:853–6.
55. ArgyelanM, CarbonM, NiethammerM, et al. Cerebellothalamocortical connectivity regulates penetrance in dystonia. J Neurosci 2009;29:9740–7.
56. GaribottoV, RomitoLM, EliaAE, et al. In vivo evidence for GABA(A) receptor changes in the sensorimotor system in primary dystonia. Mov Disord 2011;26:852–7.
57. CarbonM, NiethammerM, PengS, et al. Abnormal striatal and thalamic dopamine neurotransmission: genotype-related features of dystonia. Neurology. 2009;72:2097–103.
58. CalneDB, de la Fuente-FernándezR, KishoreA. Contributions of positron emission tomography to elucidating the pathogenesis of idiopathic parkinsonism and dopa responsive dystonia. J Neural Transm Suppl 1997;50:47–52.
59. RinneJO, IivanainenM, MetsähonkalaL, et al. Striatal dopaminergic system in dopa-responsive dystonia: a multi-tracer PET study shows increased D2 receptors. J Neural Transm, 2004;111:59–67.
60. AsanumaK, MaY, HuangC, et al. The metabolic pathology of dopa-responsive dystonia. Ann Neurol 2005;57:596–600.

References

1. DeLongMR, WichmannT. Circuits and circuit disorders of the basal ganglia. Arch Neurol 2007;64:20–4.
2. EvartsEV, TeräväinenH, CalneDB. Reaction time in Parkinson’s disease. Brain 1981;104:167–86.
3. JahanshahiM, BrownRG, MarsdenCD. Simple and choice reaction time and the use of advance information for motor preparation in Parkinson’s disease. Brain 1992;115:539–64.
4. BerardelliA, RothwellJC, ThompsonPD, HallettM. Pathophysiology of bradykinesia in Parkinson’s disease. Brain 2001;124:2131–46.
5. KangSY, WasakaT, ShamimEA, et al. Characteristics of the sequence effect in Parkinson’s disease. Mov Disord 2010;25:2148–55.
6. BeneckeR, RothwellJC, DickJP, DayBL, MarsdenCD. Performance of simultaneous movements in patients with Parkinson’s disease. Brain 1986;109:739–57.
7. BeneckeR, RothwellJC, DickJP, DayBL, MarsdenCD. Disturbance of sequential movements in patients with Parkinson’s disease. Brain 1987;110:361–79.
8. AgostinoR, BagnatoS, DinapoliL, ModugnoN, BerardelliA. Neither simple nor sequential arm movements are bradykinetic in parkinsonian patients with peak-dose dyskinesias. Clin Neurophysiol 2005;116:2077–82.
9. AgostinoR, BolognaM, DinapoliL, et al. Voluntary, spontaneous, and reflex blinking in Parkinson’s disease. Mov Disord 2008;23:669–75.
10. AgostinoR, BerardelliA, CruccuG, StocchiF, ManfrediM. Corneal and blink reflexes in Parkinson’s disease with “on–off” fluctuations. Mov Disord 1987;2:227–35.
11. CookeSF, BlissTV. Plasticity in the human central nervous system. Brain 2006;129:1659–73.
12. BattagliaF, GhilardiMF, QuartaroneA, et al. Impaired long-term potentiation-like plasticity of the trigeminal blink reflex circuit in Parkinson’s disease. Mov Disord 2006;21:2230–3.
13. MaoJB, EvingerC. Long-term potentiation of the human blink reflex. J Neurosci 2001;21:RC151(1–4).
14. BerardelliA, SabraAF, HallettM. Physiological mechanisms of rigidity in Parkinson’s disease. J Neurol Neurosurg Psychiatry 1983;46:45–53.
15. MeunierS, PolS, HouetoJL, VidailhetM. Abnormal reciprocal inhibition between antagonist muscles in Parkinson’s disease. Brain 2000;123:1017–26.
16. Simonetta-MoreauM, MeunierS, VidailhetM, et al. Transmission of group II heteronymous pathways is enhanced in rigid lower limb of de novo patients with Parkinson’s disease. Brain 2002;125:2125–33.
17. BallangerB, LozanoAM, MoroE, et al. Cerebral blood flow changes induced by pedunculopontine nucleus stimulation in patients with advanced Parkinson’s disease: a [(15)O] H2O PET study. Hum Brain Mapp 2009;30:3901–9.
18. ChenR, CrosD, CurraA, et al. The clinical diagnostic utility of transcranial magnetic stimulation: report of an IFCN committee. Clin Neurophysiol 2008;119:504–32.
19. BerardelliA, AbbruzzeseG, ChenR, et al. Consensus paper on short-interval intracortical inhibition and other transcranial magnetic stimulation intracortical paradigms in movement disorders. Brain Stim 2008;1:183–91.
20. RiddingMC, InzelbergR, RothwellJC. Changes in excitability of motor cortical circuitry in patients with Parkinson’s disease. Ann Neurol 1995;37:181–8.
21. BerardelliA, InghilleriM, RothwellJC, et al. Facilitation of muscle evoked responses after repetitive cortical stimulation in man. Exp Brain Res 1998;122:79–84.
22. GilioF, CurraA, InghilleriM, et al. Repetitive magnetic stimulation of cortical motor areas in Parkinson’s disease: implications for the pathophysiology of cortical function. Mov Disord 2002;17:467–73.
23. SuppaA, IezziE, ConteA, et al. Dopamine influences primary motor cortex plasticity and dorsal premotor-to-motor connectivity in Parkinson’s disease. Cereb Cortex 2010;20:2224–33.
24. BuhmannC, GorslerA, BaumerT, et al. Abnormal excitability of premotor–motor connections in de novo Parkinson’s disease. Brain 2004;127:2732–46.
25. MirP, MatsunagaK, GilioF, et al. Dopaminergic drugs restore facilitatory premotor–motor interactions in Parkinson’s disease. Neurology 2005;64:1906–12.
26. BagnatoS, AgostinoR, ModugnoN, QuartaroneA, BerardelliA. Plasticity of the motor cortex in Parkinson’s disease patients on and off therapy. Mov Disord 2006;21:639–45.
27. UekiY, MimaT, Ali KotbM, et al. Altered plasticity of the human motor cortex in Parkinson’s disease. Ann Neurol 2006;59:60–71.
28. MorganteF, EspayAJ, GunrajC, LangAE, ChenR. Motor cortex plasticity in Parkinson’s disease and levodopa-induced dyskinesias, Brain 2006;129:1059–69.
29. HuangYZ, EdwardsMJ, RounisE, BhatiaKP, RothwellJC. Theta burst stimulation of the human motor cortex. Neuron 2005;45:201–6.
30. EggersC, FinkGR, NowakDA. Theta burst stimulation over the primary motor cortex does not induce cortical plasticity in Parkinson’s disease. J Neurol 2010;257(10):1669–74.
31. SuppaA, MarsiliL, BelvisiD, et al. Lack of LTP-like plasticity in primary motor cortex in Parkinson’s disease. Exp Neurol 2011;227:296–301.
32. ConteA, BelvisiD, BolognaM, et al. Abnormal cortical synaptic plasticity in primary motor area in progressive supranuclear palsy. Cereb Cortex 2011; doi: 10.1093/cercor/bhr149.
33. AbbruzzeseG, BerardelliA. Sensorimotor integration in movement disorders. Mov Disord 2003;18:231–40.
34. BoeckerH, Ceballos-BaumannA, BartensteinP, et al. Sensory processing in Parkinson’s and Huntington’s disease: investigations with 3D H(2)(15)O-PET. Brain 1999;122:1651–65.
35. GeorgiouN, IansekR, BradshawJL, et al. An evaluation of the role of internal cues in the pathogenesis of parkinsonian hypokinesia. Brain 1993;116:1575–87.
36. GeorgiouN, BradshawJL, IansekR, et al. Reduction in external cues and movement sequencing in Parkinson’s disease. J Neurol Neurosurg Psychiatry 1994;57:368–70.
37. CurràA, BerardelliA, AgostinoR, et al. Performance of sequential arm movements with and without advance knowledge of motor pathways in Parkinson’s disease. Mov Disord 1997;12:646–54.
38. ArtiedaJ, PastorMA, LacruzF, ObesoJA. Temporal discrimination is abnormal in Parkinson’s disease. Brain 1992;115:199–210.
39. ConteA, ModugnoN, LenaF, et al. Subthalamic nucleus stimulation and somatosensory temporal discrimination in Parkinson’s disease. Brain 2010;133:2656–63.
40. BathiaKP, MarsdenCD. The behavioural and motor consequences of focal lesions of basal ganglia in man. Brain 1994;117:859–76.
41. BerardelliA, RothwellJC, HallettM, et al. The pathophysiology of primary dystonia. Brain 1998;121:1195–212.
42. CurràA, BerardelliA, AgostinoR, et al. Movement cueing and motor execution in patients with dystonia: a kinematic study. Mov Disord 2000;15:103–12.
43. CurràA, AgostinoR, DinapoliL, et al. Impairment of individual finger movements in patients with hand dystonia. Mov Disord 2004;19:1351–7.
44. BerardelliA, RothwellJC, DayBL, MarsdenCD. Pathophysiology of blepharospasm and oromandibular dystonia. Brain 1985;108:593–608.
45. TolosaE, MontserratL, BayesA. Blink reflex studies in patients with focal dystonias. Adv Neurol 1988;50:517–24.
46. QuartaroneA, SiebnerHR, RothwellJC. Task-specific hand dystonia: can too much plasticity be bad for you?Trends Neurosci 2006;29:192–9.
47. QuartaroneA, Sant’AngeloA, BattagliaF, et al. Enhanced long-term potentiation-like plasticity of the trigeminal blink reflex circuit in blepharospasm. J Neurosci 2006;26:716–21.
48. DayBL, MarsdenCD, ObesoJA, RothwellJC. Reciprocal inhibition between the muscles of the human forearm. J Physiol 1984;349:519–34.
49. BerardelliA, DayBL, MarsdenCD, RothwellJC. Evidence favouring presynaptic inhibition between antagonist muscle afferents in the human forearm. J Physiol 1987;391:71–83.
50. NakashimaK, RothwellJC, DayBL, et al. Reciprocal inhibition between forearm muscles in patients with writer’s cramp and other occupational cramps, symptomatic hemidystonia and hemiparesis due to stroke. Brain 1989;112:681–97.
51. PrioriA, BerardelliA, InghilleriM, et al. Electrical stimulation over muscle tendons in humans. Evidence favouring presynaptic inhibition of Ia fibres due to the activation of group III tendon afferents. Brain 1998;121:373–80.
52. LorenzanoC, PrioriA, CurràA, et al. Impaired EMG inhibition elicited by tendon stimulation in dystonia. Neurology 2000;55:1789–93.
53. RiddingMC, SheeanG, RothwellJC, InzelbergR, KujiraiT. Changes in the balance between motor cortical excitation and inhibition in focal, task specific dystonia. J Neurol Neurosurg Psychiatry 1995;59(5):493–8.
54. GilioF, SuppaA, BolognaM, et al. Short-term cortical plasticity in patients with dystonia: a study with repetitive transcranial magnetic stimulation. Mov Disord 2007;22:1436–43.
55. MuraseN, RothwellJC, KajiR, et al. Subthreshold low-frequency repetitive transcranial magnetic stimulation over the premotor cortex modulates writer’s cramp. Brain 2005;128:104–15.
56. QuartaroneA, BagnatoS, RizzoV, et al. Abnormal associative plasticity of the human motor cortex in writer’s cramp. Brain 2003;126:2586–96.
57. QuartaroneA, MorganteF, Sant’angeloA, et al. Abnormal plasticity of sensorimotor circuits extends beyond the affected body part in focal dystonia. J Neurol Neurosurg Psychiatry 2008;79:985–90.
58. EdwardsMJ, HuangYZ, MirP, RothwellJC, BhatiaKP. Abnormalities in motor cortical plasticity differentiate manifesting and nonmanifesting DYT1 carriers. Mov Disord 2006;21:2181–6.
59. BelvisiD, SuppaA, MarsiliM, et al. Abnormal experimentally- and behaviorally-induced LTP-like plasticity in focal hand dystonia. Mov Disord in press.
60. QuartaroneA, RizzoV, BagnatoS, et al. Homeostatic-like plasticity of the primary motor hand area is impaired in focal hand dystonia. Brain 2005;128:1943–50.
61. BienenstockEL, CooperLN, MunroPW. Theory for the development of neuron selectivity: orientation specificity and binocular interaction in visual cortex. J Neurosci 1982;2:32–48.
62. SiebnerHR, LangN, RizzoV, et al. Preconditioning of low-frequency repetitive transcranial magnetic stimulation with transcranial direct current stimulation: evidence for homeostatic plasticity in the human motor cortex. J Neurosci 2004;24:3379–85.
63. Bara-JimenezW, SheltonP, SangerTD, HallettM. Sensory discrimination capabilities in patients with focal hand dystonia. Ann Neurol 2000;47(3):377–80.
64. TinazziM, FiorioM, BertolasiL, AgliotiSM. Timing of tactile and visuo-tactile events is impaired in patients with cervical dystonia. J Neurol. 2004;251:85–90.
65. FiorioM, GambarinM, ValenteEM, et al. Defective temporal processing of sensory stimuli in DYT1 mutation carriers: a new endophenotype of dystonia?Brain 2007;130:134–42.
66. ScontriniA, ConteA, DefazioG, et al. Somatosensory temporal discrimination in patients with primary focal dystonia. J Neurol Neurosurg Psychiatry 2009;80:1315–19.
67. ThompsonPD, BerardelliA, RothwellJC, et al. The coexistence of bradykinesia and chorea in Huntington’s disease and its implications for theories of basal ganglia control of movement. Brain 1988;111:223–44.
68. BerardelliA, NothJ, ThompsonPD, et al. Pathophysiology of chorea and bradykinesia in Huntington’s disease. Mov Disord. 1999;14:398–403.
69. AgostinoR, BerardelliA, CruccuG, et al. Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington’s chorea. Mov Disord 1988;3:281–9.
70. CrupiD, GhilardiMF, MosielloC, et al. Cortical and brainstem LTP-like plasticity in Huntington’s disease. Brain Res Bull 2008;75: 107–14.
71. ModugnoN, CurràA, GiovannelliM, et al. The prolonged cortical silent period in patients with Huntington’s disease. Clin Neurophysiol 2001;112:1470–4.
72. SchipplingS, SchneiderSA, BhatiaKP, et al. Abnormal motor cortex excitability in preclinical and very early Huntington’s disease. Biol Psychiatry 2009;65:959–65.
73. LorenzanoC, DinapoliL, GilioF, et al. Motor cortical excitability studied with repetitive transcranial magnetic stimulation in patients with Huntington’s disease. Clin Neurophysiol 2006;117:1677–81.
74. OrthM, SchipplingS, SchneiderSA, et al. Abnormal motor cortex plasticity in premanifest and very early manifest Huntington disease. J Neurol Neurosurg Psychiatry 2010;81:267–70.
75. NothJ, PodollK, FriedemannHH. Long-loop reflexes in small hand muscles studied in normal subjects and in patients with Huntington’s disease. Brain 1985;108:65–80.
76. LeckmanJF, KnorrAM, RasmussonAM, CohenDJ. Basal ganglia research and Tourette’s syndromes. Trends Neurosci 1991;14:94.
77. LeckmanJF. Tourette’s syndrome. Lancet 2002;360:1577–86.
78. RobertsonMM. Tourette syndrome, associated conditions and the complexities of treatment. Brain 2000;123:425–62.
79. RobertsonMM, EapenV, CavannaAE. The international prevalence, epidemiology, and clinical phenomenology of Tourette syndrome: a cross-cultural perspective. J Psychosom Res 2009;67:475–83.
80. JankovicJ. Tourette’s syndrome. New Engl J Med 2001;345:1184–92.
81. BerardelliA, Curra`A, FabbriniG, GilioF, ManfrediM. Pathophysiology of tics and Tourette syndrome. J Neurol 2003;250:781–7.
82. MinkJW. The basal ganglia and involuntary movements: impaired inhibition of competing motor patterns. Arch Neurol 2003;60:1365–8.
83. MinkJW. Neurobiology of basal ganglia and Tourette syndrome: basal ganglia circuits and thalamocortical outputs. Adv Neurol 2006;99:89–98.
84. GeorgiouN, BradshawJL, PhillipsJG, BradshawJA, ChiuE. Advance information and movement sequencing in Gilles de la Tourette’s syndrome. J Neurol Neurosurg Psychiatry 1995;58:184–91.
85. SheppardDM, BradshawJL, GeorgiouN, BradshawJA, LeeP. Movement sequencing in children with Tourette’s syndrome and attention deficit hyperactivity disorder. Mov Disord. 2000;15:1184–93.
86. AvanzinoL, MartinoD, BoveM, et al. Movement lateralization and bimanual coordination in children with Tourette syndrome. Mov Disord 2011;26:2114–18.
87. PalminteriS, LebretonM, WorbeY, et al. Dopamine-dependent reinforcement of motor skill learning: evidence from Gilles de la Tourette syndrome. Brain 2011;134:2287–301.
88. SmithSJ, LeesAJ. Abnormalities of the blink reflex in Gilles de la Tourette syndrome. J Neurol Neurosurg Psychiatry 1989;52:895–8.
89. SuppaA, BelvisiD, BolognaM, et al. Abnormal cortical and brain stem plasticity in Gilles de la Tourette syndrome. Mov Disord 2011;26:1703–10.
90. OrthM. Transcranial magnetic stimulation in Gilles de la Tourette syndrome. J Psychosom Res. 2009;67:591–8.
91. KurlanR, LichterD, HewittD. Sensory tics in Tourette’s syndrome. Neurology. 1989;39:731–4.
92. KarpBI, HallettM. Extracorporeal ‘phantom’ tics in Tourette’s syndrome. Neurology 1996;46:38–40.