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Neurophysiologic Correlates of Hypersomnia

This study is not yet open for participant recruitment.
Verified October 2012 by University of Wisconsin, Madison
Sponsor:
Information provided by (Responsible Party):
David Plante, University of Wisconsin, Madison
ClinicalTrials.gov Identifier:
NCT01719315
First received: October 24, 2012
Last updated: October 29, 2012
Last verified: October 2012
History of Changes
  Purpose

The goal of this project is to examine the neurophysiology of hypersomnia during sleep and wakefulness, to identify biomarkers for excessive sleepiness in neuropsychiatric disorders, and pilot acoustical slow wave induction during sleep in patients with hypersomnolence, to determine if this decreases daytime sleepiness in these patients. The primary study hypotheses are that individuals with hypersomnolence will have reduced slow wave activity (SWA) during sleep and increased waking theta/alpha activity during wake in specific brain regions. A secondary hypothesis is that acoustical slow wave induction in hypersomnolent patients will increase SWA during sleep, reduce theta/alpha activity during wake, and improve subjective sleepiness.


Condition Intervention
Major Depressive Disorder
Primary Hypersomnia
Bipolar Disorder
Narcolepsy
Primary Insomnia
 Other: Acoustical slow wave induction

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: Neurophysiologic Correlates of Hypersomnia: a High Density EEG Investigation

Resource links provided by NLM:

U.S. FDA Resources

Further study details as provided by University of Wisconsin, Madison:

Primary Outcome Measures:
  • Nocturnal Slow Wave Activity [ Time Frame: Individual nights of sleep recorded within an average of 4 weeks of enrollment ] [ Designated as safety issue: No ]
    EEG recordings during sleep will be analyzed to assess slow wave activity in the 1-4.5Hz range.


Secondary Outcome Measures:
  • Waking theta/alpha activity [ Time Frame: Individual days of waking EEG will be recorded within an average of 4 weeks of enrollment ] [ Designated as safety issue: No ]
    Waking EEG activity across the 1-12Hz range will be analyzed.


Estimated Enrollment: 240
Study Start Date: November 2012
Estimated Study Completion Date: June 2018
Estimated Primary Completion Date: June 2018 (Final data collection date for primary outcome measure)
Groups/Cohorts Assigned Interventions
MDD with Hypersomnia
Participants with Major Depressive Disorder and co-morbid hypersomnia
 Other: Acoustical slow wave induction
Brief tones (50 millisecond duration) at a frequency of 0.8 and 2 Hz, a rate that approximates the natural cellular oscillations of cortical neurons during sleep, will be played in blocks of 15-20 during non-rapid eye movement (NREM) sleep. Blocks of active acoustic slow wave induction will be followed by blocks of equal duration without induction, in order to make comparisons between stimulation periods (ON) and no stimulation periods (OFF). Tone intensity will be manually adjusted so as to be above an individual participant's auditory threshold during waking, but still quiet enough as not to awaken the subject from sleep. Sham slow wave induction will consist of auditory tones played prior to sleep, and during sleep of insufficient timing and intensity to alter slow wave activity.
MDD without hypersomnia
Participants with Major Depressive Disorder but without co-morbid hypersomnia
BPAD with hypersomnia
Participants with Bipolar Affective Disorder and co-morbid hypersomnia
 Other: Acoustical slow wave induction
Brief tones (50 millisecond duration) at a frequency of 0.8 and 2 Hz, a rate that approximates the natural cellular oscillations of cortical neurons during sleep, will be played in blocks of 15-20 during non-rapid eye movement (NREM) sleep. Blocks of active acoustic slow wave induction will be followed by blocks of equal duration without induction, in order to make comparisons between stimulation periods (ON) and no stimulation periods (OFF). Tone intensity will be manually adjusted so as to be above an individual participant's auditory threshold during waking, but still quiet enough as not to awaken the subject from sleep. Sham slow wave induction will consist of auditory tones played prior to sleep, and during sleep of insufficient timing and intensity to alter slow wave activity.
BPAD without hypersomnia
Participants with Bipolar Affective Disorder without co-morbid hypersomnia
Primary Hypersomnia
Patients with primary hypersomnia (idiopathic hypersomnia)
 Other: Acoustical slow wave induction
Brief tones (50 millisecond duration) at a frequency of 0.8 and 2 Hz, a rate that approximates the natural cellular oscillations of cortical neurons during sleep, will be played in blocks of 15-20 during non-rapid eye movement (NREM) sleep. Blocks of active acoustic slow wave induction will be followed by blocks of equal duration without induction, in order to make comparisons between stimulation periods (ON) and no stimulation periods (OFF). Tone intensity will be manually adjusted so as to be above an individual participant's auditory threshold during waking, but still quiet enough as not to awaken the subject from sleep. Sham slow wave induction will consist of auditory tones played prior to sleep, and during sleep of insufficient timing and intensity to alter slow wave activity.
Primary Insomnia
Patients with primary insomnia
Narcolepsy
Subjects with narcolepsy
 Other: Acoustical slow wave induction
Brief tones (50 millisecond duration) at a frequency of 0.8 and 2 Hz, a rate that approximates the natural cellular oscillations of cortical neurons during sleep, will be played in blocks of 15-20 during non-rapid eye movement (NREM) sleep. Blocks of active acoustic slow wave induction will be followed by blocks of equal duration without induction, in order to make comparisons between stimulation periods (ON) and no stimulation periods (OFF). Tone intensity will be manually adjusted so as to be above an individual participant's auditory threshold during waking, but still quiet enough as not to awaken the subject from sleep. Sham slow wave induction will consist of auditory tones played prior to sleep, and during sleep of insufficient timing and intensity to alter slow wave activity.
Healthy Controls
healthy participants

  Eligibility

Ages Eligible for Study:   18 Years to 60 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   Yes
Sampling Method:   Non-Probability Sample
Study Population

Subjects will be recruited from the greater Madison, WI area. Hypersomnolent subject groups (n=30 in each group) may include unipolar MDD with hypersomnolence, primary hypersomnia (idiopathic hypersomnia), bipolar disorder with hypersomnolence, and narcolepsy. Non-hypersomnolent comparison groups (n=30 in each group) will include: MDD without hypersomnolence, bipolar disorder without hypersomnolence, primary insomnia, and healthy controls.

Criteria

Inclusion Criteria:

  • Meet Diagnostic and Statistical Manual edition IV criteria for neuropsychiatric disorders enumerated in study population description

Exclusion Criteria:

Exclusionary criteria for all subjects will include: evidence of a clinically significant sleep disorder that would cause hypersomnolence (e.g. moderate to severe obstructive sleep apnea, restless legs syndrome, shift-work sleep disorder), history of significant head trauma or loss of consciousness > 30 minutes; current smoking of more than 15 cigarettes per day; >3 caffeinated beverages per day; significant neurologic or medical illness; active drug/alcohol abuse/dependence (within 6 months of enrollment), women who are pregnant, <6 months post-partum, nursing or planning to become pregnant during the study; left-handedness (due to effects on sleep topography); and imminent risk for self-harm or suicide.

  Contacts and Locations
Please refer to this study by its ClinicalTrials.gov identifier: NCT01719315

Contacts
Contact: David T Plante, MD 608-232-3333 dplante@wisc.edu

Locations
United States, Wisconsin
University of Wisconsin-Madison, Department of Psychiatry Not yet recruiting
Madison, Wisconsin, United States, 53719
Contact: David T Plante, MD     608-232-3333     dplante@wisc.edu    
Sponsors and Collaborators
University of Wisconsin, Madison
Investigators
Principal Investigator: David T Plante University of Wisconsin, Madison
  More Information

No publications provided

Responsible Party: David Plante, Assistant Professor of Psychiatry (CHS), University of Wisconsin, Madison
ClinicalTrials.gov Identifier: NCT01719315     History of Changes
Other Study ID Numbers: 2012-0201
Study First Received: October 24, 2012
Last Updated: October 29, 2012
Health Authority: United States: Institutional Review Board

Additional relevant MeSH terms:
Narcolepsy
Bipolar Disorder
Depressive Disorder
Depression
Disorders of Excessive Somnolence
Sleep Initiation and Maintenance Disorders
Depressive Disorder, Major
Affective Disorders, Psychotic
 Mood Disorders
Mental Disorders
Behavioral Symptoms
Sleep Disorders, Intrinsic
Dyssomnias
Sleep Disorders
Nervous System Diseases

ClinicalTrials.gov processed this record on June 18, 2013