Judy Fetterolf, RPSGT & Michael Bowdish, RPSGT
Conflicts of Interest X
1. We do not have any potential conflicts of interest to disclose, OR 2. I wish to disclose the following potential conflicts of interest:
Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support Consultant Speakers’ Bureaus Financial support Other 3. The material presented in this lecture has no relationship with any of these potential conflicts, OR 4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
The Impact of Artifact on Event Identification
What is Artifact? • Any recorded signal that does not represent the physiologic activity of interest. • Examples: False positive events, marked physiologic events, Distorted physiologic signals
• Artifact can cause • Incorrect scoring • Incorrect PAP Titrations • Incorrect Diagnosis
Universal Artifact Troubleshooting Framework 1.
Correlate
2.
Localize
3.
Verify
4.
Correct
5.
Reassess
Questions to ask: • Is it physiological? • Is it reproducible? • Does it correlate with another channel? • Does it disappear with intervention?
The Two Categories of Artifact: Internal Artifact or External Artifact Internal Artifact – Originates from the patient • ECG • Cardio-ballistic • Muscle • Tremors • Implanted Stimulators External Artifact – Originates from outside of the patient • 60 Hz interference • Electrode popping • Sweat Artifact • Poor electrode contact • Equipment Malfunction
ECG Artifact Can Mimic: • Sharp Waves • EEG Spikes • Arousals • Rhythmic Cerebral Activity Quick Clue: “If it marches exactly with the QRS, it isn’t brain activity”
Mechanical Aortic Replacement Valve
Muscle Artifact (EMG Contamination) • Appearance • Fast Frequency • Irregular • Increased with Arousal • Common Locations • Temporal EEG • Frontal EEG • Chin EMG Contamination • Can Mimic • Beta Activity • EEG Activation • Troubleshooting • Patient relaxation (sleep onset) • Electrode Re-prep • Secure any loose leads
60-Hz Artifact • Appearance • Uniform rhythmic pattern • Consistent Frequency • Causes • Broken ground • Nearby electrical equipment • Poor electrode Contact • Troubleshooting • Check impedances • Verify ground electrodes • Remove electrical source • Inspect power cords
“The PLMs That Weren’t” What we see • Apparent bilateral periodic limb movements • Repetitive movement activity in both leg channels • The signal persists despite the patient appearing asleep and motionless • The waveform morphology is nearly identical What clues would tell us this is external artifact rather than true PLMs?
The Mirror-Leg Artifact
The Mirror-Leg Artifact What we are seeing • Limb movement appearing in both leg channels simultaneously • Perfectly synchronized activity Troubleshooting • Verify hookups • Confirm channel assignment before lights out • Investigate unusual symmetry Teaching point • True bilateral limb movements are possible. Perfect symmetry should always raise suspicion.
Respiration in the Leg leads?
The “Snore” that wouldn’t go away…
The Heated Blanket (Electrical Interference + Secondary Thermal Effects)
After the Fact
What do you do when asked, “Is this artifact?”
You Play Detective, Of course!
But How? The Study Is Already Over! Follow a sequence of steps just like would be done when acquiring the study. Does the signal or pattern appear unusual?
Compare with related signals, notes, video, previous studies and patient’s history. Decide whether clues suggest artifact, normal physiology, or a clinical event. Determine if artifact vs. physiological activity can be confidently distinguished. If artifact is present, are there alternate ways to view the obscured signal.
Modify the Montage
How are they making these sounds? Are these sounds during inspiration or expiration?
What’s wrong with the left eye and why wasn’t it fixed?
What is causing this artifact?
Arrhythmias in the Sleep Lab R a ke s h L atc h a m s e tt y, M D, F H RS U n i ve rs i t y o f M i c h i ga n A n n A r b o r, M I
Conflicts of Interest 1. I do not have any potential conflicts of interest to disclose, OR X
2. I wish to disclose the following potential conflicts of interest:
Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support
Abbott, Biosense Webster, Biotronik, Medontronic
Consultant Speakers’ Bureaus
Abbott, Biosense Webster, Biotronik, Medontronic, Zoll
Financial support Other X
3. The material presented in this lecture has no relationship with any of these potential conflicts, OR 4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
Learning Objectives
Systematically Interpret Rhythm on ECG
Correlate ECG Findings to Cardiac Anatomy
Differentiate Benign & Malignant Arrhythmias
Outline Bradyarrhythmias o Sinus Node Dysfunction o Heart Block Tachyarrhythmias o Supraventricular Tachyarrhythmias o Ventricular Tachyarrhythmias Myocardial Ischemia/Infarction o STEMI Case Examples
Competition in the Heart
Pacing and Clinical Electrophysiology, Volume: 33, Issue: 11, Pages: 1392-1406, First published: 14 October 2010, DOI: (10.1111/j.1540-8159.2010.02838.x)
Bradycardia
Signal Generation
Resting Bradycardia
Chronotropic Incompetence
Signal Propagation
Pauses
Conduction Delay or Block
Sick Sinus Syndrome Causes • Idiopathic degenerative • Ischemic • Autonomic Dysfunction • HTN • Infiltrative Disorder • Inflammatory Disease • OSA • Congenital • Atrial Fibrillation J Am Coll Cardiol. 2019 Aug, 74 (7) e51–e156
• Drugs • Electrolyte Abnormalities • Hypothermia • Hypothyroidism • Infectious • Trauma • High Endurance Athletes • Heart Failure • Etc.
Class I/IIa Pacemaker Indications for Sinus Bradycardia
J Am Coll Cardiol. 2019 Aug, 74 (7) e51–e156
Class III Pacemaker Indications for Sinus Bradycardia
J Am Coll Cardiol. 2019 Aug, 74 (7) e51–e156
Sinus Bradycardia
What is this rhythm?
What is this rhythm?
A) Sinus Bradycardia B) Junctional Rhythm C) Ectopic atrial rhythm
Steps to Establish Rhythm and Conduction Identify and March Out Atrial Activity Establish Sequence of Ventricular Activity
Establish Relationship Between Atrial & Ventricular Activity
Correlate to Anatomy
Establish Atrial Activity
Establish Ventricular Activity
Correlate Atrial & Ventricular Activity
Types of Heart Block
1st Degree Block
3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
Types of Heart Block
1st Degree Block 3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
Types of Heart Block
Mobitz Type I Block Wenckebach
1st Degree Block
3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
Types of Heart Block
Mobitz Type II Block
1st Degree Block
3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
Types of Heart Block
1st Degree Block
3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
Types of Heart Block
1st Degree Block
3rd Degree Block
2:1 Block
2nd Degree Type I Block
2nd Degree Type II Block
What is the pattern of AV conduction?
What is the pattern of AV conduction? A) 1st degree AV block B) 2nd degree type I block C) 2nd degree type II block D) Complete heart block
SVT vs VT
AVNRT
Focal AT
AVRT
Atrial Flutter
Atrial Fibrillation
Determining VT
Capture Beats
Fusion Beats AV Dissociation Concordance
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Evolution of an MI on ECG
Nable JV, Brady W. Et al. Am J Emerg Med. 2009 Jul;27(6):734-46.
Case Examples: To worry, or not to worry?
A.
B.
Which finding is more concerning? A.
B.
A) A B) B C) Both equally concerning D) Neither concern me
A.
B.
Adapt, Improve and Pivot: Incorporating AI in Sleep Medicine Matthew Anastasi, RPSGT, FAAST, FAASM Championship Updates in Sleep Medicine September 17, 2026
I do not have any relevant conflicts to disclose
AI is already in the room. Is it assisting you, or deciding for you?
1. The AI Landscape Today 2. The Hype Cycle Where Do We Stand? 3. How AI Works 4. AI in Sleep Medicine 5. What’s Next Using AI Responsibly
This study was conducted by SSRS on its Opinion Panel Omnibus platform. The SSRS Opinion Panel Omnibus is a national, twice-per-month, probability-based survey. The survey was conducted via web (n=977) and telephone (n=30). The margin of error for total respondents is +/-3.5 percentage points at the 95% confidence level.
Breakdown of Physician AI Use Cases (AMA 2025/2026 survey) Summaries of medical research and standards of care: 39% Creation of discharge instructions, care plans and/or progress notes: 30% Documentation of billing codes, medical charts or visit notes: 28% Generation of draft responses to patient portal messages: 19% Translation services: 18% American Medical Association. Augmented Intelligence Research. Physician sentiment survey results. Chicago, IL: American Medical Association; 2024. Available at: https://www.amaassn.org/system/files/physician-ai-sentiment-report.pdf Accessed May 8, 2026.
Technology “Hype Cycle”
Kemp, J. (2007). [Gartner Research's Hype Cycle diagram] [Graphic]. Wikimedia. https://commons.wikimedia.org/wiki/
Telehealth adoption surged over 30-fold 86% of healthcare orgs increased AI investment FDA medical device authorizations surged Acceleration of AI-based sleep scoring tools
Why has AI entered the conversation at your sleep lab?
How would you rate your knowledge of AI?
How did AASM members rate their knowledge?
How did AAST members rate their knowledge? (2026)
A.I. terminology
A.I. terminology
Salto O. What is the difference between AI, ML and deep learning? Laptops Magazine. https://laptopsmagazine.com/what-is-the-difference-between-ai-ml-and-deep-learning/. Published February 11, 2019.
HOW DOES AI SEE?
¹"cat-original" by JustJohnny is licensed under CC BY-SA 2.0 ²Meskó, B., Görög, M. A short guide for medical professionals in the era of artificial intelligence. npj Digit. Med. 3, 126 (2020). https://doi.org/10.1038/s41746-02000333-z
Iriondo R. What is machine learning? Towards AI - The World's Leading AI and Technology Publication. https://towardsai.net/p/machine-learning/what-is-machine-learning-mlb58162f97ec7. Published October 22, 2021.
AI TERMINOLOGY: TWO LEARNING METHODS A. SUPERVISED LEARNING • •
INPUT DATA IS LABELLED ALGORITHM TRAINED TO MAP AN INPUT X TO AN OUTPUT Y
B. UNSUPERVISED LEARNING • •
INPUT DATA IS UNLABELED FINDING PATTERNS IN A SET OF INPUTS, WITH NO LABELED OUTPUT VARIABLES PROVIDED
Yan, Ma & Liu, Kang & Guan, Zhibin & Xinkai, Xu & Qian, Xu & Bao, Hong. (2018). Background Augmentation Generative Adversarial Networks (BAGANs): Effective Data Generation Based on GAN-Augmented 3D Synthesizing. Symmetry. 10. 734. 10.3390/sym10120734.
ARTIFICIAL INTELLIGENCE AND PSG SCORING
COMMERCIALLY AVAILABLE, FDA CLEARED, CLINICAL AI / AUTOMATED SCORING OPTIONS FOR TYPE I IN-LAB POLYSOMNOGRAPHY Company
Software
Hardware Integration
The Siesta Group
Somnolyzer
Scoring Software-only
EnsoData, Inc.
EnsoSleep
Neurovirtual
BWAnalysis Sleep Diagnostic Suite
Scoring Software-only Acquisition Add-on
Philips RS N.A.
Sleepware G3 w/ Somnolyzer
Acquisition Add-on
Neurotronics
Polysmith
Acquisition Add-on
SOMNOmedics AG
SOMNOscreen system / Domino software
Acquisition Add-on
Compumedics
Profusion Sleep Software
Acquisition Add-on
REMware
DreamClear--autoscoring by EnsoData
Nox Medical, LLC
Noxturnal Software System
Acquisition Add-on Acquisition Add-on
Natus
SleepWorks PSG Software
Acquisition Add-on
Cadwell Ind. Inc.
Easy III PSG – autoscoring by EnsoData
Natus Embla
RemLogic PSG Software
Acquisition Add-on Acquisition Add-on
AASM Pilot Stage Certified?
X X X
COMMERCIALLY AVAILABLE, FDA CLEARED, CLINICAL AI / AUTOMATED SCORING OPTIONS FOR TYPE III or IV IN-HOME HSAT
Company
Device // Software
Company
Device // Software
Acurable
AcuPebble
Huxley Medical
SANSA
Advanced Brain Monitoring Sleep Profiler & PSG2
Natus Medical Inc
Embletta MPR-PG
Belun Technology BRAEBON Med. Corp. Cadwell CleveMed Compumedics Dormotech Medical EnsoData General Sleep Corp.
Belun Ring BLR-100X MediByte ApneaTrak SleepView Somfit DormoVision EnsoSleep v.3 Zmachine Synergy
Neurovirtual USA Inc Nihon Kohden Nox Medical Onera Health PranaQ Resmed SleepImage Snap Diagnostics
BWMini HST Compass NomadAir Nox T3s Onera STS TipTraQ NightOwl SleepImage Ring Sleep Apnea Monitor (SAM)
Wesper
Wesper Lab 1.0
SOMNOmedics
SOMNOtouch RESP
X-Trodes
SmartSkin
Sunrise
Sunrise
ZOLL Itamar
WatchPAT 300 / ONE
Virtuox
Sleepifi Dream / EnsoSleep
ARTIFICIAL INTELLIGENCE AND MASK FITTING
Commercially Available Mask Selection Tools Program
Distinguishing Features
Masks
MaskFit AR
Via app or browser; does not store images; available to consumers
Various
SleepGlad AI Mask Fitter
Uses selfie
Various
Heartstrong
Direct to consumer; free
Various
sovaSage TherapistAssist
Uses selfie and questionnaire to rank and size masks; not direct to consumer; Connects to AI-powered coach to monitor compliance and communicate with patient and DME
Various
Philips Respironics Mask Selector
Uses 3-D scans in office or 2-D scans at home; not direct to consumer
Philips Respironics only
ResMed Mask Selector
Facial scan or facial measurements; not direct to consumer
ResMed only
F&P myMask
Clinician sends link to patient for the app, but also available to F&P only consumer; addresses fitting, fine tuning, and cleaning
Utilizing Artificial Intelligence to Automatically Generate an Encounter Note
AI Medical Scribe & Documentation Platforms Enterprise
Emerging
EHR / General
Abridge
Freed AI
AWS HealthScribe
Ambience
Heidi Health
Epic AI Scribe
Augmedix
Kensho Health
Google MedLM
DeepScribe
Nabla Copilot
GPT Copilots
Dragon Medical One
SOAP Health
MEDITECH Expanse
Notable Health
Tali AI
Oracle Cerner
Nuance DAX Suki AI
Emerging Use Cases Diagnostic Tools
Next Gen Consumer Devices
Sleep Population Health
Follow up care
AI TERMINOLOGY: LEARNING VS TESTING
TRAINING DATA
TO BUILD ALGORITHM
TESTING DATA
TO CHECK CORRECTNESS OF ALGORITHM
• TRAINING SET
• A SUBSET OF DATA USED TO DEVELOP THE MACHINE LEARNING MODEL
DATA
• TESTING SET
• A SUBSET OF DATA USED TO TEST THE MODEL PERFORMANCE
Goldstein CA, Berry RB, Kent DT, et al. Artificial intelligence in sleep medicine: background and implications for clinicians. J Clin Sleep Med. 2020;16(4):609–618.
AI TERMINOLOGY: HOW LEARNING CAN GO AWRY
• TRAINING SET #1
• TRAINED ONLY ON PATIENTS WITH CENTRAL SLEEP APNEA • CSA ≠ OSA • POOR PERFORMANCE
• TRAINING SET #2 • TRAINED ONLY ON MEN WITH SEVERE OSA • SEVERE OSA ≠ REPRESENTATIVE POPULATION • POOR PERFORMANCE
• SOLUTION?
• ENSURE DIVERSITY IN TRAINING DATASET
Goldstein CA, Berry RB, Kent DT, et al. Artificial intelligence in sleep medicine: background and implications for clinicians. J Clin Sleep Med. 2020;16(4):609–618.
Algorithmic Bias: Correct Pneumonia Identification?
Algorithmic Bias: Algorithm Looked for Hospital Markings on Scan
2023 AMA Principles for AI Development, Deployment, and Use Clinical decision-support functions should be implemented by clinical experts [such as sleep technologists] AI developers must disclose information to improve clinician and patient knowledge of these products. Use of AI tools must be disclosed to patients and documented in the EMR. Medical specialty societies, clinical experts, and informaticists are best positioned to set the standard of care.
AI in Sleep Medicine: Updated (2025) AASM Position Statement It is the position of the American Academy of Sleep Medicine that responsible AI integration into sleep medicine has the potential to enhance clinical care and research but requires careful consideration to overcome clinical validation challenges, ensure ongoing accuracy after implementation, and incorporate clinically relevant and user-friendly tools into practice, while also upholding standards of safety, appropriateness, and transparency. Oks M, Sachdeva R, Davenport MA, et al. Artificial intelligence in sleep medicine: an updated American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2025;21(11):1953–1955.
COLLECT DIVERSE SLEEP RECORDS
HAND SCORE EACH PSG
EXPOSE RECORDS TO AI SOFTWARE FOR SCORING
COMPARE AI PERFORMANCE TO MANUAL SCORING
POTENTIAL TO ACHIEVE AASM CERTIFICATION
ADOPT AN AI GOVERNANCE CHECKLIST
MEASURE LOCALLY
HARDEN YOUR INFRASTRUCTURE
5 Principled Ways to Use AI Responsibly KEEP THE CLINICIAN IN THE LOOP
PLAN FOR EQUITY
Sleep Lab AI Implementation Checklist
manastasi@aasm.org
Questions for your sleep center
Have we defined the problem for AI?
Direct patient care vs “back end” processes
AI model > existing practices?
Would AI disrupt current workflows?
Questions for your AI vendor What does this system reinforce?
Algorithm trained using a standard of reference?
How does the AI algorithm make decisions?
Compared with experts in my field?
Applied to same context that it was trained in?
Is the algorithm publicly available?
Tested in diverse locations and populations?
Training dataset match what we expect in real life?
Monitor and maintain for “prediction drift”?
Threats to Training and Skill Development
Overreliance on AI may reduce development of core sleep skills, especially in low-expertise settings.
Solutions include clearly defined boundaries between AI output and human verification. Maintain competencies.
Practical Workflow Considerations to Get the Most Out of AI
Maximize
Maximize AI Usage Where it Performs Best
Leverage
Leverage Human Oversight Where AI Has Known Limitations
Document
Document AI Usage
Preserve
Preserve the Workforce Skill Set
Are we Sleep Pilots? • Both fields center on human safety and expert oversight • Human judgment remains essential for complex, real-world decision making
46
Challenge the known and embrace the unknown
• THANK YOU FOR LISTENING! Acknowlegements • Championship Updates in Sleep Medicine - Organizing Committee • Barrett Leverette and Dr. Neeraj Kaplish
Matthew Anastasi, RPSGT FAAST FAASM
manastasi@aasm.org
Sleep Medicine Meets Social Media Opportunities & Challenges Christopher J. Allen, MD | @sleepdrchris Board-Certified Sleep Medicine & Pediatric Neurology Championship Updates in Sleep Medicine | September 17-18, 2026
Conflicts of Interest 1. I do not have any potential conflicts of interest to disclose, OR x
2. I wish to disclose the following potential conflicts of interest: Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support
None
Consultant
None
Speakers’ Bureaus
None
Financial support
Brand partnerships via @sleepdrchris social media (FTC-disclosed)
Other
CEO, Quality Sleep & Neurology PC; Sweet Dreams Society community
3. The material presented in this lecture has no relationship with any of these potential conflicts, OR 4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
Title Slide 2 Myself" REEL 1: "Reintroducing instagram.com/reel/DJZeKZZx6hT
184,345 views · 164,363 reach · 19.4s avg watch · 563 shares The reel that replaced my bio slide Scan to watch
Who's Teaching America About Sleep? • "Sleepmaxxing": tens of millions of posts across TikTok,
Instagram, and X • Mouth taping, nostril expanders, neck-swinging "insomnia cures," melatonin gummies • Misinformation researchers call the techniques evidence-free and potentially harmful • Platform moderation is shrinking while the trend grows
Case Study: Mouth Taping • Promoted for better sleep, snoring, oral health, even jawline definition • 2025 systematic review: no consistent benefit for sleep-disordered breathing • 4 of 10 studies flag asphyxiation risk with significant nasal obstruction • Highest risk in undiagnosed OSA, the very patients drawn to the trend • Sleep medicine organizations urge caution Source: Rhee J, et al. Breaking social media fads... a systematic review. PLoS One. 2025;20(5):e0323643.
Your Patients arrive Pre-educated The question isn't whether social media affects sleep medicine. It's who does the talking.
The Case for Physicians Online • Social platforms now shape patient understanding and
participation in care (Int J Acad Med, 2025) • A decade ago, 60% of physicians already said social media improved the quality of care they delivered — and adoption has only grown since • 85% of U.S. medical schools now have social media policies (Cureus, 2025) • Yet physicians remain underrepresented where patients actually look Sources: Hasham MA, et al. Int J Acad Med. 2025;11(1):4-9. · Miller JJ, et al. J Med Internet Res. 2012. Knopf E, et al. Cureus. 2025;17(7):e87134.
It Moves Outcomes, Not Just Awareness • Controlled trial: social media-delivered education for type 2
diabetes • Significant gains in health literacy AND HbA1c vs. control (Front Public Health, 2025) • A biological endpoint moved by content delivered through a feed • Patient education at scale is a clinical intervention Source: Safdari A, et al. Front Public Health. 2025;13:1507726.
SlideNormal?" 2 REEL 2: Title "Is Snoring instagram.com/reel/Dau1arpRp45
10,288 views · 8,212 reach · 14.4s avg watch 103 saves · 183 shares in two weeks Scan to watch
Anatomy of a Viral Medical Reel • Hook (0-2 s): a question every patient asks — "Is
snoring normal?" • Middle: myth correction plus simple airway anatomy, zero jargon • Pattern interrupt: "...even erectile dysfunction. I said it." • CTA: "Ask your partner tonight: do I snore?"
183 shares = 183 screenings A 2.23% share rate means viewers sent this reel to a bed partner who snores. That is OSA case-finding at scale.
2 REEL 3:Title WHOSlide Collaboration instagram.com/reel/DYIE-gnMdWZ
Co-created with the World Health Organization Sleep quality: the overlooked third pillar of health Scan to watch
Credibility Has Entered the Chat • The World Health Organization now co-creates sleep
content with physician creators • Public health communication has moved to where the public already is • Institutional collaboration answers the "is this professional?" question • A Saginaw practice reaching a global audience
What It Does for a Practice • Patient education at scale: patients arrive informed,
visits go deeper • Referral pipeline and cross-specialty visibility • Diversified revenue: partnerships, speaking,
community, remote monitoring • Geography stops limiting a subspecialty practice
Guardrails • HIPAA: written authorization before any identifiable patient
content • FTC: every paid partnership clearly disclosed; there is no
physician exemption • AMA and state boards: professionalism standards apply to
personal accounts • Clinical claims stay evidence-based; entertainment never
outranks accuracy
Your First 90 Days • Pick one platform; post consistently: consistency beats
perfection • Answer the questions your patients ask you in clinic • Debunk one viral sleep myth per week; the content writes
itself • Measure shares and saves, not likes
Sleepmaxxing influencers are posting tonight. So should we.
Christopher J. Allen, MD @sleepdrchris · sleepdrchris.com Quality Sleep & Neurology PC 2172 Hemmeter Rd. Saginaw, MI 48603
Uncommon Tests in Clinical Sleep Medicine & Research
Advanced Diagnostic Sleep Assessments: Translating Clinical Measurements to Legal and Safety Standards
Ahmed Ghanim, M.B.B.Ch Championship Updates in Sleep Medicine September 17, 2026
Conflicts of Interest 1. I do not have any potential conflicts of interest to disclose, OR 2. I wish to disclose the following potential conflicts of interest: Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support Consultant Speakers’ Bureaus Financial support Other 3. The material presented in this lecture has no relationship with any of these potential conflicts, OR 4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
Clinical & Scientific Breakthroughs in Diagnostic Sleep Medicine Advanced Diagnostic Sleep Assessments: Translating Clinical Measurements to Legal and Safety Standards
Advanced Sleep Biomarkers Extending Diagnostic Capabilities Beyond Standard Polysomnography Standard polysomnography provides essential nocturnal data but often fails to quantify daytime functional impairment or circadian misalignment. Modern clinical practice requires evolving paradigms to capture a complete patient profile.
Daytime vigilance testing quantifies occupational safety risks.
Motor and circadian rhythm tracking enable precision chronotherapy.
Multi-organ diagnostic extensions identify complex comorbidities and clinical mimickers.
Maintenance of Wakefulness Test (MWT) Objectively measures the ability to maintain wakefulness under standardized conditions.
Clinical Advisory
40 MIN
Maximum Trial Duration Interpretation
Test Definition Measures the ability to remain awake under standardized conditions.
Protocol ● ●
Four 40-minute wake trials.
● ●
Patient sits/reclines in dim light.
First trial 1.5–3 h post-wake; others 2 h apart.
●
<8 min: Abnormal
●
8–40 min: Intermediate values require clinical context
●
Normal-control mean ≈ 30.4 ± 11.2 min
Clinical & Safety Utility
●
40 min: Maximum ceiling; provides strongest evidence of wakefulness.
Objectively measures wakefulness; interpret with clinical context rather than as a stand-alone fitnessfor-duty test.
Ends at defined EEG sleep onset or 40 minutes
Psychomotor Vigilance Test (PVT) Lapse Threshold
>500 ms
Standard Lapse Threshold Responses ≥500 ms are conventionally classified as lapses of attention, a sensitive marker of impaired vigilance. Sleep loss increases lapses, reaction-time variability, and response slowing.
Neurobehavioral Assessment Measures sustained attention and reaction time and is highly sensitive to the neurobehavioral effects of sleep loss.
Protocol ●
Standard 10-minute simple reaction-time task.
●
Visual stimuli appear at random 2–10-second intervals.
●
Participant responds as quickly as possible.
Research & Operational Utility ●
Highly sensitive to sleep loss and circadian misalignment.
● ●
Minimal practice effects. Repeated assessment of behavioral alertness.
The OSLER Test A simplified, EEG-free behavioral test of wakefulness maintenance
EEG-Free Behavioral Protocol EEG-Free Behavioral Protocol Assesses the ability to maintain wakefulness through behavioral responses to visual stimuli without continuous EEG.
Clinical & Safety Utility A simple, portable approach to objectively assessing wakefulness with substantially less technical infrastructure than the MWT.
●
Validated against EEG: Behavioral sleep latency has demonstrated good agreement with EEG-defined sleep onset.
●
Relationship to MWT: Results show agreement with MWT in some studies, although correlation varies; MWT remains the gold standard.
●
Similar testing environment and objective to the MWT.
●
A dim LED illuminates for 1 second every 3 seconds; the subject responds by pressing a button.
●
Seven consecutive missed stimuli (21 seconds) terminate the trial, indicating sleep onset.
●
Maximum test duration is typically 40 minutes per trial.
Minimal Instrumentation: Does not require continuous EEG acquisition or sleep staging.
●
Occupational Utility: Simple, portable approach that may be useful for assessing wakefulness in professional drivers and other safety-sensitive settings.
●
Circadian, Motor & Longitudinal Assessments Evaluating endogenous biological rhythms, nocturnal motor activity, and longitudinal homebased sleep variability.
DLMO Precision Circadian Mapping Dim Light Melatonin Onset (DLMO) is the gold-standard biomarker of circadian phase, providing an objective estimate of the timing of the central circadian pacemaker.
nights_stay01
science02
healing03
Phase 1: Preparation
Phase 2: Serial Sampling
Maintain dim-light conditions (<10 lux), typically beginning ~6 hours before habitual bedtime. Control light exposure and other factors that may influence melatonin measurement.
Collect saliva (or plasma) every 30–60 minutes across approximately 6–8 hours. DLMO is defined as the time melatonin rises above a predefined threshold (~3 pg/mL).
Phase 3: Clinical Application Identifies circadian phase misalignment to support evaluation of DSWPD, ASWPD, and Non-24, guiding appropriately timed light and melatonin interventions.
Suggested Immobilization Test (SIT) The SIT provokes and quantifies RLS symptoms and leg movements during enforced immobility, providing an objective adjunct to clinical assessment
Testing Protocol Setup & Environment Patient remains reclined and awake with legs extended during a 60-minute period of enforced immobility, typically performed in the evening.
Symptom Assessment RLS sensory discomfort and urge to move are rated repeatedly during the test, typically every 5–10 minutes.
EMG Monitoring Bilateral anterior tibialis EMG records leg movements, allowing calculation of the Periodic Limb Movement Index during Wakefulness (PLMWI).
Clinical Applications Supports RLS Assessment Combines provoked sensory symptoms with objectively measured leg movements to support clinical assessment and quantify severity.
Treatment & Research Utility Can objectively quantify changes in RLS symptoms and leg movements in clinical trials and treatmentresponse studies.
Ambulatory EEG Assessments Multi-night ambulatory EEG characterizes sleep architecture and night-to-night variability in the patient’s habitual sleep environment, complementing single-night laboratory polysomnography.
sensors01
timeline02
psychology03
Protocol
Longitudinal Tracking
Portable or wearable EEG systems record sleep over multiple nights in the home environment. Depending on the device, additional signals may include movement, heart rate, respiratory signals, or snoring.
Repeated recordings characterize night-to-night variability in sleep duration, timing, continuity, and architecture, reducing reliance on a single-night snapshot.
Microstructural Biomarkers EEG-derived measures can quantify features such as sleep spindles, slow-wave activity, and spectral power, providing quantitative markers of sleep physiology and potential research biomarkers of brain health.
Multi-Organ System & Neuromodulation PSG Extensions Exploring anatomical and therapeutic enhancements to standard polysomnography, including genitourinary, gastrointestinal, and neurostimulatory assessments.
Specialized PSG Extensions Specialized physiologic monitoring integrated with polysomnography
Nocturnal Penile Tumescence & Rigidity (NPTR) Sleep-Related Erectile Physiology
Mechanism: Penile tumescence and rigidity are continuously measured using strain-gauge monitoring (e.g., RigiScan), with events correlated with sleep stages. Clinical Utility: Preserved nocturnal erections support intact neurovascular erectile function; abnormal findings may support an organic contribution to erectile dysfunction.
Dual-Channel pH Monitoring Gastrointestinal PSG Integration
Mechanism: Proximal and distal esophageal pH sensors identify acid reflux events, synchronized with PSG-defined sleep, arousals, and respiratory events. Clinical Utility: Evaluates the temporal relationship between acid reflux, sleep disruption, and respiratory events, helping determine whether reflux events precede or follow PSG-defined arousals and respiratory disturbances.
Synchronizing PSG & Vagus Nerve Stimulation Time-locking VNS activation with PSG to identify stimulation-related sleep-disordered breathing.
Telemetry Sync Protocol
Clinical Risk & Mitigation
PSG Synchronization
Parameter Optimization
Implanted Vagus Nerve Stimulation (VNS) can alter upper-airway function, breathing patterns, and sleep continuity during stimulation.
Clinical Takeaway: VNS activation can produce stimulation-linked airflow limitation, apneas/hypopneas, and, in rare cases, stridor, potentially through laryngeal effects.
Protocol: PSG respiratory channels are synchronized with VNS ON/OFF cycles, allowing airflow, respiratory effort, oxygen saturation, arousals, and sleep stage to be correlated with stimulation.
Optimization: PSG may guide adjustments in stimulation frequency, output current, or cycling time to reduce VNS-related respiratory events while balancing seizure control.
Choosing the Right Test for the Right Clinical Question From physiologic measurement to clinically meaningful answers
"Advanced sleep assessments can bridge the gap between nocturnal physiology, daytime function, and real-world clinical outcomes when used in the right patient."
Safety & Functional Assessment Use objective daytime tests (MWT, PVT, OSLER) to complement clinical assessment of wakefulness, vigilance, and safety-sensitive performance.
Precision Phenotyping Use targeted assessments (DLMO, SIT) to characterize circadian phase or RLS-related symptoms and guide appropriately timed or individualized interventions.
Integrated Physiologic Assessment Synchronize specialized physiologic signals with PSG to clarify relationships among sleep, comorbid physiology, and implanted-device effects.
Managing Complex PAP Devices in the Clinic Aneesa M. Das, MD, FCCP, FAASM Professor of Internal Medicine Division of Pulmonary Critical Care and Sleep Medicine
Disclosures: Medscape UpToDate
2
Indications for Devices Beyond CPAP Central Sleep Apnea
Restrictive Thoracic Disorders
Severe COPD
Hypoventilation Syndrome 3
Which device is the right device? Home Non-Invasive Ventilators (NIV)
Respiratory Assist Devices (RAD) E0470/0471 • • • • • •
BPAP-S
BPAP-Auto BPAP-ASV BPAP-ST BPAP-STA(iVAPS)/AVAPs
G3 BPAP 30VT S/T
• • • • •
ResMed Astral Lowenstein→Movair Luisa Ventec→React V-Home Breas Vivo 45 LS
Philips Trilogy Evo
4
Parsonage Turner Syndrome 70 year old man found to have nocturnal hypoxemia and was using 4lpm of supplemental oxygen at night. Diagnostic evaluation yielded a diagnosis of phrenic nerve palsy secondary to Parsonage Turner Syndrome, a brachial plexus neuropathy
Image from: Meiling, James B. et al. Mayo Clinic Proceedings, Volume 99, Issue 1, 124 - 140 9
70-year-old male with Parsonage Turner Syndrome
ABG was pH 7.39/ PCO2 47.4/bicarb 31
AHI was 4.5/hour overall and 40/hour in REM Noted hypoxemia with an open airway (TST SaO2 < 90%: 44.5 minutes)
10
He was initially put on intelligent Volume Assured Pressure Support (iVAPS)
Goal alveolar ventilation (accounts for deadspace)
Variable Pressure Support
11
iVAPS Recommended Settings iVAPS suggested settings
COPD
Restrictive
min
Medium (STA)
Low (STA)
Parsonage Turner Syndrome Airsense STA Initial Settings with 2lpm oxygen bled in: Set Mode to iVAPS Set EPAP to 5.0 cmH2O Set Min PS to 5.0 cmH2O Set Max PS to 20.0 cmH2O Set Target patient rate to 15 bpm Set Target alveolar ventilation to 4.7 L/min
https://ivapscalculator.resmed.com/
Parsonage Turner Syndrome Residual AHI on download 6 events/hr
•Mode iVAPS •Increased EPAP to 8.0 cmH2O •Min PS to 5.0 cmH2O •Max PS to 20.0 cmH2O •Target patient rate to 15 bpm •Increase Target alveolar ventilation to 5.8 L/min
O2 sats <=88% for 35.7 min Serum Bicarbonate 31
→ Oxygen was increased by PCP to 4lpm 14
Parsonage Turner Syndrome Persistent hypoxemia on current settings Bilevel STA in iVAPS mode with 4 lpm bled in Residual AHI 1.7/hr
•Mode iVAPS •EPAP to 8.0 cmH2O •Set Min PS to 5.0 cmH2O •Set Max PS to 20.0 cmH2O •Set Target patient rate to 15 bpm •Increase Target alveolar ventilation 6.9 L/min
O2 sats <=88% for 28 min on 4lpm
Serum bicarb 32
→ Continue oxygen at 4lpm 15
Parsonage Turner Syndrome 4lpm supplemental oxygen
•Mode to iVAPS •EPAP to 8.0 cmH2O •Min PS to 5.0 cmH2O •Max PS to 20.0 cmH2O •Target patient rate at 15 bpm •Target alveolar ventilation 6.9 L/min O2 sats <=88% for 4.1 min
→ Decrease oxygen to 2lpm
16
Parsonage Turner Syndrome Bilevel STA in iVAPS mode with 2lpm bled in
•EPAP to 8.0 cmH2O •Set Min PS to 5.0 cmH2O •Set Max PS to 20.0 cmH2O •Set Target patient rate to 15 bpm •Target alveolar ventilation 6.9 L/min
Currently has repeat oximetry on RA pending O2 sats <=88% for 4.8 min 17
65yo with mitochondrial myopathy (TWNK Gene) causing ptosis and neuromuscular weakness
• Pulmonary Function Tests • FVC 2.57L 52% • FEV1 2.43L 65% • FEV1/FVC% 125% • MIP -33 • MEP +40 • ABG pH 7.38, pCO2 64, PaO2 74
18
Mitochondrial Myopathy •Set Mode to iVAPS •Set EPAP to 4.0 cmH2O •Set Min PS to 4.0 cmH2O •Set Max PS to 20.0 cmH2O •Set Target patient rate to 15 bpm •Set Target alveolar ventilation to 5.0 L/min •(Vt of 6.6cc/Kg IBW)
• ABG pH 7.38, pCO2 64, PaO2 74
• ABG pH 7.41, pCO2 44.8, PaO2 85.3
19
Mitochondrial Myopathy His daytime sleepiness and energy levels have improved. He feels he is sleeping better but his wife notices spells of tachypnea during the night.
20
Mitochondrial Myopathy Set Mode to iVAPS Set EPAP to 4.0 cmH2O Set Min PS to 4.0 cmH2O Set Max PS to 20.0 cmH2O Set Target patient rate to 15 bpm Set Target alveolar ventilation to 5.0 L/min Comfort settings were set to default Ti Min to 0.3 sec Ti Max to 2.0 sec Trigger Medium Cycle Sensitivity Medium
21
Mitochondrial Myopathy
Goal Rapid Shallow Breathing Index <=40
22
60%
25%
23
Volume-assured pressure support modes (VAPS) AVAPS (assured volume assured pressure support;) targets expiratory tidal volume iVAPS (intelligent volume assured pressure support) targets alveolar ventilation (minute ventilation minus dead space ventilation)
Modified from: Selim, Bernardo J. et al. CHEST, Volume 153, Issue 1, 251 - 265
24
iVAPS Recommended Settings iVAPS suggested settings
COPD
Restrictive
min
Medium (STA)
Low (STA)
Mitochondrial Myopathy
Set Mode to iVAPS Set EPAP to 4.0 cmH2O Set Min PS to 4.0 cmH2O Set Max PS to 20.0 cmH2O Set Target patient rate to 15 bpm Set Target alveolar ventilation to 5.0 L/min Set Start EPAP to 4.0 cmH2O Set Ti Min to 0.3 sec → 1.2 sec Set Ti Max to 2.0 sec Set Trigger to Medium → High Set Cycle Sensitivity to Medium → Low
26
Home Noninvasive Ventilation (NIV) in COPD A 57-year-old man was referred for optimization of home NIV. He had a 35 pack-year smoking history and had quit 1 year prior. BMI of 25 kg/m2 FEV1 of 0.6 L (19% predicted) Receiving bronchodilator and oxygen therapy. He had undergone multiple hospitalizations for hypercapnic respiratory failure over the past 2 years, maximal PVCO2 of 136 mm Hg and requiring NIV acutely several times and intubation once. His ABG 3 years prior showed pH 7.4 and PaCO2 59 mm Hg. Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
27
Home Noninvasive Ventilation (NIV) in COPD Optimal initiation location is unclear In lab NIV titration: high cost, delay of care, safety of achieving rapid normocapnia over a single night, and proficiency of personnel European studies used in hospital initiation over days with progressive optimization. Not currently feasible in most US centers. Home initiation has been found do be noninferior to hospital initiation (resource intensive protocol) Parameters used and tolerated during an acute exacerbation can be a useful starting point. Macrea, M. et al. Am J Respir Crit Care Med. 2020; 202:e74-e87 Murphy, P.B et al. JAMA. 2017; 317:2177-2186 Duiverman, M.L et al. Thorax. 2020; 75:244-252
28
Home Noninvasive Ventilation (NIV) in COPD He had been started on nocturnal NIV along with 3lpm at the referring center • BPAP-ST mode • IPAP 16 cmH2O Despite symptomatic • EPAP 10 cmH2O • BUR 12/min improvement, he was • Rise time 300 ms re-hospitalized briefly • Ti minimum 0.8 s with PVCO2 of 102 mm Hg. • Ti maximum 1.6 s • Trigger sensitivity high • Cycling sensitivity medium Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
29
Home Noninvasive Ventilation (NIV) in COPD • BPAP-ST mode • IPAP 16 cmH2O • EPAP 10 cmH2O What are the problems here? • BUR 12/min • rise time 300 ms • Ti minimum 0.8 s • Ti maximum 1.6 s • Trigger sensitivity high • Cycling sensitivity medium
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
30
Home Noninvasive Ventilation (NIV) in COPD BPAP-ST mode
IPAP 16 cmH2O
EPAP 10 cmH2O
Volume assured pressure support can be a good option here (6-8cc/kgIBW)
Not optimal because of low IPAP and low driving pressure (Δ = IPAP – EPAP) IPAP 18-30 cmH2O is more typically required to optimize CO2
EPAP is traditionally set at low (4-5 cmH2O) in patients with COPD without obesity
Rise time 300 ms Rise time should be faster
31
Home Noninvasive Ventilation (NIV) in COPD On his second discharge his settings were: BPAP-ST mode • IPAP 16 cmH2O → 19 cmH2O • EPAP 10 cmH2O • BUR 12/min
• Rise time 300 ms → fastest • Ti minimum 0.8 s • Ti maximum 1.6 s • Trigger sensitivity high • Cycling sensitivity medium
The patient reported good subjective sleep quality A few days later, a routine follow-up Pvco2 measurement obtained at home was 119 mm Hg.
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
32
Home Noninvasive Ventilation (NIV) in COPD Are there still issues??? BPAP-ST mode • IPAP 19 cmH2O • EPAP 10 cmH2O • BUR 12/min • Rise time fastest • Ti minimum 0.8 s • Ti maximum 1.6 s • Trigger sensitivity high • Cycling sensitivity medium
Still a low driving pressure for COPD
Not optimally set for a COPD patient
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
33
ST mode (spontaneous/timed)
Modified from: Selim, Bernardo J. et al. CHEST, Volume 153, Issue 1, 251 - 265
34
Normal Physiology
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
35
Normal Physiology
COPD Physiology
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
36
NIV Settings in COPD • Driving pressure 18 to 30 cm H2O • Rise time: fast • Ti minimum: 0.2-0.8 s • Ti maximum: 1.0-1.5 s • Trigger sensitivity: medium • Cycling sensitivity: medium to high
37
Home Noninvasive Ventilation (NIV) in COPD BPAP-ST mode
• IPAP 19 cmH2O → Slowly titrated to 25 cmH2O remotely • EPAP 10 cmH2O • BUR 12/min • Rise time fastest • Ti minimum 0.8 s • Ti maximum 1.6 s → Decreased to 1.3 s • Trigger sensitivity high 9 months after starting NIV: • Cycling sensitivity → high • Overnight oximetry on NIV and O2 at 3 L/min showed SpO2 of < 90% for 0.8% of the night • 3 lpm supplemental oxygen with mean SpO2 of 95% • Daytime transcutaneous CO2 was 58 mm Hg Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
38
Home Noninvasive Ventilation (NIV) in COPD • IPAP 25 cmH2O → attempted increase but not tolerated • EPAP 10 cmH2O → reduced to 8 cmH2O • BUR 12/min • Rise time fastest • Ti minimum 0.8 s • Ti maximum 1.3 s → decreased to 1.1 s • Trigger sensitivity high • Cycling sensitivity high • 3 lpm supplemental oxygen→ decreased • Due to increased daytime use mouthpiece ventilation added Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
39
Home Noninvasive Ventilation (NIV) in COPD Overnight transcutaneous CO2 showed a mean of 54 mm Hg, fluctuating depending on leak (incompletely controlled) 24 months after initiating NIV, despite exacerbations requiring antibiotic and corticosteroid treatment, he was able to avoid any further rehospitalizations.
Kaminska, Marta et al. CHEST, Volume 165, Issue 6, 1372 - 1379
40
Let’s test our new skills…. 63 year-old man with paraplegia due to a T3 spinal cord injury due to a spinal cord infarct. Overnight oximetry • oxygen desaturation index of 14.3/hour • TST ≤88% was 166 minutes He was initially put on 1.5 lpm of supplemental oxygen.
After spirometry showed restriction with a reduced FEV1 and MIP, he was put on BPAP-STA iVAPS
Restrictive Thoracic Disorders Criteria A. Documentation in the medical record of a neuromuscular disease (for example, amyotrophic lateral sclerosis) or a severe thoracic cage abnormality. B. One of the following: a) An arterial blood gas PaCO2, done while
awake and breathing prescribed FIO2 is ≥ 45 mm Hg, or b) Oxygen saturation ≤ 88% for greater than or equal to 5 minutes of nocturnal recording time, done while breathing the prescribed FIO2, or c) For a neuromuscular disease (only): i. ii.
Maximal inspiratory pressure is less than 60 cm H20, or Forced vital capacity is less than 50% predicted
C. COPD does not contribute significantly to the beneficiary’s pulmonary limitation.
41
Oxygen 1.5 LPM
iVAPS
He reports dyspnea with the device and has his own oximeter. He notes significant worsening of his oxygen on the PAP versus oxygen alone.
42
What do you do next? A. Bleed in more supplemental oxygen B. Check the iVAPS settings C. Switch to ST mode D. Switch to CPAP and supplemental oxygen
43
What is the most important thing to change? •EPAP to 5.0 cmH2O •Min PS to 3.0 cmH2O •Max PS to 15.0 cmH2O •Target patient rate to 15 bpm •Target alveolar ventilation to 1.5 L/min •Start EPAP to 4.0 cmH2O •Height to 72.0 in •Ti Min to 0.3 sec •Ti Max to 2.0 sec •Rise time to Min •Trigger to Medium •Cycle Sensitivity to Medium 44
iVAPS Recommended Settings iVAPS suggested settings
COPD
Restrictive
min
Medium (STA)
Low (STA)
•EPAP to 5.0 cmH2O •Min PS to 3.0 cmH2O •Max PS to 15.0 cmH2O •Target patient rate to 15 bpm •Target alveolar ventilation to 1.5 L/min (3.1ml/Kg) •Start EPAP to 4.0 cmH2O •Height to 72.0 in •Ti Min to 0.3 sec •Ti Max to 2.0 sec •Rise time to Min •Trigger to Medium •Cycle Sensitivity to Medium
•EPAP to 5.0 cmH2O •Min PS to 5.0 cmH2O •Max PS to 20.0 cmH2O •Target patient rate to 15 bpm •Target alveolar ventilation to 4.7 L/min (6 ml/Kg) •Start EPAP to 4.0 cmH2O •Height to 72.0 in •Ti Min to 0.8 sec •Ti Max to 2.5 sec •Rise time to 300ms •Trigger to High •Cycle Sensitivity to Medium 46
Oximetry on the old and new settings
47
He acclimated to the augmented settings and provided an updated oximetry on room air a week later.
48
Increased alveolar ventilation from: 4.7 L/min (6 ml/kg) to 6.4 L/min (7.6 ml/kg)
49
What are our options now?
50
Astral/Aircurve-STA Recommended Settings iVAPS suggested settings
COPD
Restrictive
min
Medium (STA)
Low (STA)
•EPAP to 5.0 cmH2O •Min PS to 5.0 cmH2O •Max PS to 20.0 cmH2O •Target patient rate to 15 bpm •Target alveolar ventilation to 6.4 L/min •Start EPAP to 4.0 cmH2O •Height to 72.0 in •Ti Min to 0.8 sec •Ti Max to 2.5 sec •Rise time to 300ms •Trigger to High •Cycle Sensitivity to Medium → LOW 52
He continues to do well on iVAPS at night.
53
Epilepsy in Sleep: Avoiding Pitfalls in Diagnosing Nocturnal Seizures Sikawat Thanaviratananich, MD, MSc
Disclosures • Nothing to disclose
Learning Objectives • Review the relationship between sleep and epileptogenesis, sleep-related hypermotor epilepsy (SHE), disorders of arousal (DoA)
• Discuss the distinguishing features between SHE and DoA from history and vPSG • Discuss the shared pathophysiology of SHE and DoA • Case illustrations
Confusion between Seizures and Parasomnia • Like parasomnias, sleep-related seizures • Occur during entry into sleep, within sleep, or during arousals from sleep • Share broad range of semiology including autonomic nervous system changes, skeletal muscle activation, and seemingly purposeful, goal-directed complex behaviors outside consciousness • Have ill-defined EEG manifestation • Activate by sleep deprivation and stress • Share genetic background
Sleep and Epileptogenesis •
NREM sleep facilitates interictal epileptiform discharges (IEDs) and seizure1,2 - Peak frequency of IEDs during N3 (exclusively during up-state of slow wave sleep) -
•
IEDs – extensive field of distribution3 • Related to physiological hypersynchrony and thalamocortical oscillatory neural activity during NREM sleep
REM sleep inhibits IEDs and seizures4 - 80% fewer focal sz and 30% fewer generalized sz relative to wakefulness5 1.Malow, et al. Epilepsia. 1998 2.Sammaritano M, et al. Neurology. 1991 2 - IEDs-more localizing 3.Rocamora, et al. Epilepsy Behav. 2013 4.Kumar P. Brain Res. 2001 5.Ng M, Pavlova M. Epilepsy Res. 2013
Sleep and Epileptogenesis •
Clinical seizures occur most frequently during N1 and N21,2
•
Propensity for seizures during sleep varies according to brain regions - Extratemporal sz (esp. frontal lobe origin) – more likely to have nocturnal sz3
•
Focal temporal lobe seizures during sleep are more likely to evolve into bilateral tonic-clonic seizures than during wakefulness4 - First-time seizures are often present following a witnessed nocturnal convulsion 1. 2. 3. 4.
Herman, et al. Neurology. 2001 St Louis EK, et al. Epilepsia. 2004 Crespel A, et al. Epilepsia. 1998 Bazil CW, et al. Arch Neurol. 2000
Epilepsy and Circadian Pattern Occipital – 16:00 – 19:00 Parietal – 4:00 - 7:00 Frontal – 4:00– 7:00 Mesial temporal bimodal (7:00-10:00 and 16:00-19:00) Neocortical temporal – 13:00
Durazzo TS, t al. Neurology. 2008
Sleep-related Epilepsies Pure sleep epilepsies
Sleep-accentuated epilepsies
Arousal/awakeningrelated epilepsies
Seizures occur exclusively or predominantly during sleep
Seizures occur during both wakefulness and sleep, but epileptiform activities is potentiated during sleep
Seizures are most common in the period following awakening from sleep
• Benign epilepsy of childhoold with centrotemporal spikes
Epileptic encephalopthies • Lennox-Gasstaut syndrome
• Juvenile myoclonic epilepsy
• Panayiotopoulos syndrome
• Landau-Kleffner syndrome
• Sleep-related hypermotor epilepsy (SHE)
• West syndrome
• Epilepsy with grand mal seizures on awakening
Ekizoglu E, et al. Epilepsy Behav. 2011
Sleep-related Hypermotor Epilepsy: Epidemiology •
12% of focal epileptic patients 1,2 - Seizures occur exclusively or predominantly (>90%) during sleep1,2 - Primarily frontal lobe epilepsy (30%-extra-frontal epilepsy)
•
Male: female ratio = 7:33
•
Non-lesional forms are the most common
•
Positive family history in ~ 25% of cases3 - Autosomal-dominant inheritance pattern is rarely recognizable
•
Seizure onset before the age of 20 years4 - Mean age of onset: 14± 10 years
•
Delay in diagnosis of 12.8±10.1 years in 53.7% of SHE cases - Parasomnias being the most frequent misdiagnosis (55.5%)4 - 30% have comorbid parasomnias and ~half have a +FHx of parasomnia5,6 (shared pathophysiology) 1.Thomas RH, et al. JNNP. 2010 2.Derry CP. Ep behave. 2013 3.Menghi V, et al. Nature and Sci of Sleep. 2018 4.Licchetta, et al. Neurology. 2017 5.Bisulli F, et al. epilepsia. 2015
Sleep-related Hypermotor Epilepsy •
Different names: -
Hypnogenic paroxysmal dystonia
-
Nocturnal paroxysmal dystonia (NPD) Nocturnal frontal lobe epilepsy (NFLE)
-
•
no correlated EEG epileptiform abnormalities
• • •
Not exclusively frontal lobe epilepsy Not exclusively during nighttime Typical/prominent semiology = hypermotor seizure
Sleep-related hypermotor epilepsy (SHE) – 2014 (the hypermotor sz is not the sole semiology)
Menghi V, et al. Nat Sci Sleep. 2018
Clinical Manifestations •
Abrupt onset and offset
•
Stereotyped motor patterns -
-
Hypermotor (hyperkinetic) semiology – the most common motor patterns • +/-vocalization, emotional expressions • +/- asymmetric tonic or dystonic posturing ±Impaired awareness
•
±Postictal confusion
•
Usually brief (<2 min in duration)
•
Frequent episodes per night - Range from 1-20x/night
Hypermotor (Hyperkinetic) Seizure • Characteristics: - Axial or proximal limbs involvement - Violent movement
• ±Emotional components • ±Vocalization Body rocking, cycling, distal stereotypy, axial rotation, bi-manual movements, etc.
Sleep-related Hypermotor Epilepsy (SHE) Clinical spectrums
Minor motor events 2-4 sec (2/3 with correlated ED) -movement related to arousal
Seizure with paroxysmal arousal (SPA, PAs) <20 sec (median 5 sec) (all with correlated ED)
Hypermotor seizure 20-30 sec (±epileptic nocturnal wandering aka, agitated somnambulism)
ED= epileptiform discharges on sEEG Gibbs SA, Sleep Med Rev. 2016
Derry CP, et al. Sleep. 2009
Seizure with Paroxysmal Arousal (SPA)
Hypermotor Seizure video
Simple Arousal Movement (SAM)
Semiology patterns
Inclusion charateristics
Exclusion characteristics
SP1 Early elementary motor signs
• • •
Asymmetric tonic seizure Early clonic signs Proximal/distal contralateral tonic posture Contralateral versive signs
•
• • • •
Ictal pouting Non-verbal vocalization Axial tonic posturing Rotatory hypermotor seizure
• •
SP3 Integrated hypermotor movements
•
Hypermotor movement (rocking, kicking, pedaling) and distal sterotypies
Elementary motor signs
SP4 Gestural behaviors with high emotional content
•
Integrated gestural behaviors with negative emotions and speech production Epileptic wandering Strong autonomic signs high proportion of postictal confusion was associated with SP4 (48%),
Elementary motor signs
•
SP2 Unnatural hypermotor movements
• • •
• •
•
Hyperkinetic motor behaviors Integrated gestural motor behaviors Feeling of fear/anxiety/rage Early clonic signs Distal stereotypies Integrated gestural motor behaviors
Frontal SHE
• SP 4 was only observed in F and T subgroups • Emotional manifestations were observed only in frontal and temporal SHE.
F=frontal, T=temporal, OI= operculo-insular, P=posterior
Sleep Fragmentation • Frequent seizures per night -
Minor motor events or paroxysmal arousals may be even more frequent
Sleep deprivation
further seizures
• Patients with SHE have more -
Nighttime arousals1 Tiredness after awakening1 sleep instability (analysis of the cyclic alternating pattern (CAP)2,3 Not sleepier than controls 1.Vignatelli L, et al. Epilepsia. 2006 2.Zucconi M, et al. J Clin Neurophysiol. 2000 3.Parrino L, et al. Sleep Med Rev. 2012
Gibbs SA, et al. Sleep Med Rev. 2016
Semiological analysis of Disorders of Arousals
Three different motor patterns of •
SAMs most common type (93% of all captured DoA vPSG) >RAM (39%) >CAM (15%)
•
These patterns are not seen in healthy controls
•
Controls showed body movements related to body position change (mean duration 13±9 vs 27±30 s of SAMs)
•
DoA episodes were not stereotyped, different patterns in 1 night, not associated with tonic/dystonic posture, hyperkinetic movements, but showed the typical waxing/waning progression and motor arrests during the episode
•
DoA events could be temporally halted in 72%
SAM could represent a basic diagnostic element for AD to establish the diagnosis when clinical history is suggestive bu the vPSG does not capture episodes
Three behavioral patterns of DoA •
Arousal behavior (92%) - Eye oepning, head lifting, looking around, face rubbing, stretching, mumbling
•
Non-agitated motor behavior (72%) - Sitting up, manipulating objects, calm semipurposeful movements, standing/walking
•
Distressed emotional behavior (51%) - Sitting/standing with fearful expression, distressed vocalization, autonomic features Derry C. Sleep. 2009
Sleep-related seizure vs Parasomnia
NREM parasomnia
REM parasomnia
SHE
Age at onset
Usually <10 years
Over 50 years
Variable; usually childhood or adolescence
Attacks per night (mean)
1-2
1-2
≥3 and clustering
Onset and offset
gradual
sudden
sudden
Clinical course (over year)
Tends to disappear by adolescence
Worse over years
Often stable with increasing age
Episode duration
Seconds to 30 min (mostly minutes)
Seconds to 2 min
Seconds to 2 min (often less than 1-2 min)
Semiology
Variable complexity; not highly sterotyped (on video)
Not highly stereotyped, vocalizations with self-protective behaviors and dream recall
Stereotyped (on video), often hyperkinetic vigorous movements, asymmetric tonic/dystonic
Level of consciousness
variable
Poorly-responsive
Usually preserved
Postictal confusion
Present
Absent
Typically absent
Event recollection
No recollection, or vague recollection of “something” having happened. Hazy recollection of a sense of fear, or a sinister “shape” in the room
Dream recollection
Clear recollection
Time of episodes during sleep
First third of night, but usually after 90 min of sleep
Last third of sleep period
Any time, but may occur within first 30-60 min. Can occur during naps.
Sleep stages when events occur
N3
REM
N2> N1 or sleep-wake transitions
EEG
Slow waves-rhythmic delta
REM sleep without atonia
Often normal, or obscured by
•
Other features: - Speech: • SHE- words or very brief phrases • NREM Parasomnia – interactive speech -
•
Interaction with environment: • NREM parasomnia - high degree of interaction with the environment (conversation with people, opening the cupboards, turning on lights, etc) • SHE – basic interaction
Other DDx: nocturnal panic attack, PNES
FLEP Scale
Frontal Lobe Epilepsy and Parasomnia” (FLEP) Scale Score ≤0 ->parasomnia ≥3 -> SHE To diagnose SHE • Specificity = 100% • Sensitivity = 71% • Uncertain diagnosis in ~30% Usefulness: -non-epileptologist -limited vEEG access Limitations: • ~1/3 of SHE were misinterpreted as DOA(esp. nocturnal epileptic wandering) • Recall question adds a point to RBD • 1/3 of RBD scored 1-3 Manni R, et al. Epilepsia. 2008
From Video-EEG Analysis
120 nocturnal events (57 parasomnias and 63 seizures during sleep) in 44 patients
Onset
Progression Interactive behaviors
NREM Parasomnia
Seizure
Internal or external triggers in 39%
Internal or external triggers in 8%
Start with paroxysmal arousals in 79%
Start with paroxysmal arousals in 49%
+Tachycardia is common
+Tachycardia is common
Progressive complex interactive Non-progressive complex behaviors behaviors in 11%
Speech
Coherent speech
Incoherent/non-interactive speech
Modification
Modifiable by witnesses in 33% (being either exacerbated or terminated)
Not being modifiable
Waxing/waning in intensity
Waxing/waning in intensity in 39%
Not waxing/waning
Indistinct offset (clear offset in only 16%)
Clear offset in 76%
Offset
• Increased SWS and slow/mixed arousals were associated with DoA, with optimal cutoffs 6.8/h & 2.5/h, respectively • Combined EEG and ≥1 recorded event yielded correct classification>91%
At least 1 major event outside N3->SHE At least 1 minor event in N3->DoA DoA and SHE distributed differently; DoA more common in first half of sleep
Halasz P. Epilepsy & Behavior Reports. 2024
sleep terrors’ activation zones overlap with the seizure onset zones of sleep-related hypermotor sz
Case Illustration •
23-year-old male with anxiety p/w “nocturnal paroxysmal episodes” for the past 2 months, both during sleep and daytime naps
•
The episodes occur 1-2 times per night
•
Chart review “rhythmic hand and feet motions as if bicyling. Very sweaty. Bed partner tried to move him, but he grabbed onto her arm. His breathing was irregular. Some oral secretions/drool came out. Then, he awoke and asked what happened. No post-ictal confusion, and no incontinence or tongue biting”
Case Illustration • video
Treating Chronic Insomnia when CBT-I Fails: Know Your Hypnotics Xinhang Tu, MD 9/17/26 xinhangt@med.umich.edu Sleep Disorders Center, Michigan Medicine, University of Michigan, Ann Arbor, MI
Conflicts of Interest x
1. I do not have any potential conflicts of interest to disclose, OR 2. I wish to disclose the following potential conflicts of interest:
Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support Consultant Speakers’ Bureaus
Financial support Other x
3. The material presented in this lecture has no relationship with any of these potential conflicts, OR 4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
Learning Objectives 1
2
3
4
Review the current guideline framework for insomnia pharmacotherapy
Compare drug classes by mechanism, efficacy, and safety
Apply evidence to special populations: older adults, comorbid psychiatric disorders, comorbid OSA, pregnancy
Understand the AASM 2026 guideline on combination CBT-I + pharmacotherapy
Definition of Chronic Insomnia Disorder — ICSD-3-TR Criteria A–F must ALL be met: • A. Sleep Complaint — The patient reports, or the parent/caregiver observes, ≥1 of the following: • Difficulty initiating sleep • Difficulty maintaining sleep • Waking up earlier than desired
• B. Daytime Consequences — ≥1 of the following related to the nighttime sleep difficulty: • Fatigue / malaise • Attention, concentration, or memory impairment • Impaired social, familial, occupational, or academic performance • Mood disturbance / irritability • Daytime sleepiness
Refs: ICSD-3-TR
Definition of Chronic Insomnia Disorder — ICSD-3-TR • Behavioral problems (e.g., hyperactivity, impulsivity, aggression)
• Reduced motivation / energy / initiative • Proneness for errors / accidents • Concerns about or dissatisfaction with sleep • C. Adequate Opportunity — Complaints cannot be explained purely by inadequate opportunity or inadequate circumstances for sleep • D. Frequency — Sleep disturbance and daytime symptoms occur ≥3 times per week • E. Duration — Sleep disturbance and daytime symptoms present for ≥3 months
• F. Exclusion — Not better explained by another sleep disorder
Refs: ICSD-3-TR
Epidemiology and Burden • Chronic insomnia disorder: 10–15% of adults; associated with cardiovascular disease, hypertension, diabetes, depression, work disability • Commonly co-occurs with OSA, chronic pain, psychiatric disorders • Diagnosis is clinical --no objective testing required for insomnia only • CBT-I = first-line for chronic insomnia — strong recommendation across all major guidelines Refs: Buysse et al., JCSM 2026; Furukawa et al., Psychiatry Clin Neurosci 2024
Treatment Framework — Where Does Pharmacotherapy Fit? • Long-term remission with CBT-I alone (~41%) vs. pharmacotherapy alone (~28%) as initial treatment • Pharmacotherapy is recommended as an alternative (when CBT-I unavailable/unsuccessful) or short-term adjunctive treatment • AASM 2017 guideline: all pharmacotherapy recommendations were conditional (weak) • AASM 2026 NEW: CBT-I alone ≥ CBT-I + medication > medication alone • Shared decision-making approach Refs: Morin & Buysse, NEJM 2024; Perlis et al., Lancet 2022; Buysse et al., JCSM 2026; Mysliwiec et al., Ann Intern Med 2020
Overview of Drug Classes and Mechanisms Drug Class
Mechanism
FDA-Approved Examples
Benzodiazepines
GABA-A receptor allosteric modulation
Triazolam, temazepam
Z-drugs
GABA-A receptor (α1 selectivity)
Zolpidem, zaleplon, eszopiclone
Novel GABA modulators
Partial positive allosteric modulator GABA-A
Dimdazenil (approved China 2023)
Melatonin receptor agonists MT1/MT2 agonism
Ramelteon, melatonin
Sedating antidepressants
variable
Doxepin 3–6 mg
DORAs
Block wake-promoting OX1R/OX2R
Suvorexant, lemborexant, daridorexant
Selective OX2R antagonist
OX2R blockade
Seltorexant (investigational)
Refs: Morin & Buysse, NEJM 2024; Syed, Drugs 2024; Mesens et al., JAMA Psychiatry 2025
SECTION I: BENZODIAZEPINE RECEPTOR AGONISTS (BZRAs)
BZRAs — Efficacy Data • Consistent evidence for sleep onset and maintenance; highest acute effect sizes among all drug classes • Pan et al. (Drugs 2023, 153 RCTs, n=46,412): non-BZDs improved, SOL, and WASO vs. placebo • De Crescenzo et al. (Lancet 2022, 154 RCTs): BZDs very effective acutely; eszopiclone best long-term Z-drug; no long-term BZD data available • Eszopiclone: only Z-drug with 6-month nightly efficacy data without tolerance Refs: De Crescenzo et al., Lancet 2022; Pan et al., Drugs 2023; Yue et al., Sleep Med Rev 2023; Morin & Buysse, NEJM 2024
BZRAs — Efficacy Data Drug / Subclass
Type
SMD vs. Placebo (95% CI)
Short-acting BZDs (e.g., triazolam)
Benzodiazepine
0.83 (0.62–1.04)
High
Intermediate-acting BZDs (e.g., temazepam)
Benzodiazepine
0.67 (0.52–0.82)
High
Long-acting BZDs (e.g., nitrazepam)
Benzodiazepine
0.58 (0.42–0.73)
Moderate
Eszopiclone
Z-drug
0.51 (0.35–0.68)
Moderate
Zolpidem
Z-drug
0.45 (0.36–0.56)
High
Zopiclone
Z-drug
0.36 (0.17–0.55)
Moderate
Zaleplon
Z-drug
0.19 (0.00–0.37)
Moderate
Refs: De Crescenzo et al., Lancet 2022;
Certainty (CINeMA)
BZRAs — Efficacy Data Outcome
Non-BZDs (Z-drugs) vs. Placebo: MD (95% CI)
Certainty
Objective TST
+22.34 min (7.64–37.05)
High
Subjective TST
+25.07 min (15.49–34.64)
Low
Objective SOL
−12.11 min (−19.31 to −4.90)
Moderate
Subjective SOL
−10.12 min (−13.84 to −6.40)
Moderate
Objective WASO
−13.92 min (−22.71 to −5.14)
Moderate
Subjective WASO
−16.67 min (−21.79 to −11.56)
Moderate
Refs: Pan et al., Drugs 2023
Refs: De Crescenzo et al., Lancet 2022
Refs: De Crescenzo et al., Lancet 2022;
BZRAs — Safety Concerns • Short-term: next-day sedation (5–10%), anterograde amnesia (< 5%), complex sleep behaviors (3–5%) → FDA boxed warning • Tolerance and physiological dependence in 20–50% with repeated nightly use; rebound insomnia on discontinuation
• Long-term: falls, hip fractures, possible dementia association, depression • Long-term BZD use in Europe: commonly exceeds recommended ≤4 weeks; associated with increased risk of opioid use disorder Refs: Morin & Buysse, NEJM 2024; De Crescenzo et al., Lancet 2022; Soyka et al., Front Psychiatry 2023; Fung et al., JAMA Intern Med 2024
SECTION II: DUAL OREXIN RECEPTOR ANTAGONISTS (DORAs)
Refs: Morin & Buysse, NEJM 2024
SECTION II: DUAL OREXIN RECEPTOR ANTAGONISTS (DORAs) • Orexin (hypocretin) neurons in the lateral hypothalamus stimulate wake-promoting nuclei; DORAs block OX1R/OX2R → reduce wake drive and promote sleep
• Three FDA-approved agents: • Suvorexant (Belsomra) — t½ 12 h • Lemborexant (Dayvigo) — t½ 18 h • Daridorexant (Quviviq) — t½ 8 h
• All approved for insomnia with sleep onset and/or maintenance difficulties • Contraindicated in narcolepsy type 1
Refs: Morin & Buysse, NEJM 2024
DORAs — Network Meta-Analysis Evidence • Yue et al. (Sleep Med Rev 2023, 69 RCTs, n=17,319): ORAs ranked best overall — SUCRA: SL 0.84, WASO 0.93, TST 0.86, SE 0.96; superior to Z-drugs for WASO and SE • Pan et al. (Drugs 2023, 153 RCTs, n=46,412): DORAs improved subjective TST (MD 21.6 min) and objective TST (MD 31.8 min); doxepin, suvorexant, and lemborexant had best efficacy-tolerability balance • De Crescenzo et al. (Lancet 2022, 154 RCTs): lemborexant most efficacious ORA short- and long-term; seltorexant and suvorexant had better tolerability Refs: Yue et al., Sleep Med Rev 2023; Pan et al., Drugs 2023; De Crescenzo et al., Lancet 2022; Liu et al., Sleep Med 2025
DORAs — Head-to-Head Comparison • Kishi et al. (Transl Psychiatry 2025, 8 RCTs, n=5,198) — first NMA comparing all 3 DORAs: • All DORAs outperformed placebo on all efficacy outcomes • Lemborexant 10 mg: greatest reduction in subjective time to sleep onset (SMD −0.43) • Daridorexant 50 mg: greatest increase in subjective TST (SMD −0.48)
• Somnolence higher with daridorexant 25 mg, lemborexant 10 mg, and suvorexant vs. placebo • No evidence of tolerance, withdrawal, or rebound insomnia with abrupt discontinuation for any DORA
• Sleep architecture not adversely affected Refs: Kishi et al., Transl Psychiatry 2025
Daridorexant — Deep Dive • Mignot et al. (Lancet Neurol 2022) — two phase 3 RCTs: daridorexant 50 mg improved LPS, WASO, sTST, and daytime functioning (IDSIQ) at months 1 and 3; effect stable across adults and older adults (≥65 y)
• At month 3: daridorexant 50 mg improved sleep onset and maintenance by ~30 min each → TST increase of ~1 hour (mean 6.5 h) • Preserves normal sleep architecture (unlike BZRAs) • Kunz et al. (CNS Drugs 2023) — 40-week extension (total 12 months): efficacy maintained; no withdrawal or rebound on discontinuation • Jiang et al. (Medicine 2023) and Albadrani et al. (Int Clin Psychopharmacol 2023) meta-analyses: 50 mg superior to placebo on all endpoints; slightly higher somnolence and fatigue
Refs: Mignot et al., Lancet Neurol 2022; Kunz et al., CNS Drugs 2023; Jiang et al., Medicine 2023; Albadrani et al., Int Clin Psychopharmacol 2023
Figure 2 Night-time efficacy endpoints
Refs: Mignot et al., Lancet Neurol 2022
Refs: Mignot et al., Lancet Neurol 2022
Lemborexant — Deep Dive (SUNRISE Trials) • SUNRISE-1 (Rosenberg et al., JAMA Netw Open 2019) — phase 3, n=1,006, age ≥55 y: • LEM 5 mg and 10 mg significantly improved LPS, WASO, and SE vs. placebo
• LEM superior to zolpidem for WASO in the second half of the night (LEM 10 mg: −8.0 min vs. ZOL; P<.001) • Well tolerated; no treatment-related serious AEs with lemborexant
• SUNRISE-2 (Yardley et al., Sleep Med 2021) — 12-month data: efficacy maintained at 12 months; no rebound insomnia or withdrawal on discontinuation
• Moline et al. (JCSM 2021): lemborexant increased REM sleep and decreased REM latency vs. placebo and zolpidem — may address age-related sleep architecture changes • Alsaied et al. (Naunyn-Schmiedeberg's 2025) meta-analysis (n=1,976): LEM reduced SOL (−9.2 min 5 mg; −12.6 min 10 mg) and WASO (−19.9 min; −22.2 min) vs. placebo
Refs: Rosenberg et al., JAMA Netw Open 2019; Yardley et al., Sleep Med 2021; Moline et al., JCSM 2021; Alsaied et al., 2025
Lemborexant — Deep Dive (SUNRISE Trials) •
Refs: Rosenberg et al., JAMA Netw Open 2019
Lemborexant — Deep Dive (SUNRISE Trials)
Refs: Sleep Medicine. 2022. Roth T, Rosenberg R, Morin CM, et al
SECTION III: SEDATING ANTIDEPRESSANTS
Drug
Efficacy Evidence
Key Safety Concerns
Trazodone (25–100 mg)
TST +40 min, LPS −19 min, ↑N3 (Zheng 2022); PSQI Somnolence (OR 7.3), SMD −0.83 in depression blurred vision (OR 17.5), (Hameed 2026); effect size orthostatic hypotension 0.52 (NEJM 2024)
Mirtazapine (7.5–15 mg)
↑TST ~30 min, ↑N3, ↓awakenings 35–40% (Karsten 2017); ↑TST, SWS%, SE% in depression (Zhang 2026)
No RCTs in primary Weight gain (major), insomnia; reasonable if sedation, metabolic effects comorbid depression/anxiety
Quetiapine (25–150 mg)
Sleep quality SMD −0.57, TST +48 min (Lin 2023); only 1 RCT (n=13) in primary insomnia — no benefits
Weight gain, metabolic syndrome, QTc prolongation, EPS
Gabapentinoids
Inconclusive for insomnia Sedation, dizziness, (Hong 2022); improves respiratory depression, sleep in neuropathic pain dependence (pregabalin) (SMD 0.39, Kapustin 2020)
Refs: Zheng et al., Sci Rep 2022; Hameed et al., Psychopharmacology 2026; Everitt et al., Cochrane 2018; Pochiero et al., Clin Ther 2022; Morin & Buysse, NEJM 2024; Karsten et al., J Psychopharmacol 2017; Zhang et al., J Affect Disord 2026; Lin et al., Eur Neuropsychopharmacol 2023; Thompson et al., Sleep Med 2016; Hong et al., Mol Psychiatry 2022; Kapustin et al., Pain 2020
Guideline Position AASM: against; widely used off-label (17.7% of insomnia patients)
VA/DoD: against; NEJM: avoid except comorbid psychiatric disorders
Not recommended for primary insomnia; consider if comorbid pain/RLS
Low-Dose Doxepin (3–6 mg) • FDA-approved at 3 mg and 6 mg for insomnia (distinct from antidepressant doses 75–300 mg)
• Mechanism: potent H1 receptor antagonism at low doses • Effective for sleep maintenance — reduces WASO, improves SE by ~5–7% • Adverse event rates comparable to placebo (OR 0.85 vs. placebo — lowest among all insomnia drugs) • Liu et al. (Sleep Med 2025): doxepin 3 mg significantly superior to placebo for WASO (SMD −0.50) • Limitations: less effective for sleep onset; limited long-term data beyond 12 weeks
Refs: Morin & Buysse, NEJM 2024; Pan et al., Drugs 2023; Liu et al., Sleep Med 2025; Perlis et al., Lancet 2022
Refs: De Crescenzo et al., Lancet 2022;
SECTION IV: MELATONIN AND MELATONIN RECEPTOR AGONISTS
Melatonin • Melatonin (OTC supplement — NOT FDA-approved for insomnia) • Mechanism: Endogenous pineal hormone; act on MT1/MT2/MT3 receptors; t½ ~20–50 min (IR), variable (PR) • Efficacy: SOL −5 to −7 min; TST +8 min (inconsistent); optimal dose ~4 mg, 3 h before bedtime; PR melatonin may benefit adults ≥55 y (↑ sleep efficiency) • Side effects: Generally well tolerated (daytime sleepiness 1.7%, headache 0.7%, dizziness 0.7%) • Guideline: weak AGAINST (variable quality, critical outcomes not assessed) Morin & Buysse, NEJM 2024 | Ferracioli-Oda et al., PLoS ONE 2013 | Choi et al., Sleep Med Rev 2022 | Maruani et al., J Sleep Res 2023 | Cruz-Sanabria et al., J Pineal Res 2024 | Kuriyama et al., Sleep Med 2014 | Mayer et al., Sleep 2009 | Johnson et al., Arch Gen Psychiatry 2006 | De Crescenzo et al., Lancet 2022 | Ha et al., J Pineal Res 2024 | Rozerem FDA Label | Sateia et al. (AASM), JCSM 2017 | Mysliwiec et al. (VA/DoD), Ann Intern Med 2020
Ramelteon • Ramelteon (Rozerem) — FDA-approved for sleep-onset insomnia • Mechanism: Selective MT1/MT2 agonist (3–16× higher affinity than melatonin); 8 mg qhs; t½ ~1–2.6 h • Efficacy: SOL −4 to −14 min; TST +12 to +18 min (at 4 wk); effective for sleep onset only • Side effects: Placebo-like AE profile; no abuse potential ; no rebound insomnia (confirmed up to 6 months); no next-day impairment • Guideline: AASM — weak FOR sleep-onset insomnia ("benefits > minimal potential harms")
Morin & Buysse, NEJM 2024 | Ferracioli-Oda et al., PLoS ONE 2013 | Choi et al., Sleep Med Rev 2022 | Maruani et al., J Sleep Res 2023 | Cruz-Sanabria et al., J Pineal Res 2024 | Kuriyama et al., Sleep Med 2014 | Mayer et al., Sleep 2009 | Johnson et al., Arch Gen Psychiatry 2006 | De Crescenzo et al., Lancet 2022 | Ha et al., J Pineal Res 2024 | Rozerem FDA Label | Sateia et al. (AASM), JCSM 2017 | Mysliwiec et al. (VA/DoD), Ann Intern Med 2020
Melatonin and Ramelteon Feature
Melatonin (OTC)
Regulatory status
Dietary supplement (not FDA-regulated FDA-approved for sleep-onset for insomnia) insomnia
Receptor selectivity
Non-selective (MT1, MT2, MT3 + other targets)
Highly selective MT1/MT2 agonist
Binding affinity
Lower; variable by formulation
3–16× higher affinity than melatonin for MT1/MT2
Half-life
20–50 min (IR); variable (PR)
~1–2.6 h (active metabolite M-II: ~2–5 h)
SOL reduction
−5 to −7 min vs. placebo
−4 to −14 min vs. placebo
TST increase
+8 min (inconsistent)
+12 to +18 min (at 4 weeks)
Dose standardization
Highly variable; content may differ from label
Standardized 8 mg tablet
Abuse potential
None reported
None (not a controlled substance)
Rebound insomnia
Not reported
None (confirmed up to 6 months)
Guideline position
AASM: weak against
AASM: weak for (sleep onset); VA/DoD: insufficient evidence
Refs: Maruani et al., J Sleep Res 2023; Morin & Buysse, NEJM 2024; Liu et al., Sleep Med 2025
Ramelteon (Rx)
SECTION V: EMERGING AGENTS
Seltorexant — Selective OX2R Antagonist • First selective orexin-2 receptor antagonist studied clinically • May preserve normal sleep architecture better than DORAs • Mesens et al. (JAMA Psychiatry 2025) — phase 2b RCT, n=364, 14 days: • Seltorexant 10 mg and 20 mg: significant dose-response for LPS and WASO-6 on night 1 (P<.001) • Seltorexant 20 mg outperformed zolpidem on LPS (night 1) and maintained efficacy at night 13, while zolpidem efficacy diminished
• Night 13 vs. zolpidem: seltorexant 10 mg and 20 mg improved LPS by 30% and 28%; seltorexant 20 mg improved WASO-6 by 31% • TEAEs lower with seltorexant (33.8%) than placebo (49.3%) or zolpidem (42.5%)
• Phase 3 trial underway for depression + insomnia; no registered phase 3 for insomnia alone
Refs: Mesens et al., JAMA Psychiatry 2025
Refs: Mesens et al., JAMA Psychiatry 2025
Dimdazenil — Novel Partial GABA-A Modulator • Mechanism: Partial positive allosteric modulator of the GABA-A receptor with α1/α5 selectivity— designed to reduce tolerance/dependence risk vs. full agonists (BZDs, Zdrugs) • Status: Approved in China for short-term insomnia treatment; not FDA-approved and no announced U.S. submission. • Efficacy: Phase 2/3 RCTs show significant, dose-dependent improvements-- ↑ total sleep time, ↓ WASO, ↓ sleep latency, and ↑ sleep efficiency. • Safety: Generally well tolerated; long-term and real-world comparative safety data remain limited. • Comparative data: Better than placebo for WASO, but may be less effective than daridorexant 25 mg. Refs: Syed, Drugs 2024; Huang et al., Sleep 2024; Li et al., Sleep 2024; Dun et al., J Affect Disord 2026; Liu et al., Sleep Med 2025
Refs: Huang et al., Sleep 2024
SECTION VI: COMPARATIVE EFFICACY SUMMARY Drug Class
Representative ↓ SOL Agent(s)
BZDs
Triazolam, Temazepam
+++
↓ WASO
++
↑ TST
Safety / Dependence
++
Dependence ↑↑; AASM: weak falls, cognitive FOR; avoid in impairment elderly (Beers)
Z-drugs
Zolpidem, Eszopiclone
+++
++
++
DORAs
Suvorexant, Lemborexant, Daridorexant
++
+++
++
Melatonin RA
Ramelteon (8 mg)
+
−
+
Dependence ↑; parasomnias (FDA boxed warning) No dependence/tol erance; somnolence, sleep paralysis (rare)
Guideline
AASM: weak FOR; eszopiclone best long-term AASM: weak FOR (maintenance); best efficacytolerability balance
Safest profile (≈ AASM: weak placebo AEs) FOR (onset only)
SECTION VI: COMPARATIVE EFFICACY SUMMARY Drug Class
Representative ↓ SOL Agent(s)
↓ WASO
↑ TST
Low-dose doxepin
Doxepin (3–6 mg) −
++
++
Sedating Trazodone, antidepressants Quetiapine
Gabapentinoids
Gabapentin, Pregabalin
Emerging
Seltorexant (OX2R), Dimdazenil
±
±
++
±
+ (↑SWS)
++
Safety / Dependence Safe; no anticholinergic effects at low dose
Guideline AASM: weak FOR (maintenance)
±
Trazodone: priapism, orthostasis; AASM/VA-DoD: Quetiapine: weak AGAINST metabolic, ↑ mortality in elderly dementia
+ (pain pop.)
Dizziness, sedation; pregabalin Schedule V
++
Favorable in phase 2b; not yet Investigational FDA-approved
No guideline rec for insomnia
SECTION VII: SPECIAL POPULATIONS
Older Adults (≥65 years) • AVOID (AGS Beers Criteria 2023)
•
Benzodiazepines (all) — >2× risk of falls, hip fractures, cognitive impairment, delirium, motor vehicle accidents
•
Z-drugs (zolpidem, eszopiclone, zaleplon) — similar adverse event profile to BZDs in older adults; HR 3.11 for hip fractures with zolpidem
•
First-generation antihistamines (diphenhydramine, doxylamine) — anticholinergic burden; cognitive impairment, urinary retention
•
Tricyclic antidepressants (amitriptyline, doxepin >6 mg) — anticholinergic, orthostatic hypotension, cardiac conduction effects
•
Barbiturates — high abuse potential, narrow therapeutic index
Refs: Steinman, JAGS 2025 (AGS Beers Criteria Alternatives); AGS Choosing Wisely 2013; Gotfried et al., Drugs Aging 2024; Rollo et al., Sleep 2026; Kishi et al., Transl Psychiatry 2025
Older Adults (≥65 years) • SAFER ALTERNATIVES (AGS Beers Criteria 2023 + Trial Evidence) •
Low-dose doxepin (3–6 mg) — best for sleep maintenance; AE rates comparable to placebo; FDAapproved
•
DORAs (lemborexant, daridorexant, suvorexant) — efficacy for onset + maintenance; no tolerance/dependence/rebound; no impairment of postural stability, memory, or driving
•
Ramelteon (8 mg) — modest efficacy for sleep onset; low AE profile; low abuse potential
•
PR melatonin — option if patient requests "natural remedy"; limited evidence of meaningful benefit; no FDA oversight of supplements
• INSUFFICIENT EVIDENCE in older adults:
• Trazodone, mirtazapine, melatonin (OTC), gabapentinoids
Refs: Steinman, JAGS 2025 (AGS Beers Criteria Alternatives); AGS Choosing Wisely 2013; Gotfried et al., Drugs Aging 2024; Rollo et al., Sleep 2026; Kishi et al., Transl Psychiatry 2025
Comorbid Psychiatric Disorders • DORAs (suvorexant, lemborexant, daridorexant) — improve sleep + modest antidepressant benefit in comorbid MDD • Low-dose doxepin (3–6 mg) — FDA-approved for insomnia; safe in MDD/anxiety • Trazodone (25–100 mg) — improves sleep quality + reduces depression severity in comorbid patients
• Seltorexant 20 mg (investigational) — dual insomnia + antidepressant effect in MDD; lower AEs vs. quetiapine XR • Ramelteon — prevents depressive relapse in bipolar disorder; no mania risk • Melatonin (adjunctive) — may reduce manic symptoms in bipolar mania
Refs: Vasudeva et al., J Psychiatr Res 2025; Hameed et al., Psychopharmacology 2026; Mesens et al., Mol Psychiatry 2025; Pinter et al., Int J Neuropsychopharmacol 2026; Meshkat et al., J Affect Disord 2025; Kishi et al., Neuropsychiatr Dis Treat 2019; McGowan et al., CNS Drugs 2022; Morin & Buysse, NEJM 2024; AASM CPG 2017
Comorbid Insomnia and Sleep Apnea (COMISA) • COMISA is the most common co-occurring sleep disorder combination • BZRAs: concern for respiratory depression, especially in moderate-to-severe OSA; significant decreases in minimum SpO₂ with zolpidem 20 mg(not 10 mg) and triazolam 0.25 mg • DORAs: should not cause respiratory depression; exert sleep promotion by antagonizing orexin, not by global sedation
• Eszopiclone: did not worsen AHI; one study showed reduced AHI — may merit further assessment • Ramelteon: did not worsen OSA in older adults with comorbid insomnia • Concurrent CBT-I + PAP is superior to PAP alone for insomnia outcomes in COMISA; may improve PAP adherence Refs: Mason et al., Cochrane 2015; Javaheri et al., JACC 2024; Ong et al., Chest 2021
Pregnancy and Peripartum • Pharmacotherapy (with shared decision-making): • Diphenhydramine / doxylamine — first generation H1 antihistamines acceptable for PRN use; benefit over placebo for insomniarelated depression in pregnancy (AAFP 2023) • Trazodone (low-dose) — no consistent evidence of increased major congenital malformations or stillbirth risk ; possible association with spontaneous abortion • BZDs and zolpidem: associated with ↑ risk of adverse obstetric outcomes: spontaneous abortion, low birth weight, preterm birth, SGA. Not teratogenic. Reassuring for inadvertent first-trimester exposure; not recommended for chronic use throughout pregnancy. • Melatonin: crosses placenta; insufficient human safety data • DORAs, doxepin: no adequate pregnancy data; generally avoided Refs: Palagini et al., Arch Women's Ment Health 2022; Felder et al., JAMA Psychiatry 2020; Kalmbach et al., Sleep Med 2025; Powers et al., Am Fam Physician 2023
SECTION VIII: GUIDELINES AND CLINICAL ALGORITHM
AASM 2026 Guideline — Combination Treatment (NEW) • First guideline to address CBT-I + pharmacotherapy combined • Recommendation 1 (Conditional FOR): CBT-I + medication suggested over medication alone — improves insomnia severity and sleep continuity • Recommendation 2 (Conditional AGAINST): CBT-I + medication not suggested over CBT-I alone • Clinical hierarchy: CBT-I alone > Combination > Pharmacotherapy alone • Combination may be appropriate when: rapid symptom relief needed, safety-sensitive occupations, CBT-I acceptable but not immediately available Refs: Buysse et al., JCSM 2026
Practical Prescribing Algorithm • Step 1: Establish diagnosis; address comorbidities and contributing factors • Step 2: CBT-I as first-line (strong recommendation) • Step 3: If CBT-I unavailable, unsuccessful, or as adjunct → pharmacotherapy via shared decision-making
• Step 4: Start at lowest effective dose; reassess efficacy and side effects regularly • Step 5: Consider combination CBT-I + medication over medication alone (AASM 2026) Refs: Buysse et al., JCSM 2026
Take Home Points 1. CBT-I is the foundation — start behavioral, add pharmacotherapy if needed
2. DORAs should be considered as the preferred pharmacotherapy class for chronic insomnia
3. Tailor pharmacotherapy to the patient population
4. Novel agents are expanding the treatment landscape
• Questions?
Unrecognized Psychological Factors in Parasomnias Alan S. Eiser, Ph.D. Sept. 17, 2026
Conflict of Interest Disclosures for Speakers 1. I do not have any relationships with any entities producing, marketing, reselling, or distributing health care goods or services consumed by, or used on, patients, OR 2. I have the following relationships with entities producing, marketing, reselling, or distributing health care goods or services consumed by, or used on, patients.
Type of Potential Conflict
Details of Potential Conflict
Grant/Research Support Consultant Speakers’ Bureaus
Financial support Other 3. The material presented in this lecture has no relationship with any of these potential conflicts, OR
4. This talk presents material that is related to one or more of these potential conflicts, and the following objective references are provided as support for this lecture:
Purpose of Talk • To identify and delineate a significant gap in current Sleep Medicine understanding and approach to certain parasomnias
Thesis • In certain parasomnias involving complex behavior arising out of sleep, psychological factors often play an integral role, in addition to the familiar sleep-related factors • The Sleep Medicine literature generally shows no awareness of the role of these factors, with rare exceptions
Plan for Presentation 1. Review of Relevant Parasomnias 2. Two Illustrative Cases: 1. Brief Simple Case Illustration 2. In-Depth Complex Case Illustration
3. Supportive Findings in Literature 4. Implications for Clinical Work: Diagnosis and Treatment
Which Parasomnias? • Among the broader category of NREM Parasomnias: –Disorders of Arousal (Confusional Arousals, Sleepwalking, Sleep Terrors) –Sleep Related Eating Disorder
3 Categories of Complex Behavior Arising out of NREM Sleep 1. 2.
3.
Sleep Related Eating Disorder Sleep Related Abnormal Sexual Behavior Violence Associated with Sleepwalking/Sleep Terrors
Disorders of Arousal (From NREM Sleep)
• 3 Disorders: Confusional Arousals, Sleepwalking, Sleep Terrors • Most often occur during arousals from deeper NREM sleep, stage 3, early in the night • The person remains “stuck” between sleep and wakefulness, with some features of each • Unresponsive, confused, disoriented
Disorders of Arousal II • Relatively amnestic afterward • Disorders tend to cluster together in individuals and within families • Strong genetic predisposition • Occurrence primed by factors that deepen sleep: sleep deprivation • Sleep disorders that cause arousals, e.g. obstructive sleep apnea (OSA), can be important triggering factors
Disorders of Arousal III • Confusional Arousals – Period of mental confusion or confusional behavior following arousal from sleep – Common in young children; diminish after age 5
• Sleepwalking or Somnambulism – Complex behavior that includes walking around in a confused state with impaired judgment following partial arousal from sleep – Eyes usually open – Peak prevalence ages 8-12, as high as 17%; usually spontaneously resolves in adolescence
Disorders of Arousal IV • Sleep Terrors – Commence with a sudden cry or scream out of sleep – Behavioral and autonomic nervous system evidence of intense fright – Typically recall just a single frightening image or no content at all – Usually sit up in bed, may bolt from bed, can have fight-flight response – Usually emerges ages 4-12, spontaneously resolves in adolescence
SPECT in Sleepwalking • 16-year-old boy with frequent sleepwalking • Scanned during undisturbed delta sleep, and following an episode of sleepwalking out of delta sleep • When sleepwalking, showed activation of thalamo-cingulate circuits (posterior cingulate), with deactivation of prefrontal cortex • Conclusion: Sleepwalking characterized by selective activation of thalamo-cingulate cortex in context of overall deactivation of other thalamo-cortical systems1 1Bassetti et al, 2000
Neurophysiology of Sleepwalking/Disorders of Arousal • Heidbreder et al (2017). MRI: Decreased gray matter volume in sleepwalkers in left dorsal posterior cingulate cortex • Castelnovo et al (2016). High Density EEG: Locally decreased delta power during slow wave sleep at cingulate, motor, and sensorimotor associative cortices – also present in REM and wakefulness
3 Categories of Complex Behavior Arising out of NREM Sleep 1. 2.
3.
Sleep Related Eating Disorder Sleep Related Abnormal Sexual Behavior Violence Associated with Sleepwalking/Sleep Terrors
Sleep Related Eating Disorder • First systematically described by Schenck and Mahowald (1991), later John Winkelman (1998) • Recurrent, frequent episodes of involuntary eating during arousals from nocturnal sleep, most often with partial awareness and partial recall • Degree of consciousness can vary from virtual unconsciousness, with little or no recall, to partial awareness with some recall, to considerable alertness and recall, but with inability to resist eating
Sleep Related Eating Disorder II • Frequency: typically nightly, often several times per night • Episodes may occur throughout the night, not just in the first third • High calorie foods, fats and carbohydrates, sweets typically eaten – Almost never alcohol
• Can consume bizarre or dangerous items, e.g. uncooked frozen foods, raw bacon, cat food, buttered cigarettes, salt sandwiches
Sleep Related Eating Disorder III • Absence of feeling of hunger or thirst • Sloppy, careless eating – Find mess in morning – Turn on oven and return to bed
• Female predominance: 66-83% • Most often begins late teens, early adulthood • Course usually unremitting
Sleep Related Eating Disorder IV • Complications – Weight gain/obesity – Inadequate sleep and daytime fatigue – Awaken with distended abdomen, no appetite – Lacerations, burns from careless food preparation – Danger from eating toxic substances
• Prevalence: 4.6% in general sample of university students, 8.7% in outpatient eating disorders, 16.7% in inpatient eating disorders2 2Winkelman at el, 1999
Sleep Related Eating Disorder V • Most patients with SRED do not have daytime eating disorders; a minority do • Sleepwalking/confusional arousals most often found – Other patients have restless legs syndrome and/or periodic limb movements of sleep – Obstructive sleep apnea may trigger episodes
• Precipitants may be noted – Daytime dieting, smoking abstinence, cessation of alcohol/substance abuse – Major separations from important others
Sleep Related Eating Disorder VI • Can be secondary to medication use, esp. zolpidem • Appears to be hybrid sleep/eating disorder: – Occurs at night, during arousals from sleep, with altered consciousness, at times bizarre behavior, as in a sleep disorder – Excessive, compulsive eating, female predominance, late adolescence/young adulthood onset, association with daytime eating disorders, suggest an eating disorder
Treatment of Sleep Related Eating Disorder • Withdraw causative medications • Treat any underlying sleep disorder – OSA – Restless legs syndrome: some cases of SRED may actually have RLS improperly treated with sedative/hypnotics for insomnia
• Topiramate effective in majority of cases – Has appetite-suppressing effect, as well as sleep-enhancing property
Sexual Behavior During Sleep • First systematically described by Guilleminault et al (2002) • Wide spectrum of sexual behaviors has been reported – Sexual moaning and vocalizations – Masturbation, sometimes violent, with or without orgasm – Sexual fondling of another person – Sexual intercourse, at times forced and violent and experienced as rape-like assault
Sexual Behavior During Sleep II •
The behavior is often reported to be coarser, more forceful and violent than during wakefulness – At least one report of homosexual activity in a heterosexual individual
•
Usually occurs out of NREM sleep, as a form of confusional arousal/sleepwalking – May be triggered by OSA
•
Lack of awareness during episode; subsequent amnesia
Sexual Behavior During Sleep III • Often begins in early adulthood • Male predominance – Female cases usually confined to sexual moaning and masturbation – Male cases more often fondling, intercourse
• May not come to clinical attention for many years – embarrassment about reporting • Prevalence unknown
Sexual Behavior During Sleep IV • Injuries can occur, especially bruises, lacerations of bed partner due to forceful quality of sex • Forensic consequences – Unwanted sexual activity – Sexual activity with minor, especially where parents take children into bed
Sexual Behavior During Sleep V • Often have history of sleepwalking, sleep terrors, confusional arousals • Dispute whether sexual behavior can occur in RBD • A number of reported cases complicated by significant alcohol/drug use
Treatment of Sexual Behavior During Sleep • Treat any underlying sleep disorder, e.g. OSA • Clonazepam usually effective in controlling episodes
Violence in Sleepwalking and Sleep Terrors • Most extensively studied by Schenck and Mahowald group (1989) • Overall prevalence of violence in sleep was 2.1% in one population study1 – SW/ST cases constituted the majority • May lash out at person who interrupts activity or is near, repeatedly attack bed partner, wield weapons (e.g. knife, loaded shotgun) • Both short frenzied episodes, and slow, lengthy, complex episodes 1Ohayon et al, 1997
Violence in Sleepwalking and Sleep Terrors II • Often have fragmentary mental images: a looming figure, an attacking person, a fire; but may have more elaborate, dreamlike images • Symptoms often begin in young adulthood • Male predominance: 61% vs 39% • Sleepwalking/Sleep Terrors usually have childhood onset, but in this group 1/3 have de novo onset at age 16 or later • Sleep disorders that cause arousals, e.g. OSA, may be significant triggering factors • Legal cases of ‘homicidal somnambulism’ have attracted much attention
Treatment of Violence in Sleepwalking/Sleep Terrors • Treat any associated sleep disorder that may precipitate episodes • Clonazepam usually effective in controlling the behavior
Psychological Factors: Brief Case Illustration • Man in his late 20s presented to sleep clinic with symptoms of masturbation in his sleep • Was extremely distressed by this symptom, which violated strongly-held religious beliefs – Bound his arms and legs to the bed at night to prevent the masturbation
• Hx: He had been treated for daytime obsessional thoughts of a sexual and aggressive nature with an SSRI, which eliminated the daytime symptoms but was followed by the appearance of the nocturnal masturbation
Psychological Factors: Brief Case Illustration (cont.) • The medication was discontinued, but the sleeprelated masturbation persisted • Sleep studies did not show seizures, OSA, loss of REM atonia, or abrupt arousals from N3 sleep • Family hx of parasomnias was present • Was diagnosed with sleep-related sexual behavior (sexsomnia) and was prescribed nightly clonazepam • Also referred for psychological evaluation
Psychological Factors: Brief Case Illustration (cont.) • Returned for followup in 3 months and indicated he had discontinued the clonazepam due to sedation. • Did not pursue the psychological evaluation • However, he reported he had gotten married and his symptoms resolved with initiation of regular sexual intercourse with his new wife1
1Dredla, Dunn, Kaplish (2017)
Detailed Case Illustration • Female patient presented with frequent episodes of eating during sleep • Awareness ranged from little or none to almost full alertness • Symptoms had persisted over many years • In addition, frequently masturbated during sleep • Concerned re weight gain, sleep disruption, tiredness
Case Illustration (Cont.) • No psychotropic medications • Two PSGs, one with Pes, were negative for OSA or PLMs • REM atonia was preserved • Case of sleep-related eating and sexual behavior • Referred for in-depth psychological evaluation
Case Illustration (Cont.) • Childhood environment involving very strict prohibitions against pleasure-seeking of any kind • Harsh, physical discipline • Parental behavior that was overstimulating in unacknowledged sexual and aggressive ways, in stark contradiction to the family’s “official” values
Case Illustration (Cont.) • Bleak sense of emotional deprivation permeating childhood • The eating and sexual behavior during sleep represented forbidden pleasureseeking behaviors emerging at a time when agency can be denied, as well as a reaction to emotional hunger and deprivation
Case Illustration (Cont.) • Of special interest, both the eating and sexual behavior during sleep had conscious childhood antecedents.
Case Illustration (Cont.) • The psychological factors in question, e.g. this patient’s conflicted pleasure-seeking desires and emotional hunger, are directly involved in her sexual and eating behavior during the parasomnia episodes • They are not simply “associated psychopathology”, or contributors to an overall level of “stress” that then potentiates parasomnia events
Supportive Findings in Literature • Schenck et al (1989). “A Polysomnographic and Clinical Report on Sleep-Related Injury in 100 Adult Patients” • 54 patients diagnosed with sleepwalking/ sleep terrors – 48.1% had an Axis I psychiatric disorder – Of those who completed a valid MMPI profile, 64% had abnormal profiles and one-third had personality disorders
Supportive Findings in Literature (cont.) • Patients with sleep related eating disorder: 47% had Axis I disorder in original Schenck et al (1991) study • 53% of patients in their followup study of sleep related eating disorder (Schenck et al,1993) had past history of repeated abuse, and Dissociative Experience Scale scores approaching those seen in PTSD
Supportive Findings in Literature (cont.) • In Winkelman et al (1999) sample of sleep related eating disorder, increased levels of depression and dissociation were found
Supportive Findings in Literature (cont.) • Guilleminault et al (2002). “Atypical Sexual Behavior During Sleep” • 11 patients comprehensively evaluated and treated • The majority had psychopathology (anxiety, affective, and personality disorders) – 2 with NREM parasomnia had major sexual traumas – 2 others had disturbing sexual factors in development
• Treatment addressed all facets of the patients’ disorders, including sleep and psychiatric
Supportive Findings in Literature (cont.) • Béjot et al (2010) “Sexsomnia: An uncommon variety of parasomnia” • Two women, aged 36 and 40, with elaborate assaultive sexual behavior apparently out of NREM sleep – One patient was sexually abused at age 16 – The other witnessed her mother’s rape at age 15 – Both women had alcoholic mothers and experienced emotional deprivation in childhood
Summary of Findings in Literature • A great deal of associated psychopathology • History of childhood trauma and other factors potentially related to parasomnia behaviors may be present • Evidence of dissociative mechanisms in some cases
Dissociative Mechanisms in These Parasomnias • Dissociation in Psychiatric sense: “A disconnection from mainstream consciousness of significant areas of such mental functions as memory and identity.” In extreme cases, there is a fragmentation of central consciousness. – Dissociative amnesia – Dissociative fugue – Dissociative identity disorder
Dissociative Mechanisms in These Parasomnias • This is very different from “dissociation” in the Sleep Medicine sense of “wake/sleep state dissociation”, in which elements of one of the three major states of being, wakefulness, NREM sleep, and REM sleep, persist or emerge in one of the other major states. • Example: In cataplexy, the muscle paralysis of REM sleep emerges during wakefulness.
Dissociative Mechanisms in These Parasomnias (Cont.) • Evidence suggests dissociative mechanisms may come into play in some cases of NREM parasomnias involving complex behavior arising out of sleep • The impaired awareness, sense of identity, and agency during parasomnia episodes may provide a channel for dissociative tendencies to come to expression in some patients with NREM parasomnias
Dissociative Mechanisms in These Parasomnias (Cont.) • Sleep-related dissociative disorder (ICSD-2) – Dissociative episode emerges in association with the main sleep period – On PSG, the dissociative episode emerges from sustained EEG wakefulness either during transition to sleep or upon awakening from NREM or REM sleep
Dissociative Mechanisms in These Parasomnias (Cont.) • ICSD-2 propounds a sharp distinction between NREM parasomnias and sleep-related dissociative episodes, the former arising from partial arousal from NREM sleep, the latter arising from sustained wakefulness at night • Evidence suggests dissociative psychiatric mechanisms may come into play in some cases of NREM parasomnias involving complex behavior arising out of sleep
Common Positions in Sleep Medicine • “I’ve never seen a case” [of psychological factors coming into play in parasomnias] • 53% rate of prevalence of repeated abuse in sleep-related eating patients “probably just what is seen in the general population” • Referring to 4 cases of homicides purportedly committed during sleepwalking: “These examples add to our growing view that there is no pathology in such cases”
Importance of Appreciating Psychological Factors in Parasomnias • To develop a comprehensive understanding of the clinical problems the patient is presenting • To formulate a treatment plan that addresses all facets of the patient’s presenting problems
Clinical Approach • Be alert to indications the patient’s sleeprelated symptoms may have correlates in their waking psychological functioning and/or antecedents in their childhood development • If so, refer for in-depth psychological assessment for potentially relevant psychodynamic factors • Psychodynamically informed psychotherapy if indicated
Bibliography 1. Béjot Y et al (2010). Sexsomnia: an uncommon variety of parasomnia. Clin Neuro Neurosurg 112: 72-75. 2. Broughton R et al (1994). Homicidal somnambulism: a case report. Sleep 17: 253-264. 3. Dredla BK, Dunn A, Kaplish N (2017). Sexsomnia: onset of sleep related masturbation after successful treatment of daytime obsessive-compulsive disorder. Sleep 40 Abstract Supplement: A458. 4. Eiser AS (2013). Sleep-related dissociative disorders. In: Kushida CA, ed. The Encyclopedia of Sleep, Volume 4. Waltham, MA: Academic Press, 225-228. 5. Guilleminault C et al (2002). Atypical sexual behavior during sleep. Psychosom Med 64: 328-336.
Bibliography (Cont.) 6. Ohayon MM et al (1997). Violent behavior during sleep. J Clin Psychiatry 58: 369-376. 7. Schenck CH et al (1989). A polysomnographic and clinical report on sleep-related injury in 100 adult patients. Am J Psychiatry 146: 1166-1173. 8. Schenck CH et al (1991). Sleep-related eating disorders: polysomnographic correlates of a heterogeneous syndrome distinct from daytime eating disorders. Sleep 14: 419-431. 9. Schenck CH et al (1993). Additional categories of sleeprelated eating disorders and the current status of treatment. Sleep 16: 457-466.
Bibliography (Cont.) 10. Schenck CH (2005). Paradox Lost: Midnight in the Battleground of Sleep and Dreams. Minneapolis, MN: Extreme-Nights, LLC (www.parasomnias-rbd.com). 11. Schenck CH et al (2007). Sleep and sex: what can go wrong? A review of the literature on sleep related disorders and abnormal sexual behaviors and experiences. Sleep 30: 683-702. 12. Schenck CH (2015). Update on sexsomnia, sleep related sexual seizures, and forensic implications. NeuroQuantology 13: 518-541.
Bibliography (Cont.) 13. Winkelman JW (1998). Clinical and polysomnographic features of sleep-related eating disorder. J Clin Psychiatry 59: 14-19. 14. Winkelman JW et al (1999). The prevalence of sleeprelated eating disorder in psychiatric and nonpsychiatric populations. Psychol Med 29: 1461-1466.
Contact Information Alan S. Eiser, Ph.D. aeiser@med.umich.edu 734-761-2772