Parkinson DiseaseNCT02200887
Sleep Homeostasis in Parkinson's Disease
An observational study of Parkinson Disease, run by Salvatore Galati at 1 site in Switzerland.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 45 to 75 yearsHealthy volunteers can take part
- Conditions the study is for
- Parkinson Disease
- How many people
- 48 participants
- Where
- 1 siteSwitzerland
- Study dates
- Sep 2013to Jun 2015
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 45 to 75 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Study population: Healthy volunteers and patients with parkinson disease
Who may be able to join
- clinical characteristics of the patients must be according the UK (United Kingdom) Brain Bank
Who cannot join
- 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)
Trial locations and contacts
1 site in 1 country.
Switzerland1 site
Ospedale Regionale di Lugano
Lugano, Canton Ticino, 6903
About this study
Official title: Role of Sleep Homeostasis in the Development of the L-Dopa Induced Dyskinesias in Patients With Parkinson's Disease
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.
Read the detailed description
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:
- 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.
- 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.
- 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
- Parkinson Disease
- Keywords
- Dyskinesia, Slow Wave Sleep
- Medical subject headings
- Parkinson Disease, Dyskinesias
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Advanced Parkinsons Disease | Polysomnogram | |
| Parkinsons Disease with Dyskinesia | Polysomnogram | |
| De novo Parkinsons Disease | Polysomnogram | |
| Healthy Volunteers | Polysomnogram |
What is being measured
The primary outcome is the main question the study is designed to answer.
Slow wave sleep
Percentage of total sleep classified as slow wave sleep
Measured: 1 night
Secondary outcomes (1)
Amplitude of slow waves during sleep
Reduction of homeostatic synaptic plasticity during the time of sleep
Measured: 1 Night
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted25 Jul 2014 (estimated)
- Study startSep 2013
- Primary completionJun 2015
- Study completionJun 2015
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (33)Papers the sponsor has linked to this study.
- Other trials for Parkinson DiseaseStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Enrolment
- 48 participants (actual)
Sponsor and investigators
- Lead sponsor
- Salvatore Galati
- Sponsor type
- Other government
- Responsible party
- Sponsor-investigator, Salvatore Galati, Ospedale Civico, Lugano
- Investigators
- Salvatore Galati, MD, Principal investigator, Ospedale Regionale di Lugano
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT02200887
- Sponsor's protocol ID
- EOC-NSI.12.01
- Status last verified
- Apr 2018
- First submitted
- 24 Jul 2014
- Last updated
- 9 Apr 2018
- Results posted
- No
- Data monitoring committee
- No
Publications
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.
PubMed 10970059Rye DB, Jankovic J. Emerging views of dopamine in modulating sleep/wake state from an unlikely source: PD. Neurology. 2002 Feb 12;58(3):341-6. doi: 10.1212/wnl.58.3.341. No abstract available.
PubMed 11839829Moller JC, Rethfeldt M, Korner Y, Stiasny-Kolster K, Cassel W, Meindorfner C, Rissling I, Kruger HP, Oertel WH. Daytime sleep latency in medication-matched Parkinsonian patients with and without sudden onset of sleep. Mov Disord. 2005 Dec;20(12):1620-2. doi: 10.1002/mds.20630.
PubMed 16078226Moller 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.
PubMed 18619893Valko PO, Waldvogel D, Weller M, Bassetti CL, Held U, Baumann CR. Fatigue and excessive daytime sleepiness in idiopathic Parkinson's disease differently correlate with motor symptoms, depression and dopaminergic treatment. Eur J Neurol. 2010 Dec;17(12):1428-36. doi: 10.1111/j.1468-1331.2010.03063.x.
PubMed 20491889Benninger DH, Michel J, Waldvogel D, Candia V, Poryazova R, van Hedel HJ, Bassetti CL. REM sleep behavior disorder is not linked to postural instability and gait dysfunction in Parkinson. Mov Disord. 2010 Aug 15;25(11):1597-604. doi: 10.1002/mds.23121.
PubMed 20629146Unger MM, Belke M, Menzler K, Heverhagen JT, Keil B, Stiasny-Kolster K, Rosenow F, Diederich NJ, Mayer G, Moller JC, Oertel WH, Knake S. Diffusion tensor imaging in idiopathic REM sleep behavior disorder reveals microstructural changes in the brainstem, substantia nigra, olfactory region, and other brain regions. Sleep. 2010 Jun;33(6):767-73. doi: 10.1093/sleep/33.6.767.
PubMed 20550017Claassen DO, Josephs KA, Ahlskog JE, Silber MH, Tippmann-Peikert M, Boeve BF. REM sleep behavior disorder preceding other aspects of synucleinopathies by up to half a century. Neurology. 2010 Aug 10;75(6):494-9. doi: 10.1212/WNL.0b013e3181ec7fac. Epub 2010 Jul 28.
PubMed 20668263Bassetti CL. Nonmotor disturbances in Parkinson's disease. Neurodegener Dis. 2011;8(3):95-108. doi: 10.1159/000316613. Epub 2010 Dec 23.
PubMed 21196687Currie LJ, Bennett JP Jr, Harrison MB, Trugman JM, Wooten GF. Clinical correlates of sleep benefit in Parkinson's disease. Neurology. 1997 Apr;48(4):1115-7. doi: 10.1212/wnl.48.4.1115.
PubMed 9109914Bateman DE, Levett K, Marsden CD. Sleep benefit in Parkinson's disease. J Neurol Neurosurg Psychiatry. 1999 Sep;67(3):384-5. doi: 10.1136/jnnp.67.3.384. No abstract available.
PubMed 10449564Stefani 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.
PubMed 16328297Diederich 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.
PubMed 15946897Romigi 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.
PubMed 18484989Dodel 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.
PubMed 11735671
Study at a glance
From the registry record, last updated by the sponsor on 9 Apr 2018. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Role of Sleep Homeostasis in the Development of the L-Dopa Induced Dyskinesias in Patients With Parkinson's Disease
- ClinicalTrials.gov ID
- NCT02200887
- Acronym / sponsor ID
- EOC-NSI.12.01
- Conditions
- Parkinson Disease
- Keywords
- Dyskinesia, Slow Wave Sleep
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 48 participants (actual)
- Lead sponsor
- Salvatore GalatiOther government
- Study start
- Sep 2013
- Primary completion
- Jun 2015 (actual)
- Study completion
- Jun 2015 (actual)
- First posted
- 25 Jul 2014 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed description
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:
- 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.
- 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.
- 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.
Study design
- Observational model
- Case-control
- Time perspective
- Cross-sectional
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| Advanced Parkinsons Disease | – | –Polysomnogram |
| Parkinsons Disease with Dyskinesia | – | –Polysomnogram |
| De novo Parkinsons Disease | – | –Polysomnogram |
| Healthy Volunteers | – | –Polysomnogram |
Who may qualify
- Ages
- 45 to 75 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
- Study population
- Healthy volunteers and patients with parkinson disease
Key inclusion criteria (1 listed)
- clinical characteristics of the patients must be according the UK (United Kingdom) Brain Bank
Key exclusion criteria (3 listed)
- 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)
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Slow wave sleep
Time frame: 1 night
Percentage of total sleep classified as slow wave sleep
1 secondary outcome
Amplitude of slow waves during sleep
Time frame: 1 Night
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 9 Apr 2018.
- Background: PubMed 10970059Poewe 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.
- Background: PubMed 11839829Rye DB, Jankovic J. Emerging views of dopamine in modulating sleep/wake state from an unlikely source: PD. Neurology. 2002 Feb 12;58(3):341-6. doi: 10.1212/wnl.58.3.341. No abstract available.
- Background: PubMed 16078226Moller JC, Rethfeldt M, Korner Y, Stiasny-Kolster K, Cassel W, Meindorfner C, Rissling I, Kruger HP, Oertel WH. Daytime sleep latency in medication-matched Parkinsonian patients with and without sudden onset of sleep. Mov Disord. 2005 Dec;20(12):1620-2. doi: 10.1002/mds.20630.
- Background: PubMed 18619893Moller 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.
- Background: PubMed 20491889Valko PO, Waldvogel D, Weller M, Bassetti CL, Held U, Baumann CR. Fatigue and excessive daytime sleepiness in idiopathic Parkinson's disease differently correlate with motor symptoms, depression and dopaminergic treatment. Eur J Neurol. 2010 Dec;17(12):1428-36. doi: 10.1111/j.1468-1331.2010.03063.x.
- Background: PubMed 20629146Benninger DH, Michel J, Waldvogel D, Candia V, Poryazova R, van Hedel HJ, Bassetti CL. REM sleep behavior disorder is not linked to postural instability and gait dysfunction in Parkinson. Mov Disord. 2010 Aug 15;25(11):1597-604. doi: 10.1002/mds.23121.
- Background: PubMed 20550017Unger MM, Belke M, Menzler K, Heverhagen JT, Keil B, Stiasny-Kolster K, Rosenow F, Diederich NJ, Mayer G, Moller JC, Oertel WH, Knake S. Diffusion tensor imaging in idiopathic REM sleep behavior disorder reveals microstructural changes in the brainstem, substantia nigra, olfactory region, and other brain regions. Sleep. 2010 Jun;33(6):767-73. doi: 10.1093/sleep/33.6.767.
- Background: PubMed 20668263Claassen DO, Josephs KA, Ahlskog JE, Silber MH, Tippmann-Peikert M, Boeve BF. REM sleep behavior disorder preceding other aspects of synucleinopathies by up to half a century. Neurology. 2010 Aug 10;75(6):494-9. doi: 10.1212/WNL.0b013e3181ec7fac. Epub 2010 Jul 28.
- Background: PubMed 21196687Bassetti CL. Nonmotor disturbances in Parkinson's disease. Neurodegener Dis. 2011;8(3):95-108. doi: 10.1159/000316613. Epub 2010 Dec 23.
- Background: PubMed 9109914Currie LJ, Bennett JP Jr, Harrison MB, Trugman JM, Wooten GF. Clinical correlates of sleep benefit in Parkinson's disease. Neurology. 1997 Apr;48(4):1115-7. doi: 10.1212/wnl.48.4.1115.
- Background: PubMed 10449564Bateman DE, Levett K, Marsden CD. Sleep benefit in Parkinson's disease. J Neurol Neurosurg Psychiatry. 1999 Sep;67(3):384-5. doi: 10.1136/jnnp.67.3.384. No abstract available.
- Background: PubMed 16328297Stefani 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.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Salvatore Galati, MD principal investigator
Ospedale Regionale di Lugano
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Parkinson Disease, run by Salvatore Galati at 1 site in Switzerland.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 9 Apr 2018. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Switzerland. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Slow wave sleep (time frame: 1 night). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT02200887, which also lists 33 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 9 Apr 2018.