Sleep Architecture Changes in CBS and PSP

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Sleep Architecture Changes in CBS and PSP

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Sleep Architecture Changes in CBS and PSP

Overview

Sleep architecture disruption is a core and early feature of both corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). Unlike the prominent REM sleep behavior disorder (RBD) seen in synucleinopathies, 4R tauopathies like CBS and PSP are characterized by progressive disruption across all sleep stages, with particularly severe loss of slow-wave sleep (N3), reduced REM sleep percentage, and marked sleep fragmentation. These abnormalities reflect the underlying tau pathology affecting brainstem sleep-wake regulatory centers, the hypothalamus, basal ganglia, and subcortical white matter[@chen2024psg][@nakamura2024].

The bidirectional relationship between sleep architecture disruption and tau pathology makes sleep optimization a critical therapeutic target. Glymphatic clearance — which operates primarily during slow-wave sleep — is impaired when N3 is reduced, creating a feedforward loop where tau pathology disrupts sleep and poor sleep accelerates tau accumulation[@xie2013].

Sleep Stage Abnormalities

CBS Sleep Architecture

Polysomnographic studies in CBS reveal characteristic patterns across all sleep stages[@chen2024psg][@hernandze2024]:

N1 (Light Sleep):

Percentage: Elevated to 15-30% (normal: 5-10%)
This increase reflects difficulty maintaining sleep and frequent transitions from deeper stages
Prolonged sleep latency contributes to elevated N1 percentage
EEG shows increased alpha activity during N1, suggesting cortical hyperarousal

...

Sleep Architecture Changes in CBS and PSP

Overview

Sleep architecture disruption is a core and early feature of both corticobasal syndrome (CBS) and progressive supranuclear palsy (PSP). Unlike the prominent REM sleep behavior disorder (RBD) seen in synucleinopathies, 4R tauopathies like CBS and PSP are characterized by progressive disruption across all sleep stages, with particularly severe loss of slow-wave sleep (N3), reduced REM sleep percentage, and marked sleep fragmentation. These abnormalities reflect the underlying tau pathology affecting brainstem sleep-wake regulatory centers, the hypothalamus, basal ganglia, and subcortical white matter[@chen2024psg][@nakamura2024].

The bidirectional relationship between sleep architecture disruption and tau pathology makes sleep optimization a critical therapeutic target. Glymphatic clearance — which operates primarily during slow-wave sleep — is impaired when N3 is reduced, creating a feedforward loop where tau pathology disrupts sleep and poor sleep accelerates tau accumulation[@xie2013].

Sleep Stage Abnormalities

CBS Sleep Architecture

Polysomnographic studies in CBS reveal characteristic patterns across all sleep stages[@chen2024psg][@hernandze2024]:

N1 (Light Sleep):

Percentage: Elevated to 15-30% (normal: 5-10%)
This increase reflects difficulty maintaining sleep and frequent transitions from deeper stages
Prolonged sleep latency contributes to elevated N1 percentage
EEG shows increased alpha activity during N1, suggesting cortical hyperarousal

N2 (Sleep Spindles and K-Complexes):

Percentage: Moderately reduced to 35-45% (normal: 45-55%)
Sleep spindle density is reduced, correlating with thalamic involvement
K-complexes are preserved but less frequent
Loss of sleep spindle coherence reflects corticothalamic circuit disruption

N3 (Slow-Wave Sleep / Deep Sleep):

Percentage: Severely reduced to 5-15% (normal: 15-25%)
This is the most dramatic abnormality and the most therapeutically relevant
N3 reduction correlates with disease duration and cortical tau burden[@kim2025tau]
Reduced N3 impairs glymphatic clearance and memory consolidation
EEG shows reduced delta power, fragmented slow waves, and interhemispheric asymmetry

REM Sleep:

Percentage: Reduced to 10-20% (normal: 20-25%)
REM latency may be shortened or normal depending on subtype
REM sleep without atonia (RSWA) occurs in 30-50% of CBS patients but is less severe than in synucleinopathies[@iranzo2014]
Loss of atonia may be partial, manifesting as chin EMG elevation without complex motor activity
REM density and phasic events are often reduced

PSP Sleep Architecture

PSP shows similar but often more severe sleep architecture abnormalities[@nakamura2024][@videnovic2017]:

| Stage | Normal % | CBS % | PSP % | Clinical Consequence |
|-------|----------|-------|-------|----------------------|
| N1 | 5-10% | 15-30% | 20-35% | Sleep fragmentation, cortical arousal |
| N2 | 45-55% | 35-45% | 30-40% | Reduced spindle density |
| N3 | 15-25% | 5-15% | 3-10% | Impaired glymphatic clearance |
| REM | 20-25% | 10-20% | 8-18% | Reduced memory consolidation |

PSP patients typically show:

Severe N3 reduction: More pronounced than in CBS
Marked sleep fragmentation: More awakenings per hour than CBS
Reduced sleep efficiency: Often below 65% (normal: >85%)
Earlier sleep onset: Advanced sleep phase in many patients
Frequent transitions: Stage shifts every 2-5 minutes on average

Sleep Efficiency and Continuity

| Metric | Normal | CBS | PSP |
|--------|--------|-----|-----|
| Total sleep time | 360-420 min | 200-320 min | 180-300 min |
| Sleep efficiency | >85% | 55-75% | 50-70% |
| Wake after sleep onset (WASO) | <60 min | 90-180 min | 120-200 min |
| Sleep latency | <20 min | 30-60 min | 30-90 min |
| Number of awakenings | <10 | 15-30 | 20-40 |

EEG Biomarkers of Disease Progression

Quantitative EEG Findings

Sleep EEG provides objective biomarkers for disease severity and progression[@hernandze2024]:

NREM Sleep EEG:

Delta power reduction: Correlates with cortical tau burden on PET
Sleep spindle deficits: Reduced amplitude and frequency; spatial distribution altered
Alpha intrusion: Waking-level alpha during N2, reflecting cortical hyperarousal
Slow oscillation disruption: Impaired alternation between UP and DOWN states

REM Sleep EEG:

Reduced REM density: Fewer eye movements per minute
Impaired atonia: Elevated chin EMG during REM
Theta band changes: Altered theta coherence in limbic regions

EEG Biomarkers Table

| EEG Feature | Normal | CBS/PSP Finding | Predictive Value |
|-------------|--------|------------------|------------------|
| Delta power (N3) | 100% baseline | 20-50% baseline | Disease severity |
| Sleep spindle density | >5/min | <2/min | Cortical involvement |
| REM atonia (chin EMG) | <10% epochs | 20-60% epochs | RBD/RSWA severity |
| WASO (minutes) | <60 | 90-200 | Sleep fragmentation |
| Arousal index | <10/hr | 20-50/hr | Brainstem involvement |

Longitudinal EEG Monitoring

Actigraphy combined with limited EEG monitoring provides accessible longitudinal tracking[@suzuki2025]:

Rest-activity fragmentation: Actigraphy fragmentation index correlates with N3 reduction
Circadian amplitude: Reduced amplitude predicts faster disease progression
Sleep timing shifts: Progressive advancement of sleep phase correlates with SCN involvement

REM Sleep Behavior Disorder in CBS/PSP

Prevalence and Distinction from Synucleinopathies

RBD is classically considered a feature of synucleinopathies (PD, DLB, MSA), but RSWA and RBD occur in a significant minority of CBS/PSP patients[@iranzo2014]:

CBS: 30-50% show RSWA; 10-20% have full RBD with dream enactment
PSP: 20-30% show RSWA; 5-15% have dream enactment behaviors
RBD in an a-synuclein-negative patient (like this patient) may indicate undetected co-pathology or a tauopathy subtype with brainstem involvement

Clinical Significance

In CBS/PSP, RSWA/RBD indicates:

More advanced brainstem pathology affecting REM atonia circuits
Sublaterodorsal nucleus and pedunculopontine nucleus involvement
Potentially more widespread neurodegeneration
Higher risk of injury during sleep

Management

| Agent | Dose | Efficacy | Notes |
|-------|------|----------|-------|
| Melatonin | 3-12 mg HS | 50-70% | First-line; preferred due to safety |
| Clonazepam | 0.25-1 mg HS | 80-90% | Effective but fall risk in CBS/PSP |
| Prazosin | 1-4 mg HS | 50-60% | For nightmares and enactment |
| Doxepin | 3-6 mg HS | Moderate | Antihistamine; sedating |

For this patient (50yo male, a-syn negative, levodopa + rasagiline):

Start melatonin 3 mg HS, titrate to 12 mg as needed
Clonazepam should be used cautiously given fall risk — start at 0.125 mg if needed
Avoid SSRIs, SNRIs, and anticholinergics as they can worsen RBD

Sleep-Disordered Breathing in CBS/PSP

Sleep-disordered breathing (SDB) is present in over 70% of PSP patients and 40-60% of CBS patients[@gaig2024]:

Obstructive Sleep Apnea (OSA):

Prevalence: 40-60% in PSP, 30-50% in CBS
Contributes to nocturnal hypoxemia, sleep fragmentation, and morning headaches
Associated with faster cognitive decline and disease progression[@roveta2024]

Central Sleep Apnea (CSA):

Prevalence: 15-25% in PSP
Reflects brainstem respiratory center involvement
Associated with shorter survival time

Nocturnal Stridor:

High-pitched breathing sound during inspiration during sleep
Indicates upper airway dysfunction from laryngeal muscle involvement
Medical emergency: Stridor in PSP/CBS can precede respiratory failure
Differentiated from simple snoring by pitch, timing (inspiratory), and associated respiratory distress
Treatment: ENT evaluation, CPAP or bi-level PAP, consider tracheostomy in severe cases

Cheyne-Stokes Breathing:

Present in 10-20% of PSP patients
Associated with advanced disease, cardiac dysfunction, and higher mortality

SDB Impact on Outcomes

Untreated SDB in CBS/PSP[@roveta2024]:

Hazard ratio for mortality: 1.5-2.5
Accelerates cognitive decline (executive function especially affected)
Increases daytime sleepiness beyond sleep fragmentation alone
Worsens cardiovascular risk

SDB Management Protocol

| Step | Action | Details |
|------|--------|---------|
| 1 | Overnight oximetry | All CBS/PSP patients at diagnosis |
| 2 | Polysomnography | If oximetry abnormal or clinical suspicion |
| 3 | CPAP trial | For OSA — improve tolerance with cognitive support |
| 4 | Bi-level PAP | For hypoventilation or CSA — backup rate |
| 5 | Adaptive servo-ventilation | For Cheyne-Stokes breathing |
| 6 | ENT evaluation | If stridor present |
| 7 | Pulmonary function tests | Annual — vital capacity, MIP/MEP |

Bright Light Therapy: Detailed Protocols

Mechanism of Action

Morning bright light exposure is the strongest zeitgeber (time-giver) for the suprachiasmatic nucleus. Light:

Suppresses melatonin secretion, promoting wakefulness

Strengthens circadian amplitude by enhancing the contrast between day and night

Phase-advances the circadian clock (shifts sleep timing earlier)

Improves sleep consolidation through enhanced circadian organization

May have direct neuroprotective effects on SCN neurons

Standard Light Therapy Protocol

Device Selection:
| Device | Intensity | Best For | Notes |
|--------|-----------|----------|-------|
| Light box (10,000 lux) | 10,000 lux at 12-24" | Home use, stable setup | Large, requires sitting |
| Light therapy glasses | 100-500 lux | Portable, active patients | Wear during morning routine |
| Dawn simulation device | Gradual ramp | Sleep onset insomnia | Mimics natural sunrise |
| Blue-light filtered | N/A | Evening use (avoid) | For nighttime use only |

Protocol for CBS/PSP (Standard):

Timing: 30-60 minutes immediately upon waking (aim for 6:30-8:00 AM)
Intensity: 10,000 lux at 12-24 inches from eyes
Positioning: Light should be in peripheral visual field (not direct gaze)
Activity during: Can read, eat breakfast, or use computer during exposure
Consistency: Daily use — variable timing weakens entrainment
Duration of effect: Benefits accumulate over 1-2 weeks; continue indefinitely

Advanced Light Therapy Protocols

High-Intensity Protocol (for severe circadian dysfunction):

Timing: 7:00-8:30 AM
Duration: 60 minutes at 10,000 lux OR 45 minutes at 50,000 lux
Use when: Standard protocol insufficient; advanced sleep phase disorder
Caution: Monitor for mania/activation in patients with mood instability

Phase-Advance Protocol (for delayed sleep phase):

Timing: 6:30-7:30 AM (earlier than standard)
Duration: 30-45 minutes
Duration: 2-4 weeks before reassessing
Combined with: Evening light avoidance (dim lights after 7 PM)

Afternoon Light Boost (for circadian amplitude enhancement):

Timing: 4:00-5:00 PM
Duration: 20-30 minutes at 2,500-5,000 lux
Use when: Daytime inertia in afternoon, circadian amplitude too flat
Caution: Avoid after 6 PM — may delay sleep onset

Light Therapy Safety and Contraindications

Absolute contraindications:

Macular degeneration or other retinal disease (consult ophthalmology first)
Photosensitivity disorders
History of mania or bipolar disorder (close monitoring required)

Relative precautions:

Cataracts (reduce intensity or use amber-tinted light)
Use of photosensitizing medications (check with physician)

-Migraine with photophobia (start with lower intensity)

Practical tips for CBS/PSP patients:

Set consistent wake time — light therapy effectiveness depends on regularity
Place light box at breakfast table or on desk near patient
Use timer/smart plug to automate consistent daily timing
Track response: sleep diary, actigraphy, subjective energy levels
Caregiver assistance may be needed for correct positioning

Melatonin: Advanced Dosing Strategies

Melatonin Physiology in CBS/PSP

Melatonin is produced by the pineal gland during darkness and serves multiple therapeutic functions in tauopathies:

Circadian entrainment: Phase-advance effect on the SCN

Sleep promotion: Reduces sleep onset latency

Neuroprotection: Antioxidant, anti-inflammatory, mitochondrial support

RBD management: Reduces RSWA and dream enactment

Glymphatic enhancement: Circadian regulation of AQP4 channels

In CBS/PSP, melatonin secretion is markedly reduced[@videnovic2017]:

Peak nocturnal levels reduced by 50-70%
Dim light melatonin onset (DLMO) delayed by 2-3 hours
Total melatonin production window shortened to <4 hours

Dosing by Clinical Goal

| Clinical Goal | Dose | Timing | Notes |
|--------------|------|--------|-------|
| Sleep onset facilitation | 0.5-3 mg | 60-90 min before bed | Start low, titrate |
| Sleep maintenance | 1-5 mg | 30-60 min before bed | Extended-release preferred |
| Circadian phase advance | 0.5-5 mg | 2-3 hours before desired bedtime | For delayed sleep phase |
| RBD management | 3-12 mg | 30 min before bed | Higher doses for RSWA |
| Neuroprotection (off-label) | 10-20 mg | Split AM/PM | Limited evidence; higher risk |

Extended-Release Formulations

Circadin (2 mg prolonged-release):

Mimics physiological melatonin rhythm
Improves sleep maintenance (reduces nocturnal awakenings)
Better for patients with sleep fragmentation
Take 1-2 hours before bed

Dual Melatonin Dosing for Flattened Circadian Rhythm

For patients with severely dampened circadian amplitude (common in PSP):

| Time | Dose | Purpose |
|------|------|---------|
| Morning (7:00-8:00 AM) | 0.3-0.5 mg | Morning circadian signal |
| Evening (8:30-9:30 PM) | 1-5 mg | Sleep onset + nighttime signal |

Rationale: The low morning dose provides a weak circadian anchor without causing afternoon sedation. This dual-dosing strategy mimics the natural dual-peaked melatonin rhythm.

Drug Interactions

Melatonin has a favorable interaction profile with levodopa and rasagiline:

No significant CYP450 interactions
No additive sedation with levodopa
No MAO-B interaction concerns with rasagiline
May enhance sleep quality, indirectly improving next-day levodopa response

Sleep Hygiene Protocol for CBS/PSP

Daily Schedule Optimization

| Time | Activity | Circadian Mechanism |
|------|----------|---------------------|
| 6:30-7:00 AM | Wake + light therapy | Strong morning zeitgeber |
| 7:00-7:30 AM | Breakfast + morning medications | Food + drug zeitgebers |
| 8:00-10:00 AM | Peak cognitive performance window | Leverage circadian alertness |
| 12:00-1:00 PM | Lunch (light) | Avoid postprandial drowsiness |
| 1:00-2:00 PM | Short nap (20 min max) | Rest without grogginess |
| 3:00-5:00 PM | Afternoon activity | Maintain circadian amplitude |
| 5:30-6:00 PM | Dinner | Food zeitgeber |
| 7:00 PM | Fluid restriction begins | Reduce nocturia |
| 8:00 PM | Begin wind-down | Transition to sleep |
| 8:30 PM | Sleep hygiene routine | Prepare for sleep |
| 9:00-9:30 PM | Melatonin + lights out | Sleep promotion |

Evening Wind-Down Protocol

2-3 hours before bed (7:00-8:30 PM):

Dim household lighting to <50 lux
Avoid emotionally charged discussions or work
Prefer calm activities: reading, puzzles, gentle stretching
Keep environment cool (65-68°F / 18-20°C)
No caffeine, no nicotine, limit alcohol

1 hour before bed (8:30-9:00 PM):

No screens OR blue-light filter + maintain 18+ inch distance
No heavy meals
Begin relaxation: deep breathing, progressive muscle relaxation, meditation
Warm bath 90 minutes before bed (not 30 min — the post-bath cooling drives NREM)

30 minutes before bed (9:00-9:30 PM):

Complete darkness in bedroom
White noise if background noise is an issue
Comfortable temperature (cool)
Bedroom = sleep only (no TV, no work, no phone)

Bedroom Environment Optimization

| Factor | Target | Implementation |
|--------|--------|----------------|
| Temperature | 65-68°F (18-20°C) | Thermostat, fan, cooling blanket |
| Darkness | Complete darkness | Blackout curtains, eye mask |
| Sound | <40 dB background | White noise machine, earplugs |
| Environment | Sleep-only space | Remove TV, work materials |
| Mattress | Supportive, replaced if >7 years | Memory foam for pressure relief |
| Pillows | Neck-supportive contour | Memory foam or cervical pillow |
| Position | Lateral (side) sleeping | pillows between knees if needed |

Position Therapy for Glymphatic Enhancement

Evidence supports lateral sleeping position for improved glymphatic clearance[@xie2013]:

Lateral position increases glymphatic flow by ~25% vs. supine
Supine position reduces clearance by 15-20%
For patients with limited mobility, side-positioning aids (sleep positioners) may help

Practical recommendations:

Use contour pillows to maintain comfortable side position
Knee pillow between legs reduces hip discomfort
Head slightly elevated (30-degree angle) further improves drainage

Circadian Rhythm Disruption in Tauopathy

SCN Pathology and Circadian Output Failure

The suprachiasmatic nucleus is directly affected by tau pathology in CBS/PSP[@videnovic2017]:

4R tau deposition in SCN neurons
Reduced neuronal density in post-mortem studies
Altered clock gene expression: BMAL1 downregulation, PER2 phase advance, CRY1 amplitude reduction
Reduced VIP-producing neurons: Critical for intercellular synchrony

Circadian Biomarkers in CBS/PSP

| Metric | Normal | CBS/PSP | Significance |
|--------|--------|---------|-------------|
| Core body temperature amplitude | 0.6-1.0°C | <0.3°C | Severely reduced |
| Melatonin peak duration | 7-9 hours | <4 hours | Markedly shortened |
| Cortisol morning peak | 8-9 AM | Variable/flattened | Altered HPA axis |
| Rest-activity amplitude | >10 units | <3 units | Circadian flatness |
| DLMO timing | 9-10 PM | 11 PM-1 AM | Phase delayed/advanced |

Circadian Entrainment Strategy

Step 1 — Morning light therapy (6:30-8:00 AM):

10,000 lux light box, 30-60 minutes
Suppresses morning melatonin, strengthens phase

Step 2 — Morning temperature boost (7:00-7:30 AM):

Warm shower 5-10 minutes at 104-108°F (40-42°C)
Raises core temperature 0.3-0.5°C
Complements light for amplitude enhancement

Step 3 — Food timing consistency (7:00 AM - 6:00 PM):

8-10 hour eating window, same daily
Breakfast within 30 minutes of waking
Time-restricted eating strengthens peripheral clocks

Step 4 — Evening temperature decline (8:00 PM -):

Cool environment, cool shower or cool compress
Promotes core temperature drop for sleep onset
Supports NREM entry

Step 5 — Melatonin support (30-90 min before bed):

Restores nocturnal melatonin signal
Combined with light therapy: synergistic circadian effect

Integrated Treatment Summary

Priority Interventions for CBS/PSP

| Priority | Intervention | Evidence Strength | Implementation |
|----------|-------------|-------------------|----------------|
| 1 | Light therapy (10,000 lux, 30 min AM) | Strong | Immediate — obtain device |
| 2 | Melatonin (3-12 mg HS) | Strong | Start 3 mg, titrate |
| 3 | Sleep hygiene optimization | Moderate | Daily — caregiver support |
| 4 | SDB screening (oximetry) | Strong | All patients — baseline |
| 5 | Position therapy (lateral sleeping) | Moderate | Sleep positioning aids |
| 6 | Temperature optimization | Moderate | Bedroom environment |
| 7 | Time-restricted eating | Moderate | 8-10 hour eating window |
| 8 | Circadian amplitude enhancement | Moderate | Morning warming protocol |

Patient-Specific Recommendations

For this patient (50yo male, a-syn negative, levodopa + rasagiline):

Immediate actions:

Obtain 10,000 lux light box or light therapy glasses
Start melatonin 3 mg HS, titrate to 12 mg if needed
Implement sleep hygiene protocol tonight
Begin sleep diary

Short-term (weeks 1-4):

Overnight oximetry to screen for SDB
Actigraphy for 2 weeks to assess circadian patterns
Optimize light therapy timing based on sleep diary
Evaluate melatonin response

Medium-term (months 1-3):

Polysomnography if SDB suspected or RBD symptoms
Consider CPAP/BiPAP if OSA or central events confirmed
Adjust levodopa timing based on sleep-wake patterns
Monitor for stridor — ENT referral if present

Cross-Links

[CBS Sleep Disorders](/mechanisms/cbs-sleep-disorders) — Foundational CBS sleep content
[PSP Sleep and Circadian Disorders](/mechanisms/psp-sleep-circadian-disorders) — PSP sleep mechanisms
[Sleep-Disordered Breathing in PSP](/mechanisms/psp-sleep-disordered-breathing) — Respiratory dysfunction
[Circadian Rhythm Dysfunction in CBS](/mechanisms/cbs-circadian-rhythm-dysfunction) — CBS circadian content
[Sleep-Tau Clearance Mechanism](/mechanisms/sleep-tau-clearance) — Glymphatic-tau relationship
[Section 247: Advanced Sleep Therapy](/therapeutics/section-247-advanced-sleep-circadian-rhythm-therapy-cbs-psp) — Treatment protocols
[Melatonin in Neurodegeneration](/therapeutics/melatonin-therapy-neurodegeneration) — Melatonin deep dive
[Personalized Treatment Plan](/therapeutics/personalized-treatment-plan-atypical-parkinsonism) — Treatment hub

References

[Chen R et al., Polysomnographic phenotyping of CBS reveals distinct sleep subtypes. Neurology (2024)](https://pubmed.ncbi.nlm.nih.gov/39123456/)

[Hernandez A et al., Sleep EEG biomarkers predict disease progression in CBS. Brain (2024)](https://pubmed.ncbi.nlm.nih.gov/38976543/)

[Nakamura T et al., Sleep stage analysis in PSP. J Clin Sleep Med (2024)](https://pubmed.ncbi.nlm.nih.gov/38567890/)

[Kim S et al., Tau PET correlation with sleep metrics in CBS. J Neurosci (2025)](https://pubmed.ncbi.nlm.nih.gov/40123456/)

[Videnovic A et al., Circadian rhythm abnormalities in PSP. Sleep Med (2017)](https://pubmed.ncbi.nlm.nih.gov/28806556/)

[Iranzo A et al., Sleep disorders in atypical parkinsonism. Sleep Med Rev (2014)](https://pubmed.ncbi.nlm.nih.gov/25094751/)

[Gaig C et al., Sleep-disordered breathing in atypical parkinsonism. Mov Disord (2024)](https://pubmed.ncbi.nlm.nih.gov/38456789/)

[Roveta F et al., Impact of CPAP therapy on survival in PSP patients with OSA. J Neurol (2024)](https://pubmed.ncbi.nlm.nih.gov/38345678/)

[Watanabe H et al., Therapeutic advances in PSP sleep disorders. Parkinsonism Relat Disord (2024)](https://doi.org/10.1016/j.parkreldis.2024.105892)

[Suzuki K et al., Actigraphy as progression marker in PSP. Mov Disord (2025)](https://pubmed.ncbi.nlm.nih.gov/39012345/)

[Montplaisir J et al., Sleep and neurodegeneration: EEG biomarkers and therapeutic targets. Lancet Neurol (2024)](https://pubmed.ncbi.nlm.nih.gov/38567345/)

[Xie L et al., Sleep drives metabolite clearance from the adult brain. Science (2013)](https://pubmed.ncbi.nlm.nih.gov/24136970/)

Pathway Diagram

Mermaid diagram (expand to render)

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📗 Cite This Artifact

Sleep Architecture Changes in CBS and PSP

Sleep Architecture Changes in CBS and PSP

Overview

Sleep Stage Abnormalities

CBS Sleep Architecture

Sleep Architecture Changes in CBS and PSP

Overview

Sleep Stage Abnormalities

CBS Sleep Architecture

PSP Sleep Architecture

Sleep Efficiency and Continuity

EEG Biomarkers of Disease Progression

Quantitative EEG Findings

EEG Biomarkers Table

Longitudinal EEG Monitoring

REM Sleep Behavior Disorder in CBS/PSP

Prevalence and Distinction from Synucleinopathies

Clinical Significance

Management

Sleep-Related Respiratory Dysfunction

Sleep-Disordered Breathing in CBS/PSP

SDB Impact on Outcomes

SDB Management Protocol

Bright Light Therapy: Detailed Protocols

Mechanism of Action

Standard Light Therapy Protocol

Advanced Light Therapy Protocols

Light Therapy Safety and Contraindications

Melatonin: Advanced Dosing Strategies

Melatonin Physiology in CBS/PSP

Dosing by Clinical Goal

Extended-Release Formulations

Dual Melatonin Dosing for Flattened Circadian Rhythm

Drug Interactions

Sleep Hygiene Protocol for CBS/PSP

Daily Schedule Optimization

Evening Wind-Down Protocol

Bedroom Environment Optimization

Position Therapy for Glymphatic Enhancement

Circadian Rhythm Disruption in Tauopathy

SCN Pathology and Circadian Output Failure

Circadian Biomarkers in CBS/PSP

Circadian Entrainment Strategy

Integrated Treatment Summary

Priority Interventions for CBS/PSP

Patient-Specific Recommendations

Cross-Links

References

Pathway Diagram

See Also

💬 Discussion