Neuroplastic Alterations of the Motor Cortex by Caffeine
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|ClinicalTrials.gov Identifier: NCT04011670|
Recruitment Status : Recruiting
First Posted : July 8, 2019
Last Update Posted : October 10, 2019
Caffeine is a psychostimulant drug. It acts as a competitive antagonist at adenosine receptors, which modulate cortical excitability as well. In deep brain stimulation (DBS), the production of adenosine following the release of adenosine triphosphate (ATP) explains the reduction of tremor. Binding of adenosine to adenosine A1 receptors suppresses excitatory transmission in the thalamus and hereby reduces both tremor-and DBS-induced side effects. Also, the effect of adenosine was attenuated following the administration of the 8-Cyclopentyl-1,3-dipropylxanthine (DPCPX) adenosine A1 receptor antagonist. Therefore, the presence of a receptor antagonist such as caffeine was suggested to reduce the effectiveness of deep brain stimulation (DBS) in treating tremor and other movement disorders.
Based on this finding, the investigators hypothesize that the antagonistic effect of caffeine can tentatively block the excitatory effects of transcranial alternating current stimulation (tACS). The plasticity effects might differ among caffeine users and non- caffeine users depending on the availability of receptor binding sites.
Apart from that, a major issue in NIBS studies including those studying motor-evoked potentials is the response variability both within and between individuals. The trial to trial variability of motor evoked potentials (MEPs) may be affected by many factors. Inherent to caffeine is its effect on vigilance. In this study, the investigator shall monitor the participant's vigilance by pupillometry to (1) better understand the factors, which might cause variability in transcranial excitability induction studies and (2) to separate the direct pharmacological effect from the indirect attentional effect of caffeine.
|Condition or disease||Intervention/treatment||Phase|
|Cortical Excitability Brain Stimulation Caffeine||Other: 200 mg caffeine tablet Other: Non-active tablet||Not Applicable|
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||30 participants|
|Intervention Model:||Crossover Assignment|
|Intervention Model Description:||15 participants are assigned to caffeine group and another 15 are assigned to placebo group. Then, the participants who were initially in the caffeine group now be in placebo group and those who were in the placebo group were assigned to caffeine group. Finally, all participants received both placebo and caffeine|
|Masking:||Double (Participant, Investigator)|
|Masking Description:||A statistician prepares a randomization list. Only the pharmacist knows the medication type (caffeine or placebo) and the type of electrical stimulation. The researcher knows only the vigilance conditions (**passive or *active) . An investigator is blinded to the type of electrical stimulation and medication. In addition, all participants are naive to electrical stimulation and do not know if they receive placebo or verum drug.|
|Primary Purpose:||Basic Science|
|Official Title:||Neuroplastic Alterations of the Motor Cortex by Caffeine: Differences Between Caffeine and Non-caffeine Users and Influence of Vigilance During Stimulation|
|Actual Study Start Date :||July 15, 2019|
|Estimated Primary Completion Date :||May 30, 2020|
|Estimated Study Completion Date :||May 30, 2020|
Active Comparator: Caffeine group
Participants will receive a caffeine tablet and all electrical stimulations in a random order (tACS 140 Hz at 1 mA and sham tACS). Participant's vigilance status will be monitor based on active vigilance condition or passive vigilance condition.
Other: 200 mg caffeine tablet
Placebo Comparator: Placebo group
Participants will receive a placebo tablet and all electrical stimulations in a random order (tACS 140 Hz at 1 mA and sham tACS). Participant's vigilance status will be monitor based on active vigilance condition or passive vigilance condition.
Other: Non-active tablet
- Neuroplastic changes of the cortical areas [ Time Frame: Baseline (pre-measurement), immediately after intervention, 5 minutes, 10 minutes, 15 minutes, 20 minutes, 25 minutes, 30 minutes ]Motor cortex plasticity is measured from the changes in the amplitude of the motor evoked potentials (MEPs) at different time points. Transcranial magnetic stimulation (TMS) will be used to measure MEP amplitudes.
- The influence of vigilance during stimulation [ Time Frame: 10 minutes ]Participant's level of vigilance is monitored from pupil diameter and pupil unrest index (PUI) using pupillometer. This measurement is carried out during 10 minutes of transcranial alternating current stimulation (tACS)
- Genetic polymorphism [ Time Frame: 1 year ]Brain-derived neurotrophic factor (BDNF) gene polymorphisms on cortical plasticity
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT04011670
|Contact: Mohd Faizal Mohd Zulkifly, MClinPsych||4955139 ext email@example.com|
|Contact: Walter Paulus||4955139 ext firstname.lastname@example.org|
|Prof. Dr. Walter Paulus||Recruiting|
|Goettigen, Lower Saxony, Germany, 37075|
|Contact: Walter Paulus 551396650|
|Principal Investigator:||Walter Paulus||University Medical Center Goettingen, Goettingen|