Study Results
Results pending
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Basic Information
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Recruitment Status
COMPLETED
Total Enrollment
48 participants
Study Classification
OBSERVATIONAL
Study Start Date
2013-09-30
Study Completion Date
2015-06-30
Brief Summary
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Parkinson's disease is characterized in the advanced phases by an altered response to dopaminergic therapy for the occurrence of abnormal movements called dyskinesias, that worsens the quality of life of the patient and exposes him to comorbidities. Several data show a reduction in the amount of slow wave sleep that correlates inversely with disease duration. Since this stage of sleep is linked to mechanisms of deletion of superfluous information the investigators hypothesize that the onset of dyskinesias is related to such alteration of sleep.
-This study is aimed to investigate, by means of high-density electroencephalography (hd-EEG), the sleep and in particular the slow wave in order to clarify the relations with the development of dyskinesias.
-This study is aimed to investigate, by means of high-density electroencephalography (hd-EEG), the sleep and in particular the slow wave in order to clarify the relations with the development of dyskinesias.
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Detailed Description
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Wakefulness in PD is frequently interrupted by sleep episodes, even rapid eye movement sleep (REM), whilst nocturnal sleep is disturbed by abnormal motor activity interference, such as REM sleep behaviour disorder (RBD) or periodic limb movements (PLMS). Several lines of evidence have suggested a close relation between sleep-wake changes and dopaminergic degeneration in PD(1-7) while sleep disorders commonly precede the clinical motor onset by many years (8,9). On the other hand, morning motor performance improvement is frequently mentioned by patients, mainly in those with long disease duration and motor fluctuation (10,11). Of note, the same state of vigilance can profoundly influence some clinical PD features (for instance rigidity) as well as basal ganglia neuronal activity(12).
Few reports have shown changes in sleep architecture: a reduction of the amount of SWS in parallel with disease duration (13-15) has been observed, but no study, so far, has addressed how sleep may impact on LID. Once these abnormal movements develop, they are difficult to treat and negatively affect the quality of life and the treatment costs of PD patients (16,17). Although levodopa represents, so far, the more effective treatment for PD patients (18,19) to ameliorate the cardinal signs such as bradykinesia/akinesia and rigidity (20), as the disease progresses, these benefits are in some measure abolished by the emergence of dyskinesia (21). During the early stages PD patients experience a rather satisfying quality of life that is impeded in the advanced stages by the emerging of these involuntary movements frequently at the peak of the levodopa effect (16,22,23). In other words, when the patients experience these motor complications (shortening motor response and development of dyskinesia) the delivery of levodopa without inducing dyskinesia becomes increasingly difficult (21,24-27).
Several efforts have been made in order to find "pure" anti-dyskinetic drugs that are able to uncouple the anti-akinetic effect from the dyskinetic response. Serotoninergic receptor agonists were claimed to be drugs against dyskinesia (28), however, it was observed that they may also impair levodopa efficacy (29-31). As of today, no clinical effective therapies are able to alleviate dyskinesia without worsening parkinsonism.
Great efforts have been made to clarify LID pathogenesis, emphasizing the role of pulsative stimulation of striatal receptors by dopaminergic treatment (25) and more recently, on molecular changes of postsynaptic (32,33) or presynaptic mechanisms (34). Although no conclusive results on LID pathogenesis have been achieved, indeed disease duration (i.e. the degree of dopaminergic degeneration) rather than long-term use of levodopa, seems to play a crucial role (22,23). This notion can be inferred from clinical practice, but is also evident in MPTP-induced parkinsonism in humans in which the extended dopaminergic lesion caused within a few days the development of dyskinesias undistinguishable from those in the idiopathic form (35).
General Aim:
The study is aimed 1) to define abnormal cortical synaptic homeostasis, measured by means of SWS and waking EEG evoked responses, as key components for the development of LID; 2) to analyse the impact of anti-dyskinetic effect of rTMS on the SWA in additional ten PD patient with LID.
Specific aims:
1. To compare, in the four groups of subjects (control, de novo, advanced without dyskinesia, and advanced with dyskinesia), changes of the EEG features of NREM sleep: slow wave/slow oscillation and sleep spindles. A significant reduction of the physiological reduction of SWA in dyskinetic patients in comparison with the other groups is expected.
2. To identify the homeostatic reduction of cortical synaptic strength (downscaling) in the four categories of subjects by comparing late sleep (i.e. towards morning) SWA with early sleep (i.e. at the beginning of the night) SWA as well as by comparing the overnight changes in the amplitude of EEG somatosensory, auditory and visual evoked responses recorded before and after sleep. The study is aimed to demonstrate the reduction/absence of a physiological downscaling in dyskinetic patients versus the other groups.
3. To analyse the effect of rTMS on SWA of PD patients with LID in order to demonstrate a recovery of physiological downscaling of SWA in these patients parallel to the reduction of dyskinesia.
Few reports have shown changes in sleep architecture: a reduction of the amount of SWS in parallel with disease duration (13-15) has been observed, but no study, so far, has addressed how sleep may impact on LID. Once these abnormal movements develop, they are difficult to treat and negatively affect the quality of life and the treatment costs of PD patients (16,17). Although levodopa represents, so far, the more effective treatment for PD patients (18,19) to ameliorate the cardinal signs such as bradykinesia/akinesia and rigidity (20), as the disease progresses, these benefits are in some measure abolished by the emergence of dyskinesia (21). During the early stages PD patients experience a rather satisfying quality of life that is impeded in the advanced stages by the emerging of these involuntary movements frequently at the peak of the levodopa effect (16,22,23). In other words, when the patients experience these motor complications (shortening motor response and development of dyskinesia) the delivery of levodopa without inducing dyskinesia becomes increasingly difficult (21,24-27).
Several efforts have been made in order to find "pure" anti-dyskinetic drugs that are able to uncouple the anti-akinetic effect from the dyskinetic response. Serotoninergic receptor agonists were claimed to be drugs against dyskinesia (28), however, it was observed that they may also impair levodopa efficacy (29-31). As of today, no clinical effective therapies are able to alleviate dyskinesia without worsening parkinsonism.
Great efforts have been made to clarify LID pathogenesis, emphasizing the role of pulsative stimulation of striatal receptors by dopaminergic treatment (25) and more recently, on molecular changes of postsynaptic (32,33) or presynaptic mechanisms (34). Although no conclusive results on LID pathogenesis have been achieved, indeed disease duration (i.e. the degree of dopaminergic degeneration) rather than long-term use of levodopa, seems to play a crucial role (22,23). This notion can be inferred from clinical practice, but is also evident in MPTP-induced parkinsonism in humans in which the extended dopaminergic lesion caused within a few days the development of dyskinesias undistinguishable from those in the idiopathic form (35).
General Aim:
The study is aimed 1) to define abnormal cortical synaptic homeostasis, measured by means of SWS and waking EEG evoked responses, as key components for the development of LID; 2) to analyse the impact of anti-dyskinetic effect of rTMS on the SWA in additional ten PD patient with LID.
Specific aims:
1. To compare, in the four groups of subjects (control, de novo, advanced without dyskinesia, and advanced with dyskinesia), changes of the EEG features of NREM sleep: slow wave/slow oscillation and sleep spindles. A significant reduction of the physiological reduction of SWA in dyskinetic patients in comparison with the other groups is expected.
2. To identify the homeostatic reduction of cortical synaptic strength (downscaling) in the four categories of subjects by comparing late sleep (i.e. towards morning) SWA with early sleep (i.e. at the beginning of the night) SWA as well as by comparing the overnight changes in the amplitude of EEG somatosensory, auditory and visual evoked responses recorded before and after sleep. The study is aimed to demonstrate the reduction/absence of a physiological downscaling in dyskinetic patients versus the other groups.
3. To analyse the effect of rTMS on SWA of PD patients with LID in order to demonstrate a recovery of physiological downscaling of SWA in these patients parallel to the reduction of dyskinesia.
Conditions
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Parkinson Disease
Study Design
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Observational Model Type
CASE_CONTROL
Study Time Perspective
CROSS_SECTIONAL
Study Groups
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Advanced Parkinsons Disease
Polysomnogram
No interventions assigned to this group
Parkinsons Disease with Dyskinesia
Polysomnogram
No interventions assigned to this group
De novo Parkinsons Disease
Polysomnogram
No interventions assigned to this group
Healthy Volunteers
Polysomnogram
No interventions assigned to this group
Eligibility Criteria
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Inclusion Criteria
* clinical characteristics of the patients must be according the UK (United Kingdom) Brain Bank
Exclusion Criteria
* anamnestic obstructive sleep apneas syndrome
* known cognitive deterioration or with MMSE (Mini-Mental State Examination) ≤24/30
* depression ≥ 20 of the BDI scale (Beck Depression Inventory)
* known cognitive deterioration or with MMSE (Mini-Mental State Examination) ≤24/30
* depression ≥ 20 of the BDI scale (Beck Depression Inventory)
Minimum Eligible Age
45 Years
Maximum Eligible Age
75 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
Yes
Sponsors
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Salvatore Galati
OTHER_GOV
Sponsor Role
lead
Responsible Party
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Salvatore Galati
MD, head of service
Responsibility Role
SPONSOR_INVESTIGATOR
Principal Investigators
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Salvatore Galati, MD
Role: PRINCIPAL_INVESTIGATOR
Ospedale Regionale di Lugano
Locations
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Ospedale Regionale di Lugano
Lugano, Canton Ticino, Switzerland
Site Status
Countries
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Switzerland
References
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Poewe W, Hogl B. Parkinson's disease and sleep. Curr Opin Neurol. 2000 Aug;13(4):423-6. doi: 10.1097/00019052-200008000-00009. No abstract available.
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Moller JC, Unger M, Stiasny-Kolster K, Kaussner Y, Penzel T, Oertel WH, Hemmeter U. Continuous sleep EEG monitoring in PD patients with and without sleep attacks. Parkinsonism Relat Disord. 2009 Mar;15(3):238-41. doi: 10.1016/j.parkreldis.2008.05.009. Epub 2008 Jul 10.
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BACKGROUND
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BACKGROUND
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Bassetti CL. Nonmotor disturbances in Parkinson's disease. Neurodegener Dis. 2011;8(3):95-108. doi: 10.1159/000316613. Epub 2010 Dec 23.
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BACKGROUND
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Reference Type
BACKGROUND
Stefani A, Galati S, Peppe A, Bassi A, Pierantozzi M, Hainsworth AH, Bernardi G, Orlacchio A, Stanzione P, Mazzone P. Spontaneous sleep modulates the firing pattern of parkinsonian subthalamic nucleus. Exp Brain Res. 2006 Jan;168(1-2):277-80. doi: 10.1007/s00221-005-0175-y. Epub 2005 Nov 18.
Reference Type
BACKGROUND
Diederich NJ, Vaillant M, Mancuso G, Lyen P, Tiete J. Progressive sleep 'destructuring' in Parkinson's disease. A polysomnographic study in 46 patients. Sleep Med. 2005 Jul;6(4):313-8. doi: 10.1016/j.sleep.2005.03.011.
Reference Type
BACKGROUND
Romigi A, Placidi F, Peppe A, Pierantozzi M, Izzi F, Brusa L, Galati S, Moschella V, Marciani MG, Mazzone P, Stanzione P, Stefani A. Pedunculopontine nucleus stimulation influences REM sleep in Parkinson's disease. Eur J Neurol. 2008 Jul;15(7):e64-5. doi: 10.1111/j.1468-1331.2008.02167.x. Epub 2008 May 15. No abstract available.
Reference Type
BACKGROUND
Dodel RC, Berger K, Oertel WH. Health-related quality of life and healthcare utilisation in patients with Parkinson's disease: impact of motor fluctuations and dyskinesias. Pharmacoeconomics. 2001;19(10):1013-38. doi: 10.2165/00019053-200119100-00004.
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BACKGROUND
Devos D; French DUODOPA Study Group. Patient profile, indications, efficacy and safety of duodenal levodopa infusion in advanced Parkinson's disease. Mov Disord. 2009 May 15;24(7):993-1000. doi: 10.1002/mds.22450.
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BACKGROUND
Mercuri NB, Bernardi G. The 'magic' of L-dopa: why is it the gold standard Parkinson's disease therapy? Trends Pharmacol Sci. 2005 Jul;26(7):341-4. doi: 10.1016/j.tips.2005.05.002.
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Poewe W, Antonini A, Zijlmans JC, Burkhard PR, Vingerhoets F. Levodopa in the treatment of Parkinson's disease: an old drug still going strong. Clin Interv Aging. 2010 Sep 7;5:229-38. doi: 10.2147/cia.s6456.
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Katzenschlager R, Lees AJ. Treatment of Parkinson's disease: levodopa as the first choice. J Neurol. 2002 Sep;249 Suppl 2:II19-24. doi: 10.1007/s00415-002-1204-4.
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Reference Type
BACKGROUND
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BACKGROUND
Melamed E, Zoldan J, Galili-Mosberg R, Ziv I, Djaldetti R. Current management of motor fluctuations in patients with advanced Parkinson's disease treated chronically with levodopa. J Neural Transm Suppl. 1999;56:173-83. doi: 10.1007/978-3-7091-6360-3_11.
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Antonini A, Ursino G, Calandrella D, Bernardi L, Plebani M. Continuous dopaminergic delivery in Parkinson's disease. J Neurol. 2010 Nov;257(Suppl 2):S305-8. doi: 10.1007/s00415-010-5714-1.
Reference Type
BACKGROUND
Stefani A, Galati S, Brusa L, Pierantozzi M, Peppe A, Stanzione P. Pathological gambling from dopamine agonist and deep brain stimulation of the nucleus tegmenti pedunculopontine. BMJ Case Rep. 2010 Nov 18;2010:bcr0220102774. doi: 10.1136/bcr.02.2010.2774.
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BACKGROUND
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BACKGROUND
Olanow CW, Kieburtz K, Stern M, Watts R, Langston JW, Guarnieri M, Hubble J; US01 Study Team. Double-blind, placebo-controlled study of entacapone in levodopa-treated patients with stable Parkinson disease. Arch Neurol. 2004 Oct;61(10):1563-8. doi: 10.1001/archneur.61.10.1563.
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Calabresi P, Di Filippo M, Ghiglieri V, Tambasco N, Picconi B. Levodopa-induced dyskinesias in patients with Parkinson's disease: filling the bench-to-bedside gap. Lancet Neurol. 2010 Nov;9(11):1106-17. doi: 10.1016/S1474-4422(10)70218-0. Epub 2010 Sep 27.
Reference Type
BACKGROUND
Galati S, Stanzione P, D'Angelo V, Fedele E, Marzetti F, Sancesario G, Procopio T, Stefani A. The pharmacological blockade of medial forebrain bundle induces an acute pathological synchronization of the cortico-subthalamic nucleus-globus pallidus pathway. J Physiol. 2009 Sep 15;587(Pt 18):4405-23. doi: 10.1113/jphysiol.2009.172759. Epub 2009 Jul 21.
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BACKGROUND
Langston JW, Ballard P. Parkinsonism induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP): implications for treatment and the pathogenesis of Parkinson's disease. Can J Neurol Sci. 1984 Feb;11(1 Suppl):160-5. doi: 10.1017/s0317167100046333.
Reference Type
BACKGROUND
Other Identifiers
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EOC-NSI.12.01
Identifier Type: -
Identifier Source: org_study_id
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